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低睾酮和高瘦素激活过氧化物酶体增殖物激活受体信号通路诱导去势公鹅脂肪生成和脂肪沉积。

Low Testosterone and High Leptin Activate PPAR Signaling to Induce Adipogenesis and Promote Fat Deposition in Caponized Ganders.

机构信息

Institute of Animal Science, Jiangsu Academy of Agricultural Sciences, Nanjing 210014, China.

Key Laboratory of Crop and Livestock Integration, Ministry of Agriculture, Institute of Animal Science, Jiangsu Academy of Agricultural Sciences, Jiangsu Province Engineering Research Center of Precision Animal Breeding, Nanjing 210014, China.

出版信息

Int J Mol Sci. 2024 Aug 9;25(16):8686. doi: 10.3390/ijms25168686.

DOI:10.3390/ijms25168686
PMID:39201373
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11354323/
Abstract

Low or insufficient testosterone levels caused by caponization promote fat deposition in animals. However, the molecular mechanism of fat deposition in caponized animals remains unclear. This study aimed to investigate the metabolomics and transcriptomic profiles of adipose tissues and study the effect of testosterone and leptin on the proliferation of adipocytes. We observed a significant enlargement in the areas of adipocytes in the abdominal fat tissues in capon, as well as increased luciferase activity of the serum leptin and a sharp decrease in the serum testosterone in caponized gander. Metabolomics and transcriptomic results revealed differentially expressed genes and differentially expressed metabolites with enhanced PARR signal pathway. The mRNA levels of peroxisome proliferators-activated receptor γ, fatty acid synthase, and suppressor of cytokine signaling 3 in goose primary pre-adipocytes were significantly upregulated with high leptin treatment and decreased significantly with increasing testosterone dose. Hence, reduced testosterone and increased leptin levels after caponization possibly promoted adipocytes proliferation and abdominal fat deposition by altering the expression of PPAR pathway related genes in caponized ganders. This study provides a new direction for the mechanism through which testosterone regulates the biological function of leptin and fat deposition in male animals.

摘要

去势导致的低水平或不足的睾酮会促进动物脂肪沉积。然而,去势动物脂肪沉积的分子机制尚不清楚。本研究旨在研究脂肪组织的代谢组学和转录组学特征,并研究睾酮和瘦素对脂肪细胞增殖的影响。我们观察到,去势公鹅的腹部脂肪组织中脂肪细胞的面积明显增大,血清瘦素的荧光素酶活性增加,血清睾酮急剧下降。代谢组学和转录组学结果显示,具有增强 PARR 信号通路的差异表达基因和差异表达代谢物。鹅原代前体脂肪细胞中过氧化物酶体增殖物激活受体 γ、脂肪酸合酶和细胞因子信号转导抑制因子 3 的 mRNA 水平随着高瘦素处理而显著上调,随着睾酮剂量的增加而显著下降。因此,去势后睾酮水平降低和瘦素水平升高可能通过改变去势公鹅中 PPAR 通路相关基因的表达,促进脂肪细胞增殖和腹部脂肪沉积。本研究为睾酮调节雄性动物瘦素生物学功能和脂肪沉积的机制提供了新的方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3195/11354323/dd7ac9696ee1/ijms-25-08686-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3195/11354323/90b0f4e6d120/ijms-25-08686-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3195/11354323/e29d77bf0ac0/ijms-25-08686-g002.jpg
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