ArticleBMB reports2022
UCP2 KO mice exhibit ameliorated obesity and inflammation induced by high-fat diet feeding.
Article in BMB reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Uncoupling Protein 2 and Nitric Oxide Deficiency Favor Glycolytic Pathways and Organ Growth in the Rat Spleen.Current issues in molecular biology · 2026Article
- Exercise reverses high-fat diet-induced perivascular adipose tissue dysfunction through modulation of UCP2 and TXNIP/NLRP3 pathways.Journal of physiology and biochemistry · 2026Article
- New Horizons in Metabolic Health: Unveiling the Future of Drug Discovery and Development.Endocrine, metabolic & immune disorders drug targets · 2026Review
- Novel perspectives on the link between obesity and cancer risk: from mechanisms to clinical implications.Frontiers of medicine · 2024Review
- Article
- Differential chromatin accessibility and Gene Expression Associated with Backfat Deposition in pigs.BMC genomics · 2024Article
- Uncoupling Protein 3 Promotes the Myogenic Differentiation of Type IIb Myotubes in C2C12 Cells.Genes · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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. [BMB Reports 2022; 55(10): 500-505].
Indexed as
Identifiers
35725013PMC9623237W4283261397What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.