Extrahepatic inflammation and metabolic disorders contribute to NAFLD development
| Metabolic diseases | Factors or regulators | Hepatic inflammation and steatosis | References |
|---|---|---|---|
| Obesity | Production of adipokines (e.g., increase of leptin levels and decrease of adiponectin levels) | Induce hepatic inflammation | [21] |
| Adipose tissue insulin resistance | Increase hepatic TG accumulation | [27] | |
| Production of FFAs | Increase hepatic steatosis | [28] | |
| Insulin resistance | High levels of FPG | Increase liver DNL | [33, 36] |
| Downregulation of CYP7B1 expression | Increase hepatic cholesterol accumulation | [34] | |
| T2DM | Continual hyperglycemia | Cause hepatic liver accumulation | [39, 41] |
| Insulin resistance | |||
| CKD | High circulating levels of IL-6 and TNFR2 | Cause liver inflammation | [47] |
| CVD | Increased levels of proinflammatory cytokines such as IL-1β and TNF | Cause liver inflammation | [53–55] |
| Dysregulation metabolism of lipids and lipoproteins | Increase hepatic steatosis | [58, 59] |
CZ: Conceptualization, Investigation, Writing—original draft, Writing—review & editing. YS and SL: Investigation, Writing—original draft, Writing—review & editing. MY: Conceptualization, Validation, Writing—review & editing, Supervision. All authors read and approved the submitted version.
The authors declare that they have no conflicts of interest.
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© The Author(s) 2023.