Insulin Resistance - Science topic
Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS. It can be caused by the presence of INSULIN ANTIBODIES or the abnormalities in insulin receptors (RECEPTOR, INSULIN) on target cell surfaces. It is often associated with OBESITY; DIABETIC KETOACIDOSIS; INFECTION; and certain rare conditions. (from Stedman, 25th ed)
Questions related to Insulin Resistance
I was going through different ways to calculate insulin resistance, I came across the eGDR equation. It is a very good and easy reliable way to calculate insulin resistance. But, I am confused a little about how to decide the threshold for a population. also, I came across various studies where a modified version of eGDR was used, how do authors decide that they might need modified version of eGDR?
Sorry if I ask but i dont understand.
Type 2 diabetes is known to be due to insulin resistance, dysfunctional insulin sensitivity and impaired insulin secretion. Induction of autophagy has been reported to ameliorate type 2 diabetes complications via TFEB, mTORC1, AMPK and other pathways. Late onset autophagy was also been reported to be detrimental rather than being beneficial. I did like to know how induction of autophagy affects insulin secretion especially as it affects the beta cell biology.
How it is possible to be insulin resistant and sensitive, and at same time AN adaptations of insulin metabolism is characterised by a decrease in basal insulin levels and increase in metabolic clearance to avoid hypoglycaemia (Zuniga-Guajardo et al., 1986)?
Zuniga-Guajardo, S., Garfinkel, P., & Zinman, B. (1986). Changes in insulin sensitivity and clearance in anorexia nervosa. Metabolism, 35(12), 1096–1100. https://doi.org/10.1016/0026-0495(86)90021-1
The literature indicates that yoghurt contains live bacteria that have major effects on gut dysbiosis, metabolism, insulin resistance and neurodegeneration. Gram negative bacteria release bacterial lipopolysaccharides (LPS) that have critical effects on insulin resistance and amyloid beta aggregation with relevance to diabetes and Alzheimer’s disease. The use of yoghurt, cheese and milk should be used to reduce gram negative bacteria and reduce plasma LPS levels that are markedly elevated in the developing and third world individuals.
1. Le Roy CI, Kurilshikov A, Leeming ER, et al. Yoghurt consumption is associated with changes in the composition of the human gut microbiome and metabolome [published correction appears in BMC Microbiol. 2022 Feb 28;22(1):66]. BMC Microbiol. 2022;22(1):39.
2. Lisko DJ, Johnston GP, Johnston CG. Effects of Dietary Yogurt on the Healthy Human Gastrointestinal (GI) Microbiome. Microorganisms. 2017;5(1):6.
3. Aslam H, Marx W, Rocks T, et al. The effects of dairy and dairy derivatives on the gut microbiota: a systematic literature review. Gut Microbes. 2020;12(1):1799533.
4. Le Roy, C.I., Kurilshikov, A., Leeming, E.R. et al. Yoghurt consumption is associated with changes in the composition of the human gut microbiome and metabolome. BMC Microbiol 22, 39 (2022).
5. V Yu Kontareva et al. Yogurt enriched to correct intestinal microflora in dysbiosis. 2020 IOP Conf. Ser.: Earth Environ. Sci. 548 082051.
6. Suzuki Y, Ikeda K, Sakuma K, Kawai S, Sawaki K, Asahara T, Takahashi T, Tsuji H, Nomoto K, Nagpal R, Wang C, Nagata S, Yamashiro Y. Association between Yogurt Consumption and Intestinal Microbiota in Healthy Young Adults Differs by Host Gender. Front Microbiol. 2017 May 11;8:847.
7. LPS Regulates Apolipoprotein E and Aβ Interactions with Effects on Acute Phase Proteins and Amyloidosis. Advances in Aging Research 03/2015; 4(2):69-77.
8. Unhealthy Diets Determine Benign or Toxic Amyloid Beta States and Promote Brain Amyloid Beta Aggregation. Austin J Clin Neurol 2015;2(7): 1060-66.
9. Overnutrition Determines LPS Regulation of Mycotoxin Induced Neurotoxicity in Neurodegenerative Diseases. Int J Mol Sci. 2015;16(12): 29554–29573.
10. The Role of Clinical Proteomics, Lipidomics, and Genomics in the Diagnosis of Alzheimer’s Disease. Proteomes, 2016. 4(2) 1-19.
11. Food quality induces a miscible disease with relevance to Alzheimer’s disease and Neurological diseases, J Food Research, vol. 5, pp.45-52, 2016.
12. Bacterial Lipopolysaccharides Change Membrane Fluidity with Relevance to Phospholipid and Amyloid Beta Dynamics in Alzheimer’s Disease. J Microb Biochem Technol. 2016; 8: 322-324.
13. The Future of Genomic Medicine Involves the Maintenance of Sirtuin 1 in Global Populations. Int J Mol Biol . 2017. 2(1): 00013.
14. Bacterial Lipopolysaccharides and Neuron Toxicity in Neurodegenerative Diseases. Neurology Research and Surgery. 2018; 1(1): 1-3.
Diabetes is a multifactorial disease characterised by chronic hyperglycemia as the baseline symptom. However, specific dietary components have been implicated as classic independent risk factors. Scientific investigations of these on-switches with respect to the pathogenesis of types I and II diabetes is very vital in preventive clinical practice. What is the distinguished "nutritional sword of Damocles" that usually precipitate insulin deficiency/pancreatic beta cell destruction as well as insulin resistance? How do these dietary agents instigate molecular cascades to initiate and also sustain lifelong hyperglycemia?
I am interested in creating insulin-resistant 3T3-L1 adipocytes using TNF-alpha, and I have the following questions:
1. Would it be best to use human TNF-alpha or mouse TNF-alpha?
2. What is an appropriate buffer to prepare the stock solution of TNF-alpha?
3. If I aliquot and freeze the solution, how long can I keep it in -20C. And for an aliquot that I thaw and dilute, how long can it stay in a 4C fridge?
4. For testing glucose uptake, can I use an indirect glucose assay (measuring how much glucose is left in the medium)? Or would you recommend using 2-NBDG?
Thank you very much
One of mode for treating type-2 diabetes is insulin injection. As per the pathophysiology there is insulin resistance to insulin for extra-hepatic tissues resulting in hyperglycemia. Does insulin is given very high amount in comparison to physiological levels which are unable to activate GLUT-4?
Hi, somebody knows about insulin resistance mechanisms of tobacco? I would like to begin a research project. I have some ideas but I would like to read you all.
In the literature reviewed, there are several ways to determine insulin resistence, the best known being the HOMA index.
During pregnancy, maternal tissues become increasingly insensitive to insulin.
What is the best treatment for insulin resistance in a pregnant woman?
Experts in the field of metabolism, what is the appropriate fasting period prior to investigating intraperitoneal Glucose or Insulin sensitivity test? This publication: https://nature.com/articles/s42255-021-00455-y suggested 2 hours while this: https://nature.com/articles/s42255-021-00414-7 recommended 6 hours.
Does creatine supplementation increase insulin sensitivity?
What is your opinion?
I have a few articles that are examining the factors of insulin resistance amongst Type 2 DM patients. These articles are cross sectional studies that uses questionnaires and surveys in their study. The researchers did not conduct any face-to-face interview or lived experiences. Thus, to appraise these articles, I used the JBI critical appraisal for Analytic Cross-Sectional Studies. Am I on the right track?
I know there have been so many rodent animal models of type 2 diabetes, but their hyperglycemia mechanisms are various (e.g. insulin resistance, beta cell destruction). Is there any suitable model for us to evaluate the GSIS function only of pancreatic beta cells? What I want is that, when I evaluate the GSIS function of pancreatic beta cells, other factors such as ER stress, beta cell apoptosis, and insulin resistance are no need to be considered.
I am working on hepatic insulin resistance and currently looking for any accurate and cost effective ways to measure the glucose uptake within the cells and in the media. Can anyone suggest me an appropriate assay along with its detailed procedure.
What is the recommended dose of insulin to perform insulin tolerance test in C57BL/6JUnib mice (fed on chow or high-fat diet)? I have found 0.1 to 10 UI/kg in the literature. Which is an adequate fasting time?
is anyone looking to be able to measure glycated insulin? Glycation (sometimes incorrectly called non-enzymatic glycosylation) is the covalent attachment of a sugar to a protein or lipid. Typical sugars that participate in glycation are glucose, fructose, and their derivatives.
Most monosaccharides, including glucose, galactose and fructose, spontaneously bond with hemoglobin, [hgAc1]when present in the bloodstream of humans. Glycohemoglobin, hemoglobin A1c provides a three (3) month average of fasting glucose levels.
My hypothesis is the glycation of insulin is mainly responsible for cell's resistance to insulin
Is there a standardized laboratory test for glycated insulin?
I want to know what are the different cell lines available for Polycystic ovary syndrome. What cell lines can be best used to understand insulin resistance in PCOS?
I plan to treat C57BL/6J mice with a Western-type high-fat, high sugar diet for 16 weeks to induce obesity and NAFLD. I also plan to study ex-vivo central insulin resistance (Western blot in the hypothalamus). Doses of insulin range from 0.5 - 1 U/Kg BW to 5 U/mice in the published papers. I would appreciate receiving an expert opinion about the recommended insulin dose to be injected before sacrifice.
the aim is to induce insulin resistance.
The aim is to induce insulin resistance in male wistar rats weighted 200-300 grams, fed with normal chow
TFAs take on similar properties as saturated fats, and appear to be more atherogenic. High intakes of saturated fats may promote insulin resistance. Since elaidic acid (EA), the trans isomer of OA, can be found in hydrogenated cooking oils and fried foods. We aim to assess the effect of this trans fatty acid (EA) on animal model by inducing diabetes using different doses.
I'm trying to understand the causal mechanisms for Type 2 diabetes and would like to know the sufficient and necessary factors for type 2 diabetes.
Most causes of type 2 DM are secondary such as insulin function, insulin resistance, obesity, recycling of the receptors, GlucT4 trafficking, etc, even genetics impact depend on epigentics factors that includes, lifestyle, nutritional etc.
I want to apply regression analysis using SPSS. Kindly help as to how to apply the regression model in the study where i have recorded Weight, BMI, Total body fat mass, insulin resistance and nerve conduction velocity in type 2 diabetics.
To establish insulin resistance, should HOMA-IR or the triglyceride glucose index (TyG) be used?
In this case-control study, 60 patients with in vitro fertilization (IVF)/intracytoplas- mic sperm injection (ICSI) indication were subdivided into 3 groups as follow: 20 subjects were assigned to control (fertile women with male infertility history) group, 20 subjects with PCOS were insulin resistant (IR) and 20 subjects with PCOS were insulin sensitive (IS). After puncture, retrieved oocytes were classified into metaphase II (MII) as mature and in metaphase I (MI) or germinal vesicle stage (GV) as immature. Regres- sion analyses were used to explore the association between MII oocyte number and demographic and clinical variables. LH/FSH ratio was significantly higher in PCOS-IR women compared to controls but not significantly dif- ferent from that of PCOS-IS group. PCOS-IR women had lower MII oocyte number compared with that of controls. According to multiple regression analysis, the number of previous assisted reproductive technology (ART) cycles was negatively associated with the number of MII oocy
Treating children known to have metabolic disorders often includes ensuring adequate amount of calories for age and weight to avoid catabolism, that is usually by giving glucose solution 10%.
What is the long term impact of the sugary fluids on these patients?
Does it contribute to generating some degree of insulin resistance?
Can we predict the insulin resistance if so?
will HOMA-IR serve as a good predictor test?
A study by Peeters et al. (2017) suggests that sugar traps cancer in a 'vicious cycle' which make it more aggressive and harder to treat (1). On the question-and-answer site Quora, Ray Schilling, MD, concludes: "there is a connection between the consumption of sugar and starchy foods and various cancers in man. Animal experiments are useful in suggesting these connections, but many clinical trials including the Women’s Health Initiative have shown that these findings are also true in humans. It is insulin resistance due to sugar and starch overconsumption that is causing cancer" (2).
1. Peeters K, Van Leemputte F, Fischer B, Bonini BM, Quezada H, Tsytlonok M, Haesen D, Vanthienen W, Bernardes N, Gonzalez-Blas CB, Janssens V, Tompa P, Versées W, Thevelein JM. Fructose-1,6-bisphosphate couples glycolytic flux to activation of Ras. Nat Commun 2017; 8: 922. doi: 10.1038/s41467-017-01019-z. https://www.nature.com/articles/s41467-017-01019-z.pdf
2. Schilling R. Why isn't sugar portrayed as bad like cigarettes? https://www.quora.com/Why-isnt-sugar-portrayed-as-bad-like-cigarettes
We knew from research that chromium is essential element to millions of peoples,
Chromium is an essential mineral that appears to have a beneficial role in the regulation of insulin action, metabolic syndrome, and cardiovascular disease. There is growing evidence that chromium may facilitate insulin signaling and chromium supplementation therefore may improve systemic insulin sensitivity. Tissue chromium levels of subjects with diabetes are lower than those of normal control subjects, and a correlation exists between low circulating levels of chromium and the incidence of type 2 diabetes. Controversy still exists as to the need for chromium supplementation. However, supplementation with chromium picolinate, a stable and highly bioavailable form of chromium, has been shown to reduce insulin resistance and to help reduce the risk of cardiovascular disease and type 2 diabetes. Since chromium supplementation is a safe treatment, further research is necessary to resolve the confounding data. The existing data suggest to concentrate future studies on certain forms as chromium picolinate and doses as at least 200 mcg per day.so why we dont take chromium tablets?
Vitamin-D plays role in maintaining insulin secretion from pancreatic beta cells. Vitamin-D deficiency contributes to the development of insulin resistance and onset of diabetes. Does vitamin-D supplementation in deficient patients prevent the development of diabetes? If so, what will be the minimum daily/weekly amount to be supplemented?
I am planning antidiabetic study laboratory study using Wistar albino rats. Aim of the study is to evaluate antidiabetic potential, quality of life, herb-herb, herb-drug interaction of two polyherbal formulations present in the local market and metformin will be standard. We plan to study liver, kidney, heart, pancrea protection by these formaltions in addition to antihyperglycemic, antihyperlipidemic effect and effect on oxidative stress. OGTT will be performed before and after the study.
Need advise - should we perform insulin sensitivity and insulin resistance, both test in preclinical diabetic studies?
I am not sure whats the best way to "control" for pubertal stage and gender in my analysis.
Actually, puberty is classified in 5 stages (1=prepubertal to 5=fully grown). To make it easier and also get more or less two groups with the same size, I also classified them into 1=prepubertal and 2=pubertal(stages2-5), which is valid from a clinical perspective.
So, what I want to do:
I want to see how continous marker X correlates with Insulin resistance (continous) AND if continous marker X is able to predict insulin resistance.
However, I am a bit stuck how to best implement pubertal status and gender in this analysis. it is likely that pubertal stage is somehow a confounding factor (since it is associated with insulin resistance), and maybe also gender.
--> How do I solve this? do a partial correlation with gender and puberty as cofactors? add them as first independent variables in a logistic regression model? how do I see/can say that puberty really influences the relation between marker X and insulin resistance?
If puberty is a confounder, it would then be possible to do two subgroup-analysis seperately evaluating the marker in prepubertal and pubertal children. (?)
thanks in advance!
I have completed a study collecting demographics, sleep data and measures of glucose homeostasis in older adults. I have fasting glucose, fasting insulin and Hba1c for each participant. I wanted to use HOMA-IR as a measure of insulin resistance in the population but I am struggling to find consensus regarding HOMA-IR cut-offs. Ethnicity and race seem to have a significant effect. My population is based in Australia (however I would expect have mixed heritage though I did not collect that data). Any advice on what HOMA-IR cutoff would be acceptable and any literature to support same?
Happy new year researchers! I was wondering if you knew of any reported cases of Medullary thyroid Ca in patients on Liraglutide (a GLP-1 agonist that's used for diabetes, insulin resistance, as well as help with weight loss). There is a theoretical increased risk of Medullary thyroid Ca in patients with a history of MEN2 (study was done in rats I believe), but I couldn't see any in human studies. We have been using this drug more in our practice due to the increased rate of diabetes and obesity in general in our patient population and not all patients are able to provide a dependable family history.
I was wondering whether high-fat diet or high-sugar-high-fat diets are more commonly used for diet induced obesity in rodents? And the reasoning behind using one or the other.
When i do a pub-med search i see more hits for 'high-fat diet' for rodents, although there are many different terms for a high-sugar-high fat diet, so its hard to say. I would have expected that HFHS would be more effective.
I'm interested in which is the most effective at inducing obesity, and in particular i'm interested in the effect of the quality of the diet on inducing overeating behaviour. (i'm not planning on conducting experiments, rather looking at the findings in the literature). In general, I'm hoping to get impressions of 'experts in the field' as to what researchers generally use and why...
In the clinical world, GLP1 agonists and SGLT2 inhibitors are not commonly co-prescribed, though given the benefit of weight loss, cardiovascular benefits, and blood glucose control in patients with insulin resistance as well as obesity, should this be more commonly used? Thank you!
As per available records, PCOD develops due to imbalance of the two female hormones (estrogen and progesterone) where estrogen taking the upper hand.
Common symptoms are:
1. Menstrual irregularities,
3. Increased risk of Endometrial (inner lining of the uterus) cancer,
4. Increased risk of Breast cancer,
5. Insulin resistance,
6. Obesity and increase in weight (mainly around the waist),
7. Unwanted excess hair growth on face and body,
9. Dark pigmentation of skin around the neck etc.
What are the actual reasons works behind development of that dangerous disease?
Is it curable?
How can it be prevented?
Diabetics is attacking millions in the universe, magnesium deficiency has been linked to insulin resistance, which is central to the development of type 2 diabetes, research shows. On the flip side, increasing your intake of magnesium has been shown to possibly lower your risk of developing the chronic disease. Research suggests consuming 100 milligrams (mg) of magnesium through eating foods rich in the mineral may decrease the risk of diabetes by 15 percent. Researchers noted more study would be needed before recommending a magnesium supplement to prevent diabetes.
Not as many studies have looked into the relationship between type 2 diabetes and magnesium once you have already been diagnosed, though one study published in August 2015 in the World Journal of Diabetes noted that people with the disease who are deficient in magnesium may be more likely to have complications, such as issues with heart health. According to the Centers for Disease Control and Prevention (CDC), people with diabetes are about twice as likely to die of heart disease as people without diabetes.,but now what is link between diabetic and magnesium?
I would like to measure Hepatic insulin sensitivity both in vivo and cultured cells. Thus, I am looking for new methods other than traditional previous approaches such as (glucose clamp, IPGTT, IPITT, radiolabeled 2-deoxyglucose).
Your cooperation is highly appreciated.
I'm asking for the most common PAI-1 gene polymorphism related to metabolic syndrome or any of its Pillars ( diabetes - obesity - insulin resistance ).
i need RS and the primer.
Fructose is found in many processed foods and beverages
There are putative mechanisms for Insulin resistance, induced by fructose
eg https://www.mdpi.com/2072-6643/9/3/230 see diagram from article
Its association with complications of insulin resistance, eg NAFLD [fatty liver] and the potential magnitude of its health effect on populations should point us to regulating its usage.
Should we be doing more to control the use of fructose: is there enough evidence?
So, let's say some subject body presented these characteristics:
- β-cell life-span increased (SOD, Cat, GSH-Px expression increased, no abnormalities with them afterwards)
- β-cell insulin secretion increased (increased cell signals)
- GLUT4 expression increased and thus, achieving cell insulin resistance reduction (I have written GLUT2 before, but it was a typo)
- All of the above bringing the blood glucose to somewhere between 60 - 99 mg/dL (2 hours or so, after meal)
Given the subject is a T2DM affected, if the above could be achieved, can the subject be considered as cured?
It is easy to find references about diabetic-hypertensive animal models, but hard to find some infomation about the cell model. In addition, I may focus on type 2 diabetes with insulin resistance more than other types of diabetes.
I've find a phD dissertation named In Vitro Diabetic-Hypertensive Cellular-Response Evaluation Model for In-Stent Restenosis, which used FlexCell-3000TM system (Flexcell International, NC) and a peristaltic pump (Cole-Parmer) to help building the cell model. Since my lab doesn't have these machine, I would like to know whether there are other useful methods. Any idea about this topic is welcome. :)
Hello there, genotype matters is not something I know much about, so I decided ask about my situation here hoping that I could get some insights.
I am working on some immune receptor and I am using 2 KO strains; one obtained by CRISPR and the other one is more traditional ES mice. Apart from that, the strain (C57), diet, age, gender, housing... Everything is the same! Interestingly, these 2 KO mice show different metabolic phenotype. One put more body weight, more insulin resistance, etc. than other counterpart.
I am really confused what might be the reason to that. Is it do you think some changes by the CRISPR off-target effects?
I am talking to a sequencing service. Maybe I will send some samples for whole-genome sequencing, but it is pretty expensive. Do you think how many mice do I need to sequence for a healthy comparison? 1 from each enough? Or is there any other way you could suggest apart from sequencing?
I appreciate any comment, thank you very much.
Why is polycystic ovary syndrome (PCOS) rising all over the world?
The role of hyperglycemia, saturated fatty acids, oxidative stress, inflammatory cytokines have been investigated in causing insulin resistance. However, is hyperinsulinemia itself not likely to cause insulin resistance as a negative feedback mechanism?
Are all patients with congenital generalized lipodystrophy suffer from insulin resistance or it is a consequence that could happen later in the course of the disease?
Previously there has been evidence to suggest an inflammatory response to endotoxaemia inhibiting the insulin signalling cascade. Is there any new evidence either way supporting or conflicting this potential metabolic effect through the gut?
I am having problems with my animals, because they aren't insulin resistance.
I started giving HFD 60% (54% land and 6% oil) for them with 6 week old and with 12 weeks of HFD they are not insulin resistance. I'm using C57Bl/6J mice and I have already found many articles in literature that use this model and they become insulin resistance, in some cases with 8 weeks of high-fat feeding.
What could be happening? I'm really woried, because they need to be insulin resistance for me to start the treatment with a ligand!!
According to common soil hypothesis metabolic diseases are associated with each other due to underlying insulin resistance.
What is your take on that?
I am looking for papers or evidences for loss of insulin receptor in case of diabetes. I am interetsed to know more about insulin resistance development based on insulin receptor loss. Please give your comments on the same.
Thanks and reagrds,
Diabetes mellitus has two distinct but quite differet forms. Type 1 due to lack id insulin production and type 2 an excess of glucose that insulin production can no longer control. Insulin resistance is cited as an issue when the physiological issue is too much glucose. Until glucose consumption is targetted in the management of type 2 diabetes mellitus, the underlying cause will not be addressed, contributing to phararmacologic and surgical interventions when diet modifiction is what is needed
I would like to induce diabetes in swiss mice by fructose in the drinking water, but it is hard to find literature about it. Protocols are scarce. Also, in the studies that have attempted the protocols vary too much regarding the lenght of time to induce diabetes and fructose concentration. Also, does anyone knows if there are differences in the time to achieve glucose/ insulin resistance among male and female mice?
I had met with the statement that Alzheimer's disease is type 3 diabetes and that the insulin resistance damages brain cells. While in the literature the brain is described as an insulin independent organ.
What is your opinion?
Do you know some papers that can dispell doubts?
Does anyone have papers relating fasting insulin levels and associated CVD risks?
I would like to calculate the hepatic insulin resistance index proposed by Abdul-Ghani et al., (2007) using the following formula with values from an OGTT:
HIRI = (glucose0–30[AUC] x insulin0–30[AUC]).
I have calculated the AUC between baseline and 30 minutes using the trapezoid rule, with glucose expressed in mmol/L and insulin expressed in pmol/L. Is this correct? or do I need to use other units of measurements?
I am asking this questions as I have seen this formula used in numerous research articles but there is great discrepancy between the results in each.
Thank you in advance.
Insulin resistance condition in which the receptor is mutated is it just a feedback mechanism of less use of ATP??
Insulin resistance is considered as an important contributor, if not he sole cause of PCOS. But i believe there must be other tangible factors which cause insulin resistance. There are features of ladies and young girls which have all features of PCOS but no insulin resistance. Yes congenital adrenal hyperplasia can be one but still there are patients with PCOS like symptoms but no insulin resistance.
So what else can cause such features?
Insuli-Resistance and 2NBDG glucose uptake
Does the increased levels of Insulin is always associated with Insulin resistance?
What are the best studies in this field?
i have read several articles and there were contradictions. The main problem was about adipose tissue and obesity. As adipocyte grows, it would secrete MCP-1 or other adipokine that attract macrophages. Consequently attracted macrophages would secrete various inflammation cytokines such as TNF-alpha. Those cytokines would decrease insulin sensitivity in adipose tissue and muscle. On top of that it would also decrease ppar gamma gene expression and increase lipolysis. As a result concentration of free fatty acid increases. However, the obese are getting more fat and have a larger adipose tissue than lean subject or mouse. Can anyone solve this contradiction
I have to measure the lactate concentration in mouse blood over time. There seems to be several lactameters on the market (more or less similar to glycometers), however, the manufactures are not typical lab providers. Thus, it is difficult to know which to go for/trust.
As diabetes (type 1 diabetes and type 2 diabetes) is metabolic disease and very complex, it involved in dysregulation of carbohydrates, proteins and fats metabolisms. So, there is macro- & microvascular complications in the body like cardiovacular problems, coronary artery diseases, retinopathy, nephropthy and peripheral neuropthy, some others etc, furthermore, its mechanism involved hyperglycemia, insulin resistance and some other factors responsible for these complications. Please provide review articles and publications latest to cover all these situations.
Beyond checking Glycated hemoglobin (Hb A1C) I want to start checking both glycated albumin and insulin. Glycated albumin will indicate the risk of rising amounts of ionized calcium; glycated insulin will establish the risk of insulin resistance that develops into type II Diabetes
Whether diabetes management is a problem but there is lack of diagnosis of complications, how should it be emphasized on the early basis and manage with special criteria. i think many factors are there if we restricted hyperglycemic control and insulin resistance, there are unknown factors that can cause these problems with restricted control too, so if early diagnosis is made then there is chance to further inhibit the complications of diabetes.
Is it possible for insulin sensitivity to change within 5 hours of consuming an antioxidant nutritional intervention?
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?
I am currently studying the db/db K strain and have a project with updates regarding my transmission electron microscopic findings
and I have found that in this obese insulin resistant model with persistent elevations of glucose making it a definite type 2 DM model that has preexisting obesity and insulin resistance that the astrocyte
become separated from the NVU Endothelial basement membrane and become retracted as well. These TEM finding obliterate the normal astrocyte corona as found in control models regarding studies of the NVU (neurovascular unit). Do you think these findings are compatible with impaired signaling of the other NVU in the midbrain cortex as in my project findings.
M. R. (Pete) Hayden, MD
firstname.lastname@example.org - if you would prefer to answer by e-mail correspondence.
Some researchers claim that it happens, some other not.
What analytes will you be recording? Will you be recording blood type; insulin resistance; urine ketone levels; glycated albumin; would you consider dong an OPG [panoramic- x-ray of the mandibles]; HS- C reactive protein; triglycerides?
1- How can insulin resistance be measured in diabetic rats?
2- Why is HOMA-IR not valid for rodents?