Nonalcoholic fatty liver disease (NAFLD), which has recently undergone a change in its definition and acronym to “metabolic dysfunction associated fatty liver disease (MAFLD),” is clinically significant as an increasingly prevalent independent risk factor for cardiovascular diseases. Insulin resistance is considered to be a key mechanism in the development and progression of NAFLD/MAFLD, and fatty liver disease itself may exacerbate insulin resistance. In this review, we describe the mechanisms underlying the interaction between insulin resistance and fatty liver, and we summarize the therapeutic attempts based on those mechanisms.
Increased inflammation and insulin resistance are commonly observed in obesity and diabetes. Inflammatory mediators secreted by the adipose tissue contribute to the pathogenesis of diabetes and cardiovascular diseases. Free fatty acids and pro-inflammatory cytokines from adipose tissue inhibit the intracellular insulin signaling pathway, further contributing to the progression of diabetes. Meta-analysis studies show that high sensitivity C-reactive protein can be used as a predictor of future all-cause mortality, including cardiovascular and cancer mortality. In addition to the discovery of novel therapeutic methods targeting inflammatory mediators, basic lifestyle interventions, such as regular exercise, healthy eating, and proper weight control, are absolutely crucial for reducing inflammation and preventing mortality.
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Links between oral microbiome and insulin resistance: Involvement of MAP kinase signaling pathway Yi-Ru Chang, Wen-Chi Cheng, Ya-Chun Hsiao, Guan-Wei Su, Shan-Jen Lin, Yu-Shan Wei, Hsiu-Chuan Chou, Hsiu-Ping Lin, Guan-Yu Lin, Hong-Lin Chan Biochimie.2023; 214: 134. CrossRef