title: Effects of prolonged treatment of lactating goats with bovine somatotropin on aspects of adipose tissue and liver metabolism.
abstract: The effects of prolonged (22 weeks) treatment of lactating goats with bovine somatotropin on the metabolism of adipose tissue and liver has been investigated. Somatotropin treatment resulted in smaller adipocytes, decreased rate of fatty acid synthesis and decreased total acetyl-CoA carboxylase activity of adipocytes, but with no change in the proportion of this enzyme in the active state. The rate of acylglycerol glycerol synthesis from glucose of adipocytes tended to decrease as did total glucose utilization by the tissue. Glucose conversion to lactate was unchanged by somatotropin treatment but glucose conversion to other products was decreased. Maximum response of adipose tissue to insulin was unchanged but the sensitivity to insulin decreased on somatotropin treatment. Treatment with somatotropin had no effect on basal lipolysis and decreased maximum response to the beta-agonist isoproterenol, but this probably reflects the rate of isoproterenol-stimulated lipolysis varying with cell volume in adipocytes. No apparent change in response either to alpha 2-adrenergic agonists or to adenosine was apparent. The number of beta-adrenergic receptors was unchanged in adipocyte membranes but the number of alpha 2-adrenergic receptors increased. The rate of hepatic gluconeogenesis in vitro, the activity of key gluconeogenic enzymes and the modulation of the rate of gluconeogenesis by butyrate were unchanged except for the effect of this latter agent on gluconeogenesis from propionate. Hepatic ketogenic activity, as indicated by the activity of carnitine palmitoyl-CoA-transferase-1 and the concentrations of carnitine and acyl carnitines, was unchanged by treatment. Thus at the end of a prolonged period of treatment with somatotropin in lactating goats, lipid synthesis in adipose tissue is still decreased but no effects on liver lipid and carbohydrate metabolism were apparent.
authors.affiliation: Hannah Research Institute, Ayr, UK.
authors.forename: R G
authors.initials: RG
authors.lastname: Vernon
authors.forename: A
authors.initials: A
authors.lastname: Faulkner
authors.forename: E
authors.initials: E
authors.lastname: Finley
authors.forename: P W
authors.initials: PW
authors.lastname: Watt
authors.forename: V A
authors.initials: VA
authors.lastname: Zammit
mesh_terms: D000103:Acetyl-CoA Carboxylase / Q000378:metabolism; D017667:Adipocytes / Q000166:cytology; D000273:Adipose Tissue / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D048429:Cell Size; D002478:Cells, Cultured; D005227:Fatty Acids / Q000096:biosynthesis; D005260:Female; D005947:Glucose / Q000008:administration & dosage / Q000378:metabolism; D006041:Goats / Q000378:metabolism*; D013006:Growth Hormone / Q000494:pharmacology*; D007773:Lactates / Q000378:metabolism; D007774:Lactation; D019344:Lactic Acid; D008066:Lipolysis / Q000187:drug effects; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism; D011768:Pyruvate Dehydrogenase Complex / Q000378:metabolism
chemical_list: D005227:Fatty Acids; D007773:Lactates; D011768:Pyruvate Dehydrogenase Complex; D019344:Lactic Acid; D013006:Growth Hormone; D000103:Acetyl-CoA Carboxylase; D005947:Glucose