Oleic acid-esterified octacosanol supplementation significantly reduced high-fat diet-induced weight gain and adipose tissue expansion in mice by promoting lipolysis and thermogenesis via PPAR activation.
Does octacosanol and its esterified derivatives improve lipid dysregulation and reduce weight gain in high-fat diet-fed mice?
Structural modification of octacosanol, particularly oleic acid esterification, enhances its metabolic activity in lipid catabolism and thermogenesis, offering a potential functional ingredient for obesity-associated metabolic regulation.
Absolute Event Rate: 10.61% vs 14.59%
p-value: p=<0.05
Octacosanol, a major constituent of policosanol, exhibits lipid-lowering activity, particularly when esterified with fatty acids. Although its cholesterol-lowering actions have been linked to the modulation of fatty acid and cholesterol biosynthesis, its functions within adipose tissue remain poorly defined. Here, we examined nonesterified octacosanol (NO), lauric acid-esterified octacosanol (LEO), and oleic acid-esterified octacosanol (OEO) in high-fat diet-fed mice for 11 weeks. Target prediction and molecular docking identified PPARα and PPARδ as putative targets of octacosanol, guiding downstream mechanistic analyses in adipose tissue. Both NO and OEO enhanced lipolysis; NO preferentially increased fatty acid β-oxidation, whereas OEO specifically promoted thermogenic remodeling, indicating distinct metabolic consequences driven by ester chemistry. Together, these findings demonstrate that structural modification, particularly oleic acid esterification, substantially augments the metabolic activity of octacosanol in lipid catabolism and thermogenesis, underscoring its potential relevance in obesity-associated metabolic regulation.
Koh et al. (Tue,) conducted a other in Obesity-associated lipid dysregulation (n=48). Oleic acid-esterified octacosanol (OEO) vs. High-fat diet (HFD) control was evaluated on Weight gained (g) (p=<0.05). Oleic acid-esterified octacosanol supplementation significantly reduced high-fat diet-induced weight gain and adipose tissue expansion in mice by promoting lipolysis and thermogenesis via PPAR activation.