OBJECTIVE: The influence of growth hormone (GH) on the regulation of lipolytic response to specific agonists to beta-adrenoceptors and several post-receptor steps in the lipolytic cascade were investigated. RESEARCH METHODS AND PROCEDURES: Adipose tissues from rats were incubated with or without GH (1.38 nM). After a 24-hour incubation, isolated adipocytes were prepared for different assays. Rats were hypophysectomized. One week after operation, L-thyroxine and hydrocortisone acetate was given to hypophysectomized rats. One group of rats was treated with GH (1.33 mg/kg, daily). After 1 week of hormonal treatment, adipose tissues were removed for different studies. RESULTS: GH treatment increased both basal lipolysis and lipolytic sensitivity to dobutamine and CGP 12177 in adipocytes. The lipolytic sensitivity to terbutaline was not influenced by GH treatment. GH treatment increased the maximal lipolytic response to dobutamine and CGP 12177, but not to terbutaline as determined with absolute values of lipolysis. Forskolin-induced lipolysis was increased by addition of GH to tissues. Moreover, GH treatment resulted in enhanced expression of hormone-sensitive lipase. GH treatment in hypophysectomized rats influenced neither the expressions of G alpha s protein and cholera toxin-catalyzed adenosine diphosphate-ribosylation of G alpha s protein, nor cholera toxin-induced 3',5'-cyclic adenosine monophosphate accumulation. However, the expression of G alpha i protein was decreased after GH treatment. DISCUSSION: These and previous results suggest that GH increases lipolysis in rat adipocytes partly through the beta-adrenergic system, including increases in both beta(1)- and beta(3)-adrenergic receptor function, and partly through enhanced adenylate cyclase function, and expression of hormone-sensitive lipase, perhaps via a decrease in G alpha i protein expression.
OBJECTIVE: The influence of growth hormone (GH) on the regulation of lipolytic response to specific agonists to beta-adrenoceptors and several post-receptor steps in the lipolytic cascade were investigated. RESEARCH METHODS AND PROCEDURES: Adipose tissues from rats were incubated with or without GH (1.38 nM). After a 24-hour incubation, isolated adipocytes were prepared for different assays. Rats were hypophysectomized. One week after operation, L-thyroxine and hydrocortisone acetate was given to hypophysectomized rats. One group of rats was treated with GH (1.33 mg/kg, daily). After 1 week of hormonal treatment, adipose tissues were removed for different studies. RESULTS: GH treatment increased both basal lipolysis and lipolytic sensitivity to dobutamine and CGP 12177 in adipocytes. The lipolytic sensitivity to terbutaline was not influenced by GH treatment. GH treatment increased the maximal lipolytic response to dobutamine and CGP 12177, but not to terbutaline as determined with absolute values of lipolysis. Forskolin-induced lipolysis was increased by addition of GH to tissues. Moreover, GH treatment resulted in enhanced expression of hormone-sensitive lipase. GH treatment in hypophysectomized rats influenced neither the expressions of G alpha s protein and cholera toxin-catalyzed adenosine diphosphate-ribosylation of G alpha s protein, nor cholera toxin-induced 3',5'-cyclic adenosine monophosphate accumulation. However, the expression of G alpha i protein was decreased after GH treatment. DISCUSSION: These and previous results suggest that GH increases lipolysis in rat adipocytes partly through the beta-adrenergic system, including increases in both beta(1)- and beta(3)-adrenergic receptor function, and partly through enhanced adenylate cyclase function, and expression of hormone-sensitive lipase, perhaps via a decrease in G alpha i protein expression.
Authors: Pamela U Freda; Wei Shen; Steven B Heymsfield; Carlos M Reyes-Vidal; Eliza B Geer; Jeffrey N Bruce; Dympna Gallagher Journal: J Clin Endocrinol Metab Date: 2008-03-18 Impact factor: 5.958