title: Deficiency of CKIP-1 aggravates high-fat diet-induced fatty liver in mice.
abstract: Casein kinase 2 interacting protein-1(CKIP-1) is widely expressed in a variety of tissues and cells, and plays an important role in various critical cellular and physiological processes including cell growth, apoptosis, differentiation, cytoskeleton and bone formation. Here, we found: (1) CKIP-1 deficient mice exhibited increased body weight, liver weight, number and size of lipid droplets, and TG content comparing with WT mice after being exposed to high fat diet (HFD); (2) the levels of serum insulin, liver glycogen, phosphorylated C-Jun-N-terminal kinase-1 (pJNK1) and phosphorylated insulin receptor substrate -1(pIRS1) in CKIP-1-/-mice were higher than those of WT mice; (3) CKIP-1 interacted with JNK1 in vitro. Our results indicate that CKIP-1 deficiency in mice aggravates HFD-induced fatty liver by upregulating JNK1 phosphorylation and further upregulating IRS-1 phosphorylation and RI.
authors.affiliation: Department of Gastroenterology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.
authors.forename: Yutao
authors.initials: Y
authors.lastname: Zhan
authors.affiliation: Physical Examination Centre, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
authors.forename: Ping
authors.initials: P
authors.lastname: Xie
authors.affiliation: Department of Biochemistry and Molecular Biology, Beijing Key Laboratory of Cancer & Metastasis Research, Capital Medical University, Beijing 100069, China.
authors.forename: Dongnian
authors.initials: D
authors.lastname: Li
authors.affiliation: Department of Gastroenterology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.affiliation: Department of Gastroenterology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Chen
authors.affiliation: Department of Cell Biology, Municipal Laboratory for Liver Protection and Regulation of Regeneration, Capital Medical University, Beijing 100069, China.
authors.forename: Wei
authors.initials: W
authors.lastname: An
authors.affiliation: State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing 102206, China.
authors.forename: Lingqiang
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Department of Gastroenterology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China. Electronic address: digestivezhang@163.com.
authors.forename: Chuan
authors.initials: C
authors.lastname: Zhang
mesh_terms: D000818:Animals; D002352:Carrier Proteins / Q000235:genetics* / Q000378:metabolism; D059305:Diet, High-Fat / Q000009:adverse effects*; D005234:Fatty Liver / Q000139:chemically induced / Q000209:etiology* / Q000378:metabolism*; D017353:Gene Deletion; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D047908:Intracellular Signaling Peptides and Proteins
chemical_list: D002352:Carrier Proteins; C000620556:PLEKHO1 protein, mouse; D047908:Intracellular Signaling Peptides and Proteins
keywords: Casein kinase 2 interacting protein-1 (CKIP-1); High fat diet (HFD); Insulin receptor substrate −1(IRS-1); Non-alcoholic fatty liver disease (NAFLD); c-Jun NH2-terminal kinase 1 (JNK1)