BMB Reports 2022; 55(10): 500-505  https://doi.org/10.5483/BMBRep.2022.55.10.056
UCP2 KO mice exhibit ameliorated obesity and inflammation induced by high-fat diet feeding
Do Hyun Kim1,2,3, Hye Jin Kim2,3 & Je Kyung Seong1,2,3,4,*
1The Research Institute for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul 08826, 2Laboratory of Developmental Biology and Genomics, BK21 Program for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul 08826, 3Korea Mouse Phenotyping Center (KMPC), Seoul National University, Seoul 08826, 4Interdisciplinary Program for Bioinformatics, Program for Cancer Biology, BIO-MAX/N-Bio Institute, Seoul National University, Seoul 08826, Korea
Correspondence to: Tel: +82-2-885-8395; Fax: +82-2-885-8397; E-mail: snumouse@snu.ac.kr
Received: March 23, 2022; Revised: April 19, 2022; Accepted: June 7, 2022; Published online: October 31, 2022.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

cc This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
ABSTRACT
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.
Keywords: Adipose, High fat diet, Inflammation, Mouse, Obesity, UCP2

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Funding Information
  • Research Institute for Veterinary Science, Seoul National University
     
  • National Research Foundation of Korea
      10.13039/501100003725
      NRF-2013M3A9D5072550
  • Ministry of Science and ICT, South Korea
      10.13039/501100014188
      NRF-2013M3A9D5072550

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