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卵巢激素调节骨髓来源细胞中脂肪细胞的生成。

Ovarian Hormones Regulate the Production of Adipocytes From Bone Marrow-Derived Cells.

作者信息

Gavin Kathleen M, Sullivan Timothy M, Kohrt Wendy M, Majka Susan M, Klemm Dwight J

机构信息

Division of Geriatric Medicine, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.

Charles C. Gates Center for Regenerative Medicine and Stem Cell Biology, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.

出版信息

Front Endocrinol (Lausanne). 2018 May 28;9:276. doi: 10.3389/fendo.2018.00276. eCollection 2018.

DOI:10.3389/fendo.2018.00276
PMID:29892267
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5985395/
Abstract

Sex differences in body fat distribution and menopause-associated shifts in regional adiposity suggest that sex hormones play an important role in regulating the differentiation and distribution of adipocytes, but the underlying mechanisms have not been fully explained. The aim of this study was to determine whether ovarian hormone status influences the production and distribution of adipocytes in adipose tissue arising from bone marrow-derived cells. Nine- to ten-week-old ovariectomized (OVX), surgery naïve (WT), and estrogen receptor alpha knockout (αERKO) mice underwent bone marrow transplantation from luciferase or green fluorescent protein expressing donors. A subset of OVX animals had estradiol (E) added back. Eight-weeks posttransplant, whole body and gonadal fat BM-derived adipocyte production was highest in OVX and αERKO mice, which was attenuated in OVX mice by E add-back. All groups demonstrated the highest bone marrow derived adipocyte (BMDA) production in the gonadal adipose depot, a visceral fat depot in mice. Taken together, the loss of ovarian hormones increases the production of BMDAs. If translatable across species, production of BMDA may be a mechanism by which visceral adiposity increases in estrogen-deficient postmenopausal women.

摘要

体脂分布的性别差异以及与更年期相关的局部肥胖变化表明,性激素在调节脂肪细胞的分化和分布中起着重要作用,但其潜在机制尚未完全阐明。本研究的目的是确定卵巢激素状态是否会影响源自骨髓细胞的脂肪组织中脂肪细胞的产生和分布。对9至10周龄的去卵巢(OVX)、未接受过手术的野生型(WT)和雌激素受体α基因敲除(αERKO)小鼠进行了来自表达荧光素酶或绿色荧光蛋白的供体的骨髓移植。一部分OVX动物补充了雌二醇(E)。移植后8周,OVX和αERKO小鼠的全身和性腺脂肪中源自骨髓的脂肪细胞生成量最高,而在补充E的OVX小鼠中这一量有所减弱。所有组在性腺脂肪库(小鼠的一个内脏脂肪库)中骨髓源性脂肪细胞(BMDA)的生成量最高。综上所述,卵巢激素的缺失会增加BMDA的生成。如果这种现象可以跨物种转化,那么BMDA的产生可能是雌激素缺乏的绝经后女性内脏肥胖增加的一种机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/881f/5985395/ed222b161d3b/fendo-09-00276-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/881f/5985395/6783384a5d1c/fendo-09-00276-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/881f/5985395/bdaf1680e607/fendo-09-00276-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/881f/5985395/567fecfe6464/fendo-09-00276-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/881f/5985395/ed222b161d3b/fendo-09-00276-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/881f/5985395/6783384a5d1c/fendo-09-00276-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/881f/5985395/bdaf1680e607/fendo-09-00276-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/881f/5985395/567fecfe6464/fendo-09-00276-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/881f/5985395/ed222b161d3b/fendo-09-00276-g004.jpg

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