The GCGR is expressed by islet β cells and supraphysiological amounts of glucagon stimulate insulin release in vitro and in vivo. In isolated human and rat islets studied in culture, antagonism of the GCGR impairs insulin secretion in response to increased media glucose, suggesting a physiological role for islet glucagon action to maintain normal β- cell stimulus–secretion coupling. Consistent with local control of insulin secretion mediated by α- cell products, dispersed β cells are more responsive to glucose when attached to an α cell. Thus, paracrine regulation mediated by α- to- β- cell communication (Figure 1) is increasingly accepted and has gained additional support from recent studies. Several groups, using complementary approaches, have shown that glucagon acts through both glucagon and GLP- 1 receptors on β cells to stimulate insulin release, an effect that is apparent in both mouse and human islets. One proposed effect of α- cell products on systemic homeostasis is regulation of the glycaemic set- point – that is, the normal basal concentration of blood glucose – through effects on β- cell tone and responsiveness to glucose . However, a recent demonstration that stimulation of α- cell secretion by gastric inhibitory polypeptide (GIP), a hormone released episodically after meals, promotes glucose tolerance through α- to- β- cell communication suggests that proglucagon peptides are also a component of prandial insulin responses.

Fig1. he integration of the incretin system and nutrient sensing in α and β cells in the post- prandial state. Feeding increases the plasma concentrations of glucose, amino acids, and glucose- dependent insulinotropic polypeptide (GIP). GIP potentiates glucose- stimulated insulin secretion in β cells and amino acid–stimulated glucagon secretion in α cells. The rise in glucagon, and potentially glucagon- like peptide 1 (GLP- 1), secretion in α cells enhances α- to- β- cell communication, which is mediated by both the GLP-1 receptor (GLP- 1R) and glucagon receptor (GCGR). The combined activation of GLP- 1R, GCGR, and GIP in β cells produces maximal insulin secretion and glucose homeostasis.

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مواضيع ذات صلة

Early β-cell dysfunction

Physiological insulin secretion

Hypoglycemia in Diabetes

Mouse genetics reveal tissue- integrated insulin signalling

Heterologous regulation and insulin resistance

Abnormalities of glucagon secretion and action in diabetes

Glucagon actions in the liver: amino acid metabolism and the hepatic–α- cell axis

Glucagon actions in the liver: glucose and lipid metabolism

Regulation of α- cell secretion

Regulation of insulin secretion by non- nutrients

Regulation of insulin secretion

Islet structure and function