关键词: ATGL CTRP9 UCP-1 brown adipocytes lipolysis

Mesh : Animals Lipolysis Diet, High-Fat / adverse effects Adipose Tissue, Brown / metabolism Mice, Inbred C57BL Male Mice Adiponectin / metabolism genetics Insulin Resistance Lipase / metabolism genetics Cell Differentiation Adipogenesis / genetics Perilipin-1 / metabolism genetics Acyltransferases Glycoproteins

来  源:   DOI:10.31083/j.fbl2906236

Abstract:
BACKGROUND: This study aimed to elucidate the molecular mechanism through which C1q/tumor necrosis factor (TNF)-related protein 9 (CTRP9) acts in the formation and differentiation of brown adipose tissue (BAT).
METHODS: Adenovirus particles encoding CTRP9 and green fluorescent protein were inoculated into the scapula of C57BL/6J mice and fed a high-fat diet for 8 weeks; the body weight, lipid droplet morphology, glucose tolerance, insulin tolerance, and protein expression levels were analyzed. In addition, CTRP9 adenovirus was transfected into brown preadipocytes, and differentiation was induced to identify the effect of CTRP9 overexpression on adipocyte differentiation.
RESULTS: CTRP9 overexpression significantly increased the weight gain of mice. Additionally, the CTRP9 overexpression group exhibited significantly increased adipose tissue weight and glucose clearance rates and decreased insulin sensitivity and serum triglyceride levels compared to the control group. Furthermore, CTRP9 overexpression significantly upregulated the adipose triglyceride lipase (ATGL) and perilipin 1 protein expression levels in BAT. The cell experiment results confirmed that CTRP9 overexpression significantly inhibited the adipogenesis of brown adipocytes as evidenced by the downregulation of uncoupling protein 1, beta-3 adrenergic receptor, ATGL, and hormone-sensitive lipase mRNA levels and the significant suppression of uncoupling protein 1, ATGL, and perilipin 1 protein levels in brown adipocytes.
CONCLUSIONS: The finding of this study demonstrated that CTRP9 promotes lipolysis by upregulating ATGL expression in vivo and inhibits the differentiation of brown preadipocytes in vitro.
摘要:
背景:本研究旨在阐明C1q/肿瘤坏死因子(TNF)相关蛋白9(CTRP9)在棕色脂肪组织(BAT)的形成和分化中起作用的分子机制。
方法:将编码CTRP9和绿色荧光蛋白的腺病毒颗粒接种到C57BL/6J小鼠的肩胛骨中,饲喂高脂饮食8周;体重,脂滴形态,葡萄糖耐量,胰岛素耐受,和蛋白质表达水平进行分析。此外,CTRP9腺病毒转染棕色前脂肪细胞,并诱导分化以鉴定CTRP9过表达对脂肪细胞分化的影响。
结果:CTRP9过表达显著增加了小鼠的体重增加。此外,与对照组相比,CTRP9过表达组的脂肪组织重量和葡萄糖清除率显著增加,胰岛素敏感性和血清甘油三酯水平降低.此外,CTRP9过表达显着上调BAT中脂肪甘油三酯脂肪酶(ATGL)和perilipin1蛋白的表达水平。细胞实验结果证实,CTRP9过表达显著抑制棕色脂肪细胞的脂肪生成,解偶联蛋白1β-3肾上腺素能受体的下调证明了这一点,ATGL,和激素敏感性脂肪酶mRNA水平和解偶联蛋白1,ATGL,和棕色脂肪细胞中的perilipin1蛋白水平。
结论:这项研究的发现表明,CTRP9通过体内上调ATGL表达促进脂肪分解,并在体外抑制棕色前脂肪细胞的分化。
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