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UCP2 KO mice exhibit ameliorated obesity and inflammation induced by high-fat diet feeding

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Uncoupling protein 2 (Ucp2) was first introduced as a memberof Uncoupling protein family and a regulator of ROS formation;however, its role in adipose tissue is not fully understood. Inthe present study, we have investigated the role of Ucp2 againsthigh-fat diet (HFD)-induced obesity in epididymal white adiposetissue (eWAT) and browning of inguinal white adipose tissue(iWAT). Diet-induced obesity is closely related to macrophageinfiltration and the secretion of pro-inflammatory cytokines. Macrophagessurround adipocytes and form a crown-like-structure(CLS). Some reports have suggested that CLS formation requiresadipocyte apoptosis. After 12 weeks of HFD challenge, Ucp2knockout (KO) mice maintained relatively lean phenotypes comparedto wild-type (WT) mice. In eWAT, macrophage infiltration,CLS formation, and inflammatory cytokines were reduced in HFDKO mice compared to HFD WT mice. Surprisingly, we foundthat apoptotic signals were also reduced in the Ucp2 KO mice. Our study suggests that Ucp2 deficiency may prevent diet-inducedobesity by regulating adipocyte apoptosis. However, Ucp2deficiency did not affect the browning capacity of iWAT.

Abstract

Uncoupling protein 2 (Ucp2) was first introduced as a memberof Uncoupling protein family and a regulator of ROS formation;however, its role in adipose tissue is not fully understood. Inthe present study, we have investigated the role of Ucp2 againsthigh-fat diet (HFD)-induced obesity in epididymal white adiposetissue (eWAT) and browning of inguinal white adipose tissue(iWAT). Diet-induced obesity is closely related to macrophageinfiltration and the secretion of pro-inflammatory cytokines. Macrophagessurround adipocytes and form a crown-like-structure(CLS). Some reports have suggested that CLS formation requiresadipocyte apoptosis. After 12 weeks of HFD challenge, Ucp2knockout (KO) mice maintained relatively lean phenotypes comparedto wild-type (WT) mice. In eWAT, macrophage infiltration,CLS formation, and inflammatory cytokines were reduced in HFDKO mice compared to HFD WT mice. Surprisingly, we foundthat apoptotic signals were also reduced in the Ucp2 KO mice. Our study suggests that Ucp2 deficiency may prevent diet-inducedobesity by regulating adipocyte apoptosis. However, Ucp2deficiency did not affect the browning capacity of iWAT.

참고문헌 (34)

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