Environmental Factors Slightly Outweigh Genetic Influences in the Development of Pancreatic Lipid Accumulation: A Classical Twin Study.

Several studies showed that lipid accumulation in the pancreas (NAFPD: nonalcoholic fatty pancreas disease) may lead to different pancreatic disorders, including beta-cell dysfunction. The role of genetic and environmental factors in pancreatic lipid accumulation is unclear. We evaluated the magnitude of genetic and environmental impact on pancreatic lipid content within a cohort of adult twin pairs. We investigated 136 twin subjects [monozygotic (MZ,  = 86) and dizygotic (DZ,  = 50) same-gender twins (age 57.7 ± 9.1 years; body mass index [BMI] 28.0 ± 4.4 kg/m; females 64.7%)] with a 256-slice computed tomography (CT)-scanner. Using nonenhanced CT images, we calculated the average value of pancreatic attenuation expressed in Hounsfield unit (HU) suggesting pancreatic lipid content. Crude data were adjusted to age, sex, BMI, and hemoglobinA1c values. Intrapair correlations were established, and structural equation models were used for quantifying the contribution of additive genetic (A), common environmental (C), and unique environmental (E) components to the investigated phenotype. The study cohort represented a moderately overweight, middle-aged Caucasian population. Average pancreatic attenuation was 48.9 ± 11.9 HU in MZ and 49.0 ± 13.0 HU in DZ twins ( = 0.934). The intrapair correlation between HU values was stronger in MZ compared to DZ twins (rMZ = 0.536,  < 0.001; rDZ = 0.115,  = 0.580). Using the structural equation model, a greater unique environmental influence [E: 54%, 95% confidence interval (CI) 19%-66%] and a moderate additive genetic dependence (A: 46%, 95% CI 34%-81%) were found. The results of our classical twin study indicate that environmental (lifestyle) influences slightly outweigh genetic effects on the phenotypic appearance of pancreatic lipid accumulation known as NAFPD.