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Title 

Crif1 deficiency reduces adipose OXPHOS capacity and triggers inflammation and insulin resistance in mice

Authors 

M J RyuS J KimY K KimM J ChoiS TadiM H LeeS E LeeH K ChungS B JungH J KimY S JoK S KimS H LeeJ M KimG R KweonK C ParkJ U LeeY Y KongChul Ho LeeJ ChungM Shong

Publisher 

Public Library of Science

Issue Date 

2013

Citation 

PLoS Genetics, vol. 9, no. 3, pp. 1003356-1003356

Abstract 

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.

ISSN 

1553-7390

Link 

http://dx.doi.org/10.1371/journal.pgen.1003356

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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