Abstract
Inflammation and immune response profoundly influence metabolic syndrome and fatty acid metabolism. To analyze influence of systemic inflammatory response to metabolic syndrome, we inoculated an attenuated vaccine strain of Mycobacterium bovis Bacillus Calmette–Guérin (BCG) into leptin-deficient ob/ob mice. BCG administration significantly decreased epididymal white adipose tissue weight, serum insulin levels, and a homeostasis model assessment of insulin resistance. Serum high molecular weight (HMW) adiponectin level and HMW/total adiponectin ratio of the BCG treated mice were significantly higher than those of control mice. Hepatic triglyceride accumulation and macrovesicular steatosis were markedly alleviated, and the enzymatic activities and mRNA levels of lipogenic-related genes in liver were significantly decreased in the BCG injected mice. We also exposed human hepatocellular carcinoma HepG2 cells to high levels of palmitate, which enhanced endoplasmic reticulum stress-related gene expression and impaired insulin-stimulated Akt phosphorylation (Ser473). BCG treatment ameliorated both of these detrimental events. The present study therefore suggested that BCG administration suppressed development of nonalcoholic fatty liver disease, at least partly, by alleviating fatty acid-induced insulin resistance in the liver.
Highlights
Obesity, especially visceral obesity, contributes to the pathogenesis of the metabolic syndrome, a cluster of metabolic abnormalities that includes hyperlipidemia, type 2 diabetes mellitus (T2DM), and hypertension [1]
We investigated the effects of Bacillus Calmette–Guérin (BCG) on the development of metabolic syndrome in ob/ob mice
These results suggest that BCG administration alleviated the Nonalcoholic fatty liver disease (NAFLD) by inhibiting fatty acid-induced endoplasmic reticulum (ER) stress in livers of the ob/ob mice which resulted in amelioration of insulin resistance (IR)
Summary
Especially visceral obesity, contributes to the pathogenesis of the metabolic syndrome, a cluster of metabolic abnormalities that includes hyperlipidemia, type 2 diabetes mellitus (T2DM), and hypertension [1]. Nonalcoholic fatty liver disease (NAFLD) is associated with metabolic syndrome. It has recently been reported that various immune cells play key roles in the development of obesity-related metabolic abnormalities [3]. Obesity-related insulin resistance (IR) is associated with elevated cytokine levels, including tumor necrosis factor (TNF)-α and interleukin (IL)-6, and elevated serum free fatty acid levels [4, 5]
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