Development of metabolic dysfunction in mice lacking chemerin. (15th September 2021)

• Record Type: Journal Article
• Authors: Fang, Penghua; Han, Long; Yu, Mei; Han, Shiyu; Wang, Mengyuan; Huang, Yujie; Guo, Wancheng; Wei, Qingbo; Shang, Wenbing; Min, Wen
• Is Part Of: Molecular and cellular endocrinology. Volume 535(2021)
• Publication Date: 2021-09-15
• Subjects: Chemerin -- Glucose metabolism -- PGC-1α -- GLUT4; AS160 AKT substrate of 160 kDa -- HFD high fat diet -- GLUT4 glucose transporter 4 -- PVDF polyvinylidene fluoride -- PGC-1α peroxisome proliferator-activated receptor-γ coactivator-1α -- Rarres2 retinoic acid receptor responder protein 2 -- TBST Tris-buffered saline with 0.1% Tween-20 -- WT wild type -- p38 MAPK p38 mitogen-activated protein kinases; Endocrinology -- Periodicals; Molecular biology -- Periodicals; Cytology -- Periodicals; Endocrinology -- Periodicals; Hormones -- Periodicals; Endocrinologie -- Périodiques; Cytology; Endocrinology; Molecular biology; Periodicals; 573.4
• DOI: 10.1016/j.mce.2021.111369
• Languages: English
• ISSNs: 0303-7207

Abstract

Abstract: Chemerin, an adipocyte-secreted adipokine, is hypothesized to participate in energy homeostasis and glucoregulation. However, the physiologic effect of endogenous chemerin on glucose metabolism is unclear. The present studies tested the hypotheses that chemerin deficiency alters whole-body glucose homeostasis following switches to high-fat diet. Adult, male chemerin knockout and C57BL/6J control wild type mice were studied. During the following 4 weeks, chow- or high-fat diet maintained chemerin knockout mice showed elevated fasting glucose levels and glucose intolerance as well as insulin intolerance. Chemerin deficiency impaired adaptation to glucose and insulin challenge, leading to increased glucose levels. Moreover, the mRNA and protein levels of GLUT4 and PGC-1α expression in both skeletal muscle and adipose tissue were significantly decreased in chemerin knockout mice relative to the wild type, respectively. Taken together, the results support the hypotheses that chemerin helps adapt glucose metabolism to changes in dietary fat and modulates glucose consumption in mice by activation of PGC-1α/GLUT4 axis. Chemerin may play a significant role in elevation of glucose uptake and insulin sensitivity to promote glucose clearance. Highlights: Chemerin knockout mice showed increased glucose intolerance as well as insulin intolerance. Chemerin deficiency impaired adaptation to glucose and insulin challenge. The GLUT4 and PGC-1α expression in skeletal muscle and adipocytes were significantly decreased in chemerin knockout mice. Chemerin modulated glucose consumption in mice by activation of PGC-1α/GLUT4 axis.