Key result
Ucp2 deficiency protected mice from high-fat diet-induced obesity and adipose tissue inflammation by reducing adipocyte apoptosis.
Why the study?
Uncoupling protein 2 regulates ROS formation, but its role in adipose tissue during high-fat diet-induced obesity was not fully understood.
Does Ucp2 deficiency prevent high-fat diet-induced obesity and adipose tissue inflammation in mice?
Does Ucp2 deficiency prevent high-fat diet-induced obesity and adipose tissue inflammation in mice?
Ucp2 deficiency protects mice from high-fat diet-induced obesity and adipose tissue inflammation by reducing adipocyte apoptosis, though it does not affect the browning capacity of white adipose tissue.
Ucp2 targeting merits human validation studies; leaves open any clinical relevance for obesity or adipose inflammation.
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. [BMB Reports 2022; 55(10): 500-505].
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Kim et al. (2022) studied Diet-induced obesity and adipose tissue inflammation. Ucp2 knockout vs. Wild-type mice was evaluated on High-fat diet-induced weight gain and adipose tissue inflammation. Ucp2 deficiency protected mice from high-fat diet-induced obesity and adipose tissue inflammation by reducing adipocyte apoptosis.
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