Short-term exposure to lauric acid promotes adipose tissue lipolysis and reduces leptin expression via a PPARγ-dependent mechanism

Coconut oil has gained popularity for its potential health benefits, particularly regarding energy metabolism. One of its key components, lauric acid (LA), has been reported to reduce body fat and improve insulin sensitivity, making it beneficial for individuals with obesity and type 2 diabetes. However, its full metabolic effects remain unclear, and further research is needed. This study investigated how LA influences fat cells (adipocytes) metabolism. Mice fed a diet containing 40% coconut oil showed elevated blood levels of glycerol and free fatty acids (FAs), indicating enhanced lipolysis. Gene expression analysis showed upregulation of pathways involved in FA uptake and metabolism. Concurrently, leptin expression in white adipose tissue (WAT), and circulating leptin levels, were reduced. Protein analysis revealed increased activation of lipid turnover regulators, including hormone-sensitive lipase (HSL) and perilipin 1 (PLIN1). In vitro, rat adipocytes treated with LA showed enhanced activity of metabolic processes that support fat oxidation, such as citrate synthase and carnitine palmitoyltransferase, along with a higher rate of oxygen consumption. Leptin production was likewise reduced by LA in vitro. The reduction in leptin levels and increased lipolysis appear to be partly mediated by the modulation of peroxisome proliferator-activated receptor gamma (PPARγ), a key regulator of lipid metabolism. While these effects support fat mobilization, the concurrent reduction in leptin expression may influence energy homeostasis, potentially counteracting the metabolic benefits of LA. These findings underscore the complex role of lauric acid in adipose tissue metabolism and raise questions about potential trade-offs.