scholarly journals Implications of Hydrogen Sulfide in Glucose Regulation: How H2S Can Alter Glucose Homeostasis through Metabolic Hormones

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Jennifer Pichette ◽  
Jeffrey Gagnon
Keyword(s):  
Hydrogen Sulfide ◽  
Glucose Homeostasis ◽  
Major Health Problem ◽  
Obesity And Diabetes ◽  
Hepatic Glucose ◽  
Important Regulator ◽  
Glucose Output ◽  
Gastrointestinal Microbes

Diabetes and its comorbidities continue to be a major health problem worldwide. Understanding the precise mechanisms that control glucose homeostasis and their dysregulation during diabetes are a major research focus. Hydrogen sulfide (H2S) has emerged as an important regulator of glucose homeostasis. This is achieved through its production and action in several metabolic and hormone producing organs including the pancreas, liver, and adipose. Of importance, H2S production and signaling in these tissues are altered during both type 1 and type 2 diabetes mellitus. This review first examines how H2S is produced both endogenously and by gastrointestinal microbes, with a particular focus on the altered production that occurs during obesity and diabetes. Next, the action of H2S on the metabolic organs with key roles in glucose homeostasis, with a particular focus on insulin, is described. Recent work has also suggested that the effects of H2S on glucose homeostasis goes beyond its role in insulin secretion. Several studies have demonstrated important roles for H2S in hepatic glucose output and adipose glucose uptake. The mechanism of H2S action on these metabolic organs is described. In the final part of this review, future directions examining the roles of H2S in other metabolic and glucoregulatory hormone secreting tissues are proposed.

The Role of Physical Exercise in Obesity and Diabetes

2018 ◽  
Vol 66 (3) ◽  
Keyword(s):  
Type 2 Diabetes ◽  
Type 1 Diabetes ◽  
Glycemic Control ◽  
Physical Exercise ◽  
Treatment Guidelines ◽  
Treatment Guideline ◽  
Obesity And Diabetes ◽  
Regular Physical Exercise

The prevalence of obesity is increasing world-wide. Obesity is associated with a plethora of metabolic and clinical constraints, which result in a higher risk for the development of cardiovascular complications and metabolic disease, particularly insulin resistance and type 2 diabetes. Obesity is an acknowledged determinant of glycemic control in patients with type 1 diabetes and accounts for the majority of premature death due to cardiovascular events. Physical exercise is generally recommended in patients with diabetes in order to prevent the development of or reduce existing obesity, as adopted by every international treatment guideline so far. Regular physical exercise has a beneficial impact on body composition, cardiovascular integrity, insulin sensitivity and quality of life. However, only a minority of patients participates in regular physical exercise, due to individual or ­disease-related barriers. In type 2 diabetes, there is robust evidence for beneficial effects of physical exercise on glycemic control, cardiovascular health and the development of diabetes-related long-term complications. In type 1 diabetes and patients treated with insulin, a higher risk for exercise-­related hypoglycemia has to be considered, which requires certain prerequisites and adequate adaptions of insulin ­dosing. Current treatment guidelines do only incompletely address the development of exercise-related hypoglycemia. However, every patient with diabetes should participate in regular physical exercise in order to support and enable ­sufficient treatment and optimal glycemic control.

scholarly journals P0950EFFECT OF THYROID HORMONE TREATMENT ON RENAL REABSORPTION OF GLUCOSE IN ALLOXAN-INDUCED DIABETIC RATS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Gireesh Dayma
Keyword(s):  
Blood Glucose ◽  
Thyroid Hormone ◽  
Glucose Homeostasis ◽  
Hepatic Glucose Production ◽  
Liver Perfusion ◽  
Glucose Production ◽  
Diabetic Rats ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
Renal Expression

Abstract Background and Aims The thyroid hormone (TH) plays an important role in glucose metabolism. Recently, we showed that the TH improves glycemia control by decreasing cytokines expression in the adipose tissue and skeletal muscle of alloxan-induced diabetic rats, which were also shown to present primary hypothyroidism. In this context, this study aims to investigate whether the chronic treatment of diabetic rats with T3 could affect other tissues that are involved in the control of glucose homeostasis, as the liver and kidney. Method Adult male Wistar rats were divided into nondiabetic, diabetic, and diabetic treated with T3 (1.5 ?g/100 g BW for 4 weeks). Diabetes was induced by alloxan monohydrate (150 mg/kg, BW, i.p.). Animals showing fasting blood glucose levels greater than 250 mg/dL were selected for the study. Results After treatment, we measured the blood glucose, serum T3, T4, TSH, and insulin concentration, hepatic glucose production by liver perfusion, liver PEPCK, GAPDH, and pAKT expression, as well as urine glucose concentration and renal expression of SGLT2 and GLUT2. T3 reduced blood glucose, hepatic glucose production, liver PEPCK, GAPDH, and pAKT content and the renal expression of SGLT2 and increased glycosuria. Conclusion Results suggest that the decreased hepatic glucose output and increased glucose excretion induced by T3 treatment are important mechanisms that contribute to reduce serum concentration of glucose, accounting for the improvement of glucose homeostasis control in diabetic rats.

scholarly journals Hepatic Glucose Output Inhibition by Mexican Plants Used in the Treatment of Type 2 Diabetes

2020 ◽  
Vol 11 ◽  
Author(s):  
Gerardo Mata-Torres ◽  
Adolfo Andrade-Cetto ◽  
Fernanda Artemisa Espinoza-Hernández ◽  
René Cárdenas-Vázquez
Keyword(s):  
Type 2 Diabetes ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Glucose Output

scholarly journals METABOLIC PHENOTYPING GUIDELINES: Assessing glucose homeostasis in rodent models

2014 ◽  
Vol 222 (3) ◽  
pp. G13-G25 ◽  
Author(s):  
James E Bowe ◽  
Zara J Franklin ◽  
Astrid C Hauge-Evans ◽  
Aileen J King ◽  
Shanta J Persaud ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Tolerance ◽  
Glucose Homeostasis ◽  
Β Cells ◽  
Advantages And Disadvantages ◽  
Autoimmune Destruction ◽  
Normal Glucose

The pathophysiology of diabetes as a disease is characterised by an inability to maintain normal glucose homeostasis. In type 1 diabetes, this is due to autoimmune destruction of the pancreatic β-cells and subsequent lack of insulin production, and in type 2 diabetes it is due to a combination of both insulin resistance and an inability of the β-cells to compensate adequately with increased insulin release. Animal models, in particular genetically modified mice, are increasingly being used to elucidate the mechanisms underlying both type 1 and type 2 diabetes, and as such the ability to study glucose homeostasisin vivohas become an essential tool. Several techniques exist for measuring different aspects of glucose tolerance and each of these methods has distinct advantages and disadvantages. Thus the appropriate methodology may vary from study to study depending on the desired end-points, the animal model, and other practical considerations. This review outlines the most commonly used techniques for assessing glucose tolerance in rodents and details the factors that should be taken into account in their use. Representative scenarios illustrating some of the practical considerations of designingin vivoexperiments for the measurement of glucose homeostasis are also discussed.

scholarly journals Intravenous AICAR administration reduces hepatic glucose output and inhibits whole body lipolysis in type 2 diabetic patients

Diabetologia ◽  
2008 ◽  
Vol 51 (10) ◽  
pp. 1893-1900 ◽  
Author(s):  
H. Boon ◽  
M. Bosselaar ◽  
S. F. E. Praet ◽  
E. E. Blaak ◽  
W. H. M. Saris ◽  
...  
Keyword(s):  
Whole Body ◽  
Diabetic Patients ◽  
Hepatic Glucose Output ◽  
Type 2 Diabetic Patients ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
Type 2 Diabetic

scholarly journals Adiposity and Glucose Intolerance in Offspring of Diabetic Mothers in India

2021 ◽  
Author(s):  
Sonali S Wagle ◽  
Sanat Phatak ◽  
Dattatraya Bhat ◽  
Kalyanaraman Kumaran ◽  
Madhura K Deshmukh ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Intolerance ◽  
Cell Function ◽  
Glucose Measurement ◽  
Insulinogenic Index ◽  
Compensatory Response ◽  
Obesity And Diabetes ◽  
Diabetic Mothers

Objective Maternal diabetes in pregnancy increases the risk of obesity and diabetes in the offspring. Our aim was to compare the offspring born to diabetic mothers (ODM) with those born in non-diabetic mothers (ONDM). Research design and methods We compared the physical characteristics, body composition (DXA) and glycemia of ODMs and matched ONDMs. Glycemic measures included capillary blood glucose measurement in children <10 years of age and a 1.75g/kg glucose OGTT in those >10 years. We evaluated insulin sensitivity (HOMA-S and Matsuda index), beta cell function (HOMA-β and insulinogenic index) and β-cell compensatory response (Disposition Index: Matsuda* Insulinogenic index). We studied the association of maternal and paternal body size and glycemia with outcomes in the child. Results We studied 200 ODMs (176 diabetic mothers - 133 GDM, 21 type 2 diabetes and 22 type 1 diabetes), 177 ONDMs, and their parents at an average period of 9.7 years after delivery. ODMs were heavier and more glucose intolerant than ONDMs. Children born to overweight or obese mothers with GDM or type 2 diabetes were more likely to be overweight or glucose intolerant, whereas those born to thin type 1 diabetic mothers were glucose intolerant but not obese. In addition, obesity or glucose intolerance in the father had an independent influence on the child′s phenotype. Conclusion: Our results show that offspring obesity and glucose intolerance are programmed independently by both parents. In addition there is an independent mirror-imaging of size and glycemia between parents and children. Further studies of genetic and epigenetic mechanisms are indicated.

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