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首页> 外文期刊>Molecular and Cellular Biology >Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity
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Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity

机译：褐色脂肪YY1缺乏激活与能量消耗有关的分泌蛋白的表达，并防止饮食引起的肥胖

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Mitochondrial oxidative and thermogenic functions in brown and beige adipose tissues modulate rates of energy expenditure. It is unclear, however, how beige or white adipose tissue contributes to brown fat thermogenic function or compensates for partial deficiencies in this tissue and protects against obesity. Here, we show that the transcription factor Yin Yang 1 (YY1) in brown adipose tissue activates the canonical thermogenic and uncoupling gene expression program. In contrast, YY1 represses a series of secreted proteins, including fibroblast growth factor 21 (FGF21), bone morphogenetic protein 8b (BMP8b), growth differentiation factor 15 (GDF15), angiopoietin-like 6 (Angptl6), neuromedin B, and nesfatin, linked to energy expenditure. Despite substantial decreases in mitochondrial thermogenic proteins in brown fat, mice lacking YY1 in this tissue are strongly protected against diet-induced obesity and exhibit increased energy expenditure and oxygen consumption in beige and white fat depots. The increased expression of secreted proteins correlates with elevation of energy expenditure and promotion of beige and white fat activation. These results indicate that YY1 in brown adipose tissue controls antagonistic gene expression programs associated with energy balance and maintenance of body weight.
机译：棕色和米色脂肪组织中的线粒体氧化和生热功能调节能量消耗的速率。然而，尚不清楚米色或白色脂肪组织如何促进褐色脂肪的生热功能或补偿该组织中的部分缺陷并防止肥胖。在这里，我们表明棕色脂肪组织中的转录因子阴阳1（YY1）激活规范的生热和解偶联基因表达程序。与此相反，YY1抑制一系列分泌蛋白，包括成纤维细胞生长因子21（FGF21），骨形态发生蛋白8b（BMP8b），生长分化因子15（GDF15），血管生成素样6（Angptl6），神经调节素B和nesfatin，与能源支出有关。尽管棕色脂肪中的线粒体产热蛋白显着降低，但在该组织中缺乏YY1的小鼠仍受到强烈保护，可抵抗饮食引起的肥胖，并在米色和白色脂肪库中表现出增加的能量消耗和氧气消耗。分泌蛋白表达的增加与能量消耗的增加以及米色和白色脂肪活化的促进有关。这些结果表明，棕色脂肪组织中的YY1控制与能量平衡和体重维持相关的拮抗基因表达程序。

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