Acute growth hormone deficiency rapidly alters glucose metabolism in rat adipocytes. Relation to insulin responses and binding.
To investigate cellular aspects of the antagonism between endogenous GH and insulin in adipose tissue, we examined glucose metabolism, insulin responses, and insulin binding in adipocytes isolated from rats made GH deficient by treatment with antibodies to rat GH (ArGH), which neutralize the biological actions of GH. Adipocytes were incubated in the presence or absence of insulin, and their ability to convert [14C] glucose to CO2 and lipid was measured. Basal glucose utilization was significantly elevated in adipocytes from ArGH-treated rats after 6, 3, or even 1 h of serum treatment compared to that in controls treated with nonimmune serum. This suggests that endogenous GH suppresses glucose metabolism in adipocytes from normal rats. In the presence of insulin, the absolute values of glucose utilization were also higher in cells from ArGH-treated rats than in controls. However, because basal glucose oxidation was higher with GH deficiency, the percent stimulation by insulin was not different in adipocytes from ArGH-treated rats and controls. In keeping with this, the binding of [125I]iodoinsulin was not altered by GH deficiency. These findings indicate that endogenous GH suppresses basal glucose metabolism in adipocytes, and that this effect is rapidly reversed by treatment of normal rats with ArGH. Furthermore, this effect of GH on adipocyte metabolism is independent of changes in insulin binding and appears to account for the enhanced responses to insulin observed with GH deficiency.
D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D005947:Glucose / Q000378:metabolism*; D013006:Growth Hormone / Q000172:deficiency* / Q000378:metabolism; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism / Q000494:pharmacology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D007328:Insulin; D013006:Growth Hormone; D005947:Glucose