Our aims were to further characterize the stimulatory effect of glucagon on brown fat and to test the hypothesis that physiological levels of hyperglucagonemia would stimulate brown fat thermogenesis. In the first set of experiments, glucagon (1 mg/kg sc twice daily) or vehicle control was administered three times in 26 h. This large dose of glucagon produced increases in GDP binding to brown fat mitochondria. In addition, Scatchard analysis indicated a glucagon-induced increase in number of GDP binding sites without evidence for alteration in binding site affinity. No consistent increase in brown fat mitochondrial GDP binding was produced 2 h after a single injection of glucagon (1 mg/kg). In the second set of experiments, glucagon was administered intraperitoneally by constant osmotic minipump infusion. Glucagon in a dose of 150 micrograms.kg-1.day-1 for 5 days produced significant increases in GDP binding to brown fat mitochondria, whereas glucagon serum levels were increased but stayed within the usual physiological range. A larger dose of glucagon administered by constant infusion virtually eliminated body weight gain over 7 days while significantly increasing nucleotide binding (GDP) to brown fat mitochondria. An important role for glucagon in thermogenic regulation is suggested.
Synthetic luteinizing hormone releasing hormone (LH-RH) provides a useful tool for the study of pituitary regulation in the hypothalamo-adenohypophysialgonadal system. Negro-Villar, Orias & McCann (1973) showed that oestradiol-17\g=b\ given 2 h before injection of LH-RH to ovariectomized rats reduced luteinizing hormone (LH) release. In male dogs, Jones & Boyns (1974) have found that oestradiol-17\g=b\ or diethylstilboestrol similarly reduces LH release in response to LH-RH given 2\m=.\5 h, but not 24 h later. Androgens were without effect in that study.We now report the gonadotrophin responses to LH-RH in healthy men 2 h after i.m. injection of either oestradiol benzoate (2 mg in 1 ml ethyl oleate), testosterone propionate (5 mg in 1 ml ethyl oleate), or with no acute steroid pretreatment.Five men volunteered for these ambulatory studies. They were 20-35 years old, had no history of endocrine disorders and were not taking medication.At least 2 weeks elapsed between experiments. Blood was taken by venepuncture, separated, and stored frozen until assayed for LH and follicle-stimulating hormone (FSH) by radioimmunoassays which have been described previously (Groom, Groom, Cooke & Boyns, 1971). The initial blood sample was always taken between 09.15 and 10.00 h. After two more samples had been removed at hourly intervals, LH-RH (100 µg in sterile water) was injected i.m. and sampling continued every 30 min for 4-5 h.Gonadotrophin responses were calculated as mean ± s.e.m. after first normalizing the data for each man, by expressing hormone concentration as a fraction of the average level within an experiment, and then scaling to make the initial sample mean equal to 100. Significance of the difference between means was given by twotailed Student's i-test.Plasma concentrations of both LH and FSH were raised by LH-RH (Fig. 1). Administration of testosterone 2 h before LH-RH was given, reduced both the LH response (2P < 0-02) and the FSH response (2P < 0-01); oestradiol-17/? reduced the LH response still further (2 < 0-001 v. testosterone; 2 < 0-001 v. control).The effect of acute oestradiol-17/? pretreatment on FSH secretion was variable. In three men, the response was the same as in the control experiment (2 > 0-98) over the period 0-1 h after LH-RH injection; the other two men showed no stimu¬ lation of FSH release. The latter belonged to a group of three who had wives in the
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