Mangiferin Ameliorates Obesity-Associated Inflammation and Autophagy in High-Fat-Diet-Fed Mice: In Silico and In Vivo Approaches

• Published in: International journal of molecular sciences Vol. 23; no. 23; p. 15329
• Main Authors: Noh, Ji-Won, Lee, Han-Young, Lee, Byung-Cheol
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 05.12.2022; MDPI
• Subjects: Adipose tissue; Adipose Tissue - metabolism; Anemarrhenae rhizoma; Animals; Apoptosis; Autophagy; Body weight; Cholesterol; Cytokines; Diabetes; Diet, High-Fat - adverse effects; Disease; Experiments; Fat metabolism; Fibroblast growth factors; Gene expression; Genes; Glucose; Glucose - metabolism; Growth factors; High density lipoprotein; High fat diet; In vivo methods and tests; Inflammation; Inflammation - pathology; Inflammatory response; Insulin; Insulin Resistance; Kinases; Kupffer cells; Lipid metabolism; Lipids; Liver; Macrophages; mangiferin; Metabolic disorders; Metabolic syndrome; Mice; Mice, Inbred C57BL; Mice, Obese; Obesity; Obesity - complications; Obesity - drug therapy; Phosphorylation; Proteins; Signal transduction; Tumor necrosis factor-TNF; Tumor necrosis factor-α; autophagy; mangiferin; inflammation; insulin resistance; Anemarrhenae rhizoma; obesity
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms232315329

Obesity-induced insulin resistance is the fundamental cause of metabolic syndrome. Accordingly, we evaluated the effect of mangiferin (MGF) on obesity and glucose metabolism focusing on inflammatory response and autophagy. First, an in silico study was conducted to analyze the mechanism of MGF in insulin resistance. Second, an in vivo experiment was conducted by administering MGF to C57BL/6 mice with high-fat-diet (HFD)-induced metabolic disorders. The in silico analysis revealed that MGF showed a high binding affinity with macrophage-related inflammatory cytokines and autophagy proteins. In the in vivo study, mice were divided into three groups: normal chow, HFD, and HFD + MGF 150 mg/kg. MGF administration to obese mice significantly improved the body weight, insulin-sensitive organs weights, glucose and lipid metabolism, fat accumulation in the liver, and adipocyte size compared to HFD alone. MGF significantly reduced the macrophages in adipose tissue and Kupffer cells, inhibited the gene expression ratio of tumor necrosis factor-α and F4/80 in adipose tissue, reduced the necrosis factor kappa B gene, and elevated autophagy-related gene 7 and fibroblast growth factor 21 gene expressions in the liver. Thus, MGF exerted a therapeutic effect on metabolic diseases by improving glucose and lipid metabolism through inhibition of the macrophage-mediated inflammatory responses and activation of autophagy.