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引用次数: 37

摘要

瘦素与体脂的关系以及激素对体脂分布的调节将会被讨论。瘦素循环水平与体脂百分比密切相关,女性瘦素值通常是男性的两倍。有人认为雄激素的作用可以解释这种性别差异。胰岛素抵抗可能导致瘦素水平的广泛变化。瘦素水平和胰岛素抵抗在妊娠末期升高,分娩后恢复正常。此外,胰岛素抵抗与血浆瘦素水平升高相关,与体脂量无关,瘦素水平与胰岛素敏感性显著相关,与BMI无关。能量限制可以强烈地影响瘦素水平,克服身体成分变化的影响。从甘油三酯储存状态到释放状态的转变可能会下调瘦素的产生。腹内水平的甘油三酯通量取决于胰岛素和皮质类固醇(具有脂肪合成活性)以及性激素和生长激素(具有脂肪分解活性)之间的平衡。荷尔蒙和身体成分都随着年龄的增长而变化,主要是由于脂肪分解活动的减少,随之而来的是脂肪合成和内脏脂肪的积累。绝经后,男性腹内脂肪细胞的增大更为缓慢,而女性腹内脂肪细胞的增大更为突然。
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Hormones and body composition in humans: clinical studies.

Leptin in relation to body fat and hormonal regulation of body fat distribution will be treated. Leptin circulating levels are strongly related to the percentage of body fat and in women leptin values are always twofold those observed in men. A role of androgens has been suggested to explain this gender difference. Insulin resistance may contribute to the wide variation in leptin levels. Leptin levels and insulin resistance are increased at the end of pregnancy and normalize after delivery. Furthermore, insulin resistance is associated with elevated plasma leptin levels independent of body fat mass and leptin levels are significantly related to insulin sensitivity independent of BMI. Energy restriction can strongly influence leptin levels, overcoming the effects of body composition changes. The shift from a state of triglycerides storage to a state of release could down-regulate leptin production. Triglyceride flux at the intra-abdominal level depends on the balance between insulin and corticosteroids, which have liposynthetic activity, and between sexual and growth hormones, which have lipolytic activity. Both hormonal and body composition change with ageing, primarily due to a decrease in lipolytic activity, with consequent prevalence of liposynthesis and visceral fat accumulation. Enlargement of intra-abdominal adipose cells is more gradual in men and more abrupt in women after menopause.

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Concept of fat balance in human obesity revisited with particular reference to de novo lipogenesis. Role of energy charge and AMP-activated protein kinase in adipocytes in the control of body fat stores. Role of glucocorticoids in the physiopathology of excessive fat deposition and insulin resistance. Fat storage in pancreas and in insulin-sensitive tissues in pathogenesis of type 2 diabetes. Ectopic fat storage in heart, blood vessels and kidneys in the pathogenesis of cardiovascular diseases.
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