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Transcript
Biological effects of GH • Somatotropic – Growth and cell proliferation • IGF-I mediated • Metabolic – Direct action of GH • IGF-I independent • Many tissues • All nutrients • Effects of GH on metabolism – Nutrient partitioning • After absorption – Independent of digestion process – Independent of nutrient expenditure Nutrient partitioning during growth • Alteration of growth by exogenous GH – Alteration in nutrient partitioning between muscles and adipose tissue • • • • Increased daily gain Increased feed efficiency Decreased fat deposition Increased protein deposition – Age-dependent response • Action of GH – Different between adipose and muscle – Growth of muscle in response to GH • Depends on availability of dietary proteins and energy • Involves IGF-I – Decreased fat accumulation • Inhibition of glucose uptake • Action of GH – Decreased fat accumulation • Inhibition of glucose utilization • Glucose diverted to muscles • Net results – Decreased adipocyte hypertrophy – Increased muscle growth Effects on adipoccytes • Chronic • Lipogenesis – Inhibited • Fatty acid synthesis • Lipolysis – Stimulated when undernutrition • Mechanism – Inhibition of insulin action on adipocytes • Decreased sensitivity of adipocytes to insulin stimulation – Decreased glucose usage by the cells – Independent of receptor number or intracellular signaling system • Inhibition of fatty acid synthase expression – Interference with insulin signaling pathway – Direct genomic effects • Effects on lipolysis – Indirect mechanism • Alteration of adipocyte responsiveness to acute lipolytic signaling pathway • Highly dependent on nutritional status of the individual • Increased hepatic gluconeogenesis – Direct effects – Inhibition of insulin action • Increased efficiency of amino acid utilization – Reduced oxidation – Results in muscle fiber hypertrophy Pancreatic hormones Pancreas • Exocrine organ – Digestive enzymes • Discovery of the first hormone (secretin) • Endocrine organ – Islets • Described by Langerhans – Islet of Langerhans • Cell composition – Two major types • Alpha – Glucagon • Beta – Insulin – Other cells • D cells (SS) • F cells (pancreatic polypeptide) Regulation of glucose metabolism • Glucose homeostasis – Movement of glucose into and out of extracellular space • Involvement of many tissues – Liver – Adipose tissue – Muscle • Two hormones – Insulin – Glucagon Regulation of glucose metabolism • Glucose homeostasis – Basic concept • Coordinated relationship between alpha (glucagon) and beta (insulin) cells under control of glucose sensor Regulation of glucose metabolism • Glucose homeostasis – Basic concept • Particular arrangement of cells within the islet • Specialized cell membrane Insulin • Required for normal growth and development • Only hormone that can lower blood glucose level – Dominant metabolic regulator • Unregulated glucose level if absent • Hypoglycemia if too high – Cause neural shock • Biochemistry – Two subunits • Alpha and beta • Linked by two disulfide bridges – Synthesized as prohormone • Preproinsulin – Proinsulin precursor • Proteolytic cleavage – Proinsulin – Formation of disulfide bridges • Insulin – Coupled with zinc within the beta cells – Very short life • Around 5 to 15 min after synthesis • Metabolized by kidneys and liver Glucagon • Biochemistry – Single peptide • 29 AA • Similar structurally to gastric inhibitory peptide and VIP • Cleaved from larger protein • Highly conserved – Identical among mammals Other pancreatic peptides • SS – Localized in D cells • Located adjacent to alpha and beta cells – Local action of SS – Affects function of intestine • Movement of nutrients • Pancreatic polypeptide – Unclear function in mammals • Suppression of SS secretion by pancreas and intestine • Inhibition of gallbladder and pancreatic enzyme secretion – Secretion affected by nutrient uptake by the intestine