Abstract
ObjectiveTo emphasize the mechanism of concurrent exercise effect on lipid disorders in insulin resistance (IR) and nonalcoholic fatty liver disease (NAFLD).Materials and methodsTwenty male ApoE knockout mice were randomly divided into two groups: HFD group (n = 10) fed a high fat diet, and HFDE group (n = 10) with high-fat diet intervention for 12 weeks and swimming exercise. Other ten healthy male C57BL/6 J mice were fed a normal diet, and included as control group. Retro-orbital blood samples were collected for biochemical analysis. Oil red O staining of liver tissues was performed to confirm the exercise effect. Western blotting was performed to evaluate the expressions of PPAR-γ, CPT-1, MCAD.ResultsThe levels of TG, TC, LDL, FFA, FIN, FPG and Homa-IRI in the HFD group were significantly higher than ND group, while these were markedly decreased in the HFDE group compared with HFD group. The Oil Red O staining of liver samples further confirmed the exercise effect on the change of lipid deposition in the liver. Western blotting showed increased expressions of PPAR-γ, CPT-1, MCAD induced by high fat diet were significantly downregulated by exercise.ConclusionA concurrent 12-week exercise protocol alleviated the lipid metabolism disorders of IR and NAFLD, probably via PPAR-γ/CPT-1/MCAD signaling.
Highlights
Type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD) are pandemic metabolic diseases
The levels of TG, Total serum cholesterol (TC), Low-density lipoprotein cholesterol (LDL), Free fatty acid (FFA), Fasting serum insulin level (FIN), Fasting plasma glucose (FPG) and Homa-Insulin resistance index (IRI) in the high fat diet (HFD) group were significantly higher than Normal diet (ND) group, while these were markedly decreased in the High fat diet plus exercise (HFDE) group compared with HFD group
Western blotting showed increased expressions of Peroxisome proliferator-activated receptors (PPAR)-γ, carnitine palmitoyl transferase-1 (CPT-1), medium-chain acyl-CoA dehydrogenase (MCAD) induced by high fat diet were significantly downregulated by exercise
Summary
Type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD) are pandemic metabolic diseases. They act in a “vicious circle” that accelerates worsening of the vascular complications of T2DM and aggravates NAFLD progression to liver cirrhosis and hepatocellular carcinoma [1]. T2DM is one of the most common chronic diseases with increasing incidence due to lifestyle changes. It is characterized by hyperglycemia mainly caused by impaired insulin. Zheng and Cai Lipids in Health and Disease. The most common independent risk factor for NAFLD is believed to be IR [5, 6]. IR is caused by an imbalance between excess nutrients or inflammatory cytokines and the cell membrane receptors [7, 8]
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