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    Impaired mitochondrial oxidative phosphorylation (OXPHOS) has been proposed as an etiological mechanism underlying insulin resistance. However, the initiating organ of OXPHOS dysfunction during the development of systemic insulin resistance has yet to be identified. To determine whether adipose OXPHOS deficiency plays an etiological role in systemic insulin resistance, the metabolic phenotype of mice with OXPHOS-deficient adipose tissue was examined. Crif1 is a protein required for the intramitochondrial production of mtDNA-encoded OXPHOS subunits; therefore, Crif1 haploinsufficient deficiency in mice results in a mild, but specific, failure of OXPHOS capacity in vivo. Although adipose-specific Crif1-haploinsufficient mice showed normal growth and development, they became insulin-resistant. Crif1-silenced adipocytes showed higher expression of chemokines, the expression of which is dependent upon stress kinases and antioxidant. Accordingly, examination of adipose tissue from Crif1-haploinsufficient mice revealed increased secretion of MCP1 and TNFα, as well as marked infiltration by macrophages. These findings indicate that the OXPHOS status of adipose tissue determines its metabolic and inflammatory responses, and may cause systemic inflammation and insulin resistance.


    Min Jeong Ryu, Soung Jung Kim, Yong Kyung Kim, Min Jeong Choi, Surendar Tadi, Min Hee Lee, Seong Eun Lee, Hyo Kyun Chung, Saet Byel Jung, Hyun-Jin Kim, Young Suk Jo, Koon Soon Kim, Sang-Hee Lee, Jin Man Kim, Gi Ryang Kweon, Ki Cheol Park, Jung Uee Lee, Young Yun Kong, Chul-Ho Lee, Jongkyeong Chung, Minho Shong. Crif1 deficiency reduces adipose OXPHOS capacity and triggers inflammation and insulin resistance in mice. PLoS genetics. 2013;9(3):e1003356

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    PMID: 23516375

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