Abstract
To determine whether endogenous GH contributes to impairments of glucose metabolism in diabetes mellitus, we examined the metabolic consequences of GH deficiency in streptozotocin (SZ)-diabetic rats. Diabetic rats were treated with a highly specific antirat GH serum (ArGH) to neutralize the activity of circulating GH, and glucose metabolism was measured in adipose tissue in vitro in the absence or presence of insulin. Short term (6-h) GH deficiency led to a 10% decrease in hyperglycemia (P = 0.002) in SZ-diabetic rats. Basal glucose oxidation and insulin responses in adipose tissue were unchanged by acute ArGH treatment. Since hyperglycemia was improved when adipose tissue metabolism was unaltered, GH-dependent changes occurring in other tissues, such as liver or muscle, most likely contribute to derangements of glucose metabolism in diabetes, even when GH is not elevated. Prolonged GH deficiency was produced by infusing ArGH into SZ-diabetic rats for 5 days. In these animals, the relative fat content (percentage of wet weight) of adipose tissue was significantly increased. In addition, the conversion of [14C]glucose to lipid and CO2 in adipose tissue was significantly increased with chronic GH deficiency in SZ-diabetic rats, but the ability of insulin to stimulate glucose metabolism in the tissue was unaffected. These results indicate that endogenous GH suppresses basal glucose utilization in adipose tissue of diabetic animals; this is reversed by prolonged (5-day), but not acute (6-h), ArGH treatment. Taken together, these findings suggest that the role of endogenous GH in the regulation of glucose metabolism in diabetic animals involves several mechanisms and multiple tissues.
Published Version
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