TY - JOUR
T1 - Insulin resistance as a mediator of the association between obesity, high-intensity binge drinking, and liver enzyme abnormalities in young and middle-aged adults
T2 - a cross-sectional study
AU - Zhu, Jiayi
AU - Duan, Yinglong
AU - Li, Ying
AU - Zhou, Yi
AU - Lu, Zitong
AU - Chen, Nandan
AU - Luo, Juan
AU - Wang, Xingxing
AU - Dong, Xiaoqian
AU - Cheng, Andy S. K.
AU - Liu, Yuan
PY - 2025
Y1 - 2025
N2 - Background: Binge drinking (BD) and obesity are well-established risk factors for liver enzyme abnormalities, but how varying intensities of BD interact with obesity to affect liver function remains unclear. This study aims to examine whether insulin resistance (IR) mediates the associations between different levels of BD, obesity, their interaction, and liver enzyme abnormalities. Methods: This cross-sectional study included 137,878 young and middle-aged adults who underwent physical examinations in southern China between August 2017 and March 2024. BD was self-reported, and IR was assessed using the triglyceride–glucose (TyG) index. Causal mediation analysis within the counterfactual framework was used to quantify the mediating role of the TyG index in the associations involving BD intensity, obesity, their interaction, and liver enzyme abnormalities. Results: The interaction between obesity and high-intensity binge drinking (HIBD) was significantly associated with liver enzyme abnormalities (OR, 1.591; 95% CI, 1.401–1.806). IR, measured by the TyG index, statistically accounted for 36.6% (OR, 1.034; 95% CI, 1.029–1.039) of this association, exceeding the proportion explained in the HIBD alone (25.9%) or obesity alone (16.7%) pathways. No significant mediating effect of IR was observed for non-BD or low-intensity BD, regardless of obesity status. Conclusion: The TyG index serves as a critical mediator in the synergistic effects of HIBD and obesity on liver enzyme abnormalities. Targeting IR and reducing the intensity of alcohol consumption may help mitigate liver injury in young and middle-aged adults with obesity.
AB - Background: Binge drinking (BD) and obesity are well-established risk factors for liver enzyme abnormalities, but how varying intensities of BD interact with obesity to affect liver function remains unclear. This study aims to examine whether insulin resistance (IR) mediates the associations between different levels of BD, obesity, their interaction, and liver enzyme abnormalities. Methods: This cross-sectional study included 137,878 young and middle-aged adults who underwent physical examinations in southern China between August 2017 and March 2024. BD was self-reported, and IR was assessed using the triglyceride–glucose (TyG) index. Causal mediation analysis within the counterfactual framework was used to quantify the mediating role of the TyG index in the associations involving BD intensity, obesity, their interaction, and liver enzyme abnormalities. Results: The interaction between obesity and high-intensity binge drinking (HIBD) was significantly associated with liver enzyme abnormalities (OR, 1.591; 95% CI, 1.401–1.806). IR, measured by the TyG index, statistically accounted for 36.6% (OR, 1.034; 95% CI, 1.029–1.039) of this association, exceeding the proportion explained in the HIBD alone (25.9%) or obesity alone (16.7%) pathways. No significant mediating effect of IR was observed for non-BD or low-intensity BD, regardless of obesity status. Conclusion: The TyG index serves as a critical mediator in the synergistic effects of HIBD and obesity on liver enzyme abnormalities. Targeting IR and reducing the intensity of alcohol consumption may help mitigate liver injury in young and middle-aged adults with obesity.
KW - binge drinking
KW - insulin resistance
KW - liver enzymes
KW - metabolic dysfunction
KW - obesity
KW - young and middle-aged
UR - http://www.scopus.com/inward/record.url?scp=105012775843&partnerID=8YFLogxK
U2 - 10.3389/fnut.2025.1554392
DO - 10.3389/fnut.2025.1554392
M3 - Article
AN - SCOPUS:105012775843
SN - 2296-861X
VL - 12
JO - Frontiers in Nutrition
JF - Frontiers in Nutrition
M1 - 1554392
ER -