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The endocrine system
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
Throughout the pancreas, endocrine are cells found in scattered clusters called islets of Langerhans. These endocrine cells can be classified into three distinct types: alpha cells that produce the hormone glucagon; beta cells that produce insulin and delta cells that produce somatostatin (see Table 11.5). The major regulator of insulin and glucagon release from the pancreas is blood glucose level. An increase in blood glucose (as occurs after a meal) will stimulate the release of insulin and inhibit the release of glucagon. Conversely, decreases in blood glucose (during fasting for example) will stimulate the release of glucagon and inhibit the release of insulin. When released, the main effect of insulin is to lower blood glucose levels by enhancing the utilization and uptake of insulin. Glucagon directly counters the effects of insulin by decreasing glucose utilization and uptake as well as stimulating the formation of new glucose from glycogen and amino acids. The major target tissues for insulin and glucagon action are liver, skeletal muscle and fat.
SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
Insulin acts via cell membrane spanning receptors which have intrinsic receptor tyrosine kinase activity. When insulin binds to the receptor, the tyrosine kinase is phosphorylated, resulting in a cascade of intracellular signalling mechanisms which results in glucose uptake into the cell. It is secreted by beta cells of the pancreas. Somatostatin is secreted by delta cells. Secretion is inhibited by somatostatin, which is always considered an inhibitory hormone. Insulin is considered an anabolic hormone; that is, it takes up glucose into the cell and converts it to larger ‘building blocks’ such as proteins and fats. Release of insulin is stimulated not only by the ingestion of glucose but also amino acids which it will convert into larger proteins.
Chronic Hyperglycemia—A Primer
Published in Robert Fried, Richard M. Carlton, Type 2 Diabetes, 2018
Robert Fried, Richard M. Carlton
Somatostatin is a hormone that inhibits the secretion of growth hormone by the pituitary gland. It is released from the δ-cells (delta-cells) under control of the same stimuli that result in insulin release and that act primarily as a regulator of insulin release, preventing insulin levels from rising too rapidly. It may also have an endocrine role as an inhibitor of nutrient absorption in the gut.
Amyloid nomenclature 2022: update, novel proteins, and recommendations by the International Society of Amyloidosis (ISA) Nomenclature Committee
Published in Amyloid, 2022
Joel N. Buxbaum, Angela Dispenzieri, David S. Eisenberg, Marcus Fändrich, Giampaolo Merlini, Maria J. M. Saraiva, Yoshiki Sekijima, Per Westermark
Somatostatin is synthesised as a 116 aa residue polypeptide from which a 24 aa signal peptide is removed. The resulting 92 aa propeptide is further processed to yield somatostatins 14 or 28, constituting the C-terminus of the precursor (prosomatostatin) [12]. Somatostatin is expressed in the D (or delta) cells of the islets of Langerhans but also in cells in the gastrointestinal canal and in the brain. Two recent papers have described somatostatin as an amyloid fibril protein in somatostatinomas. One of the reports describes 4 patients. It was not possible to determine the exact form of somatostatin in the deposits [13]. The other paper describes the analysis of amyloid in an endocrine papillary tumour of the duodenum where the fibrillary protein was derived from the somatostatin precursor [14]. The exact portion of the precursor comprising the amyloid fibrils was not determined. The name will be amyloid protein ASom.
Evidence for the existence and potential roles of intra-islet glucagon-like peptide-1
Published in Islets, 2021
Scott A. Campbell, Janyne Johnson, Peter E. Light
Glucose is an essential regulator of islet hormone secretion. Both beta and delta cells rely on glucose-stimulated secretion pathways, where hyperglycemia favors the release of insulin and somatostatin from the islet. In beta and delta cells, glucose entry and metabolism results in the closure of KATP channels, membrane depolarization, elevated intracellular calcium, and hormone secretion. This pathway in delta cells is more dependent on calcium-induced Ca2+ release, whereas beta cells depend on the activation of voltage-gated Ca2+ channels.60 The sodium-glucose transporter SGLT2 is expressed in 33–58% of human delta cells, and its current contributes to insulin-induced somatostatin secretion.108 In the presence of SGLT2 inhibitors like dapagliflozin, insulin-stimulated somatostatin secretion is modestly suppressed.108,109 As previously stated, the actions of GLP-1 in alpha cells are also glucose-dependent. In hyperglycemia, GLP-1R activation inhibits alpha cell hormone release, while receptor activation in hypoglycemia potentiates hormone secretion.100
Culture, differentiation, and transduction of mouse E12.5 pancreatic spheres: an in vitro model for the secondary transition of pancreas development
Published in Islets, 2021
Lukas Huijbregts, Virginie Aiello, Andrea Soggia, Philippe Ravassard, Latif Rachdi, Raphaël Scharfmann, Olivier Albagli
Pancreas development in mammals begins with the specification and evagination of two dorsal and ventral regions of foregut/midgut endoderm, which marks the emergence of pancreatic progenitors. The subsequent differentiation events occur in two temporally separated steps in rodent, termed primary and secondary transitions. The first transition starts just after the onset of pancreatic buds outgrowth, and spans from embryonic day 9.5 to 12.5 (E9.5 to E12.5) in mice. During this transition, the progenitors actively proliferate to form an epithelial tree, while a few of them in the dorsal bud begin to differentiate in glucagon-producing (alpha) endocrine cells.1–3 Then, during the secondary transition (mostly between E12.5 to E15.5 in mice), all other pancreatic cell types arise quite suddenly. During this period, the pancreatic progenitors differentiate into either exocrine acinar cells, which comprise the prevailing population of the pancreas, exocrine duct cells, or in various endocrine cell types, insulin-producing (beta) cells or, slightly later, somatostatin-producing (delta) cells and pancreatic polypeptide-producing (PP) cells.3,4 Together with the alpha population, which undergoes a continuous expansion during the secondary transition,3 and with the more recently described ghrelin-producing (epsilon) cells, these endocrine cells cluster in specialized « micro-organs », the islets of Langerhans. Meanwhile, the condensed mesenchymal tissue surrounding the early pancreatic bud progressively intermingles with the differentiating populations.2 Although the proper function of the pancreas requires the subsequent cell maturation until birth and in newborns, most developmental decisions are determined at the end of the secondary transition. How the secondary transition occurs and why it is delayed with respect to the first events of endocrine differentiation are major issues in pancreas development.