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脂肪组织中PI3K p110缺失导致雄性小鼠不育和青春期启动延迟。

Loss of PI3K p110 in the Adipose Tissue Results in Infertility and Delayed Puberty Onset in Male Mice.

作者信息

Nelson Victoria L Boughton, Negrón Ariel L, Reid Inefta, Thomas Justin A, Yang Leon, Lin Richard Z, Acosta-Martínez Maricedes

机构信息

Department of Physiology and Biophysics, Stony Brook University Medical Center, Stony Brook, NY, USA.

Department of Physiology and Biophysics, Stony Brook University Medical Center, Stony Brook, NY, USA; Graduate Program in Neuroscience, State University of New York at Stony Brook, Stony Brook, NY, USA.

出版信息

Biomed Res Int. 2017;2017:3756089. doi: 10.1155/2017/3756089. Epub 2017 Mar 5.

DOI:10.1155/2017/3756089
PMID:28357399
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5357525/
Abstract

Deletion of PI3K catalytic subunit p110 in adipose tissue (aP2-Cre/p110, -/- hereafter) results in increased adiposity, glucose intolerance, and liver steatosis. Because this endocrine organ releases hormones like leptin, which are important in reproductive physiology, we investigated the reproductive phenotype of -/- males. Compared to controls, -/- males displayed delayed onset of puberty accompanied by a reduction in plasma LH levels and testicular weight. At postnatal day 30, -/- mice exhibited normal body weight but elevated fasted plasma leptin levels. Testicular leptin gene expression was increased, whereas expression of the cholesterol transporter StAR and of P450 cholesterol side chain cleavage enzyme was decreased. Adult -/- males were infertile and exhibited hyperandrogenemia with normal basal LH, FSH, and estradiol levels. However, neither sperm counts nor sperm motility was different between genotypes. The mRNA levels of leptin and of 17-beta-dehydrogenase 3, and enzyme important for testosterone production, were significantly higher in the testis of adult -/- males. The mRNA levels of ER, an important regulator of intratesticular steroidogenesis, were lower in the testis of adult and peripubertal -/- males. We propose that chronic hyperleptinemia contributes to the negative impact that disrupting PI3K signaling in adipocytes has on puberty onset, steroidogenesis, and fertility in males.

摘要

脂肪组织中PI3K催化亚基p110的缺失（以下简称aP2-Cre/p110, -/-）会导致肥胖、葡萄糖耐量异常和肝脂肪变性增加。由于这个内分泌器官会释放如瘦素等在生殖生理学中很重要的激素，我们研究了-/-雄性小鼠的生殖表型。与对照组相比，-/-雄性小鼠青春期开始延迟，同时血浆促黄体生成素（LH）水平和睾丸重量降低。出生后第30天，-/-小鼠体重正常，但空腹血浆瘦素水平升高。睾丸瘦素基因表达增加，而胆固醇转运蛋白类固醇生成急性调节蛋白（StAR）和P450胆固醇侧链裂解酶的表达降低。成年-/-雄性小鼠不育，表现为高雄激素血症，基础LH、促卵泡生成素（FSH）和雌二醇水平正常。然而，不同基因型之间的精子数量和精子活力并无差异。成年-/-雄性小鼠睾丸中瘦素和17-β-脱氢酶3（一种对睾酮生成很重要的酶）的mRNA水平显著更高。雌激素受体（ER）是睾丸内类固醇生成的重要调节因子，在成年和青春期前-/-雄性小鼠的睾丸中，其mRNA水平较低。我们认为，慢性高瘦素血症导致脂肪细胞中PI3K信号通路破坏对雄性青春期启动、类固醇生成和生育能力产生负面影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0918/5357525/41bd290500ac/BMRI2017-3756089.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0918/5357525/65486f9830be/BMRI2017-3756089.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0918/5357525/2a4de91c7073/BMRI2017-3756089.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0918/5357525/1cd104a49e9a/BMRI2017-3756089.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0918/5357525/b7007eb05e3b/BMRI2017-3756089.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0918/5357525/41bd290500ac/BMRI2017-3756089.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0918/5357525/65486f9830be/BMRI2017-3756089.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0918/5357525/2a4de91c7073/BMRI2017-3756089.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0918/5357525/1cd104a49e9a/BMRI2017-3756089.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0918/5357525/b7007eb05e3b/BMRI2017-3756089.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0918/5357525/41bd290500ac/BMRI2017-3756089.005.jpg

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Targeting adipose tissue in the treatment of obesity-associated diabetes.靶向脂肪组织治疗肥胖相关性糖尿病。
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Leptin Within the Subphysiological to Physiological Range Dose Dependently Improves Male Reproductive Function in an Obesity Mouse Model.
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