This study aimed to examine the protective effect of Artemisia iwayomogi extract (AI) against hypertriglyceridemia induced by a high-fat diet (HFD) in mice and to uncover the underlying molecular mechanisms. C57BL/6N mice were fed chow, HFD, HFD + 0.1% AI, HFD + 0.25% AI, or HFD + 0.5% AI for 10 weeks. The addition of 0.25% and 0.5% AI resulted in dose-dependent improvements in the major parameters of hypertriglyceridemia, including plasma triglyceride, free fatty acids, apolipoprotein B, and lipoprotein lipase, with parallel reductions in body weight gain, hepatic lipid accumulation, and insulin resistance. These beneficial effects were accompanied by the activation of adiponectin-adenosine monophosphate-activated protein kinase (AMPK) mediated signaling cascades in the liver, which downregulated molecules involved in lipogenesis and concurrently upregulated molecules related to fatty acid oxidation. The downregulation of molecules involved in very low density lipoprotein assembly, which was associated with improved hepatic insulin signaling, also appeared to contribute to the AI-induced attenuation of hypertriglyceridemia.

Introduction: Gene expression profiles in human peripheral blood mononuclear cells (PBMCs) may act as a useful tool to better understand obesity. We investigated gene expression levels in PMBCs for possible differences between obese and non-obese subjects (19–55 years) and evaluated correlations between gene expression in PBMCs and clinical obesity indices. Methods: Body weight, BMI, fat amount, fat percentage, waist/hip ratio, leptin, and adiponectin levels were determined in 30 obese and 20 non-obese subjects. Expression levels of 19 genes, which were differentially expressed by clinical obesity indices in the PBMCs of high fat-fed rats, were determined in their PBMCs using real-time PCR. Results: The expression of 9 of 19 previously selected genes was significantly correlated with one or more clinical obesity indices. Both TFEC and CCL2 expression were negatively correlated with BMI, fat amount, fat percentage, waist/hip ratio, and leptin concentration. Similarly, TNFAIP2, VCAN, ASSI, IRF1, and HK3 expression negatively correlated with some clinical obesity indices, such as TNFAIP2 for BMI, fat amount, fat percentage, and waist/hip ratio, VCAN for fat amount, fat percentage, and waist/hip ratio, ASS1 for BMI and fat amount, IRF1 for BMI, fat amount, and fat percentage, and HK3 for fat amount. In contrast, both TNF-α and LPL expression were positively correlated with waist/hip ratio. Conclusion: We identified 9 of 19 genes in human PBMCs that significantly correlated with one or more clinical obesity indices. Because these genes have a mechanistic basis for the development or progression of obesity and its metabolic derangements, they may help to determine possible underlying mechanisms for obesity.