Exploring Gene Polymorphisms and Expression Patterns of Brown Adipose Tissue in Individuals with Obesity.

Abstract

Adipose tissue plays a central role in energy homeostasis, influencing metabolism, thermoregulation, and overall health. White adipose tissue (WAT) primarily stores energy, while brown adipose tissue (BAT) dissipates energy through heat production. This thermogenic capacity of BAT is mediated by uncoupling protein 1 (UCP1), an important therapeutic target for obesity and related metabolic disorders. The activity and function of BAT are strongly influenced by genetic factors, including genes involved in temperature regulation, mitochondrial function, and energy metabolism. Key regulators such as uncoupling protein 1 (UCP1), Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha (PGC-1α), PR Domain Containing 16 (PRDM16), and Cell Death-Inducing DFFA-Like Effector A (CIDEA) modulate BAT activation and energy expenditure, providing potential avenues for therapeutic intervention in obesity. Moreover, genetic variants in the Fat Mass and Obesity-Associated gene (FTO), ADRB3, and LEP highlight the links between BAT activity, lipid metabolism, and obesity susceptibility. Ethnic differences in adiposity traits, including body mass index (BMI) and waist-to-hip ratio, further emphasize the need for population-specific approaches in genetic studies. This review synthesizes current knowledge on the genetic regulation of BAT and explores their practical implications for obesity management. Importantly, we highlight gaps in understanding, such as obstacles to implementing BAT-targeted therapies, and recommend future studies that integrate genetic diversity, functional analyses, and translational research to enhance strategies for improving energy balance and metabolic health.