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Neuropeptide Y (NPY) is the most powerful appetite stimulant known, and rates of synthesis and release in the hypothalamus correlate closely with nutritional status. Pregnancy and lactation provide an excellent model of physiological hyperphagia. In this study the authors measured food intake, plasma glucose, insulin and luteinizing hormone (LH) and hypothalamic NPY mRNA in rats during pregnancy and in early and late lactation. The effect of food restriction (to 80% of control) during lactation was also studied. Pregnancy resulted in a modest increase in daily food intake over non-lactating controls (controls: 15·6±0·6 g, pregnant: 19·8±1·1 g, P<0·01) During lactation food intake increased dramatically to 355% of non-lactating levels by the 12th day. Insulin and glucose levels were unchanged in lactation, except in the food-restricted animals, when insulin levels were reduced to 49·5±18·4 pmol/l compared with 215±55 pmol/l (P<0·01) in lactating, non-restricted animals, and glucose was reduced to 3·7±0·2 mmol/l compared with 5·1 ± 0·2 mmol/l in non-restricted lactating animals. Hypothalamic NPY mRNA was unchanged in pregnancy, moderately increased after 5 days lactation (130±6·2% of control, P<0·01) and increased further at 14 days lactation (179 ± 14%, P<0·001). The greatest changes occurred in the animals who were food-deprived during lactation, when hypothalamic NPY mRNA levels reached 324 ± 44% (P<0·001) of non-lactating levels. Increases in hypothalamic NPY synthesis may be partly responsible for the increase in food intake seen in lactation, but unlike in food deprivation, the increase is not related to circulating insulin, suggesting involvement of other regulatory factors.
Journal of Endocrinology (1997) 152, 365–369
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Abstract
To investigate the role of cortisol in the etiology of insulin resistance in men and women, we examined 218 healthy non-hospitalized elderly, selected from the Rotterdam Study. Free cortisol was assessed by the ratio of fasting serum cortisol over corticosteroid-binding globulin (CBG), and insulin resistance was estimated by the fasting insulin level. CBG was higher in women and decreased with age. In both men and women, the early morning free cortisol level showed no association with age or waist/hip ratio. In men, an inverse association between cortisol and body mass index was observed. In women, higher cortisol levels were associated with increased insulin levels; an increase of 9·7 mU/l insulin per unit cortisol/CBG (s.e. 3·9, P=0·01). The association did not change after adjustment for age, body mass index or waist/hip ratio. The results of this study in elderly subjects suggest that in women cortisol may be implicated in the age-associated insulin resistance.
Journal of Endocrinology (1996) 149, 313–318
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Search for other papers by J. G. D. Lambert in
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ABSTRACT
Quantitative aspects of bioconversions in the testes of the African catfish (Clarias gariepinus) were studied in vitro by incubation of tissue with [3H]pregnenolone or [3H]androstenedione. During the breeding period, spawning and non-spawning animals were collected from their natural habitat, the Hula nature reserve, in northern Israel. In the same period, non-spawning animals were collected from a fish pond in the same region. It was shown that spawning was accompanied by significant changes in steroid bioconversions, i.e. a reduction in androgen synthesis, especially of 11β-hydroxyandrostenedione and 11β-hydroxytestosterone and an increase in the production of C21-steroids, especially progesterone, 17α-hydroxyprogesterone and a pregnenolone ester. These changes resulted from a decreased contribution of the cytochrome P-450 enzymes 17α-hydroxylase, C17–20-lyase and 11β-hydroxylase. A rise in plasma gonadotrophin concentration was observed only in spawning catfish. In the absence of such an increase in plasma gonadotrophin, steroid synthesis in the testes of non-spawning feral and pond catfish was primarily directed towards the production of 11-oxygenated androgens and 5β-pregnane-3α,17α,20α-triol. It is suggested that spawning is induced by gonadotrophin and the ensuing change in steroidogenesis. It is possible that husbandry conditions inhibit the necessary increase in gonadotrophin release.
J. Endocr. (1987) 112, 323–332
