Abstract
Glucagon’s ability to increase energy expenditure has been known for more than 60 years, yet the mechanisms underlining glucagon’s thermogenic effect still remain largely elusive. Over the last years, significant efforts were directed to unravel the physiological and cellular underpinnings of how glucagon regulates energy expenditure. In this review, we summarize the current knowledge on how glucagon regulates systems metabolism with a special emphasis on its acute and chronic thermogenic effects.
Highlights
Glucagon is a 29 amino acid peptide that is secreted from pancreatic α-cells in response to low levels of blood glucose
Glucagon acts through the glucagon receptor (GCGR), a G protein-coupled receptor that is most abundantly expressed in the liver
These non-glycemic effects of glucagon include the modulation of food intake and satiety [4], lipid homeostasis [5], insulin secretion [6], and energy expenditure [7]
Summary
Glucagon is a 29 amino acid peptide that is secreted from pancreatic α-cells in response to low levels of blood glucose. Often reduced to its glycemic effects, glucagon is a pleiotropic hormone with metabolic action that goes well beyond its ability to increase blood glucose These non-glycemic effects of glucagon include the modulation of food intake and satiety [4], lipid homeostasis [5], insulin secretion [6], and energy expenditure [7]. A series of preclinical [14,15,16,17] and clinical studies [18,19] have demonstrated that inhibition of glucagon signaling can have beneficial effects on glucose metabolism in individuals with type-2 diabetes Adverse effects such as increased hepatic fat accumulation and increased LDL cholesterol have been reported for these antagonists in humans [20,21]. We summarize the current knowledge on how glucagon regulates energy expenditure, with a special emphasize on acute and chronic effects
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