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Updated: Jul 6, 2026

Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
Association between dietary inflammatory index and hepatic steatosis: cross-sectional evidence from the NHANES
Zhounan Wu1,2, Yuhang Liang1,2, Li Zeng3
1Department of Orthopaedic Surgery, the Third Xiangya Hospital of Central South University, 138 Tongzipo Road, Hexi Yuelu District, Changsha City, 410013, Hunan Province, China.
Background:
Although inflammation and dietary habits have been linked to obesity-associated hepatic steatosis, the role of diet-mediated inflammation in the course of hepatic steatosis remains unclear. This study aims to investigate the association between the Dietary Inflammatory Index (DII) and hepatic steatosis in the US population.
Methods:
The cross-sectional portion of this study included participants from the National Health and Nutrition Examination Survey (NHANES) spanning from 2007 to 2020. Our investigation employed weighted logistic regression to explore the association between DII score and hepatic steatosis prevalence. Subgroup analyses were performed to identify potential confounding factors, while smooth curve fitting and threshold effect analysis were utilized to determine any non-linear relationships. Least absolute shrinkage and selection operator (LASSO) regression was used to identify the key nutrients associated with the risk of hepatic steatosis. Subsequently, a nomogram model based on these major dietary factors was constructed. The diagnostic power of the predictive model to screen for hepatic steatosis risk was evaluated using receiver operating characteristic (ROC) curves and calibration curves.
Results:
This study included a substantial cohort of 27,655 participants, representing 181 million residents in the U.S. Weighted logistic regression revealed a positive association between elevated DII scores and the risk of hepatic steatosis (DII as a continuous variable: OR = 1.07, 95% CI = 1.05-1.10; Q4 compared to Q1: OR = 1.35, 95% CI = 1.21-1.50). The nomogram model exhibited considerable power in disease risk assessment (the area under the curve (AUC) of the training set: 0.714, 95% CI = 0.706-0.721; the AUC of the validation set: 0.707, 95% CI = 0.697-0.716). The results of the sensitivity analyses indicated that a history of current or past hepatitis B infections and excessive alcohol did not interfere with the association between DII and hepatic steatosis.
Conclusions:
Our findings reveal a significant association between the DII score and hepatic steatosis. This suggests that dietary patterns with lower inflammatory potential may be associated with a reduced prevalence of hepatic steatosis. However, given the inherent limitations of the cross-sectional study design, further longitudinal studies or intervention trials are necessary to ensure such an association.
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