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本文引用的文献

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IL-1 induces mitochondrial translocation of IRAK2 to suppress oxidative metabolism in adipocytes.白细胞介素-1诱导白细胞介素-1受体相关激酶2的线粒体易位,以抑制脂肪细胞中的氧化代谢。
Nat Immunol. 2020 Oct;21(10):1219-1231. doi: 10.1038/s41590-020-0750-1. Epub 2020 Aug 10.
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Altered adipose tissue and adipocyte function in the pathogenesis of metabolic syndrome.代谢综合征发病机制中的脂肪组织改变和脂肪细胞功能障碍。
J Clin Invest. 2019 Oct 1;129(10):3990-4000. doi: 10.1172/JCI129187.
3
Macrophage LRP1 Promotes Diet-Induced Hepatic Inflammation and Metabolic Dysfunction by Modulating Wnt Signaling.巨噬细胞 LRP1 通过调节 Wnt 信号促进饮食诱导的肝炎症和代谢功能障碍。
Mediators Inflamm. 2018 Nov 4;2018:7902841. doi: 10.1155/2018/7902841. eCollection 2018.
4
Metabolic markers, regional adiposity, and adipose cell size: relationship to insulin resistance in African-American as compared with Caucasian women.代谢标志物、局部肥胖和脂肪细胞大小:与非裔美国女性和白种女性的胰岛素抵抗的关系。
Int J Obes (Lond). 2019 Jun;43(6):1164-1173. doi: 10.1038/s41366-018-0191-1. Epub 2018 Aug 20.
5
Mechanisms of Insulin Action and Insulin Resistance.胰岛素作用机制和胰岛素抵抗。
Physiol Rev. 2018 Oct 1;98(4):2133-2223. doi: 10.1152/physrev.00063.2017.
6
The interplay of canonical and noncanonical Wnt signaling in metabolic syndrome.经典和非经典 Wnt 信号通路在代谢综合征中的相互作用。
Nutr Res. 2019 Oct;70:18-25. doi: 10.1016/j.nutres.2018.06.009. Epub 2018 Jul 4.
7
Programming of central and peripheral insulin resistance by low birthweight and postnatal catch-up growth in male mice.低出生体重和出生后追赶性生长对雄性小鼠中枢和外周胰岛素抵抗的编程作用。
Diabetologia. 2018 Oct;61(10):2225-2234. doi: 10.1007/s00125-018-4694-z. Epub 2018 Jul 24.
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The cell biology of systemic insulin function.系统性胰岛素功能的细胞生物学。
J Cell Biol. 2018 Jul 2;217(7):2273-2289. doi: 10.1083/jcb.201802095. Epub 2018 Apr 5.
10
Harnessing low-density lipoprotein receptor protein 6 (LRP6) genetic variation and Wnt signaling for innovative diagnostics in complex diseases.利用低密度脂蛋白受体蛋白6(LRP6)基因变异和Wnt信号通路进行复杂疾病的创新诊断。
Pharmacogenomics J. 2018 May 22;18(3):351-358. doi: 10.1038/tpj.2017.28. Epub 2017 Jul 11.

宫内生长受限追赶生长大鼠脂肪组织中 LRP6/β-连环蛋白通路的变化。

Changes of LRP6/β-catenin pathway in adipose tissue of rats with intrauterine growth restriction with catch-up growth.

出版信息

Zhejiang Da Xue Xue Bao Yi Xue Ban. 2021 Dec 25;50(6):755-761. doi: 10.3724/zdxbyxb-2021-0178.

DOI:10.3724/zdxbyxb-2021-0178
PMID:35347917
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8931619/
Abstract

To investigate the expression of low-density lipoprotein receptor-related protein 6 (LRP6)/β-catenin pathway related proteins in adipose tissue of rats with intrauterine growth restriction with catch-up growth SD rats were randomly divided into nutrition-restriction rats and normal feed rats during pregnancy. CG-IUGR model was established by reducing the number of offspring in the nutrition-restriction rats (CG-IUGR group); while the rats in the control group were offspring of the normal feed pregnant rats. In order to exclude the interference of gender, male offspring mice were selected in both the CG-IUGR group and the control group in the following studies. The CG-IUGR group and the control group were subjected to glucose tolerance test at 12 weeks of age, and the perirenal adipose tissue samples were taken to observe the adipose structure by HE staining. Expression of LRP6, β-catenin and insulin receptor substrate 1 (IRS-1) in adipocytes were examined by confocal microscopy. Protein expression of LRP6, β-catenin and IRS-1 were measured by Western blotting. Blood glucose level and the area under the cure of CG-IUGR group were significantly higher than that of control group (both <0.05). Adipocyte size in the CG-IUGR group was significantly larger than that of control group, and the expression of LRP6, β-catenin and IRS-1 protein in adipose tissue of the CG-IUGR group was significantly lower than that of control group (all <0.05). : The expression of LRP6/β-catenin pathway related proteins is reduced in the adipose tissue in CG-IUGR rats, probably contributing to the insulin resistance in these rats.

摘要

为了研究宫内发育迟缓(IUGR)后追赶生长(CG)大鼠脂肪组织中低密度脂蛋白受体相关蛋白 6(LRP6)/β-连环蛋白通路相关蛋白的表达情况,将 SD 大鼠随机分为孕期限食组和正常喂养组。通过减少限食组大鼠的后代数量建立 CG-IUGR 模型(CG-IUGR 组);而正常喂养组的大鼠为正常喂养孕鼠的后代。为了排除性别的干扰,在以下研究中,从 CG-IUGR 组和正常喂养组中均选择雄性子代小鼠。两组子鼠于 12 周龄时行葡萄糖耐量试验,取肾周脂肪组织行 HE 染色观察脂肪组织形态学变化,激光共聚焦显微镜观察脂肪细胞中 LRP6、β-连环蛋白和胰岛素受体底物 1(IRS-1)的表达,Western blot 法检测 LRP6、β-连环蛋白和 IRS-1 蛋白的表达。CG-IUGR 组的血糖水平和曲线下面积均明显高于对照组(均<0.05)。CG-IUGR 组的脂肪细胞体积明显大于对照组,脂肪组织中 LRP6、β-连环蛋白和 IRS-1 蛋白的表达明显低于对照组(均<0.05)。

结论

CG-IUGR 大鼠脂肪组织中 LRP6/β-连环蛋白通路相关蛋白表达降低,可能导致大鼠胰岛素抵抗。