• OpenAccess
  • 2,4-Dinitrophenol Downregulates Genes for Diabetes and Fatty Liver in Obese Mice  [ICDM 2015]
  • DOI: 10.4236/jbm.2015.39007   PP.44 - 51
  • Author(s)
  • Qian Gao, Jiang He, Tao Liao, Qingping Zeng
  • Whether obesity is a disease or a risk factor of metabolic diseases including type 2 diabetes and fatty liver remains debating, we report here that a high-fat diet (HFD) alone or HFD-combined intramuscular injection with a high dose (1.2 mg/kg) of lipopolysaccharide (LPS) induces mouse peripheral noninflammatory obesity. In contrast, HFD-combined intraperitoneal injection with a low dose (0.25 mg/kg) of LPS induces mouse visceral low-grade inflammatory obesity. While the noninsulin-dependent diabetes mellitus (NIDDM) and nonalcoholic fatty liver disease (NAFLD)- related genes are globally upregulated in HFD + low-dose LPS mice, NIDDM and NAFLD genes are not extensively upregulated in HFD + high-dose LPS mice. The mitochondrial uncoupler 2,4-dini- trophenol (DNP) in the dosage of 16 mg/kg was found to exert a weight-reducing effect in obese mice by compromising NF-κB-primed inflammatory responses, thereby down regulating NIDDM and NAFLD genes. Conclusively, mouse visceral low-grade inflammatory obesity that predisposes NIDDM and NAFLD can be ameliorated by DNP via anti-inflammation.

  • Obesity, Metabolic Disease, Low-Grade Inflammation, 2,4-Dinitrophenol, Anti-Inflammation
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