Effect of omega-3 fatty acids on adipose tissue: histological, metabolic, and gene expression analyses in mice fed a high-fat diet

ω-3脂肪酸对脂肪组织的影响:高脂饮食小鼠的组织学、代谢和基因表达分析

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Abstract

Obesity is a metabolic disorder characterized by excessive fat accumulation due to energy imbalance. This study aimed to evaluate the effects of omega-3 fatty acids (n-3 FAs) on body weight, biochemical parameters, thermogenic gene expression, and adipose tissue morphology in a male C57BL/6 mice model of high-fat diet (HFD)-induced obesity initiated at 4 weeks of age. After a one-week adaptation, mice were randomly divided into four groups: a control group fed a standard diet (CD) and three experimental groups fed a HFD alone or enriched with 1.2% or 2.4% n-3 FAs. All groups were fed ad libitum for 12 weeks. Feed intake and body weight were recorded, and glucose and insulin tolerance tests were performed. Serum glucose, lipid profiles, insulin, leptin, and adiponectin levels were analyzed. Gene expression of uncoupling protein 1 (Ucp1), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (Pgc-1α), PR domain containing 16 (Prdm16), and G protein-coupled receptor 120 (Gpr120) was evaluated in brown adipose tissue (BAT), along with histological assessments of both BAT and white adipose tissue (WAT). n-3 FAs improved serum lipid profiles and glucose metabolism without significant changes in body weight or energy intake. Although no significant differences were observed in the expression of Ucp1, Pgc-1α, and Gpr120, Prdm16 expression was significantly higher in the 1.2% HFD group (p < 0.05). Histological analysis showed that n-3 FAs prevented BAT whitening, promoted WAT browning, and reduced inflammatory infiltration. Ucp1 immunoreactivity was significantly lower in the HFD group compared to the CD group (p < 0.05). These findings suggest that n-3 FAs exerts multifaceted protective effects on adipose tissue at genetic, biochemical, and histological levels, highlighting their potential in the management of diet-induced obesity.

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