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首页> 外文期刊>The Journal of Nutritional Biochemistry >SR-BI deficiency disassociates obesity from hepatic steatosis and glucose intolerance development in high fat diet-fed mice
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SR-BI deficiency disassociates obesity from hepatic steatosis and glucose intolerance development in high fat diet-fed mice

机译：SR-BI缺乏症消除了高脂饮食喂养小鼠的肝脏脂肪变性和葡萄糖不耐受发育的肥胖

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Scavenger receptor BI (SR-BI) has been suggested to modulate adipocyte function. To uncover the potential relevance of SR-BI for the development of obesity and associated metabolic complications, we compared the metabolic phenotype of wild-type and SR-BI deficient mice fed an obesogenic diet enriched in fat. Both male and female SR-BI knockout mice gained significantly more weight as compared to their wild-type counterparts in response to 12 weeks high fat diet feeding (1.5-fold; P < .01 for genotype). Plasma free cholesterol levels were 2-fold higher ( P < .001) in SR-BI knockout mice of both genders, whilst plasma cholesteryl ester and triglyceride concentrations were only significantly elevated in males. Strikingly, the exacerbated obesity in SR-BI knockout mice was paralleled by a better glucose handling. In contrast, only SR-BI knockout mice developed atherosclerotic lesions in the aortic root, with a higher predisposition in females. Biochemical and histological studies in male mice revealed that SR-BI deficiency was associated with a reduced hepatic steatosis degree as evident from the 29% lower ( P < .05) liver triglyceride levels. Relative mRNA expression levels of the glucose uptake transporter GLUT4 were increased ( + 47%; P < .05), whilst expression levels of the metabolic PPARgamma target genes CD36, HSL, ADIPOQ and ATGL were reduced 39%-58% ( P < .01) in the context of unchanged PPARgamma expression levels in SR-BI knockout gonadal white adipose tissue. In conclusion, we have shown that SR-BI deficiency is associated with a decrease in adipocyte PPARgamma activity and a concomitant uncoupling of obesity development from hepatic steatosis and glucose intolerance development in high fat diet-fed mice. <(c)> 2020 The Author(s). Published by Elsevier Inc. This is an open access article under the CC BY license ( http://creativecommons.org/licenses/by/4.0/ )
机译：清道夫受体BI（SR-BI）被认为可以调节脂肪细胞的功能。为了揭示SR-BI与肥胖和相关代谢并发症的潜在相关性，我们比较了喂食富含脂肪的肥胖饮食的野生型和SR-BI缺陷小鼠的代谢表型。与野生型小鼠相比，雄性和雌性SR-BI基因敲除小鼠在12周高脂饮食喂养后体重显著增加（1.5倍；基因型P<0.01）。两种性别的SR-BI基因敲除小鼠的血浆游离胆固醇水平均高出2倍（P<0.001），而雄性小鼠的血浆胆固醇酯和甘油三酯浓度仅显著升高。值得注意的是，SR-BI基因敲除小鼠肥胖加剧的同时，葡萄糖处理也更好。相比之下，只有SR-BI基因敲除的小鼠在主动脉根部出现动脉粥样硬化病变，而雌性小鼠更易发生这种病变。雄性小鼠的生化和组织学研究表明，SR-BI缺乏与肝脏脂肪变性程度降低有关，从肝脏甘油三酯水平降低29%（P<0.05）可以明显看出。在SR-BI基因敲除的性腺白色脂肪组织中，葡萄糖摄取转运体GLUT4的相对mRNA表达水平增加（+47%；P<0.05），而代谢性PPARGMA靶基因CD36、HSL、ADIPOQ和ATGL的表达水平降低39%-58%（P<0.01）。总之，我们已经证明，在高脂饮食喂养的小鼠中，SR-BI缺乏与脂肪细胞PPARgamma活性降低以及伴随的肥胖发展与肝脂肪变性和葡萄糖不耐受发展脱钩有关<（c） >2020作者。由爱思唯尔公司出版。这是一篇根据CC by license（http://creativecommons.org/licenses/by/4.0/ )

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    Hoekstra Menno; Ouweneel Amber B.; Price Juliet; van der Geest Rick; van der Sluis Ronald J.; Geerling Janine J.; Nahon Joya E.; Van Eck Miranda;

  • 作者单位

    Leiden Univ Gorlaeus Labs Leiden Acad Ctr Drug Res Div BioTherapeut Einsteinweg 55 NL-2333 CC Leiden Netherlands;

    Leiden Univ Gorlaeus Labs Leiden Acad Ctr Drug Res Div BioTherapeut Einsteinweg 55 NL-2333 CC Leiden Netherlands;

    Leiden Univ Gorlaeus Labs Leiden Acad Ctr Drug Res Div BioTherapeut Einsteinweg 55 NL-2333 CC Leiden Netherlands;

    Leiden Univ Gorlaeus Labs Leiden Acad Ctr Drug Res Div BioTherapeut Einsteinweg 55 NL-2333 CC Leiden Netherlands;

    Leiden Univ Gorlaeus Labs Leiden Acad Ctr Drug Res Div BioTherapeut Einsteinweg 55 NL-2333 CC Leiden Netherlands;

    Leiden Univ Gorlaeus Labs Leiden Acad Ctr Drug Res Div BioTherapeut Einsteinweg 55 NL-2333 CC Leiden Netherlands;

    Leiden Univ Gorlaeus Labs Leiden Acad Ctr Drug Res Div BioTherapeut Einsteinweg 55 NL-2333 CC Leiden Netherlands;

    Leiden Univ Gorlaeus Labs Leiden Acad Ctr Drug Res Div BioTherapeut Einsteinweg 55 NL-2333 CC Leiden Netherlands;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 生物化学;
  • 关键词

    scavenger receptor BI; obesity; glucose intolerance; hepatic steatosis; adipocyte; PPARgamma;

    机译：清除剂受体BI;肥胖;葡萄糖不耐受;肝脏脂肪变性;脂肪细胞;ppargamma;

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