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Abnormal beta cell nutrient sensing resulting from gene mutations leads to hypoglycemia or diabetes. Glucokinase (GCK) plays a key role in beta cell glucose sensing. As one form of congenital hyperinsulinism (CHI), activating mutations of<jats:italic>GCK<\/jats:italic>result in a decreased threshold for glucose\u2010stimulated insulin secretion and hypoglycemia. In contrast, inactivating mutations of<jats:italic>GCK<\/jats:italic>result in diabetes, including a mild form (MODY2) and a severe form (permanent neonatal diabetes mellitus (PNDM)). Mutations of beta cell ion channels involved in insulin secretion regulation also alter glucose sensing. Activating or inactivating mutations of ATP\u2010dependent potassium (K<jats:sub>ATP<\/jats:sub>) channel genes result in severe but completely opposite clinical phenotypes, including PNDM and CHI. Mutations of the other ion channels, including voltage\u2010gated potassium channels (K<jats:sub>v<\/jats:sub>7.1) and voltage\u2010gated calcium channels, also lead to abnormal glucose sensing and CHI. Furthermore, amino acids can stimulate insulin secretion in a glucose\u2010independent manner in some forms of CHI, including activating mutations of the glutamate dehydrogenase gene, HDAH deficiency, and inactivating mutations of K<jats:sub>ATP<\/jats:sub>channel genes. These genetic defects have provided insight into a better understanding of the complicated nature of beta cell fuel\u2010sensing mechanisms.<\/jats:p>","DOI":"10.1111\/nyas.13448","type":"journal-article","created":{"date-parts":[[2017,10,17]],"date-time":"2017-10-17T03:56:40Z","timestamp":1508212600000},"page":"65-82","source":"Crossref","is-referenced-by-count":28,"title":["Nutrient sensing in pancreatic islets: lessons from congenital hyperinsulinism and monogenic diabetes"],"prefix":"10.1111","volume":"1411","author":[{"given":"Ming","family":"Lu","sequence":"first","affiliation":[{"name":"Division of Endocrinology and Diabetes The Children's Hospital of Philadelphia Philadelphia Pennsylvania"},{"name":"Department of Pediatrics &amp; Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine University of Pennsylvania Philadelphia Pennsylvania"},{"name":"Department of Endocrinology Shandong Provincial Hospital affiliated to Shandong University Jinan Shandong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Changhong","family":"Li","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Diabetes The Children's Hospital of Philadelphia Philadelphia Pennsylvania"},{"name":"Department of Pediatrics &amp; Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine University of Pennsylvania Philadelphia Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2017,10,16]]},"reference":[{"key":"e_1_2_11_2_1","first-page":"173","article-title":"Calcium fluxes in the process of glucose\u2010induced insulin release","volume":"246","author":"Herchuelz A.","year":"1980","journal-title":"Arch. 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