Association Between Dietary Advanced Glycation End Products ( AGEs ) and Pancreatic Fat Accumulation: Evidence From a Case–Control Study

ABSTRACT Background Pancreatic steatosis (PS) is a metabolic condition associated with obesity, insulin resistance, and fatty liver disease. Advanced Glycation End Products (AGEs), abundant in processed and high‐temperature–cooked foods, have been linked to several metabolic disorders; however, their relationship with PS has not been previously examined. Methods In this case–control study, 278 individuals with gallstones, aged 55.7 ± 15.1 years, were classified as cases (with PS, n = 89) or controls (without PS, n = 189). PS was defined based on increased echogenicity of the pancreatic parenchyma relative to surrounding structures. Dietary intake was assessed using a food frequency questionnaire. Logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for PS across quartiles of dietary AGE intake. The fully adjusted model included age, sex, total energy intake, body mass index, smoking status, and alcohol consumption. Results Higher dietary AGE intake was significantly associated with an increased likelihood of PS. In the crude model, odds of PS did not differ significantly across quartiles of dietary AGE intake compared with the lowest quartile. After adjustment for age and sex, individuals in the highest quartile had higher odds of PS (OR = 3.56; CI: 1.1–11.6; p = 0.040). In the fully adjusted model, significant associations were observed for the third (OR = 2.76; CI: 1.69–11.1) and fourth (OR = 3.3; CI: 1.79–13.7) quartiles of dietary AGE intake compared with the lowest quartile. A significant positive trend in the odds of PS was observed across increasing quartiles of dietary AGE intake (p for trend = 0.024). Conclusion Our findings suggest a potential role of dietary AGEs in pancreatic fat accumulation; however, causality cannot be inferred. Larger prospective and interventional studies are needed to confirm these associations and to determine whether reducing dietary AGE exposure can beneficially influence pancreatic fat.