Direct Effects of Growth Hormone on Insulin Action in Rat Adipose Tissue Maintained in Vitro*

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Abstract
Previous studies have shown that there is impaired insulin action in states of GH excess. In the present work, an organ culture system for adipose tissue was used in an attempt to characterize those diabetogenic cellular alterations directly attributable to GH. Pieces of rat epididymal fat tissue were maintained in supplemented medium 199 for 20–44 h in the absence or presence of bovine or human GH (5.0 × 10-7 to 5.0 × 10-10 M). [125I]Insulin binding, basal and insulin-stimulated 2-deoxyglucose uptake, and glucose utilization were measured in adipocytes isolated from the cultured tissue. Prolonged exposure to GH did not influence insulin receptor number or affinity. In contrast, GH-treated cells showed reduced hexose uptake in the basal state and in response to 0.2–40 ng/ml insulin. However, insulin sensitivity was not altered, since the incremental response to maximally effective concentrations of insulin and the concentration of insulin causing half-maximal stimulation were the same in GH-treated and untreated cells. Glucose metabolism, as measured by glucose conversion to CO2 and triglycerides, was also reduced by GH treatment in the basal and maximally stimulated states, but, again, altered insulin responsivity was not apparent. Furthermore, the proportions of metabolites formed were not affected by GH, suggesting that the observed metabolic changes were due to effects on glucose transport. Of the parameters measured in adipocytes, GH in vitro only inhibits basal glucose uptake. In this circumstance, excess GH does not lead to a true state of insulin resistance or altered sensitivity.