title: CMKLR1 deficiency influences glucose tolerance and thermogenesis in mice on high fat diet.
abstract: Obesity has become a global epidemic disease, contributing to increases in the prevalence of type 2 diabetes. CMKLR1, one of the receptors for chemerin, has a wide range of functions in physiological and pathological activity, including innate and adaptive immunity, inflammation, metabolism and reproduction. In our study, CMKLR1 deficiency did not influence the gain of body weight but did exacerbate glucose intolerance, increase serum insulin level, and promote insulin resistance in mice on high fat diets. The expression of thermogenesis related genes was examined and indicated to decrease in CMKLR1 knockout (KO) mice in both normal and cold environments, which indicated CMKLR1 influence the thermogenesis process. Cold exposure induced significant body mass decrease and improved glucose tolerance and insulin resistance in wild type HFD mice but had no obvious effect on CMKLR1 KO HFD mice. In vitro, loss of CMKLR1 did not significantly influence the differentiation of stromal vascular fibroblasts (SVFs) derived from adipose tissue, but did suppress the expression of thermogenesis related genes. Collectively, these data demonstrate that CMKLR1 deficiency induces inbalance of glucose metabolism and impairs the cold induced-thermogenesis process in high diet models.
authors.affiliation: Laboratory for Reproductive Health, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, China; University of Chinese Academy of Sciences, 518055, China.
authors.forename: Chen
authors.initials: C
authors.lastname: Huang
authors.affiliation: Laboratory for Reproductive Health, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, China; Nano Science and Technology Institute, University of Science and Technology of China, 215123, China.
authors.forename: Miaomiao
authors.initials: M
authors.lastname: Wang
authors.affiliation: Shenzhen Key Laboratory of Birth Defects, Shenzhen Baoan Maternal and Child Health Hospital, Shenzhen, Guangdong 518133, China.
authors.forename: Lirong
authors.initials: L
authors.lastname: Ren
authors.affiliation: Laboratory for Reproductive Health, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, China.
authors.forename: Liang
authors.initials: L
authors.lastname: Xiang
authors.affiliation: Laboratory for Reproductive Health, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Chen
authors.affiliation: Laboratory for Reproductive Health, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, China.
authors.forename: Mengxia
authors.initials: M
authors.lastname: Li
authors.affiliation: Laboratory for Reproductive Health, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, China.
authors.forename: Tianxia
authors.initials: T
authors.lastname: Xiao
authors.affiliation: Laboratory for Reproductive Health, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, China.
authors.forename: Peigen
authors.initials: P
authors.lastname: Ren
authors.affiliation: Shenzhen Key Laboratory of Birth Defects, Shenzhen Baoan Maternal and Child Health Hospital, Shenzhen, Guangdong 518133, China. Electronic address: xionglk@sina.cn.
authors.forename: Likuan
authors.initials: L
authors.lastname: Xiong
authors.affiliation: Laboratory for Reproductive Health, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, 518055, China. Electronic address: jian.zhang@siat.ac.cn.
authors.forename: Jian V
authors.initials: JV
authors.lastname: Zhang
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D059305:Diet, High-Fat / Q000009:adverse effects*; D005786:Gene Expression Regulation; D005947:Glucose / Q000378:metabolism; D018149:Glucose Intolerance / Q000150:complications / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D007333:Insulin Resistance / Q000235:genetics*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009765:Obesity / Q000150:complications / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D019707:Receptors, Chemokine; D043562:Receptors, G-Protein-Coupled / Q000235:genetics* / Q000378:metabolism; D022722:Thermogenesis
chemical_list: C486456:CMKLR1 protein, mouse; D019707:Receptors, Chemokine; D043562:Receptors, G-Protein-Coupled; D005947:Glucose
keywords: CMKLR1; Insulin resistance; Obesity; Thermogenesis