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      Glucocorticoid Effects on the Diurnal Rhythm of Circulating Leptin Levels

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          It is known that circulating leptin shows diurnal variation with a nocturnal rise; however, the mechanisms generating this rhythm have not been fully elucidated. Glucocorticoids are a potent stimulator of leptin secretion, and there is a reciprocal relationship between circulating leptin and glucocorticoid levels. We hypothesized that glucocorticoids could modulate the diurnal rhythm of circulating leptin. We therefore explored the diurnal variation of leptin under situations in which subjects showed no or some shift of glucocorticoid diurnal rhythm, such as prednisolone-administered humans, and adrenalectomized and corticosterone-replaced (ADX+B) rats. The peak level of plasma cortisol immunoreactivity was shifted from early morning to noon by prednisolone administration. The nocturnal increment of plasma leptin in prednisolone-administered patients (71.2 ± 14.2% from 08:00 h value) was significantly greater than that in normal volunteers (12.2 ± 7.5% from 08:00 h value), but the timing of nadir and the peak of plasma leptin was not shifted. In normal rats, the plasma concentration of leptin showed the diurnal rhythm with the bottom at 16:00 h and the top between midnight and early morning. The amplitude of leptin diurnal rhythm was significantly reduced in ADX+B rats (08:00 h: 3.0 ± 0.2, 16:00 h: 2.7 ± 0.2, 00:00 h; 3.7 ± 0.2 ng/ml) compared with sham operated rats (08:00 h: 3.0 ± 0.2, 16:00 h 2.2 ± 0.2, 00:00 h: 4.7 ± 0.4 ng/ml); but ADX+B rats still retained similar timing of nadir and the peak of plasma leptin as observed in sham rats. These results indicate that glucocorticoids enhance the amplitude of leptin diurnal rhythm, and are consistent with previous findings showing that glucocorticoids increase leptin secretion. Glucocorticoids appear to play modulatory, but not essential roles in generating leptin diurnal rhythm.

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          Induction of ob gene expression by corticosteroids is accompanied by body weight loss and reduced food intake.

          Genetic studies in mice have identified the ob gene product as a potential signaling factor regulating body weight homeostasis and energy balance. It is suggested that modulation of ob gene expression results in changes in body weight and food intake. Glucocorticoids are shown to have important metabolic effects and to modulate food intake and body weight. In order to test the hypothesis that these metabolic effects of glucocorticoids are linked to changes in the expression of the ob gene, ob mRNA levels were evaluated in rats treated with different glucocorticosteroids at catabolic doses and correlated to the kinetics of changes in body weight gain and food intake. Results from time course experiments demonstrate that adipose tissue ob gene expression is rapidly induced by glucocorticosteroids. This induction is followed by a concordant decrease in body weight gain and food consumption. These data suggest that the catabolic effects of corticosteroids on body weight mass and food intake might be mediated by changes in ob expression. Modulation of ob expression may therefore constitute a mechanism through which hormonal, pharmacological, or other factors control body weight homeostasis.
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            Dexamethasone regulates obese expression in isolated rat adipocytes.

             K Shima,  M Iida,  T. Murakami (1995)
            An obese (ob) gene product, expressed specifically in adipose tissues, regulates energy balance. Here we report adipocytes in adipose tissue actually express ob mRNA and that a synthetic glucocorticoid (dexamethasone) regulates expression of the ob gene. Addition of 100 nM dexamethasone to isolated rat adipocytes rapidly induced a 4-8 fold increase in ob mRNA. This increase in ob mRNA level was apparent within 1 h, and reached a maximum at about 7 h after stimulation. The dexamethasone-stimulated increase of ob mRNA was only partially blocked by protein synthesis inhibitors cycloheximide (20 micrograms/ml) or anisomycin (200 microM). This suggests that new protein synthesis is not necessarily required for the observed dexamethasone-stimulated increase in ob mRNA.
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              Regulation of Expression ofobmRNA and Protein by Glucocorticoids and cAMP


                Author and article information

                Horm Res Paediatr
                Hormone Research in Paediatrics
                S. Karger AG
                09 March 2001
                : 54
                : 2
                : 69-73
                aSecond Department of Internal Medicine, Kochi Medical School, Kohasu, Nankoku, Kochi and bFukuyama Yuuai Hospital, Fukuyama, Hiroshima, Japan
                53234 Horm Res 2000;54:69–73
                © 2001 S. Karger AG, Basel

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                Page count
                Figures: 3, Tables: 2, References: 28, Pages: 5
                Original Paper


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