Glucagon

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.  

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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!