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SUMMARY
The effect of α-MSH on sebum secretion and preputial gland weight was examined in intact, castrated and hypophysectomized male rats and in hypophysectomized rats receiving treatment with either testosterone propionate (TP) or progesterone. After treatment with α-MSHMSH for 2 weeks, increases in sebum secretion occurred in intact, castrated and hypophysectomized rats, but larger responses were found in the hypophysectomized rats that had received treatment with either TP or progesterone, suggesting that α-MSH acts synergistically with TP and progesterone to stimulate sebum secretion. α-Melanocyte-stimulating hormone also increased preputial gland weight in intact rats, but there was no response after castration and only a small response after hypophysectomy. However, when the hypophysectomized rats received simultaneous treatment with either TP or progesterone, α-MSH increased preputial gland weight.
It is suggested that α-MSH acts directly on the sebaceous glands to stimulate lipogenesis and, together with steroid hormones, may have an important role in controlling sebaceous gland function in the rat and other hairy mammals. With the evolution of hair, certain of the MSH peptides may have lost their significance as pigmentary hormones and have developed a sebotrophic function. For this reason, it might be more appropriate to refer to these peptides as the 'sebotrophins'.
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Adipocytes contain large lipid droplets in their cytoplasm. When cultured, they float on top of the medium, clump together, and do not gain equal and sufficient access to the medium. Morphological changes cannot be observed and the majority of adipocytes undergo cell lysis within 72 h of isolation. We have used a ceiling culture method for human mature adipocytes which uses their buoyant property to allow them to adhere to a floating glass surface, where they remain viable for several weeks. Using confocal immunofluorescence microscopy we showed the cellular expression and subcellular localization of leptin in ceiling-cultured adipocytes. The secretion of leptin was increased from ceiling cultures following tumour necrosis factor-alpha treatment. Proliferation of mature human adipocytes in serum-containing medium was demonstrated by incorporation of bromodeoxyuridine, 2% of adipocytes showing positive incorporation after 4 h labelling. Proliferation was also evident from the budding of daughter cells. Apoptosis in the ceiling cultures was increased by 48 h serum deprivation (30-35 vs 10-15% in the control) and was assayed by propidium iodide staining and terminal deoxynucleotidyl transferase-mediated dUTP-fluorescein nick-end labelling. Lipolysis, analysed by liquid scintillation counting, was increased by forskolin (10 microM for 90 min) and lipogenesis, shown by autoradiography, was stimulated by insulin (10 and 100 nM for 4 h). These findings indicate that ceiling-cultured adipocytes maintain adipocyte-specific functions and that ceiling culture, which overcomes the shortcomings of adipocyte suspension culture, can be used to study adipocyte cell biology.
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Treatment of HIV infection using protease inhibitors is frequently associated with lipodystrophy and impaired lipid and glucose metabolism. We examined the effect of saquinavir, one of the protease inhibitors, on lipid metabolism and glucose transport in cultured adipocytes. Saquinavir inhibited lipoprotein lipase (LPL) activity in 3T3-F442A and 3T3-L1 adipocytes. The inhibition of LPL was 81% at a concentration of 20 microg/ml. Another closely related drug, indinavir, had a small inhibitory effect. Saquinavir also inhibited the biosynthesis of lipids from [(14)C]-acetate. Saquinavir increased the lipolysis. Saquinavir had no significant effect on the cellular protein synthesis or protein content. Saquinavir increased the basal glucose transport threefold and decreased insulin-stimulated glucose transport by 35%. These studies suggest that some HIV protease inhibitors have direct effects on lipid and glucose metabolism. This inhibition of lipogenesis and glucose transport may explain some of the lipodystrophy, dyslipidemia and disturbed glucose metabolism with the clinical use of these drugs.
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Pregnancy and progesterone treatment of ovariectomized rats decrease glucose metabolism through the pentose-phosphate pathway in isolated female rat adipocytes. As demonstrated in previous studies, progesterone directly decreases [1-14C]glucose oxidation through the pentose-phosphate pathway and lipogenesis from [6-14C]glucose; the present study therefore compared glucose-induced lipid synthesis during pregnancy (10, 16 and 20 days of pregnancy) with the effect of progesterone treatment (5 mg/rat per day for 14 days) to shed more light on the role of this steroid in glucose metabolism during pregnancy. The inhibition of [6-14C]glucose incorporation into triacylglycerols in the progesterone-treated rats was comparable to that which occurs during late (20 days) and mid-pregnancy (16 days) but not during early pregnancy (10 days). The inhibition of fatty acid synthesis was more important as pregnancy advanced and was different from the decrease in fatty acid synthesis induced by progesterone treatment. The sensitivity to insulin was comparable in virgin, ovariectomized and progesterone-treated ovariectomized rats but not in pregnant rats. This implies that progesterone and insulin affect glucose-induced lipid synthesis by distinct processes and that the impaired glucose metabolism is characterized by a reduction in basal glucose utilization rather than by an impaired insulin response.
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ABSTRACT
Inhibition of prolactin secretion with bromocriptine and neutralization of GH action with a specific antiserum to rat GH (rGH) were used to explore the modes of action of GH and prolactin in maintaining lactation in the rat. Treatment of dams with anti-rGH caused a small reduction in litter weight gain whilst bromocriptine reduced litter weight gain by 50%. When both treatments were combined, however, milk yield ceased completely and this wasaccompanied by a wide variety of effects on mammary lipid metabolism including decreases in the mRNA concentrations of acetyl CoA carboxylase, fatty acid synthase, malic enzyme and lipoprotein lipase. Activities of acetyl CoA carboxylase and lipoprotein lipase were also significantly reduced. Reciprocal changes were evident in adipose tissue with increases in acetyl CoA carboxylase and lipoprotein lipase activities. In conjunction with a decreased lipolytic response to noradrenaline in adipose tissue of animals given the combined treatment of bromocriptine and anti-rGH, this represented a co-ordinated series of changes to reduce lipid synthesis in the mammary gland and enhance lipogenesis and triglyceride storage in adipose tissue as milk production ceased. All of these effects could be prevented in part by concurrent treatment with GH, but insulin-like growth factor-I (IGF-I) and IGF-II failed to affect any of the parameters measured. Taken as a whole, these data suggest that (1) both prolactin and GH induce a co-ordinated series of changes in the mammary gland, (2) the intracellular controls involved clearly operate at the level of gene transcription although post-translational controls are also probably involved, (3) the effects of GH on the mammary gland could not be mimicked by IGFs and (4) although GH clearly regulates lipid metabolism in adipose tissue in a manner which should favour nutrient utilization by the mammary gland, these effects are probably too small to account for the effects of GH on milk production. Since GH receptors have not been reported to be present on mammary secretory cells, the precise mode of action of GH remains uncertain.
Journal of Endocrinology (1992) 135, 195–202
Center of Brain, Behavior and Metabolism, University of Lübeck, Lübeck, Germany
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Institute for Human Genetics, Epigenetics and Metabolism Lab, University of Lübeck, Lübeck, Germany
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Center of Brain, Behavior and Metabolism, University of Lübeck, Lübeck, Germany
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Center of Brain, Behavior and Metabolism, University of Lübeck, Lübeck, Germany
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Institute for Human Genetics, Epigenetics and Metabolism Lab, University of Lübeck, Lübeck, Germany
German Center for Diabetes Research (DZD), Helmholtz Zentrum München, Bayern, Germany
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Center of Brain, Behavior and Metabolism, University of Lübeck, Lübeck, Germany
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breakdown gene expression by VSG; t -tests against hypothetical mean, detected rhythmicity (R) with JTK_CYCLE P < 0.05. (E) Mean normalized expression of genes associated with lipogenesis; two-way ANOVA: group effect #### P < 0.0001, Sidak’s post hoc
University Paris sud, bat 447, 91405 Orsay Cedex, France
Faculty of Agriculture, Institute of Biochemistry, Food Science and Nutrition, The Hebrew University, Rehovot 76100, Israel
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University Paris sud, bat 447, 91405 Orsay Cedex, France
Faculty of Agriculture, Institute of Biochemistry, Food Science and Nutrition, The Hebrew University, Rehovot 76100, Israel
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University Paris sud, bat 447, 91405 Orsay Cedex, France
Faculty of Agriculture, Institute of Biochemistry, Food Science and Nutrition, The Hebrew University, Rehovot 76100, Israel
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University Paris sud, bat 447, 91405 Orsay Cedex, France
Faculty of Agriculture, Institute of Biochemistry, Food Science and Nutrition, The Hebrew University, Rehovot 76100, Israel
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University Paris sud, bat 447, 91405 Orsay Cedex, France
Faculty of Agriculture, Institute of Biochemistry, Food Science and Nutrition, The Hebrew University, Rehovot 76100, Israel
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(4) as in human, lipogenesis occurs essentially in the liver of chickens ( Leveille et al. 1968 ), however, in rodents, lipogenesis occurs in both adipose tissue and liver ( Blair et al. 1991 ). Therefore, chicken is an interesting model for
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-enriched diet. Glucose metabolism was assessed through analysis of systemic insulin sensitivity, while lipid metabolism was analyzed at the level of visceral adiposity, VAT histology and the expression of GC-target genes involved in lipogenesis. Besides GR
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metabolic homoeostasis ( Oetting & Yen 2007 ). The ability of thyroid hormones to induce anabolic and catabolic pathways, such as lipogenesis and lipolysis, contributes to thyroid hormone-induced increase in energy expenditure ( Pucci et al . 2000
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Centre for Endocrinology, Department of Endocrine Neurobiology, Division of Endocrinology, Oxford Centre for Diabetes, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK
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Centre for Endocrinology, Department of Endocrine Neurobiology, Division of Endocrinology, Oxford Centre for Diabetes, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK
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reduced adipose tissue lipid stores with inhibition of lipogenesis and also to reduced lipolysis with reduction in free fatty acid release. Interestingly, AMPK activity is lower in the adipose tissues of patients who are insulin-resistant than in those of
