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Pathogenesis of insulin resistance syndrome in Western‐style diets‐induced obese and non‐obese experimental animal models
Author(s) -
Huang Jiung-Pang,
Hung Li-Man
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.686.22
Subject(s) - insulin resistance , medicine , endocrinology , adipose tissue , pathogenesis , glut4 , protein kinase b , insulin , fructose , obesity , metabolic syndrome , chemistry , biology , phosphorylation , biochemistry
Western diet induces obesity and consequently leads to insulin resistance, diabetes, and cardiovascular disease (CVD) is threatening to become a global epidemic. Although, more than 70 % of insulin resistance patient is obese, insulin resistance also occurs in non‐obese individuals. Hence, the present study was aimed to characterize the insulin resistance syndrome in obese and non‐obese and further explore its pathogenesis. The animals were fed with different western‐styles diet for 12 week and divided into five groups: (1) chow diet control group, control; (2) high fat diet, HFat; (3) high fructose diet, HFru; (4) high cholesterol diet, HC; (5) high cholesterol diet plus with 10% fructose in drinking water, HCF. The insulin resistance syndrome was observed in both HFat‐obese and HCF‐nonobese rats. The phosphorylated Akt (thr308) protein level was increased in adipose tissues of four western‐styles diets compared to chow diet control. The phosphorylated Akt (Ser473) protein level was increased in the adipose tissues of HFat, whereas it was reduced in the adipose tissues of HC and HCF. The GLUT4 level was downregulated in the adipose tissue of HFat, HC and HCF. The crown ‐ like structures around adipocytes were observed especially in HC and HCF groups. Up‐regulated NFκB/IκB ratio showed the higher inflammation degree in HFat, HC, and HCF groups. The lower MnSOD and Cu/ZnSOD proteins exhibited a weaker antioxidative ability and resulted raising of in superoxide anion in HC and HCF adipose tissues. The cleaved caspase 3 protein increased implying that adipocytes underwent apoptosis process especially in HC groups. In conclusion, our results indicate the causal relationships between inflammation and insulin resistance in non‐obese insulin resistance.