{'fraction_non_alphanumeric': 0.014828544949026877, 'fraction_numerical': 0.0023169601482854493, 'mean_word_length': 5.5823170731707314, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
The Regulation of Amylin and Insulin Gene Expression and Secretion

Amylin and insulin are cosecreted by beta cells in the islets of the pancreas. Insulin is required for glucose homeostasis; however, the physiology of amylin and its metabolic importance are not well understood. Dysregulation of insulin and peripheral insulin resistance of skeletal muscle are the major factors responsible for diabetes. Amylin may contribute to the development of diabetes by inhibiting insulin release from the beta cells and promoting beta cell death through apoptosis. Other pathologic conditions such as pancreatic cancer and obesity are associated with elevated amylin levels and hypoglycemia. Although insulin secretion and gene expression are well understood, new factors have been discovered that affect both pathways. The regulation of amylin secretion and gene expression is less clear, but recent studies have demonstrated the complexity of amylin regulation, both in concert with insulin and in a nonparallel fashion. This review describes the current thinking behind amylin and insulin regulation by beta cells under normal physiologic conditions and during pathologic states. Insulin secretion is a complex phenomenon that is triggered by circulating metabolites and hormones as well as neural factors. Circulating glucose levels play a central role in the control of insulin secretion. However, under normal circumstances, glucose concentrations in the bloodstream do not change by more than 20% with feeding. The regulation between the gastrointestinal tract and insulin secretion is known as the enteroinsular axis. The signals of the enteroinsular axis are dependent on a small increase in circulating glucose, a process that has evolved to prevent inappropriate hypoglycemia following nutrient ingestion. The major endocrine mediators of the enteroinsular axis (incretins) are glucosedependent insulinotropic peptide (GIP) and glucagon-like peptide 1 (GLP-1). Both of these incretins activate insulin and amylin secretion through interactions with 7 transmembrane serpentine receptors that are coupled to G proteins and the cAMP second messenger system.