Body fat distribution, the menopause transition, and hormone replacement therapy.
Body fat distribution, the menopause transition, and hormone replacement therapy.
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DOI：
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发表时间：
2000-02
影响因子：
7.2
通讯作者：
A. Tchernof;E. Poehlman;J. Despres
中科院分区：
文献类型：
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作者：
A. Tchernof;E. Poehlman;J. Despres
更年期过渡引起的内分泌变化极大地改变了妇女的荷尔蒙环境。这些变化的后果不仅会导致女性生殖停止和伴随症状，还会极大地影响长期健康。雌激素的丢失与心血管疾病的发展有关。脂肪组织的集中分布和积聚以及伴随的胰岛素抵抗性血脂异常状态已成为与冠心病密切相关的一组代谢异常的重要组成部分。因此，雌激素缺乏可能会影响心血管疾病的风险，介导的变化，在身体脂肪分布。这篇文章是一个更新的文献领域的更年期，激素替代疗法，和身体脂肪分布。采用人体测量腹部脂肪分布的横断面研究往往未能检测到绝经过渡期的影响，这是独立的年龄增长和肥胖程度。然而，使用放射学技术，如DEXA和计算机断层扫描，得出的结论是，绝经过渡加速了腹腔内脂肪的选择性沉积。现有的纵向数据也支持增加中心体肥胖发生更年期。大多数关于激素替代疗法和体脂分布的干预试验表明，该疗法可预防未接受治疗或接受安慰剂的绝经后妇女的中心性肥胖增加。这些结果得到了回顾性研究的支持，这些研究表明激素使用者与非使用者相比WHR较低。可能解释绝经相关腹部脂肪积累加速的机制包括面对正能量失衡时局部脂肪组织代谢的变化。由于在研究中发现了一些不一致之处，需要使用纵向和干预设计进行进一步调查，以及更精确的方法来测量体脂分布，以明确绝经和激素替代对腹部体脂分布的影响以及伴随的心血管疾病风险增加。
Endocrine changes resulting from the menopause transition dramatically modify women's hormonal milieu. The consequences of these changes not only lead to cessation of reproduction and accompanying symptoms in women, but also dramatically impact long-term health. Loss of estrogen has been associated with the development of cardiovascular disease. Central distribution and accumulation of adipose tissue, and the concomitant insulin resistant dyslipidemic state have emerged as important components of a cluster of metabolic abnormalities that are strongly related to coronary heart disease. Thus, estrogen deficiency may affect cardiovascular disease risk by mediating changes in body fat distribution. This article is an update of the literature in the area of menopause, hormone replacement therapy, and body fat distribution. Cross-sectional studies using anthropometric measurements of abdominal fat distribution most often failed to detect an effect of the menopause transition that was independent of advancing age and degree of obesity. The use of radiologic techniques such as DEXA and computed tomography, however, led to the conclusion that the menopause transition accelerates the selective deposition of intra-abdominal fat. Available longitudinal data also support an increase in central body fatness occurring with menopause. Most intervention trials on hormone replacement therapy and body fat distribution showed that the treatment prevented the increase in central adiposity that was noted in postmenopausal women receiving no treatment or placebo. These results are supported by retrospective studies that showed a lower WHR in hormone users vs non-users. Mechanisms potentially explaining the menopause-related acceleration in abdominal fat accumulation include changes in regional adipose tissue metabolism in the face of a positive energy imbalance. As some inconsistencies were found among studies, further investigations using longitudinal and intervention designs, as well as more precise methodologies to measure body fat distribution, are needed to clearly establish the effects of menopause and hormone replacement on abdominal body fat distribution and the concomitant increase in cardiovascular disease risk.