The effect of chronic glucocorticoid therapy on serum testosterone levels was studied in men aged 67 +/- 4 (SD) years with chronic pulmonary disease. The serum testosterone level was reduced in 14 of 16 patients to a mean value of 211 +/- 93 ng/dL, compared with 449 +/- 111 ng/dL in 11 age- and disease-matched control patients (p less than 0.001). The corticosteroid dosage and the serum testosterone level were inversely related (r = -0.78). Testosterone binding to serum proteins was not significantly affected. Basal gonadotrophin levels were not elevated while their secretory responses to exogenous gonadotrophin-releasing hormone (GnRH) were intact. We conclude that glucocorticoid therapy commonly reduces serum testosterone levels in older men due to alteration of hypothalamic GnRH secretion.

The influence of different levels of inhibition of prostaglandin (PG) synthesis on the release of insulin and glucagon was investigated in the basal state (5.6 mM glucose) and in response to 30-min perfusion of 16.7 mM glucose using the isolated perfused rat pancreas model. Flurbiprofen (FLR), a potent and selective inhibitor of PG synthesis, was present in the perfusate during the entire experimental period at a concentration of 10(-8), 5 X 10(-8), or 10(-6) M; control experiments were performed without the drug. Levels of immunoreactive PGE2, PGF2 alpha, insulin, and glucagon were measured in the portal venous effluent. FLR inhibited PG synthesis in a dose-related manner; PGE2 was inhibited more than PGF2 alpha. Basal and glucose-induced secretion of insulin was augmented by FLR at 5 X 10(-8) M, but was inhibited at 10(-6) M. At 10(-6) M FLR, basal glucagon secretion was inhibited; glucose-induced suppression still occurred without any potentiation. We conclude that 1) endogenous PGs modulate the secretion of insulin and glucagon; 2) divergence of the effects of low and high levels of inhibition of PG biosynthesis on insulin release may be due to altered tissue proportions of various PGs and related autacoids; and 3) the predominant effect of endogenous PGs on glucagon release is tonic stimulation.

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