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功能丧失型肌生成抑制素突变增加了梅山猪的胰岛素敏感性和白色脂肪的褐色化。

Loss-of-function myostatin mutation increases insulin sensitivity and browning of white fat in Meishan pigs.

作者信息

Cai Chunbo, Qian Lili, Jiang Shengwang, Sun Youde, Wang Qingqing, Ma Dezun, Xiao Gaojun, Li Biao, Xie Shanshan, Gao Ting, Chen Yaoxing, Liu Jie, An Xiaorong, Cui Wentao, Li Kui

机构信息

Institute of Animal Sciences, Chinese Academy of Agricultural Sciences, Beijing, 100193, P. R. China.

State Key Laboratory of Agro Biotechnology, China Agricultural University, Beijing, 100193, P. R. China.

出版信息

Oncotarget. 2017 May 23;8(21):34911-34922. doi: 10.18632/oncotarget.16822.

DOI:10.18632/oncotarget.16822
PMID:28432282
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5471021/
Abstract

Myostatin-deficient mice showed a remarkable hypertrophy of skeletal muscle, with a decreased fat mass and enhanced insulin sensitivity. Currently, it is unclear if the inhibition of myostatin could be used as an approach to treat human obesity and insulin resistance. In this study, we investigated if the inhibition of porcine myostatin has any effect on fat deposition and insulin sensitivity using genetically engineered Meishan pigs containing a myostatin loss-of-function mutation (Mstn -/- ). Our results indicated that, when compared with wild-type pigs, the amount of subcutaneous fat and leaf fat of Mstn -/- pigs were significantly decreased mainly due to the browning of subcutaneous adipose tissue. Additionally, the serum insulin level decreased and the insulin sensitivity increased significantly in Mstn -/- pigs. Moreover, we found a significant increase in levels of insulin receptor and insulin receptor substrate proteins in skeletal muscle of Mstn -/- pigs, which then activating the insulin signaling pathway. Irisin-mediated regulation is not the only pathway for the activation of insulin signal in Mstn -/- skeletal muscle. This study provides valuable insight for the treatment of human obesity and diabetes mellitus.

摘要

肌肉生长抑制素缺陷型小鼠表现出骨骼肌显著肥大，脂肪量减少且胰岛素敏感性增强。目前，尚不清楚抑制肌肉生长抑制素是否可作为治疗人类肥胖和胰岛素抵抗的一种方法。在本研究中，我们利用含有肌肉生长抑制素功能缺失突变（Mstn -/- ）的基因工程梅山猪，研究抑制猪肌肉生长抑制素对脂肪沉积和胰岛素敏感性是否有任何影响。我们的结果表明，与野生型猪相比，Mstn -/- 猪的皮下脂肪和板油数量显著减少，这主要是由于皮下脂肪组织的褐变。此外，Mstn -/- 猪的血清胰岛素水平降低，胰岛素敏感性显著增加。而且，我们发现Mstn -/- 猪骨骼肌中胰岛素受体和胰岛素受体底物蛋白水平显著升高，进而激活胰岛素信号通路。鸢尾素介导的调节不是Mstn -/- 骨骼肌中激活胰岛素信号的唯一途径。本研究为治疗人类肥胖和糖尿病提供了有价值的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7c/5471021/9a3ac44a2aee/oncotarget-08-34911-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7c/5471021/2783da0a2e90/oncotarget-08-34911-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7c/5471021/7ec7e09df4b8/oncotarget-08-34911-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7c/5471021/49f9f64c80c2/oncotarget-08-34911-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7c/5471021/0e24bd91ad9a/oncotarget-08-34911-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7c/5471021/6608462b7530/oncotarget-08-34911-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7c/5471021/9a3ac44a2aee/oncotarget-08-34911-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7c/5471021/2783da0a2e90/oncotarget-08-34911-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7c/5471021/7ec7e09df4b8/oncotarget-08-34911-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7c/5471021/49f9f64c80c2/oncotarget-08-34911-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7c/5471021/0e24bd91ad9a/oncotarget-08-34911-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7c/5471021/6608462b7530/oncotarget-08-34911-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f7c/5471021/9a3ac44a2aee/oncotarget-08-34911-g006.jpg

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