Hormonal
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.
This research suggests that obesity is not just about calories but involves complex genetic signaling (Wnt/β-catenin) that dictates how fat cells grow and store energy. While you cannot change your genetics, understanding this helps explain why fat storage differs by body area (visceral vs. subcutaneous) and why some people are more prone to obesity. Lifestyle interventions remain relevant as they interact with these signaling pathways.
Several studies have demonstrated the crucial role of Wnt/β-catenin signaling in the development of WAT and BAT, thus targeting Wnt/β-catenin pathway to combat obesity is promising.
Why this rating
The paper is a review summarizing various genetic and animal studies; it does not present new primary clinical trial data.
Source
Wnt/β-Catenin Signaling and Obesity
Na Chen et al. · Frontiers in Physiology · 2018
DOI 10.3389/fphys.2018.00792
More from this paper
- 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
- 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.Moderate
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