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Gastrointestinal hormones and the regulation of β‐cell mass

Type 2 diabetes occurs due to a relative deficit in β‐cell mass or function. Glucagon‐like peptide 1 (GLP‐1), glucose‐dependent insulinotropic polypeptide (GIP), cholecystokinin (CCK), and gastrin are gastrointestinal hormones that are secreted in response to nutrient intake, regulating digestion, insulin secretion, satiety, and β‐cell mass. In this review, we focus upon β‐cell mass regulation. β‐cell mass expands through β‐cell proliferation and islet neogenesis; β‐cell mass is lost via apoptosis. GLP‐1 and GIP are well‐studied gastrointestinal hormones and influence β‐cell proliferation, apoptosis, and islet neogenesis. CCK regulates β‐cell apoptosis and mitogenesis, and gastrin stimulates islet neogenesis. GLP‐1 and GIP bind to G protein‐coupled receptors and regulate β‐cell mass via multiple signaling pathways. The protein kinase A pathway is central to this process because it directly regulates proliferative and anti‐apoptotic genes and transactivates several signaling cascades, including Akt and mitogen‐activated protein kinases. However, the signaling pathways downstream of G protein‐coupled CCK receptors that influence β‐cell mass remain unidentified. Gastrointestinal hormones integrate nutrient signals from the gut to the β‐cell, regulating insulin secretion and β‐cell mass adaptation.