Hormonal
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.
Fat storage is not uniform across the body. The Wnt/β-catenin signaling pathway regulates how fat cells grow differently in visceral (abdominal) versus subcutaneous (under skin) areas. High-fat diets trigger this pathway to increase the number of fat cells in the visceral area, which is more metabolically harmful. This explains why visceral fat accumulation is a key risk factor for metabolic diseases.
we highlight the regulation of updated Wnt/β-catenin signaling in obesity, especially the distinctly depot-specific roles between subcutaneous and visceral adipose tissue under high-fed diet stimulation
Why this rating
Based on review of multiple studies including mouse models and human genetic associations.
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
- 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
- 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
Related findings · Hormonal
- Initial treatment for type 2 diabetes should be a combination of metformin and either an SGLT-2 inhibitor or a GLP-1 receptor agonist to achieve cardiorenal protection, rather than monotherapy or older agents like sulfonylureas.Strong
- For patients with specific monogenic obesity syndromes (leptin deficiency, POMC/PCSK1/LEPR mutations), targeted pharmacotherapy (recombinant leptin or setmelanotide) is highly effective and should be prioritized, unlike in polygenic obesity.Strong
- Continued weekly administration of 2.4 mg subcutaneous semaglutide prevents weight regain and promotes further weight loss in adults with overweight or obesity, whereas switching to placebo results in significant weight regain.Strong
This is one finding among thousands. Every one is graded and traced to its source, so you can see what the evidence actually supports. Browse the research →