Hello. My question is regarding the rise of NEFAs as a pathogenic cause of type 2 DM. In a healthy human hormone sensitive lipase responds to epinephrine, ACTH & glucagon to release glycerol + NEFAs. I thought this enzyme would be the main culprit acting to release glycerol + NEFAs in DM2, however, several papers are saying it markedly reduced! My question is then, if HSL is reduced in type 2 DM/Obese patients, what enzyme is responsible for the lipolysis? Which hormone stimulates it? I hope someone can shed some light on this. Thanks!
almost 8 years ago
Physiology of the pancreatic α-cell and glucagon secretion: role in glucose homeostasis and diabetes
The secretion of glucagon by pancreatic α-cells plays a critical role in the regulation of glycaemia. This hormone counteracts hypoglycaemia and opposes insulin actions by stimulating hepatic glucose synthesis and mobilization, thereby increasing blood glucose concentrations. During the last decade, knowledge of α-cell physiology has greatly improved, especially concerning molecular and cellular mechanisms. In this review, we have addressed recent findings on α-cell physiology and the regulation of ion channels, electrical activity, calcium signals and glucagon release. Our focus in this review has been the multiple control levels that modulate glucagon secretion from glucose and nutrients to paracrine and neural inputs. Additionally, we have described the glucagon actions on glycaemia and energy metabolism, and discussed their involvement in the pathophysiology of diabetes. Finally, some of the present approaches for diabetes therapy related to α-cell function are also discussed in this review. A better understanding of the α-cell physiology is necessary for an integral comprehension of the regulation of glucose homeostasis and the development of diabetes.
over 5 years ago
A needle-free nasal delivery system for glucagon for use in severe hypoglycemia showed promsing results, especially compared with conventional delivery.
about 5 years ago
For reducing HbA1c levels in people with type 2 diabetes, dulaglutide once weekly, when added to metformin, was statistically superior to exenatide twice daily (both in combination with pioglitazone), statistically superior to sitagliptin and statistically non‑inferior to liraglutide 1.8 mg daily. As with the other glucagon‑like peptide‑1 (GLP‑1) receptor agonists there are limited data from randomised controlled trials (RCTs) on the effect of dulaglutide on patient‑oriented outcomes, such as rates of macrovascular or microvascular events, or on long‑term safety.
about 5 years ago
Patients admitted to the intensive care unit often develop hyperglycaemia, but the underlying mechanisms have not been fully described. The incretin effect is reduced in patients with type 2 diabetes. Type 2 diabetes and critical illness have phenotypical similarities, such as hyperglycaemia, insulin resistance and systemic inflammation. Previous studies have shown beneficial effects of exogenous glucagon-like peptide (GLP)-1 on glycaemia in critically ill patients, a phenomenon also seen in patients with type 2 diabetes. In this study, we hypothesised that the incretin effect, which is mediated by the incretin hormones GLP-1 and glucose-dependent insulinotropic peptide (GIP), is impaired in critically ill patients.
about 5 years ago
Among adults with type 1 diabetes infused with insulin to induce hypoglycemia, the ability of intranasal glucagon to raise blood glucose was similar to that of the intramuscular formulation.
almost 5 years ago
The incretin hormone glucagon-like peptide 1 (GLP-1) appears to correct the abnormal secretion of insulin and glucagon in posttransplantation diabetes (PTDM), researchers from Norway and Denmark report.
over 4 years ago