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T2D is quite a complex scenario with up- and down-regulation of cytokine expressions. In case of poor controlled T2D (contribution of hyperglycemia/high blood glucose and glycated serum proteins/AGEs, which anti-inflammatory biomarkers exhibit a downregulated expression?
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Thank you Malcolm! Downregulation of IL-4 and IL-10 has been reported in clinical studies.
However, Arginase 1 expression was found to be downregulated in the in vitro studies but upregulated in the clinical studies, which have the involvement of insulin resistance. How's your thought? Any advices would be appreciated!
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The company Hela Glucose (Movano) is developing a ring-shaped product that promises to measure blood glucose using spectroscopy. The question is whether this would be the most accurate and non-invasive way to measure blood glucose, and if not, what would be the most accurate and non-invasive method?
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I think this might be possible in the future with the great development of using artificial intelligence for biosensors
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After lapse of a few months, we recently attempted insulin-tolerance tests in C57BL/6N female mice at 6 months of age. We began, years ago, with Humulin-r at 0.75 U/kg. In our recent tests we used the same protocol, but the only response was a slight increase in blood glucose! We tried several higher doses. At 1.75 U/kg a very slight decrease was observed, but not until 60 minutes. We purchased a non-clinical preparation of insulin from a company that sells a lot of growth factors and cytokines. It produced the puzzling increase in blood glucose at both 0.75 and 1.25 U/kg. Has anyone else had a problem with insulin efficacy of late? I can't believe all our mice are suddenly insulin resistant!
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Bevacizumab and ranibizumab are human-derived anti-VEGF antibodies which doesnot have any effect on rodent retinal or choroidal neovascularization. Humulin-r is a human-derived insulin. With a possibly similar reason, it doesnot work on rodents.
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I am currently working towards developing a model for type 2 diabetes, using fructose and streptozotocin (STZ). Prior to injecting my C57BL/6 mice with STZ, we tested blood glucose with a tail-prick, using an AccuChek Instant glucometer. As per methods used in relevant literature, I fasted my mice for 4 hours prior to checking blood glucose (BG). The mean BG in my normal control, which did not receive fructose water was around 8 mmol/L, a BG akin to mild hyperglycaemia. Bear in mind, this group is not due for induction, and received a normal diet of commercially available mice pellets. For the second BG test, I fasted my animals for 6 hours, and got the same if not similar results.
Please assist.
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Stress and excess sugar with tea.insullin more, starvation , alcohol, movement of body is less than more calories, physical activities less, sleeping not properly so many causes.
Unanimous food habits,.if sugar levels mor
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My study requires the induction of STZ in 30 Sprague-Dawley rats (either sex) to develop type 2 diabetes. My protocol was:
1) Fast the rats overnight.
2) Prepared STZ solution in ice-cold citrate buffer (0.1 M, pH 4.5) and injected i.p. within 5 minutes of dissolving it. Dose used was 50 mg/kg.
3) Fed them with 10% fructose water for 24 hours post injection and gave food ad libitum.
4) Checked for blood glucose levels (BGL) 4 days after injection. Rats were fasted for 24 hours before checking the blood glucose levels.
When compared to the normal BGL, some of my rats had their BGLs around the normal fasting BGL range (4.0 - 6.5 mmol/L) while some were above 11 mmol/L.
Could there be any explanation to this? I had my supervisor's help to inject the rats as he has mastered the i.p injection technique and thus, error in the technique could be ruled out.
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One paper suggested that the damage caused by STZ is reversible so you may need to give an additional dose or try high dose of STZ. You also can detect BGL after 2 weeks of diabetes induction
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We measure the mouse blood glucose level by the normal human blood-biochemistry Roche mechanism. But we get the absolutely wrong value of the blood glucose level.
Normal 10 weeks C57BL/6 mouse (DO NOT have any treatment). Mean of the glucose level is around 40 mM. There must be something wrong.
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Qirui Liu May be this help you
To measure blood glucose levels in mice accurately, it's essential to follow a precise and appropriate methodology. If you're encountering abnormally high readings, like 40 mM, it suggests there might be an issue with the procedure or the equipment used. Here are steps to ensure accurate measurements:
  1. Choose the Right Equipment: Ensure that the glucose meter and strips are suitable for use in mice. Some human blood glucose meters may not be accurate for mouse blood due to differences in blood composition.
  2. Calibrate the Equipment: Regularly calibrate the glucose meter according to the manufacturer's instructions to ensure accuracy.
  3. Sample Collection: Blood samples can be collected from the tail vein, saphenous vein, or by making a small nick at the tip of the tail. The volume of blood needed is usually very small, often less than a drop.
  4. Handling the Mice: Handle mice gently to avoid stress, which can affect blood glucose levels. It's also important to consider the time of day and the feeding status of the mice, as these factors can influence glucose levels.
  5. Performing the Test: Apply the blood sample to the test strip and use the glucose meter to read the glucose level. Ensure that the blood sample is of adequate size and is applied correctly.
  6. Repeat Measurements: Due to the small blood volume and potential variability in readings, it's advisable to take multiple measurements and calculate the average.
  7. Consider Biological Variability: Remember that there is natural variability in glucose levels among different mice. Factors like age, strain, sex, diet, and environmental conditions can influence glucose levels.
  8. Troubleshooting: If you continue to get abnormal readings, consider testing the meter with a control solution, or use a different meter to cross-check the results.
The normal fasting blood glucose level in C57BL/6 mice is typically between 4.2 and 8.3 mM. Values significantly outside this range warrant a review of your methodology or consultation with the equipment manufacturer. If the issue persists, consulting with a veterinarian or a laboratory animal specialist could provide further insights.
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World Health Organization — Diabetes, a chronic condition, is diagnosed and monitored with blood glucose testing. Learn more about the different types of diabetes on WHO's Official Website. Advice for the public.
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"During the ongoing coronavirus disease 2019 (COVID-19) pandemic, it is critical to ensure the safety of COVID-19 vaccines. We herein report a 51-year-old Japanese woman who developed acute-onset type 1 diabetes with diabetic ketoacidosis six weeks after receiving the first dose of a COVID-19 messenger ribonucleic acid (mRNA) vaccine. Laboratory tests indicated exhaustion of endogenous insulin secretion, a positive result for insulin autoantibody, and latent thyroid autoimmunity. Human leukocyte antigen typing was homozygous for DRB1*09:01-DQB1*03:03 haplotypes. This case suggests that COVID-19 vaccination can induce type 1 diabetes in some individuals with a genetic predisposition."
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My study focuses on developing a mouse model for the type II diabetes, narrowing in on a condition resembling chronic, late-stage diabetes. As such, blood glucose levels would need to be measured consistently over the course of the 16-week experimental period. I will be using C57BL/6 mice. With the welfare of the animals at the fore, I would like to know if it is safe to perform fasting blood glucose tests on a weekly basis. Will it overstress the animals, and perhaps serve as a confound the overall development of the condition?
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congratulation
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Can one have a hyperglycemic coma? (I thought it was only for hypo)
I was back in the hospital after a syncopal episode again. Blood glucose 420-550
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Coma and syncope are two entirely different things
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We are currently using Ketamine and Xylazine to anesthetize the mice for imaging purposes. However, upon injection, we see an increase in the blood glucose levels, which in turn, prevents us from inducing glucose stimulation at our desired time point. Is there any anesthetic material that doesn't interfere with pancreatic beta cells or elevate blood glucose levels?
Any insights will be very helpful.
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TIVA
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Hi guys,
I'm working on a mouse model (using C57BL/6J) that needs high-fat diet (HFD). Recently I plan to perform ipGTT, just testing blood glucose. My colleague thought 1g of glucose/kg body mass was fine.
But some research suggested a higher amount of glucose for those mice fed with HFD.
One study recommended 1.5-2g/kg. (doi:10.2147/DMSO.S234665)
Another study suggested 2g/kg, but orally. (doi:10.1152/ajpendo.90617.2008) Can anyone explain the reason why we should choose a higher dose of glucose? Or maybe 1g/kg is also appropriate?
Many thanks. .
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I read some papers and there are different methods. Some choose 1.5g/kg and others choose 2g/kg.
But my colleague adopted 2g/kg before and she found the blood glucose was so high that she couldn't measure the glucose levels from the meter. Maybe I choose 1.5g/kg to check it. Thank u so much. Mohammed Kaleem
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Hello.
We are currently observing the in vivo environment of mice at different glucose levels and
For this reason, we are currently measuring blood glucose levels in mice that have been administered anesthesia beforehand and treated with an open abdomen.
When we perform the laparotomy, we inject 30% glucose through a needle into the stomach of the mice.
However, the blood glucose level did not rise at all even after waiting 30 minutes after administration, and the mice died during the procedure after being warmed up to the 38°C range with a heater.
We are looking for a way to raise the blood glucose level in order to finally observe the glucose uptake in the pancreas, but do you have any good ideas on how to administer it?
Incidentally, we are currently considering direct glucose administration via tail vein, but no one has tried it and we are still in the consideration stage.
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Applying 30% Glucose into the abdominal cavity should result in serious osmotic stress, but not in glucose uptake.
For simplicity, you could try to infuse a glucose solution by the tail vein, using a syringe pump (hospital style or homemade, e.g. taking advantage of sth like a Cavro XP-3000 with a small volume syringe, which you might find on the used market. They are quite easy to control from a laptop through a USB-to-serial converter and sending commands from a terminal program).
An alternative injection point might be the jugular vein, but this approach requires some surgery. For an example with rats, please refer to this paper:
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I will collect blood samples from streptozotocin induced diabetic model mice and I want to measure their blood glucose level from plasma. Which tube is best without any interference specially I will then use the GOD-POD enzyme spectrometric method to measure the blood glucose level.
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One of analytes that is most commonly tested in labs is glucose. The sodium fluoride/potassium oxalate (NaF/KOx) tube is far from the expected standard, according to the most current studies on glucose stabilities. According to Dimenski (2015), Citrate tubes is the preferred tube type by many institutions in terms of blood glucose determination from plasma. However, since you are comparing the which is better among Heparin tubes versus the Heparin tube, the EDTA tube is better to use. This is because EDTA induces a little amount of hemolysis and RBC enlargement. When an analyte is tested colorimetrically, sample color from hemolysis may lead to an increase in false OD. If you can't check your blood sugar right away, use NaF tubes to stop the RBC from doing glycolysis.
Source:
Stability of glucose in plasma with different anticoagulants - PubMed (nih.gov)
Bonetti, G., Cancelli, V., Coccoli, G., Piccinelli, G., Brugnoni, D., Caimi, L., & Carta, M. (2015, December 4). Which sample tube should be used for routine glucose determination? Primary Care Diabetes. Retrieved September 13, 2022, from https://www.sciencedirect.com/science/article/abs/pii/S1751991815001564
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I used 0.5 mg/kg glyburide in 1%DMSO for diabetic rats but it doesnt reduce blood glucose and i dont know why ?
rats was injected by 50mg/kg stz for diabetes induction
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Thank you
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To calculate the sample size, I need to assume the smallest "r" with clinical relevance (error = 5% and power = 80%). My question is, which is that value? I searched for other papers to interpret correlation strength properly, but I had no results. Could you please suggest any?
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I am afraid that there won't be any proper interpretation of correlation strength. And there won't by any discussions of what the clinical relevance of a correlation would be.
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I have collected data from 9 participants during the phases. The first phase the participants were asked to record their sleep throughout the night and fast from the evening before the lab. Blood glucose was then tested for 3 hours following a sugary drink. The second phase the participants were asked to restrict there sleep to 4-5 hours the night before and fast as well. The no participants would then have their blood glucose tested for 2 hours after consumption of sugary drink. The third phase the participants sleep was restricted and while in the lab they were asked to consume caffeinated coffee. Their blood Glucose was tested after the consumption of the sugary drink.
This study will therefore answer two important questions: (1) Does caffeinated coffee intake further impair blood sugar control after acute sleep restriction? And (2) Does caffeinated coffee supress appetite when consumed following sleep restriction? The participants were asked to fill out a 5 question Sprite questionnaire before each blood glucose test.
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It is not easy to answer your question without knowing the data set. The number of the participants seems to be also too low to for me. You should certainly have a statistician at your University, so I advise you to contact him to address your problem. This will be the best way.
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There are plethora of data on the concordance or dis-concordance between Fasting Blood Glucose and Hb1Ac in the clinical diagnosis of Type 2 Diabetes (T2D). Which of the two assay or test is the most specific and sensitive in the diagnosis of T2D
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Implications of measuring HbA1c versus fasting glucose level
HbA1c indicates retrospectively the glycemic control and is a good predictor of long-term diabetic complications. However, fasting blood sugar is a better predictor of the current diabetic status of glycemic control.
Whereas to diagnose prediabetes, HbA1c may be enough, to diagnose someone with diabetes a combination of fasting blood glucose of 126 mg or more plus an HbA1c of 6.5% or more at two different times will be needed.
However, fasting blood glucose does not predict diabetic complications compared with a post-prandial glucose level.
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Does HOMA measure insulin sensitivity or resistance?
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Dear Dr. Terun Desai I agree with Alonso Romo-Romo HOMA can measures beta-cell function, insulin resistance and insulin sensitivity.
Please see the following links:
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My SD rats have fasting blood sugar (16-25 mmol/l) after 6 weeks of  STZ-induced diabetes (60 mg/kg) . Can anyone give me the range for FBG in STZ-induced rats?
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Hi Siti Safiah.
Find your answer here
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I am doing a machine learning project which determines the blood glucose level using laser light. I am training my data by actually measuring blood glucose levels using a glucose meter and taking the value of laser light passed through the fingertips, also taking into account the factors such as age and gender. So, during testing, my model will take 3 inputs, light intensity of laser light that has been passed through the finger, age, and gender, and will give the value of blood glucose level as output. Given that the input and output variables do not have a linear relationship, which machine learning algorithm will suit best for this problem.
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If I had to explain k-nearest neighbor classification, I'd use your case an an example. A knn classifier does not need too much memory, and the algorithm can be implemented on a tiny microcontroller.
Regards,
Joachim
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I heard a lot of rumours that cinnamon helps a lot about reducing the level of sugar in the blood. Any confirmation about this idea?
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Please also see the following RG link.
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Blood glucose testing is an integral test to measure glucose homeostasis in the body. It is commonly used both for screening and diagnosis of diabetes. In addition, serial blood glucose testing, also called "self monitoring of blood glucose (SMBG)" is a common tool performed by patients with diabetes for the assessment of their glycaemic status. However, blood glucose testing represents an unpleasant experience for many people. Can salivary glucose be used as an effective alternative to blood glucose testing for screening, diagnosis and follow-up of diabetes?
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Indeed the non-invasiveness of salivary glucose testing and its comparability with blood glucose determination make salivary glucose measurement a potentially useful alternative for the assessment of glucose homeostasis and for screening and diagnosis of diabetes instead of routine blood glucose testing.
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Hi all,
We are trying to establish a mouse model of diabetic nephropathy (DN) using the injection of 40 mg/kg of STZ in five consecutive days. Although the blood glucose levels were increased (300-600 mg/dL), they showed very low albuminuria and no sign of kidney damage in pathology passements after 3-5 months. We used two mouse strains, DBA2/j and C57 males, but we could not establish the model in none of the strains. Would you help us how to solve this problem?
Best Regards,
Maryam Abedi
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I absolutely agree with the previous respondent - pay special attention to the quality of the STZ reagent, the buffer for its dissolution (streptozotocin is extimelly capricious to the pH of preparetive solution) and the observance of use only in a freshly prepared form. Sometimes the success of diabetic complications on mice model looks like a lottery, therefore the stage of STZ administration should be especially scrupulous. Perhaps, for a more pronounced progression of diabetic nephropathy, you should use the strategy of a single high-dose STZ administration (120-150 mg/kg) instead of low-dose 40 mg/kg/5 days - as an autoimmune-mimicking one. Of course, everything depend on the goals of your research. Good luck!!!
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We perform research into diabetes using insulin that may lead to impaired awareness of hypoglycaemia. We run a protocol to induce recurrent hypoglycaemia in rats using insulin over several days (currently to a max 13 concurrent days, or four weeks of three hypos per week). This involves taking blood samples for hormone analysis at least twice on a few hypo sessions (~200 µL is considered a good volume), and performing blood glucose tests up to three or four times per hypo (lance the tail to obtain blood droplet for blood glucose meter test).
Blood samples are taken through a scalpel cut near the tail tip.
Blood glucose is through the same wound, or using a lancet, also near the tail tip.
After a few days the tail becomes very sore and makes it very difficult to get samples, and the stress to the animal may confound the results.
Is anyone else doing rat work that requires this frequency and similar blood sampling?
Do you know an approach that is less impactful for the rat, staff and results?
Many thanks
Julian
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Hi Julian Parsons if this is the main part of your experiment, you should consider putting a catheter in your rats so you have access to blood without the need to use the tail at all. It is a small surgery and small daily upkeep but worth it.
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In 2002, Dr. Kratz published a study of laboratory results from marathon runners with an average age of 49. Almost 60%or 22 out of 37 runners sampled from the Boston Marathon had a blood glucose level outside of the normal reference range (70-110 mg/dL) (Kratz)
A study from Austria of still older endurance athletes in their sixties found 47% were either prediabetic (22 out of 47) or diabetic (1 out of 47). In this small sample, these athletes had a higher proportion of hyperglycemia, compared to a heavier, age-matched group of controls, . (Haslacher)
From my review of the literature, this phenomenon may be due to increased hepatic release of glucose. Dr. Drouin found increased glucagon receptor sensitivity stemming from increased hepatic glucagon density in age-matched trained/untrained subjects.
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Almost purely genetic rather than physiologic degenerative aging process.
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I want to examine the relationship between the prevalence and risk factors of diabetics and socioeconomic factors. But doesn't able to locate Fasting Blood Glucose measurement in DHS dataset. How it is possible to measure?
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You might be able to search the DHS User Forum to see if anyone else has asked a similar question. And if you can't find an answer there, you can post your question. The link is: https://userforum.dhsprogram.com/
When you write the question there, please specify which country you are interested in. Blood glucose level assessments or diabetes-related questions aren't asked in every survey.
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Hello everyone,
In order to study the effect of a certain drug on blood glucose, 10 patients were randomly selected and their blood glucose and insulin levels were measured for 5 days in a row. If you want to know the correlation between insulin level and blood glucose, how to analyze it?
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You may consider Pearson correlation cofficent
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Hi, as stated. Can you still used an expired Fluoride-Oxalate tube for blood glucose and lactate examination?
I notice that there might be a problem in getting blood sample because the tube's vacuum might not work as well. But would the result of blood glucose and lactate examination be reliable if the tube had been expired for around 1 month?
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You must avoid using expired things.
You can use common blood tubes with anticiagulant (heparin and EDTA) for this. But to aboid glucose and lactate changes, you must immediately centrifuge the samples at 4 C and separate plasma and freeze or analyze it.
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Insulin is the only known hormone that can directly promote anabolism and reduce blood glucose levels.
I am curious as to whether there exist other hormones with the same function as insulin? If so, how would you identify and examine the effectiveness of this hormone? Please list any detailed techniques and methods if possible.
Note: I would prefer not to use algorithms as this is only a small project. Please guide me through this, thank you.
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Nurul, I'd try to characterize it the same way as insulin action is demonstrated: Firstly glucose uptake, and the signalling pathways your candidate is affecting and is expected to affect. If the action is similar to insulin, I'd expect it to trigger the same effectors (translocation of glucose transporter GLUT4, inhibition of glycogenolysis, initiation of glycogen synthesis). It would be interesting if it has its own receptor or what it actually is acting on. So one has finally to analyze the whole insulin signalling cascade (IR, IRSx, PI3K, pKB/Akt etc.) and compare with actual insulin signalling.
An elegant way for this would be differential phosphoproteomics, as this very likely would detect new/different signalling pathways.
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I gave C57BL / 6 mice a solvent containing 17% DMSO by 0.1 mL i.p injection for 28 days. I saw that their weight and blood glucose levels decreased. Does anyone know the effect of DMSO on glucose metabolism?
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There is no direct engagement of DMSO in the metabolism of glucose but DMSO with high doses promotes different body responses which are mostly toxic leading to an increase in the consumption of glucose.
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With the increasing prevalence of diabetes world wide, and with the presence of high proportions of undiagnosed diabetes, do we need to perform annual fasting blood glucose testing as a screening step for undiagnosed diabetes.
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It is my pleasure dear Dr. Salman.
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Hello. I have a dataset containing three groups: low cholesterol, medium cholesterol and high cholesterol. Each group has about twenty participants. For each participant I have their mean nocturnal blood gluocse level for 4-6 different days. I would ideally like to compare mean nocturnal blood glucose levels between the three different cholesterol groups. I'm aware that unless I take a mean nocturnal blood glucose across the 4-6 days for each participant and then compare these values then using a one way ANOVA would violate the assumption of independant samples, but doing this would lose a lot of useful data. Is there a way that I can include all of the participant's individuals nights in a comparison between the cholesterol groups? Many thanks
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you could also do a 2-way RM ANOVA, to take the different sample collection times into account. If you do not have repeated measure for each participant, a mixed model would be best.
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At what minimum levels of rabbits and rats' blood glucose will lead to a coma? How much minimum glucose levels required for rabbits and rats alertness
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Blood glucose levels between 2-3 mmol/L may cause coma or an even isoelectric EEG in experimental animals, for details see the link below. (1). The effects are more devastating with acute hypoglycemia, while chronic low glycemic levels cause log-term effects without death,
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I induced diabetes with STZ (40 mg/kg) after 4 weeks of high fat diet in Wistar rats. After 72 hours, i checked the FBG of all the rats and majority of the rats had FBG above 350 mg/dl. After a week i rechecked the FBG of the diabetes model group and i discovered that their blood glucose had dropped to normal, between 105-145, while the groups that are receiving treatment still showed higher FBG. Three days later i rechecked the non-fasting blood glucose of the diabetes model group and the least value was 480 mg/dl. Over the course of 3 weeks i discovered that their FBG is usually less than 150 mg/dl while their non fasting blood glucose is usually above 480 mg/dl. I have re-injected STZ but this phenomena is still the same. Does any one have any suggestion or experience about this situation
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Streptozotocin selectively poisons the insulin-producing beta-cells in the pancreas, resulting in a model of insulin deficiency (type 1or juvenile) diabetes. High fat and sugar diet will in the long term produce insulin resistant (type 2 or adult) diabetes. 4 Weeks on such a diet are unlikely to suffice for that, however. How old are your rats? What is their weight, compared to litter-mates on a normal diet (you did keep this control, didn't you)?
In my experience, STZ is rather unreliable as diabetogenic, only about half the rats treated will initially develop hyperglycaemia, and most of those will recover when kept for a couple of months. Therefore, you need very large treatment groups, especially for investigation of long-term effects.
After induction of type 2 diabetes, one could use STZ to model the secondary insulin deficiency that often accompanies this disease in humans. Rats without such treatment are less prone to this condition, as their amylin has mutations that prevent amyloid formation. I have never done that, so I can't tell if STZ is more reliable in this application than for induction of type 1 diabetes.
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Adherence to frequent blood glucose testing by patients with diabetes via self monitoring of blood glucose assumed critical importance as it enables both patients and their physicians to have a view on blood glucose profile. This is of utmost importance in patients treated by insulin and/ or agents with hypoglycaemic potencies. However, many patients dislike frequent traumatic blood glucose testing and find it too uncomfortable and even painful. This is especially the case in children and adolescents. For this reason patients not infrequently deny testing which may adversely affect the management of diabetes. To overcome the problem of traumatic finger pricking to test blood glucose, several non-truamatic devices for self monitoring of blood glucose, totally avoid piercing the skin, have been discovered and marketed and found their way to practical use. Can painless methods for self monitoring of blood glucose increase the adherence of patients with diabetes to blood glucose testing?
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Absolutely yes. The non invasive methods will definitely increase the compliance of frequent testing in diabetic patients. The patients which require more frequent monitoring of blood sugars esp during hypoglycemia or before or after planning for a surgery or any other such situation will find it very beneficial. The methods should have sensitivity and specificity as otherwise they will be of not much help or use.
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Can you tell me if we use a human glucometer to measure blood glucose in rats, then what is the normal blood sugar level in rats?
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Human glucometers are designed for human blood. That is why there are differences when glucose is determined spectrophotometrically. However, if you are interested only for a general view of glucose levels or to determine where a rat is diabetic or not, it is just okay. In addition, at the end of the experiment when animals are to be euthanized, you are advised to determine glucose levels spectrophotometrically in order to share reliable results. To sum up, yes, human glucometers are used in rats, not for in depth analysis, but from a general viewpoint.
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I have only female mice and blood glucose do not exceed 170 mg/dl
while male showed results more than 250 mg/dl in previous experiment
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Most researcher working with male mice because sex, and hormonal changes.
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If values of a specific feature for all samples in class A are statistically significant than values of the same feature of all samples in class B, would that give me any information or intuition regarding the outcome of classification? For example if you measure the blood glucose of 100 obese mice and in 100 normal mice and do ANOVA and find that the glucose level of obese mice is statistically significant than normal mice, would that give you any info about the output of classification?
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Zeynab Mousavikhamene finding a statistically significant difference in means between groups may or may not help with a classification problem. It likely depends more on the distributional separation.
Take for example two data sets of 100 mice.
In the first data set there are two groups of mice: group "a" with a mean weight of 20 (g) and std. dev. of 2.5 (g), and group "b" with a mean weight of 30 (g) and again a std. dev. of 2.5 (g). See histogram attached.
In the second data set there are also two groups of mice: group "aa" with mean weight of 20 (g) and std. dev. of 5 (g), and group "bb" with a mean weight of 30 (g) and again a std. dev. of 5 (g). See histogram attached.
The t-test comparing the two groups within each data set (i.e., "a" vs. "b" and "aa" vs. "bb") shows a statistically significant difference. But when using weight to distinguish between groups, say with logistic regression, the separation in distributions in the first data set allows us more accuracy.
To demonstrate, I simulated these two hypothetical data sets and ran the tests. Below are the results.
First data set:
data: a and b
t = -22.452, df = 97.951, p-value < 2.2e-16
Predicted
Truth 0 1
0 49 1
1 1 49
Second data set:
data: aa and bb
t = -11.532, df = 97.951, p-value < 2.2e-16
Predicted
Truth 0 1
0 43 7
1 6 44
*** R-code to reproduce these results ***
### Compare group means
set.seed(123)
a <- rnorm(50, 20, 2.5); b <- rnorm(50, 30, 2.5)
hist(a, xlim = c(0, 50),
main = expression(atop(mu ~ '=' ~ 20 ~ ',' ~ sd ~ '=' ~ 2.5 ~ (white),
mu ~ '=' ~ 30 ~ ',' ~ sd ~ '=' ~ 2.5 ~ (grey))))
hist(b, col = 'grey', add = T)
t.test(a, b)
set.seed(123)
aa <- rnorm(50, 20, 5); bb <- rnorm(50, 30, 5)
hist(aa, xlim = c(0, 50),
main = expression(atop(mu ~ '=' ~ 20 ~ ',' ~ sd ~ '=' ~ 5 ~ (white),
mu ~ '=' ~ 30 ~ ',' ~ sd ~ '=' ~ 5 ~ (grey))))
hist(bb, col = 'grey', add = T)
t.test(aa, bb)
### Compare classification
df_2.5 <- data.frame(id = 1:length(a), a, b)
df_2.5 <- reshape2::melt(df_2.5, id.vars = 'id',
variable.name = "group",
value.name = "weight")
df_2.5$g <- ifelse(df_2.5$group == 'a', 0, 1)
mod_2.5 <- glm(g ~ weight, data = df_2.5,
family = binomial(link = "logit"))
pred <- predict(mod_2.5, df_2.5, 'response')
t <- table(df_2.5$g, pred > 0.5,
dnn = c("Truth", "Predicted"))
colnames(t) <- c('0', '1'); t
df_5 <- data.frame(id = 1:length(aa), aa, bb)
df_5 <- reshape2::melt(df_5, id.vars = 'id',
variable.name = "group",
value.name = "weight")
df_5$g <- ifelse(df_5$group == 'aa', 0, 1)
mod_5 <- glm(g ~ weight, data = df_5,
family = 'binomial')
pred <- predict(mod_5, df_5, 'response')
t <- table(df_5$g, pred > 0.5,
dnn = c("Truth", "Predicted"))
colnames(t) <- c('0', '1'); t
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The dose I use - 65mg/kg i.p.:1.The rats were approximately 240 mg
2.they were on fasting 12-16 hrs before injection
3.After induction of diabetes they were given sucrose(15g/L) solution for 48 hrs.
3. I didnt use slow acting human insulin, while i need untreated rats for control group.In 2 days 25% of rats were dead, 75% have got blood glucose 31-33 mM/L . After 4 days of induction the most were dead.
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How you solved this problem? I've got a similar problem. When I induced diabetes on 150-200 gm body weight Long-Evans rats, (dose STZ 65mg/kg, nicotinamide 62mg/kg) most of the rats died. Iryna Palamarchuk
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If blood samples are to be stored frozen for some time till the analysis of blood glucose levels .. is it accurate to use frozen serum or it must be stored in grey tubes ? For how long ? And does it need any processing in the grey vacutainers before storage?
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I think 3 months should be fine for insulin and lipids (I've done it before). However, the quality of your plasma might depends on the storage conditions. If you're not sure of the quality of your samples and if you know what to expect (roughly) for your controls, the best thing is probably to try to run some tests on some of them to check their quality, before running all your experiment?
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Dear researchers/professors,
For my master's thesis I prepared insulin loaded nanoparticles (100 IU/kg) and gave them to rats via oral route. To compare my formulation I also gave insulin sc (2 IU/kg) to rats and collected their blood. When I measure the blood glucose level I saw the change and I put the blood in eppendorf tubes that has heparin inside. After centrifugation I collected plasma and used human insulin ELISA kit. The calibration solution created the color perfectly but my samples gave no color or absorbance so I wanted to get your opinion about what might cause this failure?
Thank you.
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I think immunoassays in general could be problematic in quantification. If blood glucose is affected as expected, then probably you have no problem with your preparation, so Danielle Dillon 's question are very important here.
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This is about a different approach to fighting cancer basically cancer cells must have glucose to survive. Following a ketogenic diet, the glucose drops and then using the administration of diabetic drugs to drop and keep blood glucose levels below 60 mg the healing process should start.
I would like to ask if you know people who tried this diet approach as detailed as possible & in the first place can somehow affect the patient they are any circumstances for that?
Can be this a way to heel cancer ? Are there researches that confirm this process or is the book written without evidence and is everything in theory?
Regards,
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Thank you
I appreciate you replay.
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What is the injectable range of insulin for daily administration to normalize high sugar level in Albino rats?
What is the Blood glucose range for rats?
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long acting insulin shots occur once or twice a day..insulin can help sickly person stabilize blood sugar levels. its important to stay consistent with general injection area. the response to insulin injection depend up case of disease and development the DM sick , if person resistance DM
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We're presently working on the effects of monosodium glutamate on body weight & blood glucose levels; the experimental animals are wistar rats.
We administered it in solution during the am hours but they didn't seem interested in drinking the MSG-laced water until during the pm hours.
How best do we feed them MSG daily and at what time of the day?
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Please check
1. Piyanard Boonnate, Sakda Waraasawapati, Wiphawi Hipkaeo, Supattra Pethlert, Amod Sharma, Carlo Selmi, Vitoon Prasongwattana, Ubon Cha’on .Monosodium Glutamate Dietary Consumption Decreases Pancreatic β-Cell Mass in Adult Wistar Rats.June 29, 2015https://doi.org/10.1371/journal.pone.0131595
2. Helen Nonye Henry-Unaeze .Update on food safety of monosodium l-glutamate (MSG) . Pathophysiology 24 (2017) 243–249
3. El-Helbawy NF, Radwan DA, Salem MF, El-Sawaf ME. Effect of monosodium glutamate on body weight and the histological structure of the zona fasciculata of the adrenal cortex in young male albino rats. Tanta Med J 2017;45:104-13
4. Hamza RZ, Al-Harbi MS. Monosodium glutamate induced testicular toxicity and the possible ameliorative role of vitamin E or selenium in male rats. Toxicol Rep. 2014;1:1037–1045. Published 2014 Oct 22. doi:10.1016/j.toxrep.2014.10.002
5. Khalaf HA, Arafat EA. Effect of different doses of monosodium glutamate on the thyroid follicular cells of adult male albino rats: a histological study. Int J Clin Exp Pathol. 2015;8(12):15498–15510. Published 2015 Dec 1.
6. Shilpi Gupta Dixit, Puja Rani, Akansha Anand, Kamlesh Khatri, Renu Chauhan & Veena Bharihoke (2014) To study the effect of monosodium glutamate on histomorphometry of cortex of kidney in adult albino rats,Renal Failure, 36:2, 266-270, DOI: 10.3109/0886022X.2013.846865
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I have a list of blood glucose levels before and after a missed dose. These are compared the optimal range. I would like to obtain a p value in order to see whether the missed dose had a significant impact on the blood glucose levels.
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Quoting Jochen Wilhelm "usually, results should be presented with an effect size, ideally including the confidence interval. So a clinician can judge if there is a potential that the effect may have clinical relevance", we should do away with the use of significance in any test involving treatment and outcome such as drug trials to stop misleading reporting.
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Estimation of HbA1c based on the blood glucose values.
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Good point
regards
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I am planning to find the integration of the blood glucose readings over time and use the result to find the HbA1c value.
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there are several ways of doing the integration. You can do it by hand or you can use available code which uses the same methods.
From my perspective using pandas Dataframes is the most convenient way dealing with data. You have to load your columns into a pandas.Series and then you can use the code given below to compute th integral. The necessary code is available here (https://nbviewer.jupyter.org/gist/metakermit/5720498), but a small change have to be made, because TimeSeries is just a Series. At first start with this code:
from scipy import integrate import pandas as pd import numpy as np def integrate_method(self, how='trapz', unit='s'): '''Numerically integrate the time series. @param how: the method to use (trapz by default) @return Available methods: * trapz - trapezoidal * cumtrapz - cumulative trapezoidal * simps - Simpson's rule * romb - Romberger's rule See http://docs.scipy.org/doc/scipy/reference/integrate.html for the method details. or the source code https://github.com/scipy/scipy/blob/master/scipy/integrate/quadrature.py ''' available_rules = set(['trapz', 'cumtrapz', 'simps', 'romb']) if how in available_rules: rule = integrate.__getattribute__(how) else: print('Unsupported integration rule: %s' % (how)) print('Expecting one of these sample-based integration rules: %s' % (str(list(available_rules)))) raise AttributeError result = rule(self.values, self.index.astype(np.int64) / 10**9) #result = rule(self.values) return result pd.Series.integrate = integrate_method
Than you can create your series object with your data and simply run ts.integrate.
Excample code with random values given here:
x = np.abs(np.random.randn(10000))
ts = pd.Series(x, pd.date_range(start='2013-05-03', periods=len(x), freq='s'))
ts.integrate()
There are several integrations methods available, but for sample data the trapz might be useful.
I hope this answers your question.
Kind regards
Sascha
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I am sure TIND is real, but I am wondering why the German guidelines of diabetes treatment seem to ignore the facts and allow freshly diagnosed patients with high Hb1Ac to reduce their blood glucose fast and risk pain, suffering and, possibly, induce severe complications of too fast reductions of blood glucose. How is it in other countries, are there more modern recommendations?
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Hi
South African Guidelines also don't address this entity, even though it is well described by clinicians.
Perhaps we need more research into successful management strategies? Do you know of any?
Most clinicians will try to reduce the rate of reduction of HbA1C, if the HbA1C is high at baseline assessment. [or the patient will reduce their medication....]
But we need more clinical trials to guide us, with the details.
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So, we are trying to induce T1DM, and need to measure the blood glucose of the pregnant female mice. Rather than cutting the tail (we were guessing this may interrupt their pregnancy), can we measure blood glucose level in amniotic fluid during the harvest if embryo instead?
We want to measure the blood glucose in amniotic fluid at E14.5.
And I'm wondering, at this stage, whether the blood glucose is more closer to the maternal BG, or the embryonic BG?
Or in other words, at what stage, the BG of amniotic fluid is still similar to mother's BG?
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You can certainly measure glucose in amniotic fluid at e14.5.
Collecting blood from pregnant mouse will not harm pregnancy as long as you handle pregnant mouse gently. Priest lab at Stanford has done at e12.5.
Third, for the last part of your question, you can collect blood before killing pregnant mouse and collect amniotic fluid after killing mouse at the same hour and compare the glucose level yourself, that data does not exist in literature, you might create, cheers and hope that helps
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Actually I had fed HFD to C57BL/6J with or without a drug. The result of that experiment I got that the drug suppresed HFD-induced metabolic syndrome according to body weight, fasting blood glucose, GTT, ITT, energy expenditure and so on. But one thing is not matched with all of other phenotypes. I fed HFD for more than 22 weeks and epididymal fat tissue mass was smaller than drug treated mice. Also HFD only fed (non drug treated) mice's eWAT show that some part of tissue looks like yellow and hard and severe inflammation. I think it is come from long-term HFD-induced fibrosis of fat tissue. Is that right?
If someone knows about it please let me know. Even already reported reference paper is also good for me.
Thank you.
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Thanky for all you guys.
Actually, the paper that Ryan Ceddia suggested had answer for my question.
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I am 33 weeks pregnant and a type 1 diabetic. I have been told by doctor's that I am already starting to have contractions but no dilation or indications of delivering soon. Since the contractions could have started my blood glucose levels have been impossible to bring down to an acceptable level or difficult to increase to an appropriate level. Any advice on how to better control the changes in my blood glucose level, as they change at random times during the day?
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Some pregnancies are complicated by an excessive amount of amniotic fluid (polyhydramnios). This extra fluid may result from high blood sugars in the mother leading to high blood sugars in the baby, which make the baby urinate more often. The fluid may stretch the uterus and cause contractions. In addition, infections (urinary, vaginal or other) may also increase the risk for premature labor. Certain medications which are used in patients without diabetes to control premature contractions should be used with extreme caution in pregnant women with diabetes because they can significantly affect blood sugar control (e.g. terbutaline/brethine).
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Dear all, I am interested in establishing model for gestational diabetes. I used alloxan (i.p. 120mg/kg) to induce diabetes in female rats. Does anyone has experience about the reversibility during pregnancy? How to maintained hyperglycemia if there is restoring of blood glucose level? Another alloxan injection?
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Please check
1. Kiss AC, Lima PH, Sinzato YK, et al. Animal models for clinical and gestational diabetes: maternal and fetal outcomes. Diabetol Metab Syndr. 2009;1(1):21. Published 2009 Oct 19. doi:10.1186/1758-5996-1-21
2. Alicia Jawerbaum Verónica White.Animal Models in Diabetes and Pregnancy.Endocrine Reviews, Volume 31, Issue 5, 1 October 2010, Pages 680–701,https://doi.org/10.1210/er.2009-0038
3. Siti Hajar Abdul Aziz, Cini Mathew John, Nur Intan Saidaah Mohamed Yusof, et al., “Animal Model of Gestational Diabetes Mellitus with Pathophysiological Resemblance to the Human Condition Induced by Multiple Factors (Nutritional, Pharmacological, and Stress) in Rats,” BioMed Research International, vol. 2016, Article ID 9704607, 14 pages, 2016. https://doi.org/10.1155/2016/9704607.
4. Claes Hellerström, Ingemar Swenne, Ulf J Eriksson.Is There an Animal Model for Gestational Diabetes?Diabetes Jun 1985, 34 (Supplement 2) 28-31; DOI: 10.2337/diab.34.2.S28
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Hypoglycemia is a condition with the blood glucose level below the threshold of 70 mg/dL [1] and is considered serious adverse effect of insulin based treatment for type1 diabetes (T1D) patients. One of the earliest manifestations of hypoglycemia is the involuntary shaking of the human body such as the fingertips.
Paper:
R. McCrimmon, “Glucose Sensing During Hypoglycemia: Lessons From the Lab,” Diabetes Care, vol. 32, no. 8, pp. 1357–1363, Aug. 2009.
American Diabetes Association Workgroup on Hypoglycemia, “Defining and Reporting Hypoglycemia in Diabetes: A report from the American Diabetes Association Workgroup on Hypoglycemia,” Diabetes Care, vol. 28, no. 5, pp. 1245–1249, May 2005.
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There have been some interesting applications to detect and quantify tremor in Parkinson's patients using simple performance tests delivered using a smartphone - for example measuring tremor based on smartphone accelerometer sensor readings recorded while the phone is held flat in the hand. A lot of work has been done by Roche Pharmaceuticals on this topic. See for example. It may be possible you can leverage the same approach to look at hypoglycaemia related tremor.
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I was looking into different literature and I want to know if there is a guideline for fasting glucose level for OGTT glucose level. It seems like mice with >8mM (fasting) and >7.8mM (OGTT) are considered diabetic 
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Depends on the animal model, eg. C57Bl/6 high fat diet: over 240 mg/dl which will be around 13.3 mmol ...
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What are the best statistical tools to analyse the reliability and validity of a diagnostic instrument?. Which gives the data in the ratio scale and the instrument is used for measuring the as body weight, blood pressure, blood glucose etc.
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The test used to verify accuracy of an instrument, when compared to its gold standard is the ROC curve.
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My research domain is "Blood glucose monitoring and insulin suggestion for diabetic patient". Is there any suitable data set OR i can generate my own by using any blood glucose model ?
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I think its better to generate own data
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I'm starting a research on mice to measure HbA1c levels and would want to get results in a few weeks (6-10weeks).
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You are most welcome, and just as a reminder their are specil kits for mice HbA1c that should be used in your research.
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Your OGTT curves suggest that 4-h blood glucose concentrations dropped below fasting even in controls? That does not look real does it?
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Hi
I'm running a small study to compare between the readings of different finger-pricking devices that measure blood glucose levels. Each study participant takes two measurments before and after their breakfast (two blood glucose readings, one from each device). So that's 4 readings per day for a total of 12 days = 48 data points for each participant.
What kinds of graphs do you suggest I plot? And what statistical analysis is applicable, aside from Bland-Altman Analysis?
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A mixed effects/multilevel model will fit.
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Hi everyone,
I would like to ask, is it possible if resistant maltodextrin or other resistant starch increases postprandial blood glucose? Is there any synergestic interaction between starch and fiber?
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Whats the reason behind the diabetes incidence (blood glucose level less than 250 g% in db/db mice (of less than 50% of the animals ) in a db /db mice on B6 background even after 8 weeks of either sex but having obese phenotype ?
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Please have a look this review papers
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Does circulating blood glucose concentration limit rates of aerobic ATP production. i.e. can supplementation of glucose result in an increased ATP availability during recovery from aerobic exercise?
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First of all, I assume you are talking about ATP levels in the active musculature. If so, it changes very little even under very heavy exercise. It is ~5 mmol/kg at rest and even during heavy exercise. Blood glucose (and liver glycogen) does not become a limiting factor for muscle ATP production until after ~2.5 hrs of heavy exercise (see Chapter 5 in Physiology of Exercise by David R. Lamb). This assumes that a carbohydrate drink/food is not being consumed during the exercise. The body does not store excess energy as ATP. That is what creatine phosphate, muscle glycogen, liver glycogen, and to a minor extent, blood glucose, is for. ATP is a relatively large muscle and thus inefficient means of storing excess energy. If you only had ATP as a means to store energy and you had to run a marathon, you would have to use roughly 180 kg of ATP.
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I am preparing for endocrine hormone lecture , I read a fact about the role of GH on muscle and fatty tissues to reduce glucose uptake by these tissues and increase glucose production by the liver .
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GH is a fasting hormone become active during sleeping that is why we recommend children sleep early, the the peak of this hormone during sleep is from 12 am to 4 am, also become active during exercise that needs source of energy (glucose). I n malnourished children it was recommended to give them growth GH next to a balanced diet to help lean body mass.
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why extract of okra lowers blood glucose and serum lipids?
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Because Okra contains, isoquercitrin and quercetin 3-O-gentiobioside which reduced blood glucose and serum insulin levels and improved glucose tolerance.
Okra loaded with pectin which can help in reducing high blood cholesterol simply by modifying the creation of bile within the intestines.
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We are running hyperinsulinemic euglycemic clamp in mice. But I have always been thinking about what does euglycemia means. Should the fasting glucose value of each individual mouse be the guide for the blood glucose you want to achieve at steady state or should you decide beforehand that every mouse should achieve the same blood glucose values at steady state of the clamp. If a group of mice have lower fasting glucose value than another group, then this first group might need lower GIR to maintain their “own” euglycemic value, but if you would have clamped all mice at the same blood glucose values the group with lower fasting glucose values will probably have a higher GIR. How do you usually do in mouse experiments using the glucose clamp technique?
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Louise, what you are thinking is absolutely right. Clamping blood glucose levels from two different mouse phenotypes should be resulted in different GIR, if there is different insulin sensitivity between groups. Euglycemia should be determined baseline blood glucose level before infusing insulin. If one group of mice show120mg/dL and another group of mice show 150mg/dL, either 120, 150, or around 130 should be okay. Bottom line is you should "clamp blood glucose level to the same range give or take 130-140. As suggested above, Vanderbilt University have invented this technique in mouse and published wonderful method articles and research articles. They also offer annual clamp class; https://labnodes.vanderbilt.edu/mmpc. Ask advice or question to them. Good luck!
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there are several methods to making animal model of diabetes, but if we want to make a model of diabetes with desirable blood glucose, how it is possible?
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I use 0,1 mL/100 g body weight alloxan to produce diabetic rats, but glucose concentration in blood plasma vary from 7-8 mM/L to 18-20 mM/L. Therefore, the glucose concentration in blood depends not only on alloxan amount, but other factors, which I cannot define now.
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rat blood glucose level
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Venous blood sampling in rat can be done by tail vein.
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I need data contains blood glucose , blood pressure and location of patients during a day.
I'll be so thankful to anyone can help me,,
here is my e-mail address:
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1. Chris Drummond and Robert C. Holte. Exploiting the Cost (In)sensitivity of Decision Tree Splitting Criteria. ICML. 2000. [View Context].
2. Kai Ming Ting and Ian H. Witten. Issues in Stacked Generalization. J. Artif. Intell. Res. (JAIR, 10. 1999. [View Context].
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10. Jan C. Bioch and D. Meer and Rob Potharst. Bivariate Decision Trees. PKDD. 1997.
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12. Jennifer A. Blue and Kristin P. Bennett. Hybrid Extreme Point Tabu Search. Department of Mathematical Sciences Rensselaer Polytechnic Institute. 1996.
13. Peter D. Turney. Cost-Sensitive Classification: Empirical Evaluation of a Hybrid Genetic Decision Tree Induction Algorithm. CoRR, csAI/9503102. 1995.
14. Rong-En Fan and P. -H Chen and C. -J Lin. Working Set Selection Using the Second Order Information for Training SVM. Department of Computer Science and Information Engineering National Taiwan University.
15. Alexander K. Seewald. Dissertation Towards Understanding Stacking Studies of a General Ensemble Learning Scheme ausgefuhrt zum Zwecke der Erlangung des akademischen Grades eines Doktors der technischen Naturwissenschaften.
16. Lawrence O. Hall and Nitesh V. Chawla and Kevin W. Bowyer. Combining Decision Trees Learned in Parallel. Department of Computer Science and Engineering, ENB 118 University of South Florida.
17. Ahmed Hussain Khan and Intensive Care. Multiplier-Free Feedforward Networks. 174.
18. Andrew Watkins and Jon Timmis and Lois C. Boggess. Artificial Immune Recognition System (AIRS): An ImmuneInspired Supervised Learning Algorithm. (abw5,jt6@kent.ac.uk) Computing Laboratory, University of Kent.
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21. Adil M. Bagirov and Alex Rubinov and A. N. Soukhojak and John Yearwood. Unsupervised and supervised data classification via nonsmooth and global optimization. School of Information Technology and Mathematical Sciences, The University of Ballarat.
22. Rudy Setiono and Huan Liu. Neural-Network Feature Selector. Department of Information Systems and Computer Science National University of Singapore.
23. Charles Campbell and Nello Cristianini. Simple Learning Algorithms for Training Support Vector Machines. Dept. of Engineering Mathematics.
24. Michael Lindenbaum and Shaul Markovitch and Dmitry Rusakov. Selective Sampling Using Random Field Modelling.
25. Prem Melville and Raymond J. Mooney. Proceedings of the 21st International Conference on Machine Learning. Department of Computer Sciences.
26. Fran ois Poulet. Cooperation between automatic algorithms, interactive algorithms and visualization tools for Visual Data Mining. ESIEA Recherche.
27. Wl odzisl/aw Duch and Rudy Setiono and Jacek M. Zurada. Computational intelligence methods for rule-based data understanding.
28. Liping Wei and Russ B. Altman. An Automated System for Generating Comparative Disease Profiles and Making Diagnoses. Section on Medical Informatics Stanford University School of Medicine, MSOB X215.
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31. Krzysztof Grabczewski and Wl/odzisl/aw Duch. THE SEPARABILITY OF SPLIT VALUE CRITERION. Department of Computer Methods, Nicolaus Copernicus University.
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35. Lena Kallin. Receiver operating characteristic (ROC) analysis Evaluating discriminance effects among decision support systems. Contents 1 The Theory of Receiver Operating Characteristic Curves 5.
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To my knowledge we use Clarke and Parke error grid analysis to see analytical accuracy or clinical accuracy of the performance of blood glucose (BG) meter with different borders of the zones. My question is, can we use Clarke and Parke grid analysis for non-invasive glucose solution prediction? I am looking forward. Many thanks
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I think you can use it. In fact, I've already done it in some previous studies. Although RMSE is the usual metric to evaluate BG prediction systems, the Clarke and Parke's error grid combines prediction error with specific knowledge of the problem, so I think it is a good complementary metric.
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I have given a bolus (drink containing sugar) and measured HOMA and QUICKI indexes post-bolus for up to 5hrs every hour.
I know both HOMA and QUICKI work on fasting insulin and glucose values, does this mean my data is invalid as I have given my participants a drink to consume?
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No, HOMA and QUICKI basically reflect hepatic insulin resistance while the measures after a glucose challenge rather reflect whole body insulin resistance (muscle, fat etc) or beta cell function. There are other indices for insulin/glucose dynamics such as insulinogenic index, matsuda etc
see
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I am estimating power for an experiment using AUC of blood glucose response over 120 minutes as the primary outcome. I'm struggling to find good quality reliability data for this, in particular I need an estimate of likely within-person variation. There's lots on GI but that isn't directly helpful.
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Variability of glycemic and insulin response to a standard meal, within and between healthy subjects
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In my laboratory we only have the conditions to use small rodents, rats or mice (or cell lines).
In your opinion, what is the best model for studying the long-term effects of gestational diabetes on the offspring? There is so much diversity of protocols and diets with such different compositions ...
is there any cut off value of blood glucose to say that a rodent is diabetic?
Thank you in advance for sharing your knowledge
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Hi 
Have a look on this :
and this :
doi:  10.1152/ajpendo.00425.2013
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I have read several articles that aloe vera has antioxidant properties that has the potential to lower blood glucose levels. I was wondering if there are other plants that could have the same properties to serve as an alternative.
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any snaps containing similar to olea vera
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In a clinical setting to measure fasting blood glucose, is it better to use serum or capillary blood?
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I have 2 rat experimental groups. Their weights were taken before and after 17-18h starvation. 
Group1 showed less body weight loss and a tendency of increasing of blood glucose level compared to the Group2.
Can anyone help me to understand what it means, please?
Thank you so much.
Best Regards,
Mario
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For group two ,insulin regulate glucose level , exceed glucose transport with insulin into liver and then converted into fat which stored in fat adpose tuess while in group one this will not happen ,therefore glucose level will increase and decrease body weight
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I need some sample papers
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Direct use of NIRS spectroscopy without any previous calibration model (for example PLS model) can't give u any information really u just get a simple spectrum.NIRS is secondary method always need to refer to primary method.Some extracted calibration models can be used for determination of certain properties about uknown samples
In ur case if u have the model for blood glucose concentration  u can use NIRS use spectral information to determine blood glucose concentration  for ur sample but if not u can not use
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animal is induced using stz (40 mg/kg) and nad(110mg/kg). when we checked the fasiting blood glucose one day it has decreased week later it has increased. pls clarify.
3 days after the induction of the dibetes using nicotinamide (110mg/kg) and streptozotocin(40mg/kg) the animal blood glucose was checked and it was treated with metformin(300 mg/kg). Glucose check was done for every 7 days with animal being fasted for 6 hours. first week FBG was found to be 168, 100 and 274. Metformin treatment was continued.   after one week when animal checked with fasting blood glucose again it showed 600+.
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Dear Gayathri,
In my view,you started your investigation sooner than diabetes establishment in the animals. Three days after STZ injection is suitable just for distinguishing diabetic from nondiabetic animals, but to confirm and establish diabetes in animal i recommend keeping diabetic animals at least for 2 weeks before starting investigation.
Regards,
Mehran
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I got a few blood glucose values below 50 mg/dl after a 16h fasting and wonder if anyone else got similar results. 
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Hey, 
I once checked blood glucose of NOD SCID females (roughly 30 weeks old) after 48h and 72h of a super low caloric diet (a fasting mimicking diet) and the blood glucose was in all three subjects 50-60mg/dl.
It also has been published that fasting of up to 72h (in 30w old mice if I remember right) should lower the blood glucose to a maximum of 50mg/dL. 
loook it up here:
Changhan Lee et al; Cancer Res. 2010 February 15; 70(4): 1564–1572.
so this seems a bit low after only 16h. Did you fast over day or night ?  as mice have rather a contrary circadian rythmn than humans so much mor active during the night and therefore 16h over nighth might have the same effect than 24h...but still it is low 
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From RBC we can calculate average levels of blood glucose levels , over three months, using the hemoglobin A1c test and we can measure somatic levels of glutathione. Several formulas exist to determine levels of ionized calcium using serum Calcium, Phosphorus, and Albumin. Using erythrocytes, I posit, would provide an average of ionized calcium levels - instrumental in managing arthritis, cardiovascular pathology, and, finally, cancer 
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Mr. Sikaris, Do you know of anyone working on a project that aims to identify a new HTN diagnostic technique that somewhat mirrors the discovery of the correlation between glycated hemoglobin and diabetes? I'm always wondering how and why we still rely on error-prone blood pressure measurement to diagnose HTN. Thanks for your help.
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I want to do an intervention. Info about web-linked test kits would be valuable.
HbA1c or glucose.
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apparently POC for HbA1c are not good, check Westgard web pages for info 
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glycated hemoglobin
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Some of the biochemistry textbooks mentioned 75-80 % of glycated HB is HbA1c but I couldn't find the exact answer. Thank you all for your responses.
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Dumoulin, E describes the usefulness of using granulised fluoride and citrate for stabilizing of plasma homocysteine levels. Are fluoride citrate granule containing vacutainers still available for use like the Greiner product, or is there an alternative?
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I do not have experience with insulin or glucose tolerance test in rats and I would like to have some advices or tips regarding how to collect blood to measure glucose levels during the ITT and GTT.
Best regards,
Rodrigo
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Dear Rodrigo,
According to my experiments, intraperitoneal glucose tolerance test (IPGTT) in rats is the following:
Rats were anesthetized with an i.p. injection of pentobarbital sodium (60 mg/kg body weight). After 12 hours fasting, rats were administrated an i.p injection of 50% dextrose at a dose of 2 g/kg body weight. Blood samples were collected from the tail tip in EDTA-containing microtubes at 0 (before glucose injection), 15, 30, 60, 90 and 120 min after glucose i.p injection. After centrifugation at 4°C, plasma was stored at -20°C until assayed.
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We measured average blood glucose levels in male Wistar rats as follows:
Age matched control animals - 124 mg/dL (non-fasting) and 83 mg/dL (fasting)
High-caloric diet fed animals - 139 mg/dL (non-fasting) and 105 mg/dL (fasting)
How will these values be classified?
I can't seem to find any published guidelines for classifying animals as normoglycemic or hyperglycemic.
I'm specifically looking for fasting and non-fasting guidelines.
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I agree with Dr. Bhansali. We have measured whole blood glucose twice daily in rats for over three years.  Non-diabetic (regardless of regular 18% fat or 40% high fat  diet) had mean glucose of 90±0.89 mg/dl and 92.34±1.15 respectively for diets and after development of diabetes all >200mg/dl (324±9.83mg/dl and 333±11.50 respectively.)
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I am working on noninvasive blood glucose monitoring method based on four near infrared spectrums and double artificial neural network analysis.We choose four near infrared wavelengths, 820 nm, 875 nm, 945 nm, 1050 nm, as transmission spectrums, and capture four fingers transmission PPG signals simultaneously.
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I would assume to measure blood glucose non-ivasively you must be sure that there are no other blood components that would be picked by the sensors at these wavelenghts, the results would just be estimates because even a pulse oximeter is not 100%  accurate. Secondly to ensure accuracy you may have to get the person or animal to ingest labelled glucose which is then picked by the sensors.
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Hello, I am attempting to determine what the limit of detection is for the current measurement of commercial blood glucometers. All of the resources that I have found seem to only focus on the limit of detection in glucose concentration, which does not help me. Are there any good journal articles (or other archival resources) describing the current range that blood glucose meters can measure? 
Thanks!
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Use some 1...100 K variable resistors to build a dummy cell and study the response curve of your device. The device is providing a constant potential of about 0.6 V.
I suggest that the measuring range is close to 0.01...1 mA and is also limited by the internal software. 
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Hello,
We know that control systems have been utilized in the biomedical field to create implanted automatic drug-delivery systems to patients. Automatic systems can be used to regulate blood pressure, blood sugar level, and heart rate. I would like to know that how closed-loop systems work and how they can control the blood glucose level in a non-invasive way?
Thanks for your attention
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Feed back theory works for many things. It has also a very good application in biomedical instrumentation. For controlling the blood-glucose concentration, we need to have a very sensitive sensor with good precision to measure the actual instantaneous concentration in the blood. This is very important to design artificial pancreas which almost could replace the natural one. The measured signal by the sensor should be conditioned by a DSP device and is compared with the reference value (set point) that the glucose level for the diabetic patient should be, and the subtracted error could be modified according to the physiological behavior, external noises (meal the patient takes) and other medications...and the final signal takes an effect on the micro valve or actuator to release the precise amount of insulin if blood sugar level is greater than the set point (hyperglycemia) other wise releases glucagon in exact amount if it is less than the normal level (hypoglycemia). However, as fast response is very crucial in this case for the safety of the patient, feed-forward control could be more practical than feedback control. This is the general concept behind but there are so many details that should be addressed to put  this technology in to practice and of course requires a profound knowledge in medicine as well as electrical control engineering.
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Which is more accurate among all commercially available personal glucometers to measure glucose concentration in water-glucose samples? Is there any rating available for personal glucometers based on the performance? 
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Hi Satish ¡ I agree with Tausif obout the use of blood glucometers  for measurement of glucose in wáter. You can be sure with the measurement of glucose in kown concentrations in wáter on   several  solutions prepared by yourself
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Hi, my experiment is on diabetic cardiomyopathy, the model is STZ-induced type 1 diabetes using rats. The whole experiment need 20W after the inducing of STZ , but at 12W or so, the blood glucose of rats is so high more than 600mg / dl (33.33mM) in mostly rats that cannot  be measured by blood glucose meter
So I urgently want to ask for your help for the following questions:
1.       Whether blood glucose exceeds 600mg / dl in rats needs insulin treatment, or no needs any treatments?
    If this is the case, whether all rats need to inject insulin (which kind of insulin), or just need to inject the rats which blood glucose is too high?
2.       At the end of the experiment, whether the need for HbA1c tests to assess blood glucose levels?
Many thanks!!!
Yong Yang
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Diabetes-associated long-term systemic damage tends to be a function of degree of hyperglycemic excursion. It seems that to study a specific parameter, cardiomyopathy, first you need to decide about the range of hyperglycemia you wish study and induce diabetes accordingly.
Use of portable consumer glucometer, though very convenient, has its limitations. If it gives you a high warning, it simply means >600mg/dl blood glucose and you wouldn't know if it is 601 or 862 mg/dl. If all or nearly all beta cells are destroyed by STZ, it will be nearly impossible for diabetic animals to survive on normal ad libitum feed without some form of insulin treatment for the duration of your experimental period.
if you decide to go with insulin injections, the long-accting version will be the most convenient option for a single injection in the evening, rodents being nocturnal. The amount of insulin you may need will depend on largely your experimental design, the target blood glucose level - just enough to preserve life versus near full correction (very difficult to achieve), and to some degree on the strain of rodents. Given all these caveats, try a range of insulin at 0.5-5 IU/kg.
best,
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I’m doing an investigate of blood glucose level to see the pre-diabetes progression. I use a form that consist of demographic characteristics related to that disease. I’m really looking suggestions in order to make all data gathered valid.
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Usually, assessment of validity and reliability are only required for attitudinal or behavioural questions. We can assume that demographic items have face validity and are likely to be consistently answered.
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The insulin secretion in the body of a Type 1 Diabetic is impaired/absent. Is there any insulin secretion in the body for a typical Type 1 Diabetic Patient? If yes then what is the level (typical value)?
  The context of the question is that when we simulate the compartmental model of Type 1 Diabetic patient, then is it necessary to include some constant basal value of insulin? But for control problem of blood glucose regulation of Type 1 Diabetes we sometimes assume that the body produce zero insulin. 
   Summarizing the query, it is that should we include some basal insulin concentration in blood plasma or consider it as zero.
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The answer to your question, as it is put, depends on the stage of T1DM along its temporal progression. If you review the literature, you will see that early on in the disease, there are some islets but eventually they are all destroyed.
A C-petide measurement on a specific patient will give you a much better idea as to how much insulin is coming from endogenous remaining islets at a given point. 
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When we recommend patients for HbA1C test, is it not necessary to convince them not to go for fasting and postprandial blood sugar level. It may reduce circumstances and routine hectic tension of patients. we can also council patients that HbA1C is enough to see improvement in their glucose profile.
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For type 1 diabetes, daily (multiple) measurement(s) of blood glucose levels is a necessity.
For type 2 diabetics, it is very useful for patients to have a good idea as to how their changes in life-style are helping them, hopefully it serves them well and keeps them motivated. In the absence of a routine test, complacency often works in the negative direction... just a matter of human nature. There are, of course, exceptions, but they tend to be less prevalent.
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I have to choose a glucometer for my research on mice. 
Many of those reported on publication are not available in Poland. I would like to know if some has experience with Accuchek Active or Accuchek Performa glucometer from Roche, as I am thinking to take this one. 
Thank you in advance
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In my lab, we use Bayer's version but at this point, I do not think that there will be drastic differences between Roche's version and other major brands. They are similarly reliable/inaccurate (depending on your outlook). I believe that all of the newer versions are also using smaller amounts of blood, which is important in mouse work. 
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Hi! Quick question: I know SD and Wistar rats have similar BG levels as humans, but I'm unable to find a model that would tolerate hypoglycemia well or had somewhat lower fasting BG levels per se. Any ideas? Thank you very much.
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Thank you very much Tausif.
You're right, I should have specified. From papers I have read the fasting BG of WIstar rats and other mouse models is slightly higher than in humans, and I was just looking for fasting BG levels around 80 mg/dl. Come to think of it, maybe it varies from animal model to animal model, and laboratory rats have generally higher BG, although they're easier to work with.
Anyway, based on what you're saying and papers about hypoglycemia, I think Wistar rats would do just fine. They were my first pick but if there is a model that naturally tolerates 40-50 mg/dl better, I would love to know.
Thank you all very much.
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Dear all, 
I am starting a new project and I need to buy a glucometer, for measurement of blood glucose during GTT. As this is a new procedure for me and we do not have in my lab, I would like to have some advice to choose the best one. 
thank you
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Hey Federica!
Evaluation of the appropriateness of using glucometers for measuring the blood glucose levels in mice is a newly published research article in nature.
Abstract for ur persual:
Glucometers are also widely used in diabetes research conducted using animal models. However, the appropriateness of measuring blood glucose levels using glucometers in animal models remains unclear. In this study, we evaluated the consistency between the blood glucose levels measured by 11 models of glucometers and plasma glucose levels measured by a laboratory biochemical test in blood samples collected by retro-orbital sinus puncture or tail-tip amputation. In both blood samples obtained by retro-orbital sinus puncture and those obtained by tail-tip amputation, 10 of the 11 models of glucometers yielded higher glucose values, while 1 yielded lower glucose values, than the plasma glucose values yielded by the laboratory test, the differences being in direct proportion to the plasma glucose values. Most glucometers recorded higher blood glucose levels after glucose loading and lower blood glucose levels after insulin loading in retro-orbital sinus blood as compared to tail vein blood. Our data suggest that the blood glucose levels measured by glucometers in mice tended to be higher than the plasma glucose levels yielded by the biochemical test under the hyperglycemic state, and that differences in the measured levels were observed according to the blood collection method depending on the glycemia status.
Have a look...
The following models of glucometers which were commonly used in clinical practice were used for the measurements: ACCU-CHECK Compact Plus® (Roche Diagnostics, Japan) (No. 1), Medisafe mini® (MS-GR102 TERUMO, Japan) (No. 2), Glutest neo alfa® (Sanwa Kagaku Kenkyusho, Japan) (No. 3), Glutest neo super® (Sanwa Kagaku Kenkyusho, Japan) (No. 4), Glutest mint® (Sanwa Kagaku Kenkyusho, Japan) (No. 5), Freestyle Freedom Lite® (NIPRO, Japan) (No. 6), LIFE CHECK® (eidia, Japan) (No. 7), ACCU-CHECK Aviva Nano® (Roche Diagnostics K K, Japan) (No. 8), Stat Strip Xpress® (Nova biomedical, USA) (No. 9), ONETOUCH Ultra Vue® (Johnson and Johnson, USA) (No. 10), and CareFast C® (NIPRO, Japan) (No. 11).
Togashi, Y. et al. Evaluation of the appropriateness of using glucometers for measuring the blood glucose levels in mice. Sci. Rep. 6, 25465; doi: 10.1038/srep25465 (2016).
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The dentist referred the patient for a diabetic workup after he saw that the patient's mandibular trabecular bone appeared to be sparse (as in a diabetic patient) in a panoramic radiograph. Her 2-hr postprandial level is within range (135mg/dl) however it is close to the upper limit. The patient is worried and wants to do further workup. Is it necessary?
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How about her 3 independent fasting blood glucose levels? It is fairly inexpensive and straightforward.
If fasting levels are questionable, it would make sense to measure HA1c.
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I have some mutant mice which show elevated blood glucose levels as compared to controls. So I just wanted to take valuable opinions of all of you about which factors relating mainly to beta-cells (e.g. beta cell mass/size, secretion of insulin, total content of insulin in pancreas, insulin synthesis, etc.) can have major impact on blood glucose levels?
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If you go through the literature, you will find that all the reasons you listed, and some additional ones, could play a role in influencing blood glucose levels.
Asking others for opinions without defining the strain of mice (or the mutation) is practically an exercise in futility.
Best,
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patient post cardiac arrest with blood sugars >300 but on insulin drip at 30 units per hour but decreasing electrolytes.  Is there research supporting permissive hyperglycemia during the maintenance phase of TTM in order to prevent severe hypokalemia
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Insulin for the treatment of hyperkalemia: a double-edged sword?
Tingting Li, MD and Anitha Vijayan, MD
See the article "Hypoglycemia in the treatment of hyperkalemia with insulin in patients with end-stage renal disease" in volume 7 on page 248.
 
Potassium plays a critical role in cellular metabolism and normal neuromuscular function. Tightly regulated homeostatic mechanisms have developed in the process of evolution to provide primary defense against the threats of hyper- and hypokalemia. The kidney plays a primary role in potassium balance, by increasing or decreasing the rate of potassium excretion. Distribution of potassium between the intracellular and the extracellular fluid compartments is regulated by physiologic factors such as insulin and catecholamines which stimulate the activity of the Na+-K+ ATPase. Only about 10% of the ingested potassium is excreted via the gut under normal physiologic conditions [1].
For more plz read at the following link.
Regards
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Type 1 diabetes was induced by a single intraperitoneal injection of STZ (60 mg/kg) in 0.1 mol/l citrate buffer (pH 4.5) to the overnight fasted rats. Normal rats were injected with a similar volume of citrate buffer alone. Two days after the STZ injection, rats with a fasting blood glucose concentration of 250 mg/dl were considered to be diabetic.
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Reference intervals of any analytes in laboratory animals are dependent on your colony. To find normal ranges you should measure any analyte in at least 35 animals with or without bootstrapping, then normal range would be mean +/- 3 standard deviations. If the cost is your issue you must compare treated group with control group.