Autophagy in adipose tissue thermogenic function.

Abstract

Brown adipose tissue (BAT) is the main site of adaptive thermogenesis, a heat-producing process essential for maintaining body temperature, especially in cold environments. While abundant in newborns, BAT is also present in adults, where it becomes activated under specific stimuli such as cold exposure or food intake. In addition, white adipose tissue (WAT) can undergo a "browning" process, generating beige adipocytes with thermogenic properties similar to classical brown adipocytes. BAT is highly innervated and vascularized, features that support its thermogenic function by facilitating sympathetic nervous system activation and efficient heat distribution. BAT activation increases energy expenditure and plays a protective role against obesity and metabolic disorders. A growing body of evidence highlights autophagy as a critical regulator of BAT and beige adipocyte function. During thermogenic activation, autophagy, especially mitophagy, is suppressed, promoting mitochondrial accumulation and heat production. Conversely, enhanced autophagy contributes to BAT whitening and functional decline, as seen in obesity and aging. Although the role of autophagy in thermogenesis remains unclear, modulating autophagic pathways represents a promising strategy to boost thermogenic activity and improve metabolic health. Understanding the molecular mechanisms underlying BAT plasticity and autophagic regulation could offer novel therapeutic avenues for combating obesity and related metabolic diseases.