ArticleFrontiers in endocrinology2026
Cytokeratin-18 increase as a signal for early liver cell changes in high-fat diet-induced obesity before overt steatohepatitis.
Article in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: The major cause of non-alcoholic fatty liver disease (NAFLD) is obesity; in fact, this condition has been defined as metabolic dysfunction-associated steatotic liver disease (MASLD). Non-invasive diagnosis and grading of NAFLD are the subjects of the studies. Cytokeratin-18 (CK-18) is particularly highlighted as an indicator of liver cell death and steatohepatitis, but its relationship with obesity remains unclear. This study aimed to evaluate the metabolic parameters, CK-18 levels, and liver histopathology in high-fat diet-induced obesity in rats. Methods: Rats were fed either a normal-fat diet (NFD) or a high-fat diet (HFD) for eight weeks. Body weights, metabolic-liver parameters and CK-18 levels were assessed at study end. The liver histopathological changes (steatosis, lobular inflammation, ballooning, fibrosis) and NAFLD activity score were examined. Results: Increased final body weight (335.8 ± 20.2 vs 291.5 ± 6.25 g; p<0.001), glucose (186.4 ± 46.9 vs 130.0 ± 16.2 mg/dL; p=0.011), insulin (4.30 ± 0.70 vs 2.23 ± 0.82 IU/L; p<0.001), HOMA-IR (2.03 ± 0.79 vs 0.73 ± 0.34; p=0.003), ALT (72.34 ± 12.35 vs 55.43 ± 5.75 U/L; p=0.009) and CK-18 (1.46 ± 0.18 vs 0.88 ± 0.18 ng/mL; p<0.001) levels and decreased AST/ALT ratio (1.16 ± 0.09 vs 1.32 ± 0.14; p=0.020) were observed in HFD group compared to NFD group. Histologically, all HFD specimens showed ballooning (8/8) and half showed steatosis (4/8). NAFLD score remained ≤3 in all specimens nevertheless CK-18 values tended to co-occur with higher ALT levels and ballooning formation within the HFD group. Conclusıon: HFD-induced obesity was associated with increased CK-18 and the hepatocellular changes as remarkable ballooning without the overt steatohepatitis. These findings support CK-18 interpreting as a signal for early hepatocellular injury in obesity.
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