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脂肪组织激素和胃饥饿素与骨代谢的关系

[Relationships of hormones of adipose tissue and ghrelin to bone metabolism].

作者信息

Zofková I

机构信息

Endokrinologický ustav Praha.

出版信息

Vnitr Lek. 2009 Jun;55(6):560-4.

PMID:19662887
Abstract

Body adipose tissue influences bone metabolism through mechanical load, as well as via hormones released into circulation. Such hormones are adipocytokines--leptin, adiponectin, TNF-alpha, IL-6, resistin and visfatin. Some of them exert an osteoanabolic effect, while the others activate bone resorption. An increasingly discussed adipocytokine is leptin, which fundamental role is regulation of food intake ensuring survival of the organism during starvation. Leptin also stimulates osteoblasts and activates bone formation. The direct osteotropic effect of leptin is modulated by interaction with hypothalamic centers and neurohormones. Apparently, the most important leptin sensitive pathway involved in bone regulation is the beta-adrenergic system. While activation of beta-1-adrenergic receptors by leptin enhances bone formation, activation of beta-2-adrenergic receptors in hypothalamus and in the skeleton increases bone resorption. In humans, an anabolic effect on the skeleton prevails. In pubertal girls, leptin extensively released into circulation at the moment when adipose tissue reaches a critical volume, stimulates synthesis of GnRH and induces puberty, which is followed by striking increases in bone mass. Low leptin levels in anorexia nervosa are associated with amenorrhoea, which slows down increase of bone mass and may induce osteopenia. Important adipocytokine with an unambiguous negative effect on bone is adiponectin. Decreased production of this hormone explains in part the lower prevalence of osteoporosis in obese persons. In this article, the osteotropic importance ofleptin-sensitive neurohormonal mechanisms and other hormones related to adipose tissue are discussed. Clinical importance of the above mentioned hormones to integrity of the skeleton has not yet been verified.

摘要

身体脂肪组织通过机械负荷以及释放到循环系统中的激素来影响骨代谢。这些激素就是脂肪细胞因子——瘦素、脂联素、肿瘤坏死因子-α、白细胞介素-6、抵抗素和内脂素。其中一些发挥骨合成代谢作用,而另一些则激活骨吸收。一种越来越受关注的脂肪细胞因子是瘦素,其基本作用是调节食物摄入,以确保机体在饥饿期间存活。瘦素还刺激成骨细胞并激活骨形成。瘦素的直接促骨作用通过与下丘脑中心和神经激素的相互作用来调节。显然,参与骨调节的最重要的瘦素敏感途径是β-肾上腺素能系统。瘦素激活β-1-肾上腺素能受体可增强骨形成,而下丘脑和骨骼中β-2-肾上腺素能受体的激活则增加骨吸收。在人类中,对骨骼的合成代谢作用占主导。在青春期女孩中,当脂肪组织达到临界体积时大量释放到循环系统中的瘦素,刺激促性腺激素释放激素的合成并诱导青春期,随后骨量显著增加。神经性厌食症患者瘦素水平低与闭经有关,闭经会减缓骨量增加并可能导致骨质减少。对骨骼有明确负面影响的重要脂肪细胞因子是脂联素。这种激素分泌减少部分解释了肥胖者骨质疏松患病率较低的原因。本文讨论了瘦素敏感的神经激素机制以及与脂肪组织相关的其他激素的促骨重要性。上述激素对骨骼完整性的临床重要性尚未得到证实。

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