Deficiency of CKIP-1 aggravates high-fat diet-induced fatty liver in mice
| Autor: | Lingqiang Zhang, Ping Xie, Wei An, Dongnian Li, Chuan Zhang, Jing Chen, Yu-Tao Zhan, Li Li |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Biology Diet High-Fat Mice 03 medical and health sciences chemistry.chemical_compound Internal medicine Lipid droplet Insulin receptor substrate medicine Animals Mice Knockout Glycogen Cell growth Fatty liver Cell Biology medicine.disease Fatty Liver Mice Inbred C57BL 030104 developmental biology Endocrinology chemistry Apoptosis Phosphorylation Casein kinase 2 Carrier Proteins Gene Deletion |
| Zdroj: | Experimental Cell Research. 355:40-46 |
| ISSN: | 0014-4827 |
| DOI: | 10.1016/j.yexcr.2017.03.033 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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