Anthocyanins and the browning of white adipose tissue: role of mitochondria and mechanisms of action

Graphical abstract Abstract Obesity is defined as a chronic disease characterized by fat accumulation excess. Obesity and consumption of high-fat diets are associated with alteration in mitochondrial function and biogenesis. Changes in lifestyle and dietary habits have been shown to improve mitochondrial function. In particular, emerging evidence supports the beneficial effects of anthocyanins, especially cyanidin and delphinidin consumption, on obesity-associated mitochondrial dysfunction. Selected anthocyanins and their gut metabolites have been shown to activate different key signaling pathways that promote the browning of white adipose tissue, a process whereby white adipose tissue develops characteristics of brown adipose tissue, which burns energy rather than storing it. Anthocyanins are shown to improve energy expenditure by increasing mitochondrial numbers and thermogenesis. Browning of white adipose tissue relies on mitochondrial dynamics (i.e. fission and fusion). Although just a few preclinical and in vitro studies showed that anthocyanins improve mitochondrial dysfunction via modulation of mitochondrial fusion, fission, and mitophagy, the outcomes are very promising. Because of the above, further research is needed to fully understand the therapeutic potential of anthocyanins in mitigating obesity-associated mitochondrial dysfunction.