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UCP2 KO mice exhibit ameliorated obesity and inflammation induced by high-fat diet feeding.
Do Hyun Kim1,2,3,# (Graduate student), Hye Jin Kim2,3 (Post Doc.), Je Kyung Seong 1,2,3,* (Professor)
1The Research Institute for Veterinary Science, College of Veterinary Medicine and 2Laboratory of Developmental Biology and Genomics and 3Korea Mouse Phenotyping Center (KMPC), Seoul National University
Uncoupling protein 2 (Ucp2) was first introduced as a member of Uncoupling protein family and a regulator of ROS formation; however, its role in adipose tissue is not fully understood. In the present study, we have investigated the role of Ucp2 against high-fat diet (HFD)-induced obesity in epididymal white adipose tissue (eWAT) and browning of inguinal white adipose tissue (iWAT). Diet-induced obesity is closely related to macrophage infiltration and the secretion of pro-inflammatory cytokines. Macrophages surround adipocytes and form a crown-like-structure (CLS). Some reports have suggested that CLS formation requires adipocyte apoptosis. After 12 weeks of HFD challenge, Ucp2 knockout (KO) mice maintained relatively lean phenotypes compared to wild-type (WT) mice. In eWAT, macrophage infiltration, CLS formation, and inflammatory cytokines were reduced in HFD KO mice compared to HFD WT mice. Surprisingly, we found that apoptotic signals were also reduced in the Ucp2 KO mice. Our study suggests that Ucp2 deficiency may prevent diet-induced obesity by regulating adipocyte apoptosis. However, Ucp2 deficiency did not affect the browning capacity of iWAT.
Abstract, Accepted Manuscript(in press) [Submitted on March 23, 2022, Accepted on June 7, 2022]
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