Open AccessThe essential function of CARD 9 in diet‐induced inflammation and metabolic disorders in mice
Author(s) -
Zeng Xuejiao,
Du Xihao,
Zhang Jia,
Jiang Shuo,
Liu Jie,
Xie Yuquan,
Shan Wei,
He Guanglong,
Sun Qinghua,
Zhao Jinzhuo
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13494
Subject(s) - insulin resistance , endocrinology , mapk/erk pathway , medicine , inflammation , obesity , type 2 diabetes , diabetes mellitus , insulin , biology , p38 mitogen activated protein kinases , signal transduction , microbiology and biotechnology
Inflammation and metabolic disorder are common pathophysiological conditions, which play a vital role in the development of obesity and type 2 diabetes. The purpose of this study was to explore the effects of caspase recruitment domain ( CARD ) 9 in the high fat diet ( HFD )‐treated mice and attempt to find a molecular therapeutic target for obesity development and treatment. Sixteen male CARD 9 −/− and corresponding male WT mice were fed with normal diet or high fat diet, respectively, for 12 weeks. Glucose tolerance, insulin resistance, oxygen consumption and heat production of the mice were detected. The CARD 9/ MAPK pathway‐related gene and protein were determined in insulin‐responsive organs using Western blotting and quantitative PCR . The results showed that HFD ‐induced insulin resistance and impairment of glucose tolerance were more severe in WT mice than that in the CARD 9 −/− mice. CARD 9 absence significantly modified O 2 consumption, CO 2 production and heat production. CARD 9 −/− mice displayed the lower expression of p38 MAPK , JNK and ERK when compared to the WT mice in both HFD ‐ and ND ‐treated groups. HFD induced the increase of p38 MAPK , JNK and ERK in WT mice but not in the CARD 9 −/− mice. The results indicated that CARD 9 absence could be a vital protective factor in diet‐induced obesity via the CARD 9/ MAPK pathway, which may provide new insights into the development of gene knockout to improving diet‐induced obesity and metabolism disorder.