The aim of this study was to investigate whether Dioscorea batatas (DB) extract attenuates high-fat diet (HFD)-induced insulin resistance in the visceral adipose tissues of mice, and by what mechanism(s). Mice were fed a HFD for 4 weeks to induce the early development of insulin resistance. The DB extract was administered to mice fed a HFD by oral gavage at a dose of 100 mg/kg body weight daily for 7 weeks. Biochemical parameters in blood were measured using enzymatic kits, and the expression levels of glucose transporter 4 (GLUT4), phosphorylated (p-)S6K1, phosphorylated v-akt murine thymoma viral oncogene homolog (p-AKT), and phosphorylated extracellular regulated kinase (p-ERK) in epididymal fat tissue were determined by western blot analyses. The DB extract effectively reversed the HFD-induced elevations in plasma glucose and insulin levels, and the homeostasis model assessment for insulin resistance and oral glucose tolerance test values. The level of p-AKT protein was up-regulated, whereas the levels of p-ERK and p-S6K1 proteins were down-regulated in the adipose tissues of DB mice compared with HFD mice. Furthermore, the DB extract significantly reversed the HFD-induced decrease in the plasma membrane GLUT4 level in the adipose tissue of mice. The DB extract improved glucose metabolism in HFD-fed mice through the up-regulation of plasma membrane GLUT4 content in the visceral adipose tissue. Activation of the insulin signaling cascade leading to GLUT4 translocation was the mechanism underlying the beneficial effects of the DB extract on early-stage obesity-induced insulin resistance.

The objective of the present study was to determine whether Artemisia iwayomogi (AI) extract reduces visceral fat accumulation and obesity-related biomarkers in mice fed a high-fat diet (HFD), and if so, whether these effects are exerted by modulation of the expression of genes associated with adipogenesis and inflammation. AI extract supplementation for 11 weeks significantly prevented HFD-induced increments in body weight, visceral adiposity, adipocyte hypertrophy, and plasma levels of lipids and leptin. Additionally, AI extract supplementation resulted in downregulation of adipogenic transcription factors (PPARγ2 and C/EBPα) and their target genes (CD36, aP2, and FAS) in epididymal adipose tissue compared to the HFD alone. The AI extract effectively reversed the HFD-induced elevations in plasma glucose and insulin levels and the homeostasis model assessment of insulin resistance index. Furthermore, the extract significantly decreased gene expression of proinflammatory cytokines (TNFα, MCP1, IL-6, IFNα, and INFβ) in epididymal adipose tissue and reduced plasma levels of TNFα and MCP1 as compared to HFD alone. In conclusion, these results suggest that AI extract may prevent HFD-induced obesity and metabolic disorders, probably by downregulating the expression of genes related to adipogenesis and inflammation in visceral adipose tissue.

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