Key result
Insulin resistance and metabolic syndrome in NAFLD are linked to tumorigenesis via inflammation and decreased adiponectin.
Why the study?
The pathogenesis of hepatocellular carcinoma in non-cirrhotic NAFLD is distinct and not fully elucidated, requiring further investigation.
This review highlights the unique metabolic and inflammatory pathways driving hepatocellular carcinoma in non-cirrhotic NAFLD patients.
Metabolic interventions may reduce HCC risk in non-cirrhotic NAFLD; leaves open prospective validation before practice change.
Although hepatocellular carcinoma (HCC) primarily arises in the background of liver cirrhosis, the development of HCC in nonalcoholic fatty liver disease (NAFLD) without cirrhosis is increasingly recognized. The pathogenesis of NAFLD associated non-cirrhotic HCC is distinct from that of cirrhotic HCC because the metabolic syndrome (MS) along with obesity and insulin resistance (IR) underlie several unique mechanisms that promote tumorigenesis. IR associated with MS, NAFLD, and type 2 diabetes mellitus lead to the release of multiple pro-inflammatory cytokines, including tumor necrosis factor alpha, interleukin-6, leptin and resistin, as well as decreased amounts of adiponectin. These processes favor the development of hepatic steatosis and inflammation within the liver, which precede HCC development. Nevertheless, further investigation is necessary to elucidate the determinants for development of HCC in patients with NAFLD in the absence of cirrhosis.
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Ryan B. Perumpail (2015) conducted a review in Hepatocellular carcinoma in non-cirrhotic nonalcoholic fatty liver disease. Insulin resistance and metabolic syndrome in non-cirrhotic NAFLD promote tumorigenesis via pro-inflammatory cytokines and decreased adiponectin, favoring hepatic steatosis and inflammation.
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