Association of BCAAs/BCKAs with pancreatic steatosis in patients with type 2 diabetes mellitus: A cross-sectional study.
To examine the association between branched-chain α-keto acids (BCKAs) and pancreatic steatosis in patients with type 2 diabetes (T2DM).
This cross-sectional study was conducted from January 2023 to March 2025. Upper abdominal computerized tomography was performed, pancreatic volume (PV), PV index (PVI), CT attenuation of pancreas (CTAP), and CTAp/s were then calculated. Levels of serum BCKAs and BCAAs were determined by ELISA kits. Partial correlation and linear regression analysis were performed to investigate the relationship between BCKA and pancreatic parameters. Mediating models were employed to explore the role of BMI in the relationship between BCKA and pancreatic parameters.
There were significant differences in median PV, PVI, CTAp, and CTAp/s according to BCKA tertiles (all p < 0.05). BCKAs were positively associated with PV and PVI but negatively correlated with CTAp and CTAp/s after adjustment for age and gender (all P < 0.05). Linear regression analysis showed that BCKA was associated with PV, CTAp, and CTAp/s after adjustment for confounders in all models (Model 1, Model 2, Model 3) (all P < 0.05). There existed no significant association of BCAA with pancreatic parameters after adjustment for confounders. Mediation analysis suggested that BMI played approximately 20% indirect effect in the relationship between BCKAs and PV or CTAp/s.
Serum BCKAs rather than BCAAs were associated with PV and CTAp in T2DM patients, indicating an association between BCAA malmetabolism and pancreatic steatosis. Additionally, obesity may serve as a mediator between BCKAs and pancreatic steatosis, which should be validated by prospective cohort.
This cross-sectional study was conducted from January 2023 to March 2025. Upper abdominal computerized tomography was performed, pancreatic volume (PV), PV index (PVI), CT attenuation of pancreas (CTAP), and CTAp/s were then calculated. Levels of serum BCKAs and BCAAs were determined by ELISA kits. Partial correlation and linear regression analysis were performed to investigate the relationship between BCKA and pancreatic parameters. Mediating models were employed to explore the role of BMI in the relationship between BCKA and pancreatic parameters.
There were significant differences in median PV, PVI, CTAp, and CTAp/s according to BCKA tertiles (all p < 0.05). BCKAs were positively associated with PV and PVI but negatively correlated with CTAp and CTAp/s after adjustment for age and gender (all P < 0.05). Linear regression analysis showed that BCKA was associated with PV, CTAp, and CTAp/s after adjustment for confounders in all models (Model 1, Model 2, Model 3) (all P < 0.05). There existed no significant association of BCAA with pancreatic parameters after adjustment for confounders. Mediation analysis suggested that BMI played approximately 20% indirect effect in the relationship between BCKAs and PV or CTAp/s.
Serum BCKAs rather than BCAAs were associated with PV and CTAp in T2DM patients, indicating an association between BCAA malmetabolism and pancreatic steatosis. Additionally, obesity may serve as a mediator between BCKAs and pancreatic steatosis, which should be validated by prospective cohort.
Authors
Gao Gao, Cheng Cheng, Jiang Jiang, Li Li, Shi Shi, Wang Wang, Wang Wang, Lei Lei, Zang Zang, Lu Lu
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