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自噬上调：作为代谢综合征WOKW大鼠脂肪组织中的一种保护因子。

Up-regulated autophagy: as a protective factor in adipose tissue of WOKW rats with metabolic syndrome.

作者信息

Kosacka J, Nowicki M, Paeschke S, Baum P, Blüher M, Klöting N

机构信息

1Department of Neurology, University of Leipzig, Liebigstraße 20, 04103 Leipzig, Germany.

2Department of Medicine, University of Leipzig, Liebigstraße 21, 04103 Leipzig, Germany.

出版信息

Diabetol Metab Syndr. 2018 Mar 2;10:13. doi: 10.1186/s13098-018-0317-6. eCollection 2018.

DOI:10.1186/s13098-018-0317-6
PMID:29507613
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5834836/
Abstract

BACKGROUND

Wistar Ottawa Karlsburg W (RT1u) rats (WOKW) are a model of the metabolic syndrome (MetS). Adipose tissue (AT) and peripheral nerves of WOKW rats exhibit up-regulated autophagy and inflammation corresponding with decreased apoptosis rate. The aim of this study was to characterize AT in WOKW rats in relation to autophagic activity.

METHODS

mRNA and protein expression of adiponectin, pro-inflammatory and pro-apoptotic markers including MCP1, TNFα, cleaved caspase-3 and RNF157, a new candidate gene regulated through autophagy, were analyzed in adipocytes isolated from visceral and subcutaneous AT of 5-month old WOKW rats with MetS and LEW.1W controls in response to pharmacological inhibition of autophagy. Immunohistochemistry was performed to detect adiponectin and RNF157 protein in cultured adipocytes.

RESULTS

Inhibition of autophagy by LY294002 was associated with a fourfold up-regulation of adiponectin expression and a decrease of RNF157 protein and pro-inflammatory markers-MCP-1 and TNFα predominantly in visceral adipocytes of obese WOKW rats compared to LEW.1W rats. Moreover, inhibition of autophagic activity correlates with an activation of cleaved caspase-3 apoptotic signaling pathway.

CONCLUSIONS

Up-regulated autophagy in obese WOKW rats contributes to the regulation of visceral AT function and involves an altered balance between pro-inflammatory and protective adipokine expression. Our data suggest that activation of AT autophagy protects against adipocyte apoptosis at least under conditions of obesity related MetS in WOKW rats.

摘要

背景

Wistar Ottawa Karlsburg W（RT1u）大鼠（WOKW）是代谢综合征（MetS）的一种模型。WOKW大鼠的脂肪组织（AT）和外周神经表现出自噬和炎症上调，且凋亡率降低。本研究的目的是表征WOKW大鼠中与自噬活性相关的脂肪组织。

方法

分析了从5月龄患有MetS的WOKW大鼠和LEW.1W对照的内脏和皮下脂肪组织分离的脂肪细胞中脂联素、促炎和促凋亡标志物（包括MCP1、TNFα、裂解的半胱天冬酶-3）以及RNF157（一个通过自噬调节的新候选基因）的mRNA和蛋白质表达，以响应自噬的药理学抑制。进行免疫组织化学检测培养脂肪细胞中的脂联素和RNF157蛋白。

结果

与LEW.1W大鼠相比，LY294002抑制自噬与肥胖WOKW大鼠内脏脂肪细胞中脂联素表达上调四倍以及RNF157蛋白和促炎标志物MCP-1和TNFα的减少有关。此外，自噬活性的抑制与裂解的半胱天冬酶-3凋亡信号通路的激活相关。

结论

肥胖WOKW大鼠中自噬上调有助于内脏脂肪组织功能的调节，并涉及促炎和保护性脂肪因子表达之间平衡的改变。我们的数据表明，至少在WOKW大鼠肥胖相关的MetS条件下，脂肪组织自噬的激活可防止脂肪细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/5834836/5df2f0493ce0/13098_2018_317_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/5834836/6c2fba32dfa2/13098_2018_317_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/5834836/a3043e0fdd05/13098_2018_317_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/5834836/472df9017b51/13098_2018_317_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/5834836/1e3cf0b7fcb5/13098_2018_317_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/5834836/00a8687676a1/13098_2018_317_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/5834836/d834be1aa0b5/13098_2018_317_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/5834836/5df2f0493ce0/13098_2018_317_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/5834836/6c2fba32dfa2/13098_2018_317_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/5834836/a3043e0fdd05/13098_2018_317_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/5834836/472df9017b51/13098_2018_317_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/5834836/1e3cf0b7fcb5/13098_2018_317_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/5834836/00a8687676a1/13098_2018_317_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/5834836/d834be1aa0b5/13098_2018_317_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/5834836/5df2f0493ce0/13098_2018_317_Fig7_HTML.jpg

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