Science topic

Diabetes Mellitus - Science topic

Diabetes Mellitus are a heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.
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what is the common cause of adhesive capsulitis in patient with diabetes mellitus? what are the managment options available for the same.
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Chronically high blood sugar levels cause sugar molecules to attach to collagen. Collagen is a major protein that makes up the connective tissue that holds your joints together. When the sugar attaches to the collagen, it gets sticky, so movement becomes restricted and the shoulder stiffens and is painful.
Best treatment for adhesive capsulitis after a trial of physiothaerpy is a distension arthrogram under image intensifier control.
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Due to its continuously increasing occurrence, more and more families are influenced by diabetes mellitus. Most diabetics know little about their health quality or the risk factors they face prior to diagnosis.
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Good Day
Greetings
Do any have observation that topical glucocorticoid (clobetasol) very prolong (over 10 years) use hand dermatitis can cause Diabetes Mellitus?
Regards.
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Please give a simple brief summary
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Causes:obesity,unhealthy diet,alcohol consumption,inactive life style,Age as crucial role&inherited genetical factor.
Prevention:reduce carb. intake&excess weight,,drink alot of H2O,excersise regularly,Quit smoking,&follow high fiber diet.
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The use of statins have been associated with the onset of diabetes mellitus in persons with risk factors for DM. In persons trying to reverse diabetes, in your experience, has the use of statins prevented or reduced the rate at ehich this DM reversal would occur?
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In many statin studies a small increase in glycemia is noted under statins which does not necessarly mean development of diabetes.
The very significant protective benifits of statins are also found in patients with diabetes, even more than in patients without diabetes.
The clinical significance of the increased glycemia is unclear. It is not an argument to omit statines in a good indication.
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Am looking at hla 2 association with diabetes mellitus and one of my objectives is to study the distribution of the alleles in my study group plus controls. What else can I do? Please help
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What are different types of anemia?
what is their molecular level description?
How anemia is caused?
What is the relationship between anemia and diabetes?
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Some researchers suggest starting an anti-diabetic treatment after 1-2 weeks of the Streptozotocin injection (single injection) in rodents models, indicating that this will mimic a later-stage of diabetes. While others suggest that there is no need to wait such time and start the treatment immediately after the confirmation of diabetes. I’m quite confused which is the best time to start the anti-diabetic treatment? is the time post the confirmation of diabetes really mimic the diabetes stages in human?
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Three days after administration of STZ to albino rats, I found them exhibiting almost all symptoms of diabetes II and a check using accu check glucometer found them to be diabetic and treatment commenced same day.
Good luck.
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Malaysian and NonMalaysian all are welcome. Sarawakian highly recommended.
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Thank you very much drs, academician team and researchgate community. Highly appreciated
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I would appreciate if you can answer whether you prepare glucose solution for injection in mice in NaCl solution or just in water and why!
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I hope this link is helpful
DOI: 10.3791/56672
Regards
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We are performing an antidiabetic assay by inducing alloxan in rats and we have to share with metformin, glibenclamide, or actrapid for the positive control.
Which of these three drugs is the best to use?
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Dear Nantenaina, thank you for sharing this very interesting technical question with the RG community. For streptozotocin-induced hyperglycemia please have a look at the following potentially useful article:
Glibenclamide or Metformin Combined with Honey Improves Glycemic Control in Streptozotocin-Induced Diabetic Rats
(please see the attached pdf file)
Also see the following interesting paper: Comparative effects of glibenclamide, metformin and insulin on fetal pancreatic histology and maternal blood glucose in pregnant streptozotocin-induced diabetic rats
This article has been posted by the authors as public full text on RG. Thus you can freely download it as pdf file. Good luck with your research and best wishes!
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Unbooked primigravida diagnosed with diabetes mellitus of 3 years duration and defaulted on taking her medication, presented with IUGR, was delivered of female infant of 1.7 kg at term. The mother has no renal pathology and the baby has no congenital anomaly.
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vasculopathy due to DM
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Does diabetic patients need to control their blood sugar before taking COVID-19 vaccine or patients with very high blood sugar can take COVID-19 vaccine safely ?
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Please check the following RG link.
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Allosteric binding sites are different from the active sites. If insulin receptor has this characteristic then it will be easy to target the receptor in insulin associated disorders.
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Yes, the insulin receptor has allosteric binding sites as described in this article (1). It is also possible to block these receptor sites by a human, allosteric monoclonal antibody (2).
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Hello all,
I want to assess the social burden of Major Non-communicable diseases (Diabetes Mellitus) and which instrument will address the societal burden of the diseases.
thanks in advance for the genuine support and advice.
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Dear Israel,
There is a wealth of literature on direct nd indirect costs of diabetes fort he individual and society alike. Two years ago, a good review has been published by Einarson TR, Acs A, Ludwig C, Panton UH (DOI:https://doi.org/10.1016/j.jval.2017.12.019 ), but there many more, worth being read, e.g.:
Zhuo X, Zhang P, Hoerger TJ. Lifetime direct medical costs of treating type 2 diabetes and diabetic complications .Am J Prev Med. 2013 Sep;45(3):253-61. doi: 10.1016/j.amepre.2013.04.017
Walker I et al. The Economic Costs of Cardiovascular Disease, Diabetes Mellitus, and Associated Complications in South Asia: A Systematic Review .Value Health Reg Issues. 2018 May;15:12-26. doi: 10.1016/j.vhri.2017.05.003. Epub 2017 Jul 3
Hex N, Bartlett C et al, Estimating the current and future costs of Type 1 and Type 2 diabetes in the UK, including direct health costs and indirect societal and productivity costs. Diabet Med. 2012 Jul;29(7):855-62. doi: 10.1111/j.1464-5491.2012.03698.x
Finally, there are quite many papers on costs in certain regions….
If you go thru these, I am sure, you find enough papers in the references to get more informations that will allow you estimates for your specific questions,
best
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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?
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Perhaps the “ESPGHAN/ESPEN/ESPR guidelines on pediatric parenteral nutrition: Carbohydrates” and related publications provide the appropriate and practical instructions for glucose infusion in children [1]. Excessive chronic glucose infusion may lead to hyperglycemia, which leads to increased lipogenesis and adipocyte fat deposition along with subsequent hepatic steatosis, elevated hepatic VLDL triglycerides, hypercholesterolemia, and may ultimately cause insulin resistance (IR) [1]. The magnitude of this effect depends individually and is affected by pre-existing metabolic stress or disease [1]. The gold standard for determining IR is the euglycemic–hyperinsulinemic clamp technique [3]. This method is considered invasive, costly, and impractical for large samples. Despite its modest specificity and sensitivity, HOMA-IR is used as an IR surrogate and alternative index in a large number of studies, including those dealing with children [4]. Other IR indexes with varied specificity and sensitivity, as well as purposes, are available [3,4].
References:
[1] Mesotten D, Joosten K, Kempen A, et al. ESPGHAN/ESPEN/ESPR guidelines on pediatric parenteral nutrition: carbohydrates. Clinical Nutrition, 2018; xxx: 1-7. http://dx.doi.org/10.1016/ j.clnu.2018.06.947.
[2] Sanchez-Garc´ıa A, Rodr´ıguez-Gutierrez R, Mancillas-Adame L. et al. Diagnostic accuracy of the triglyceride and glucose index for insulin resistance: a systematic review. International Journal of Endocrinology, 2020; ID 4678526, 7 pages. https://doi.org/10.1155/2020/ 4678526.
[3] van der Aa Marloes P, Catherijne AJK, Anthonius dB, et al. Definition of insulin resistance affects prevalence rate in pediatric patients: a systematic review and call for consensus. Journal of Pediatric Endocrinology and Metabolism, 2017; 30(2):123-131.doi:10.1515/jpem-2016-0242.
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Alloxan or streptozotocin is a common agent used for induction of diabetes mellitus in rodents. From my experience, not all rats administered alloxan or streptozotocin developed diabetes mellitus. In most cases, this cannot be attributed to drug-/administration-related factors such as potency, underdosages, route of administration, wrong administration, etc. Are there studies that have investigated the resistance of these agents in some rodents? Are there scientific explanations or reasons for this resistance?
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What I have noticed generally is that, conventionally there's no standardised dose. Inconsistent outcomes have been repeatedly reported. I hope a study into the molecular mechanism is done to confirm the underlying causes.
This article relorted similar thing.
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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?
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An observational study from the Nurses Health Study51 that included 83,779 women > 20 years of age found an increased risk of type 2 diabetes in those with low vitamin D status. A combined daily intake of > 800 IU of vitamin D and 1,000 mg of calcium reduced the risk of type 2 diabetes by 33%
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Discussion on the best options for management of hypertension, T2 diabetes mellitus in the context of macroalbuminuria is sought to get an insight into the matter.
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I would definitely include SGLT-2 inhibitors in the treatment algorithm early on in the care of such patients.
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As a public health measures to control the spread of the pandemic coronavirus, social distancing and home quarantine are implemented in some countries.
As a matter of fact, patients are absence from clinic under COVID-19, and clinic-based diabetic control monitoring becomes challenging.
Do you expect a change in diabetic control for these patients when staying home?
They have less exercise, and may eat more snacks at home.
Or in contrast, they are too bored, and have time to develop new exercise without pressure from work? Besides, they are banned from social around, and may eat drink less alcohol and eat less feast.
What do you think?
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COVID-19 will increase vascular complications
Coronavirus associated with respiratory distress and ph changes Both Quarantine &Thinking increase stress hormones so more oxidations Limited Exercise will increase blood glucose level
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Can anybody suggest me one/more plant names for doing project either in alone or combination therapy of diabetic mellitus, wound healing and anti oxidant property?
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I´m doing research on adherence to lifestyle and medication in Diabetes Mellitus Type 2 patient. I have trouble with finding the following questionnaires. I would be grateful if someone could help me with this.
o Cologne Patient Questionnaire (CPQ)
o Autonomi Preference Index (API)
o Decision Conflict Scale (DCS)
o Sherer General Self-Efficacy Scale (SGSES)
o Psychometric Evaluation of the Adherence in Diabetes Questionnaire (ADQ)
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In case you are still looking for the Cologne questionnnaire. The German version can be found here:
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1) could I use chi-square for one nominal and one ordinal variable or it uses only for nominal variables? 2) if I have only positive result can I find p-value in variables e. g. Finding relation between positive diabetes mellitus with respect of gender, race and.... Or I should report them as frequency without mentioning p-value?
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This looks more like a case where you would use logistic regression if you had a sample with and without D.M.
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We have now tried a number of commercially available antibodies to detect the receptor of AGEs (RAGE, sometimes called AGER) in parrafin embedded mouse tissue with DAB staining. As a control we have used corresponding tissues of a RAGE-KO mouse. Whereas most of these antibodies worked well in lung tissue that accumulates RAGE to a high amount, we have faced significant problems when using tissues that express only minor amounts of RAGE. In particular we observed cross reactivity with muscle cells. If anybody has had good results using an anti RAGE antibody for IHC in mouse tissue please let us know!
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Anyone has recommendation for human Rage WT antibody?
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Genomics of diabetes mellitus......can this in anyway improve nursing care for diabetic patient?
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@ uzma.... Thanks for your on the subject matter.
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n/a
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Please take a look at the following RG link.
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I need a technique or procedure that accurately diagnoses the type( I or II ) of diabetes mellitus in experimental albino rats
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I agree with you Marine, type1 manipulated by alloxan or STZ, and type2 only genetic model, even used of high fat diet could not results in type 2. But I need to highlight some studies findings in literature used alloxan or STZ and treated as type2. Also I have different idea about high fat induced hyperglycemia. If you are interest to discuss, this is my email: amarqqqu@yahoo.com.
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Diabetes mellitus type2 induction in experimental animals involves a biochemical link between diet and a chemical like streptozotocin. Is it possible to achieve the same result with a high-sucrose diet with streptozotocin and high-sucrose-high-fat-diet with streptozotocin?
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The addition of high fat diet accelerate the development of this type 2 diabetes experimental model due to pancreatic beta cells lipotoxicity, on the other hand, it may increase the plasma levels of lipids and the accumulation of fats in different tissues (in particular the liver).
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Good greeting,
The dental implant became one of the routine dental clinic work, and further patients with diabetes mellitus asking for dental implant.
Best wishes
Sarmad
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It depends whether the patient is poorly or well controlled. For uncontrolled patients, it is well known that Diabetes Mellitus (DM) jeopardizes periodontal health and is also a significant risk factor for dental implant failure. The explanations for this are:
1. The chronic hyperglycemia increases the formation and accumulation of glucose‐mediated advanced glycation end products (AGEs) in the periodontal and systemic tissues in patients with poorly controlled DM. These AGEs play a role in the pathogenesis and altered periodontal wound healing by activating the receptors for AGEs (RAGE) located on the periodontium.
2. The endothelial cells take up glucose passively in an insulin‐independent manner, thereby causing tissue damage.
3. The chronic hyperglycemia has also been associated with alterations in host resistance by defective migration of polymorphonuclear leukocytes, impairment in phagocytosis and exaggeration in inflammatory response to microbial products.
These factors may also be held responsible for the increase prevalence of peri‐implant diseases (peri‐implant mucositis and peri‐implantitis) in patients with poorly controlled DM as compared to nondiabetic controls.
For controlled DM patients, however, the recent studies that has been conducted to determine whether dental implant can remain functionally stable in patients with DM concluded that in patients with well‐controlled DM, dental implants can remain functionally stable in a manner similar to nondiabetic individuals. Optimal glycemic control plays a role in the long‐term survival of dental implants.
You can find further details of the studies conducted on this topic in this reference:
Fawad Javed and Georgios E. Romanos. Evidence‐based Implant Dentistry and Systemic Conditions, 2018. Chapter 9 “Dental Implants in Patients with Diabetes Mellitus”.
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After exposing rats to low fructose water(10%) for 2 wks and a single intraperitoneal injection of STZ (55mg/kg bw), to induce T2D, I want to compare the hypoglycaemic effect of my crude plant extract with a known standard drug.
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Thank you
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I am looking for other diagnostic marker for Type II Diabetes Mellitus. We are currently studying leptin as one of the potential diagnostic marker of this disease.
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Adiponectin, resistin and visfatin
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I work on a project to treat diabetes mellitus and need to make mouse xiabetic mouse to apply my matterial .
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Abbas Latif depending on which type you want to induce 1 or 2 you have your answers
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1 - Can continous stress induce high glicemic rates in humans and trigger diabetes type1 ou 2? How those possible stress induced problens are related to age? Can those high glicemic rates or diabetes be controled or cured by eliminating stress?
2 - Which type of individuals (comportamental behavior – fleumatic, coleric, introspective, .....) are more sensitive to high glicemic rates due to stress?
3 - Is there any conclusive study showing inducing diabetes or glicemic discontrol in humans by stress?
4 - Can high glicemic rates induced by stress or other metabolic problem be confused with diabetes melittos in children and juvenile populations?
5 - Which types of blood indicators and/or organs images (liver, pancreas, and so on) are important to assure that the diabetes mellitus be present in children and juvenile populations
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No, since in the first case there will not be antibodies involved and C-peptide would be probably high.
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There is little available information regarding the evolution and outcomes of patients with diabetes mellitus who acquire leishmaniasis, tegumentary or visceral. We are documenting a series of cases but we have been able to found significant references on that looking at medline, SCI, Scopus, SciELO and LILACS databases.
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We are the one need the link. Thanks for kindness share paper and links.
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Thank you very much Muhammad Adnan
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How can I know if in a paper they are talking about gestational diabetes (the condition what starts during pregnancy) or gestational diabetes mellitus (women who had diabetes mellitus before being pregnant?
I have seen that in some papers they talk about gestational diabetes mellitus as the condition that appears during pregnancy and sometimes about women who had DM before being pregnant. Or the two conditions are equal?
Thank you for your help
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mrs Alejandra Loyola Leyva may I read you paper on this topic for reference. Thanks for your kindness
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rapid progress is acheived in the field of diabetes researches and techn ologies. is it time to make use of revolutionary sciencessuch as proteomics,transcriptomics, metabolomics and exposomics. Associating all these multidisplinary sciences in a unified system may transform healthcare for diabetes mellitus patients including novel molecular biomarkers, new diagnosstic and therapeutic modalities.
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آسف السؤال ليس من اختصاصي
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Can Metformin use as a medicine for breast cancer?
What are the advantages and disadvantages of using Metformin in patients with breast cancer?
Is it possible to use Metformin for both diabetes mellitus and breast cancer?
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There is no known medication or therapeutic technique that is able to completely prevent malignancies, oral or otherwise. Anyone who claims that metformin completely prevents Breast cancer is either a misinformed medical lay person, or a quack practitioner.
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I am completing my M.D. in Biochemistry from JIPMER Puducherry. After this i want to work in the field of diabetes mellitus especially to understand the mechanism behind its complications.
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Hello dear.
In india, several labs such as CDRI, CSIR and ICMR are doing well known research in the field of diabetes.. To my best knowledge, Madras Diabetes Research Foundation (MDRF) is now recognized worldwide as a premier research institute for diabetes and its complications. Also they have collaboratory work with leading institute (Mayo Clinic, Rochester, U.S.A.,University of Minnesota, USA and University of Texas Southwestern Medical Centre, Dallas etc.).
We are also doing research on antidiabetic drugs and their mechanism of action..
With regards
Dharmendra Arya
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How do we tackle diabetes 2?
Obesity and diabetes are the two most debilitating and insidious diseases; and its scientifically proven, beyond any reasonable doubt, that its largely due to unhealthy lifestyle choices. In that case isn't it imperative to bring general awareness to the public about inculcating a healthy lifestyle?
Ultimately where should the lime light be focused - the never ending research or stressing on the dire need to switch over to healthy diet and active lifestyle?
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Diabetes is a metabolic and lifestyle disorder & it can be well controlled by adopting Healthy dietary pattern together with physical activity.
Following Published report discuss all the Ayurvedic dietary and lifestyle guidelines for prevention of type 2 diabetes and available factual research evidence validating it.
We also attempted several investigations to explore the role of Yoga and meditation in diabetes...Many documented works are under publication process...The following is one among our published reports in pubmed....
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A1c is now routinely recommended for diagnosis of diabetes mellitus. However, I feel A1c variation owes a lot to patient & technology specific factors. So can u generally share our experience for diagnosing DM with A1c?
Regards
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Hi Sikandar,
I cannot speak to the use of HbA1C kits as I have not used them myself, but the current literature has identified important variables based on the kits used. For the full list, refer to the following paper:
However, I did want to comment on the patient-specific factors to which you referred. Generally speaking, measuring the A1C is a great way to estimate circulating glucose levels over the past 7-8 weeks; this diagnostic window is defined by the half-life of red blood cells. In contrast, measuring a patient blood glucose is highly dependent on the time of day, their fed/fasted status, stress level, etc... For this reason, two separate recordings of fasting blood glucose are required to make a diagnosis, whereas only a single measurement of A1C (>6.5) is needed to diagnose a patient with diabetes mellitus.
You implied that exceptions exist, which is true, but is primarily based on the half-life of red blood cells. For example, patients with various forms of hemolytic anemia (G6PDH, Sickle cell, etc...) have a falsely reduced level of A1C. Other patient variables that reduce A1C include pregnancy, splenomegaly, and certain medications.
In contrast, patients receiving a blood transfusion are likely to have a higher-than-expected A1C (though this is probably based on the hyperglycemic transfusion media). The list continues, with uremia, hypertriglyceridemia, asplenia, etc...
So clearly, interpreting an A1C measurement for any patient requires context. However, lacking better alternatives, it is a great way to determine whether patients are at high risk of developing end-organ complications of chronically-elevated hyperglycemia.
Refer to this great write-up for more information on A1C measurement variability.
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I am working in area of diabetes mellitus. For in vitro study on pancreatic beta cell , we try to maintain RIN5F cell line. So, I want information about doubling time period for RIN5F cell.
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Here is the product sheet for the cell line. I do not see doubling time within the document, but tumor derived cell lines usually need to be split once a week or so. It does suggest changing the media every 3-4 days and doing a cell splits at a ratio between 1:3-1:6. Does this help? Do you have further questions?
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Fasting hyperglycemia and diabetes mellitus;
In clinical laboratory practice I had seen so many cases of type-II diabetes mellitus who gets a diagnosis of diabetes mellitus based upon raised fasting glucose but once u subject them with glucose load they easily manage there load. No doubt that fasting hyperglycemia is not not normal but i guess relying simply on fasting hyperglycemia, we may be overdoing the diagnosis part and in my personal opinion i feel w-hour postprandial glucose tolerance in an other wise healthy subject with any GIT pathology must be given to all subjects. Another thing which i have realized that once these subjects with fasting hyperglycemia reduce theri liver fat, they can overcome fasting hyperglycemia.
So fasting hyperglycemia and postprandial glucose tolerance are two varied concepts and the latter is a serious category. Then even thin, lean sometimes show poor glucose tolerance. And to me the latter category is worrisome rather than isolated fasting hyperglycemia.
So anybody wishes to comment on this? OR explain OR give some reasoning behind this?
Warm regards
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Dear All, I am trying to apply data mining and machine learning techniques in diabetes prediction. Therefore, I need more data.
I understand that, there is a Pima indian and UCI database. But this not enough, what i need.
The required data can be
e.g., Age, sex, glucose, LDL, HDL, BMI, HbA1C and other variables and short and long term outcome of the subject. Outcome can be defined by good and poor outcome.The poor outcome can be chronic disease or CVD.
I would like to collaborate.
Your cooperation will be highly acknowledged.
Waiting to hearing from you.
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Dear Md.abdul Awal,
Maybe you already know the following article and data-link on the subject:
Kavakiotis I, Tsave O, Salifoglou A, Maglaveras N, Vlahavas I, Chouvarda I. Machine Learning and Data Mining Methods in Diabetes Research. Comput Struct Biotechnol J 2017;15:104-116. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5257026/pdf/main.pdf
Selected Trend Table from Health, United States, 2011. Diabetes prevalence and glycemic control among adults 20 years of age and over, by sex, age, and race and Hispanic origin: United States, selected years 1988 - 1994 through 2003 – 2006: https://catalog.data.gov/dataset/selected-trend-table-from-health-united-states-2011-diabetes-prevalence-and-glycemic-contr-63c3a
All the best for your research,
Martin
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Diabetes induction
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Following
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Chromuria happens with DM
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Dear Entedhar, thanks for your answer;
what happens in the body?I know chromium level in urine increases, so the bodies is losing chromium with diabetes. I want to know the extent of chromuria (in µg chromium/gram creatinine) and the relation with DM.
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HbA1C shows the previous glycemic status of a patient this is understood but can it be a predictor of some other conditions where glycemic status is normal but HbA1C levels show elevations ?
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Variable effect on HbA1c:
· Fetal hemoglobin
· Methemoglobin
· Hemoglobinopathies
Inappropriately low HbA1c:
· Hemolysis
· Hemoglobinopathies
· Red blood transfusion
· Acute blood loss
· Hypertriglyceridemia
· Drug Chronic liver disease
Inappropriately high HbA1c:
· Iron deficiency
· Vitamin B12 deficiency
· Alcoholism
· Uremia
· Hyperbilirubenimia
· Drug
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Does Sugar Feed Cancer? Exploring the Sugar and Cancer Connection
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Because if consume too much, it can cause many diseases, such as diabetes which damages one person's health....
Here, people are talked to eat or drink less sugar- or fructose-added foods or drinks.
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I'm doing a research to reveal the effect of gestational diabetes on stem cells number and comparing with the non-diabetic group.
and what is the sample size formula for it?
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cross-selectional is preferable.
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Patient who is age of 65 is suffering from Hyperglycemic Hyperosmolar Nonketotic Syndrome has elevated levels of Potassium levels on serum electrolytes, But has total body potassium depletion ?
what is the mechanism ?
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In HHS , there is insulin deficiency which causes hyperglycemia , but adequate production to prevent ketosis ( different from DKA in T1DM , in which there is no insulin production ) . Insulin deficiency causes efflux of potassium from the cells causing hyperkalemia . In addition , volume depletion due to osmotic diuresis causes AKI which can cause hyperkalemia . T2DM can cause hyperglycemia due to insulin resistance & later insulin deficiency , which can cause HHS .
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Dysmenorrhea is the commonest complain in the female adolescents and affects their regular activities .It is the leading cause of absenteeism from work place, school and college, limitation on social and sports activities among that population. In some places government provided 2 days special leave for women employees. But they rarely use it for this purpose. In our state Bihar also, Bihar state government provide 2 days special leave for women
In our study 200 women between age group of 17-25yrs., participated from my clinic after getting their consent. They were not suffering from hypertension, Diabetes mellitus renal or hepatic disorders .Detail history was taken. Height and weight were recored.
2 dayU(��N "
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Dear Chandan,
It's a cross-sectional study. If you are performing both descriptive and inferential analysis, you may be more specific to say it's a descriptive-analytical cross-sectional study. Indeed, prevalence studies simply means cross-section in nature.
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The topic of my research proposal is Knowledge Attitude and Practice (KAP) about lifestyle modifications among type 2 diabetic patients attending Federal Medical Centre Katsina.
Objective
To assess the Knowledge, Attitude and Practice on life style modification amongst outpatients attending Federal Medical Centre Katsina Diabetes Mellitus clinic.
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important information, thank you
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Looking for a portable ketometer for use in dogs and cats, evaluated with a clinical trial.
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Thank you so much for the answer but I think these two studies evaluated the same sensor (Medisense Precision Xtra, Abbott) , that here in Europe is named Optium Exceed.
Thank you anyway!!
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Hypertensive patients with diabetes mellitus 2 type have more often and early renal dysfucntion due to negative influence of 2 diseases. There is a cut-off of kidney function according to GFR - lower then 60 ml/m2/1.73. But what about hypertensive patients with diabetes with 60-89ml/m2/1.73 - with mildely decrease GFR?
In patients with this GFR level can we declare about kidney organ damage?
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Dear Singh Shivakumar,
good message. I agree with you that we should start treatment even stage 1 CKD, Because it is really as preclinical target organ damage. Also if Proteinuria with normal GFR is stage 1 CKD should be treated with first line ACEI or ARB. Main goal erly start treatment - to prevent progression of CKD. Thanks.
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I would like to know where I can get diabetes data with information about patient. Thank you in advance!
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i don't have the details, but Sweden system has very comprehensive Diabetes dataset.
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Is it 10hour or 12hrs time period for finding exact blood sugar level and evaluating lipid profile.
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For fasting blood glucose 8- 10 hrs are suitable. For Lipid Profile you need 12 - 14 hrs are recommended. Its important to clarify that Total cholesterol does not need fasting, In addition, you can calculate LDL-C by Friedewald Equation ( [LDL-chol] = [Total chol] - [HDL-chol] - ([TG]/2.2) where all concentrations are given in mmol/L (note that if calculated using all concentrations in mg/dL then the equation is [LDL-chol] = [Total chol] - [HDL-chol] - ([TG]/5))
The Friedewald equation should not be used under the following circumstances: . fasting, is mandatory for teiglycerides analysis.
  • when chylomicrons are present
  • when plasma triglyceride concentration. exceeds 400 mg/dL (4.52 mmol/L)
  • in patients with dysbetalipoproteinemia
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i want critique questions on this topic
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Epidemiological and basic science evidence suggests a possible shared pathophysiology between type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD). It has even been hypothesized that AD might be ‘type 3 diabetes’. The present review summarizes some of the evidence for the possible link, putative biochemical pathways and ongoing clinical trials of anti-diabetic drugs in AD patients.
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A small percentage of people with Alzheimer’s disease (less than 1 percent) have an early-onset type associated with genetic mutations. Individuals who have these genetic mutations are guaranteed to develop the disease. An ongoing clinical trial conducted by the Dominantly Inherited Alzheimer Network (DIAN), is testing whether antibodies to beta-amyloid can reduce the accumulation of beta-amyloid plaque in the brains of people with such genetic mutations and thereby reduce, delay or prevent symptoms. Participants in the trial are receiving antibodies (or placebo) before they develop symptoms, and the development of beta-amyloid plaques is being monitored by brain scans and other tests.
Another clinical trial, known as the A4 trial (Anti-Amyloid Treatment in Asymptomatic Alzheimer’s), is testing whether antibodies to beta-amyloid can reduce the risk of Alzheimer’s disease in older people (ages 65 to 85) at high risk for the disease. The A4 trial is being conducted by the Alzheimer’s Disease Cooperative Study.
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Is plate method suitable for male and female patients?
How can educate male and females about portion size of plate?
Can plate method used for type 2 DM patient with ideal body weight?
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Hello Ehab!
We educate our population with modified plate method. It is a simple and effective way for nutritional diabetes education. We found good results both male and female. Yo can read our experience in the article.
Greetings,
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Diabetes Mellitus
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Nice Combination
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As Diabetes mellitus type 2 has increased tremendously in the world, so polyherbal formualtion (share some trade or generic names) used in some couuntries. So we should be aware of this if benefits found in some formulations. Many review articles are also available for the support of this kind of activities in plants.
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could any one please explain to me how to estimate sample size for genetic polymorphisms studies in type 2 diabetes mellitus? 
 i need to find two SNPs in diabetes mellitus type 2 patients,but i dont know how many samples i need and how to calculate sample size 
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According to my opinion you should take sample of minimum more than 30 diabetic patients because any statistical test not applicable in below 30 sample. If you increase sample 4 time your precision will double.
If you choosing sample from hospital 
 n=       Z² p(1-p)
        (e)²
Where
Z=confidence level let 95% (standard value of 1.96)
P=Estimated prevalence or proportions or sensitivity of project area
e=Allowed error
If you choosing from all diabetics considering amount of population than
•Sample size for Finite population   :
 K=       n
       1+ (n-1)
    N
Where
K= Sample size
n=sample size due to prevalence or proportions
N=Population size
i think this may helpful for you.
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I have a program that took years to develop on improving healthcare behaviors of patients with diabetes. The program is in both English and Spanish. It’s purpose is to help patients who do not have access to specialists in diabetes or to help diabetes specialist who can not spend all the time necessary for carefully managing the healthcare behaviors of their patients. I am retired and no longer can use the program. It is yours for the asking.
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Dear Dr. Hartz,
We appreciate your efforts and extended offer which I suppose will go along way in reaching out to the under privileged diabetes patient and care givers. I am Kenyan specializing in diabetes and among our greatest challenges are ensuring the underprivileged get equal specialized care as the elite.
Thank you,
Eva 
Email address; wachira.eva@ku.ac.ke
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This is a part of stem cells research project the previews the combination of GLP-1 in DM2 treatment
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No I just want to know a simple method to attach a peptide on mesenchymal stem cells
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Dear sir/madam, I have induced diabetes throgh STZ (90mg/kg) to 2 days old rat pusps, but unfortunately I have observed cannabolism. what may be the reason?
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After STZ injection, pups will develop a Hypoglycemia due to the insulin release from complete destroying of beta cells due to a high dose of stz. Automatically the pups become weak. Due to the weakness of the pups, the opposite get favour.  To avoid this, administrate glucose solution orally. 
Download  following paper it will useful
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 I am interested in determining a patient's post-prandial capacity to release GLP1. Can I use glucose or does it need a meal tolerance test? 
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I found this piece of info to be interesting:
Abstract from the ADDITION-PRO study as published in Diabetes. 2015;64(7):2513-2525
The role of glucose-stimulated release of GLP-1 in the development of obesity and type 2 diabetes is unclear. We assessed GLP-1 response to oral glucose in a large study population of lean and obese men and women with normal and impaired glucose regulation. Circulating concentrations of glucose, insulin, and GLP-1 during an oral glucose tolerance test (OGTT) were analyzed in individuals with normal glucose tolerance (NGT) (n = 774), prediabetes (n = 525), or screen-detected type 2 diabetes (n = 163) who attended the Danish ADDITION-PRO study (n = 1,462). Compared with individuals with NGT, women with prediabetes or type 2 diabetes had 25% lower GLP-1 response to an OGTT, and both men and women with prediabetes or type 2 diabetes had 16–21% lower 120-min GLP-1 concentrations independent of age and obesity. Obese and overweight individuals had up to 20% reduced GLP-1 response to oral glucose compared with normal weight individuals independent of glucose tolerance status. Higher GLP-1 responses were associated with better insulin sensitivity and β-cell function, older age, and lesser degree of obesity. Our findings indicate that a reduction in GLP-1 response to oral glucose occurs prior to the development of type 2 diabetes and obesity, which can have consequences for early prevention strategies for diabetes.
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We have a case where a 13 years old female mixed dog with insulinoma underwent surgery to remove a well-encapsulated insulinoma. After the surgery it was treated with toceranib fosfat (Palladia). Before the surgery this dog had hipoclucemic crysis and after the surgery those still appears more frequently than before. So we want to know if those attacks are real hypoglycemic crisis or are related with hipokalemia so how the serum potassium behaves? Greetings.
  
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Thank you for your answers. We looked for metastases but they must be microscopic or not large enough to be seen on ultrasound. The dose of Toceranib is 75 mg each 48 hours resting the weekends. We have realized that the problem is that one of the cornerstones of treatment, corticosteroids, were not being taken because of osteoarthritis, our patient was taking NSAIDs and stopped taking them due side effects. 
 
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Hello everyone.
I would like to assess insulin signaling in adipose tissue of mice. Do I have to starve animals prior sacrifice or not? Or may I put tissue in proper buffer/medium, right after explant, even if I did not starve animals? Perhaps I can leave adipose tissue without nutrients for a period of time to mimic starvation and then add insulin and after 15-30 minutes assess its action, does it make sense?
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Thank y'all!
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Acarbose or pioglitazone which will be more effective for diabete
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Thanks and appreciate from your all answers
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What are the differences between stz and aloxan diabetogenic agents? Which one is best for inducing type 1 diabetes in mice?
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Thank You sir.
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We are trying to establish a STZ induced T1DM rat model. Usually STZ dosage from most literature is about 50~65 mg per kg and the blood sugar after treatment is around 350~500 mg/dL in SD rat. But the blood sugar of our SD rats all exceeded 600mg/dL within one week. Then we reduced the dosage to 45 mpk and 30mpk, the blood sugar after treatment still exceeded 600 mg/dL within one week. We also used multiple shots like 15mpk for 3 days, the blood sugar raised to 200mg/dL but went back to normal soon. Are our SD rats too sensitive to STZ? Some people used insulin to control blood sugar and body weight on STZ rat, will insulin interfere the efficacy of anti-diabetic drug?
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In my previous study, I used ten week old male SD rats, weighed 250-270 g. The rats were fasted overnight before injected i.v. 45 mg/lg STZ (Sigma, St. Louis), prepared freshly in cold sterile distilled water. After 72 hours of injection, the fasting blood glucose level were measure and the rats with more than 15 mmol were considered diabetes. The rats were survived until end of the study (28 days).
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type 1.5 diabetes is the late onset of autoimmune type 1 diabetes
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Type 1.5 diabetes is a non-official term that is sometimes used to refer to a form of type 1 diabetes known as Latent Autoimmune Diabetes in Adults (LADA). The term type 1.5 refers to the fact that the condition is a form of type 1 diabetes that can share some features that are more commonly associated with type 2 diabetes.
Type 1.5 diabetes is sometimes also called as type 3 diabetes or “double diabetes,” because the adult has aspects of both Type 1 and Type 2 diabetes. Type 1.5 diabetics are said to have “double” diabetes because they show both the autoimmune destruction of beta cells of Type 1 diabetes and the insulin resistance characteristic of Type 2 diabetes. People with Type 1.5 have autoantibodies and gradually lose their insulin-producing capability, requiring insulin within 5–10 years of diagnosis. As their insulin resistance suggests, many people with Type 1.5 diabetes are obese or overweight.
Misdiagnosis as having type 2 diabetes is common. Around 15-20% of people diagnosed with type 2 diabetes may actually have Type 1.5 diabetes.
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i want to know advantages and disadvantages of using streptozotocin and alloxan or any other material beside high-fat dietary
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Male Wistar rats were fed with high-fat diet for 8 weeks, then different dosage of STZ (20 mg/kg, 25 mg/kg, 30 mg/kg) was injected intraperitoneally. Observed the body weight, fasting glucose and 2 h postload glucose for 7 weeks.
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ONLINE ARTCLE:
Heat Therapy With Relevance to the Reversal of NAFLD and Diabetes. J Diabetes Metab Disord 4: 018.
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Thank you for this question.
I knew that exercise training can be a promising target for NAFLD and diabetes treatment, but I did not know that heat therapy may be used to manage NAFLD and diabetes.
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Am starting to collect a small set of diabetes relevant (T1) time series data (movement, blood glucose, sleep, etc.) Have talked to many people who are doing such research, but few people seem to know how to process the data.  Some have suggested ARIMA modelling, perhaps with ML for a variable window, but looking for any ideas or ideally someone who wants to co-author a research paper.  Please get in touch if you have ideas, know relevant papers, or are interested.   Thanks, Dmitri
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Pca has no limiting a priori hypothesis but you must
Be very careful in the choice of variables and statistical units
Relative role so if you have (reasonably) three times of
Blood glucose at 6 12 24 your variables must be g6 g12 g24 and
Your statistical units the different subjects if you have exercise
At lets say 11 15 40 hours who care you add other three variabkes
Named e11 e15 e40 each individual so will be a row vector with his
Correspobding values for each variable pay attention to fill all the
Variables and not to have voids in the matrix then go on (before
Obviously read carefully one of the many existing introductory
Articles or books to pca)
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Does ghrelin level affect the cytokine gene expression in diabetes and prediabetes?
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Induction of diabetes to rats via streptozocin.
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Same as everybody,  it must be prepared fresh.
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I have difficulty in choosing the sink condition for in vitro release of Insulin, which is insoluble at pH 7.4. I red some articles used the combination of tween and cremaphore EL in the release medium for pH 7.4. I am wondering if there is any other way to maintain sink condition. 
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