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生长激素抵抗可减少肾脏促凋亡蛋白，但内脏脂肪清除不能。

Renal pro-apoptotic proteins are reduced by growth hormone resistance but not by visceral fat removal.

机构信息

Department of Internal Medicine, Geriatrics Research, Southern Illinois University School of Medicine, Springfield, IL 62702-4910, USA. adges7wp.pl

出版信息

Biol Chem. 2011 May;392(5):475-81. doi: 10.1515/BC.2011.051. Epub 2011 Mar 11.

DOI:10.1515/BC.2011.051
PMID:21391871
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3703833/
Abstract

Growth hormone (GH) receptor knockout (GHRKO) mice are highly insulin sensitive and long-lived. Surgical visceral fat removal (VFR) improves insulin signaling in normal mice and rats and extends longevity in rats. We have previously demonstrated decreased expression of certain pro-apoptotic genes in kidneys of GHRKO mice and suggested that this could contribute to the increased longevity of these animals. The aim of the present study was to examine the level of the following proteins: caspase-3, caspase-9, caspase-8, bax, bad, phospho-bad, bcl-2, Smac/DIABLO, Apaf-1, phospho-p53 (pp53) and cytochrome c in male GHRKO and normal (N) mice subjected to VFR or sham surgery, at approximately six months of age. The kidneys were collected two months after VFR. Caspase-3, caspase-8, bax, bad, Smac/DIABLO, Apaf-1 and pp53 levels were decreased in GHRKO mice as compared to N animals. VFR did not change the level of any of the examined proteins. The decreased renal levels of pro-apoptotic proteins could contribute to the extended life-span caused by targeted disruption of the GH receptor gene but are apparently not involved in mediating the effects of VFR.

摘要

生长激素（GH）受体敲除（GHRKO）小鼠具有高度的胰岛素敏感性和长寿性。手术内脏脂肪去除（VFR）可改善正常小鼠和大鼠的胰岛素信号，并延长大鼠的寿命。我们之前已经证明，GHRKO 小鼠肾脏中某些促凋亡基因的表达降低，并认为这可能有助于这些动物的寿命延长。本研究的目的是检查以下蛋白质的水平：在接受 VFR 或假手术的雄性 GHRKO 和正常（N）小鼠的肾脏中，大约在 6 个月大时，caspase-3、caspase-9、caspase-8、bax、bad、磷酸化 bad、bcl-2、Smac/DIABLO、Apaf-1、磷酸化 p53（pp53）和细胞色素 c。VFR 两个月后收集肾脏。与 N 动物相比，GHRKO 小鼠的 caspase-3、caspase-8、bax、bad、Smac/DIABLO、Apaf-1 和 pp53 水平降低。VFR 并未改变任何检查蛋白的水平。靶向破坏 GH 受体基因导致的肾脏促凋亡蛋白水平降低可能有助于延长寿命，但显然不参与介导 VFR 的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ad9/3703833/c48efa85201f/nihms483713f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ad9/3703833/a01e78858c90/nihms483713f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ad9/3703833/c3e244d98dc2/nihms483713f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ad9/3703833/c4d2525dee29/nihms483713f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ad9/3703833/c48efa85201f/nihms483713f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ad9/3703833/a01e78858c90/nihms483713f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ad9/3703833/c3e244d98dc2/nihms483713f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ad9/3703833/c4d2525dee29/nihms483713f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ad9/3703833/c48efa85201f/nihms483713f4.jpg

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