Exp Clin Endocrinol Diabetes 2020; 128(05): 290-296
DOI: 10.1055/a-0725-7897
Article
© Georg Thieme Verlag KG Stuttgart · New York

Angiopoietin-like 8 Improves Insulin Resistance and Attenuates Adipose Tissue Inflammation in Diet-Induced Obese Mice

Deng Luo
1   Department of Endocrinology, Renmin Hospital, Wuhan University, Wuhan, 430060, China
,
Xiaolin Chen
1   Department of Endocrinology, Renmin Hospital, Wuhan University, Wuhan, 430060, China
,
Wenqiang Yang
2   Department of Clinical Laboratory, Wuhan No. 1 Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430023, China
,
Wenzhuo Ran
2   Department of Clinical Laboratory, Wuhan No. 1 Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430023, China
,
Zhongyuan Wen
1   Department of Endocrinology, Renmin Hospital, Wuhan University, Wuhan, 430060, China
› Author Affiliations

Funding: This study was funded by grants from the application foundation planning project of Wuhan Science and Technology Bureau (2015061701011619); Independent Research Project of Wuhan University of China, No.2042017kf0084; Natural Science Foundation of Hubei Province (No. 2018CFB230).
Further Information

Publication History

received 21 March 2018
revised  24 August 2018

accepted 30 August 2018

Publication Date:
26 September 2018 (online)

Preview

Abstract

Angiopoietin-like 8 (ANGPTL8) is closely linked to obesity-associated metabolic diseases and insulin resistance. The aim of the current study was to investigate the ability of ANGPTL8 to reverse insulin resistance in obese mice. The administration of ANGPTL8 reduced weight gain and improved glucose tolerance in mice with diet-induced obesity. In addition, ANGPTL8 administration modified macrophage infiltration, reduced monocyte chemoattractant protein-1 (MCP-1) and interleukin-1β(IL-1β) levels, and increased adiponectin gene expression in inguinal white adipose tissue (iWAT). Moreover, the exposure of a cultured peritoneal macrophage line to ANGPTL8 reduced the mRNA expression of M1 macrophage markers (TNF-α and IL-1β) upon stimulation with lipopolysaccharides in a dose-dependent manner. By contrast, when incubated with IL-4, exposure of macrophages to ANGPTL8 increased the mRNA expression of M2 macrophage markers (Arg1 and Chi3l3) in a dose-dependent manner. Collectively, the results of the present study demonstrated that treatment with ANGPTL8 can attenuate adipose tissue inflammation through regulation of macrophage polarization, and thus, it could be useful for improving insulin resistance.

Supplementary Material