Abstract

Brown and beige adipose tissues (BAT and BeAT) are thermogenic fat depots that dissipate energy as heat via 
uncoupling protein-1 (UCP1) and complementary UCP1-independent mechanisms. Their activation increases 
whole-body substrate oxidation, improves insulin sensitivity, and modulates hepatic and skeletal-muscle 
metabolism through endocrine “batokines.” In humans, cold exposure and β-adrenergic stimulation acutely 
activate BAT, while repeated exposures drive the “browning” of white adipose tissue into beige adipocytes. 
Observational and interventional studies link higher BAT activity with lower fasting glucose, reduced 
triglycerides, and improved glucose tolerance, suggesting a role in preventing type 2 diabetes (T2D). This 
review summarizes the developmental origins and molecular control of BAT and beige fat, integrates evidence 
from animal and human studies on glucose homeostasis, and evaluates lifestyle, pharmacologic, and device-based 
strategies to activate thermogenic adipose tissue. We also address safety, feasibility, and knowledge gaps 
including heterogeneity of human BAT, durability of responses, and the need for clinically meaningful 
endpoints. Collectively, available data support BAT and beige adipose activation as a plausible, multifaceted 
approach to diabetes prevention, particularly when combined with diet and physical activity. However, 
translating mechanistic promise into population-level impact will require rigorous trials, standardized 
measurement, and long-term risk-benefit assessment.