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Recent studies have reported the positive association between exposure to insecticides and increased risk of obesity and type 2 diabetes, which are closely associated with non-alcoholic fatty liver disease (NAFLD). However, it is not known if insecticide exposure can contribute to NAFLD. Thus, the goal of the current study was to determine if insecticide exposures can exacerbate the physiological conditions of NAFLD by modulating hepatic lipid metabolism. The effects of 12 insecticides on triglycerides (TG) accumulation were tested using palmitic acid (PA)induced HepG2 hepatoma steatosis model. Results showed that among tested insecticides, permethrin and ivermectin significant interacted with palmitic acid to potentiate (permethrin) or decrease (ivermectin) TG accumulation. Further study showed that permethrin significantly promoted fatty acid synthesis, while suppressed lipid oxidation-related genes only under steatosis conditions. In comparison, ivermectin inhibited lipogenesis-related genes and promoted farnesoid X receptor, which upregulates fatty acid oxidation. Results in this study suggested that hepatic lipid metabolism may be more susceptible to insecticide exposure in the presence of excessive fatty acids, which can be associated with the development of NAFLD.

Mitochondria intricately modulate their energy production through the control of mitochondrial adaptation (mitochondrial biogenesis, fusion, and/or fission) to meet energy demands. Nutrient overload may result in dysregulated mitochondrial biogenesis, morphology toward mitochondrial fragmentation, and oxidative stress in the skeletal muscle. In addition, physical activity and diet components influence mitochondrial function. Exercise may stimulate mitochondrial biogenesis and promote mitochondrial fusion/fission in the skeletal muscle. Moreover, some dietary fatty acids, such as n-3 polyunsaturated fatty acids and conjugated linoleic acid, have been identified to positively regulate mitochondrial adaptation in the skeletal muscle. This review discusses the association of mitochondrial impairments and obesity, and presents an overview of various mechanisms of which exercise training and mitochondrial nutrients promote mitochondrial function in the skeletal muscle.

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Nonalcoholic fatty liver disease (NAFLD) is the prevalent liver disease resulting from metabolic disorder, which is highly associated with obesity and type 2 diabetes. Emerging evidence has shown that insecticide exposure disrupts lipid and glucose metabolism and results in obesity and type 2 diabetes. However, the potential impact of insecticide exposure on the liver functions related to NAFLD development is largely unknown. Thus, this perspective focused on the current knowledge of the effect of insecticides on the liver functions, particularly lipid and glucose metabolism, as well as other liver functions to correlate insecticide exposure and the development of NAFLD.