Berberine-induced browning and energy metabolism: mechanisms and implications.

Abstract

Obesity has become a global pandemic. The approaches researched to prevent it include decreasing energy intake and/or enhancing energy expenditure. Therefore, research on brown adipose tissue is of great importance. Brown adipose tissue is characterized by its high mitochondrial content. Mitochondrial uncoupling protein 1 (UCP1) releases energy as heat instead of chemical energy. Thermogenesis increases energy expenditure. Berberine, a phytochemical widely used in Asian countries, has positive effects on body weight control. While the precise mechanisms behind this effect remain unclear, the adenosine monophosphate-activated protein kinase (AMPK) pathway is known to play a crucial role. Berberine activates AMPK through phosphorylation, significantly impacting brown adipose tissue by enhancing lipolytic activity and increasing the expression of UCP1, peroxisome proliferator-activated receptor γ-co-activator-1α (PGC1α), and PR domain containing 16 (PRDM16). While investigating the mechanism of action of berberine, both the AMPK pathway is being examined in more detail and alternative pathways are being explored. One such pathway is growth differentiation factor 15 (GDF15), known for its appetite-suppressing effect. Berberine's low stability and bioavailability, which are the main obstacles to its clinical use, have been improved through the development of nanotechnological methods. This review examines the potential mechanisms of berberine on browning and summarizes the methods developed to enhance its effect.