Cardiovasc Prev Pharmacother.  2022 Oct;4(4):132-141. 10.36011/cpp.2022.4.e17.

The crosstalk between insulin resistance and nonalcoholic fatty liver disease/metabolic dysfunction-associated fatty liver disease: a culprit or a consequence?

Affiliations
  • 1Division of Endocrinology and Metabolism, Department of Internal Medicine, Changwon Fatima Hospital, Changwon, Korea
  • 2Division of Endocrinology and Metabolism, Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea

Abstract

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.

Keyword

Insulin resistance; Nonalcoholic fatty liver disease; Metabolic dysfunction associated fatty liver disease; Inflammation; Metabolic syndrome

Figure

  • Fig. 1. Link between insulin resistance and the development and progression of nonalcoholic fatty liver disease. ChREBP, carbohydrate response element-binding protein; CRP, C-reactive protein; DAG, diacylglycerol; DNL, de novo lipogenesis; ER, endoplasmic reticulum; FA, fatty acid; FFA, free fatty acid; FOXA2, forkhead box protein A2; IL-6, interleukin-6; JNK, c-Jun NH2-terminal kinase; NASH, nonalcoholic steatohepatitis; NF-κB, nuclear factor-κB; PAI-1, plasminogen activator inhibitor-1; ROS, reactive oxygen species; SREBP-1c, sterol receptor binding protein-1c; TG, triacylglycerol; TLR, Toll-like receptor; TNF-α, tumor necrosis factor-α; VLDL, very-low-density lipoprotein.


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