1. Biological effects of GH Somatotropic –Growth and cell proliferation IGF-I mediated Metabolic –Direct action of GH IGF-I independent Many tissues All nutrients

2. Effects of GH on metabolism –Nutrient partitioning After absorption –Independent of digestion process –Independent of nutrient expenditure

3. 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

7. 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

8. Action of GH –Decreased fat accumulation Inhibition of glucose utilization Glucose diverted to muscles Net results –Decreased adipocyte hypertrophy –Increased muscle growth

9. Effects on adipoccytes Chronic Lipogenesis –Inhibited Fatty acid synthesis Lipolysis –Stimulated when undernutrition

10. 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

11. Effects on lipolysis –Indirect mechanism Alteration of adipocyte responsiveness to acute lipolytic signaling pathway Highly dependent on nutritional status of the individual

12. Increased hepatic gluconeogenesis –Direct effects –Inhibition of insulin action Increased efficiency of amino acid utilization –Reduced oxidation –Results in muscle fiber hypertrophy

13. Pancreatic hormones

14. Pancreas Exocrine organ –Digestive enzymes Discovery of the first hormone (secretin) Endocrine organ –Islets Described by Langerhans –Islet of Langerhans

15. Cell composition –Two major types Alpha –Glucagon Beta –Insulin –Other cells D cells (SS) F cells (pancreatic polypeptide)

16. 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

17. Regulation of glucose metabolism Glucose homeostasis –Basic concept Coordinated relationship between alpha (glucagon) and beta (insulin) cells under control of glucose sensor

18. Regulation of glucose metabolism Glucose homeostasis –Basic concept Particular arrangement of cells within the islet Specialized cell membrane

19. 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

20. Biochemistry –Two subunits Alpha and beta Linked by two disulfide bridges –Synthesized as prohormone Preproinsulin –Proinsulin precursor Proteolytic cleavage –Proinsulin –Formation of disulfide bridges

22. Insulin –Coupled with zinc within the beta cells –Very short life Around 5 to 15 min after synthesis Metabolized by kidneys and liver

23. Glucagon Biochemistry –Single peptide 29 AA Similar structurally to gastric inhibitory peptide and VIP Cleaved from larger protein Highly conserved –Identical among mammals

24. 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

25. 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