A narrative review on the role of hesperidin on metabolic parameters, liver enzymes, and inflammatory markers in nonalcoholic fatty liver disease

Abstract

Insulin resistance, oxidative stress, hyperlipidemia, and inflammation play main roles in the development of nonalcoholic fatty liver disease (NAFLD). Some studies have reported that hesperidin can reduce hyperglycemia and hyperlipidemia by inhibiting inflammatory pathways. In the current study, our purpose was to evaluate whether it can influence the primary parameters in NAFLD and improve the treatment effectiveness for future trials. Various studies have found that hesperidin involves multiple signaling pathways such as cell proliferation, lipid and glucose metabolism, insulin resistance, oxidative stress, and inflammation, which can potentially affect NAFLD development and prognosis. Recent findings indicate that hesperidin also regulates key enzymes and may affect the severity of liver fibrosis. Hesperidin inhibits reactive oxygen species production that potentially interferes with the activation of transcription factors like nuclear factor-κB. Appropriate adherence to hesperidin may be a promising approach to modulate inflammatory pathways, metabolic indices, hepatic steatosis, and liver injury.

Keywords: fatty liver; hesperidin; inflammation; nonalcoholic; obesity.

FIGURE 1

Summary of the most important effects of hesperidin consumption on proposed mechanisms of action in NAFLD. CCK, cholecystokinin; CRP, C‐reactive protein; IL‐6, interleukin‐6; MCP‐1, monocyte chemoattractant protein‐1; MDA, malondialdehyde; NO, nitric oxide; PPAR, peroxisome proliferator‐activated receptors; ROS, reactive oxygen species; TG, triglyceride; UCP3, uncoupling protein 3.