Research
Hormonal
Mutations in the LGR4 gene, specifically the A750T variant, are associated with increased obesity risk, central obesity, and metabolic complications in humans, and ablation of Lgr4 in mice resists diet-induced obesity by promoting browning of visceral white adipose tissue.
Genetic variations in the LGR4 gene can predispose individuals to central obesity and metabolic issues. In mice, removing this gene prevents obesity by promoting the browning of fat, which burns energy. This suggests that targeting the LGR4 pathway could be a potential therapeutic strategy for treating obesity and its complications.
ModerateSupportsMEDIUM confidence
our group discovered in humans a novel low-frequency functional missense in LGR4 (A750T), that has been linked with increased obesity risk and metabolic disorders... ablation of Lgr4 in mice resists dietary and leptin mutant-induced obesity
Why this rating
Based on human genetic studies and mouse model data presented in the review.
Source
Wnt/β-Catenin Signaling and Obesity
Na Chen et al. · Frontiers in Physiology · 2018
DOI 10.3389/fphys.2018.00792
narrative_reviewCited 168×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Genetic mutations or activation of the Wnt/β-catenin signaling pathway, specifically involving LGR4, RSPOs, and ZNRF3/RNF43, regulate adipose tissue development and obesity risk by controlling the balance between adipocyte proliferation (hyperplasia) and differentiation (hypertrophy) in a depot-specific manner.Moderate
- Wnt/β-catenin signaling exerts depot-specific effects on white adipose tissue (WAT), where its activation in adipose precursor cells (APs) promotes proliferation (hyperplasia) in visceral WAT (vWAT) under high-fat diet conditions, while its role in subcutaneous WAT (sWAT) involves promoting differentiation and hypertrophy of mature adipocytes.Moderate
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