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Updated: May 5, 2026
Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
Non-linear relationship between the hepatic steatosis index and glycemic progression: evidence from a large-scale
Changchun Cao1,2,3, Yongyang Huo3, Yong Han3
1Department of Rehabilitation, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, No.3002, Sungang West Road, Futian District, Shenzhen, 518000, Guangdong Province, China.
Background:
The hepatic steatosis index (HSI) is a validated tool for assessing hepatic steatosis. While previous investigations have explored the link between HSI and prediabetes and diabetes, the connection between HSI and glycemic progression is still being explored. This research seeks to clarify the association between HSI and glycemic progression risk among a Chinese demographic.
Methods:
The research encompassed a group of 76,314 Chinese adults from the Rich Healthcare Group who were free of prediabetes at the outset. Cox proportional hazard models were utilized to investigate the connection between the HSI and glycemic progression. Additionally, cubic spline function and smooth curve fitting in the Cox regression framework were applied to identify potential non-linear associations between HSI and glycemic progression.
Results:
Multivariable analysis demonstrated that with each incremental unit in the HSI, there was a corresponding 5.4% rise in the risk of glycemic progression among females (HR: 1.054, 95%CI: 1.038-1.071) and a 3.7% increase in males (HR: 1.037, 95% CI: 1.028-1.046). Both genders exhibited a non-linear connection between HSI and the risk of glycemic progression. The inflection points for HSI were determined to be 36.595 for females and 34.328 for males. Within the female population, a significant positive association with glycemic progression risk was noted when HSI levels were below 36.595 (approximately 8.0% increased risk per unit) (HR: 1.080, 95%CI: 1.061-1.099, P < 0.0001), whereas this correlation was not statistically significant at HSI levels exceeding 36.595 (HR: 0.988, 95%CI: 0.960-1.016, P = 0.4010). In the male population, hazard ratios were 1.026 (95%CI: 1.013-1.038) (approximately 2.6% increased risk per unit) below the inflection point and 1.045 (95%CI: 1.034-1.056) (approximately 4.5% increased risk per unit) above it.
Conclusion:
Elevated HSI demonstrated a positive, non-linear correlation with the risk of glycemic progression, suggesting that maintaining lower HSI levels may mitigate the risk of developing glycemic progression.
