Elevated levels of somatostatin is a pathologic condition associated with which of the blood hormone levels.
Gut hormones (for a full listing, see Table I below)a. Gastrin from the gastric antrum and the duodenum stimulates gastric acid and pepsin secretion.b. Cholecystokinin from the duodenum and jejunum stimulates the contraction of the gallbladder and the secretion of pancreatic enzymes.c. Secretin from the duodenum and jejunum stimulates the secretion of bicarbonate by the pancreas.d. Ghrelin from the central nervous system, stomach, small intestine, and colon stimulates GH release under fasting conditions.e. Gastric inhibitory polypeptide (GIP) from the small bowel enhances insulin release and inhibits the secretion of gastric acid.f. Glucagon-like peptide 1 (GLP-1) from the neuroendocrine cells in the ileum, colon, and central nervous system enhances glucose disposal after meals by inhibiting glucagon secretion and stimulating insulin secretion. The actions of GIP and GLP-1 relevant to glucose control are summarized in Table II and Figure below.g. Vasoactive intestinal polypeptide from the pancreas relaxes smooth muscles and stimulates bicarbonate secretion by the pancreas.h. Somatostatin from the central nervous system, pancreatic d cells, and enteroendocrine d cells inhibits the secretion of insulin and glucagon from the pancreas; inhibits the release of gastrin, secretin, and GLP-1 from the gut; and reduces carbohydrate absorption from the gut lumen.Somatostatin, produced by the hypothalamus, inhibits growth hormone production and secretion by the anterior pituitary. Somatostatin will also reduce the secretion of TSH, insulin, and glucagon.Table I: Gastrointestinal-Derived Hormones That Affect Fuel Metabolism DirectlyHormonePrimary Cell/Tissue of OriginActionsSecretary Stimuli {and Inhibitors)AmylinPancreatic b cell, endocrine cells of stomach and small intestine1. Inhibits arginine-stimulated and postprandial glucagon secretion2. Inhibits insulin secretionCosecreted with insulin in response to oral nutrientsCalcitonin gene-related peptideEnteric neurons and enteroendocrine cells of the rectumInhibits insulin secretionOral glucose intake and gastric acid secretionGalaninNervous system, pituitary, neurons of gut, pancreas, thyroid, and adrenal glandInhibits the secretion of insulin, somatostatin, enteroglucagon, pancreatic polypeptide, and othersIntestinal distensionGastric inhibitory polypeptide/glucase-dependent Insulinatroprc polypeptide (GIP)Neuroendocrine K cells of duodenum and proximal jejunum1. Increases insulin release via an "incretin" effect2. Regulates glucose and lipid metabolismOral nutrient ingestion, especially long-chain fatty acidsGastrin-releasing peptide (GRP)Enteric nervous system and pancreasStimulates the release of cholecystokinin; GIP, gastrin, glucagon, GLP-I, GLP-2, and somatostatin GhrelinCentral nervous system, stomach, small intestine, and colonStimulates GH releaseFastingGlucagonPancreatic a cell, central nervous systemPrimary counterregulatory hormone that restores glucose levels in hypoglycemic state (increases glycogenolysis and gluconeogenesis as well as protein-lipid flux in liver and muscle)Neural and humoral factors released in response tohypoglycemiaGlucagon-like peptide 1 (GLP-1)Enteroendocrine L cells in ileum, colon, and central nervous system1. Enhances glucose disposal after meals by inhibiting glucagon secretion and stimulating insulin secretion2. Acts through second messengers in b cells to increase the sensitivity of these cells to glucose (an incretin)1. Oral nutrient ingestion2. Vagus nerve3. GRP and GIP4. Somatostatin inhibits secretionGlucagon-like peptide 2 (GLP-2)Same as for GLP-1Stimulates intestinal hexose transportSame as GLP-1Neuropeptide YCentral and peripheral nervous system, pancreatic islet cellsInhibits glucose-stimulated insulin secretionOral nutrient ingestion and activation of sympathetic nervous systemNeurotensin (NT)Small intestine N cells (especially ileum), enteric nervous system, adrenal gland, pancreasIn brain, modulates dopamine neurotransmission and anterior pituitary secretions1. Luminal lipid nutrients2. GRP3. Somatostatin inhibits secretionPituitary adenylate cyclase-activating peptide (PACAP)Brain, lung, and enteric nervous systemStimulates insulin and catecholamine releaseActivation of central nervous systemSomatostatinCentral nervous system, pancreatic d cells, and enteroendocrine 5 cells1. Inhibits secretion of insulin, glucagon and PP (islets), and gastrin, secretin, GLP-1, and GLP-2 (in gut)2. Reduces carbohydrate absorption from gut lumen1. Luminal nutrients2. GLP-33. GIP4. PACAP5. VIP6. b-Adrenergic stimulationVasoactive intestinal peptide (VIP)Widely expressed in the central and peripheral nervous systemsMay regulate the release of Insulin and pancreatic glucagon1. Mechanical stimulation of gut2. Activation of central and peripheral nervous systemsTable II: Actions of GLP-1 and GIP Relevant to Glucose Control GLP-1GIPPancreasStimulates glucose-dependent insulin release++Increase insulin biosynthesis++Inhibits glucagon secretion+-Stimulates somatostatin secretion+-Induces b-cell proliferation++Inhibits p-cell apoptosis++Gastrointestinal tractInhibits gastric emptying+-Inhibits gastric acid secretion++Central nervous systemInhibits food and water intake+-Promotes satiety and weight loss+-Cardiovascular systemImproves cardiovascular function after ischemia+-Adipose tissueInsulin-like lipogenic actions-+Lipid storage-+ The actions of selected peptides on vital tissues involved in glucose homeostasis. Both GLP-1 and GIP increase insulin secretion and b-cell survival. GLP-1 has additional actions related to glucose metabolism. In contrast, gastrin and CCK do not acutely regulate plasma glucose levels, but appear to increase b-cell proliferation. CCK, cholecystokinin; GIP, gastric inhibitory polypeptide; GLP-1, glucagon-like peptide 1.
High prolactin (PRL)
High TSH
High cortisol
Low growth hormone (GH)
Endocrinology