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首页> 外文学位 >Le role et la regulation du pyroglutamylated RF-amide peptide dans le tissu adipeux lors de l'obesite.
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Le role et la regulation du pyroglutamylated RF-amide peptide dans le tissu adipeux lors de l'obesite.

机译：肥胖期间脂肪组织中焦谷氨酰化RF-酰胺肽的作用和调节。

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摘要

Obesity is defined as an excess of fat tissue mass. Obesity is a public health problem which became pandemic in developed countries. The condition of obesity predisposes to potentially fatal diseases like type 2 diabetes, cardiovascular diseases and non-alcoholic steatohepatitis.;The increase in intra-abdominal adipose tissue mass is intimately associated with the development of insulin resistance. An increase in fat tissue mass occurs by preadipocytes hyperplasia, preadipocytes differentiation into adipocytes and adipocyte hypertrophy. The differentiation of preadipocytes occurs during adipogenesis and is regulated by multiple factors but inhibited by inflammatory stimuli that are responsible for insulin resistance and the emergence of obesity-related dysfunctions.;We identified a new autocrine/paracrine system of regulation of adipogenesis in adipose tissue cells. The pyroglutamylated RF-amide peptide (QRFP), previously known for its role in the regulation of appetite, is an activator of adipogenesis by activating its receptor, G protein-coupled receptor 103 (GPR103). QRFP is expressed in adipocytes and macrophages whereas the GPR103 subtype b is expressed in adipocytes only. Treatment of adipocytes with QRFP increases fatty acids uptake, lipid accumulation, LPL enzyme expression and activity. QRFP upregulates gene expressions of fatty acids transporters CD36 and FATP1, of the fatty acid activating enzyme ACSL1 and of transcription factors PPAR-γ and C/EBP-α, which are all involved in adipogenesis. In addition to its effects on adipogenesis, QRFP shows an inhibitory effect on lipolytic activity induced by catecholamines.;We have shown that QRFP expression is decreased in adipose tissues of obese mice. According to our results, this decrease could be explained by an increase of circulating endotoxins in obesity, called metabolic endotoxemia, which mediate its effect, in part, by the induction of interferons in macrophages. Signaling pathways of these effects have been identified. We demonstrated another example of inflammatory stimulus downregulating adipogenic signals.;Keywords : GPR103, QRFP, obesity, adipocytes, macrophages, adipogenesis, metabolic endotoxemia, interferons, inflammation.
机译：肥胖被定义为脂肪组织过多。肥胖是一种公共卫生问题，在发达国家已成为大流行病。肥胖病易患致命性疾病，如2型糖尿病，心血管疾病和非酒精性脂肪性肝炎。腹内脂肪组织量的增加与胰岛素抵抗的发生密切相关。脂肪组织质量的增加是由于前脂肪细胞增生，前脂肪细胞分化成脂肪细胞和脂肪细胞肥大引起的。前脂肪细胞的分化发生在脂肪形成过程中，并受多种因素调控，但受到炎症刺激的抑制，这些炎症刺激作用与胰岛素抵抗和肥胖相关功能障碍的出现有关。我们确定了一种新的自分泌/旁分泌系统，用于调节脂肪组织细胞中的脂肪生成。 。焦谷氨酰化RF酰胺肽（QRFP）以前因其在食欲调节中的作用而闻名，它是通过激活其受体G蛋白偶联受体103（GPR103）来激活脂肪形成的。 QRFP在脂肪细胞和巨噬细胞中表达，而GPR103 b亚型仅在脂肪细胞中表达。用QRFP处理脂肪细胞可增加脂肪酸摄取，脂质蓄积，LPL酶表达和活性。 QRFP上调参与脂肪形成的脂肪酸转运蛋白CD36和FATP1，脂肪酸活化酶ACSL1和转录因子PPAR-γ和C /EBP-α的基因表达。 QRFP除了对脂肪生成有影响外，还对儿茶酚胺诱导的脂解活性具有抑制作用。我们已经表明，肥胖小鼠脂肪组织中QRFP表达降低。根据我们的结果，这种减少可以通过肥胖中循环内毒素的增加来解释，这种代谢被称为代谢性内毒素血症，其介导其作用的部分原因在于巨噬细胞中干扰素的诱导。已经确定了这些作用的信号传导途径。我们证明了炎症刺激下调脂肪形成信号的另一个例子。关键词：GPR103，QRFP，肥胖，脂肪细胞，巨噬细胞，脂肪形成，代谢性内毒素血症，干扰素，炎症。

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  • 作者

    Jossart, Christian.;

  • 作者单位

    Universite de Montreal (Canada).;

  • 授予单位 Universite de Montreal (Canada).;
  • 学科 Health Sciences Pharmacology.
  • 学位 Ph.D.
  • 年度 2013
  • 页码 266 p.
  • 总页数 266
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 肿瘤学;
  • 关键词

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