The Journal of clinical endocrinology and metabolism · 2025
Determinants of Pancreatic Size and Fat Content in the UK Biobank: Influence of Race, Genetic Variants, and Risk Factors.
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Kongara Tanvi, Carruth Alexander, Bhat Prahlad, Virostko John
Аннотация
OBJECTIVE: Pancreas size and fat content differ in individuals with diabetes, but it is not clear how pancreas imaging features are impacted by race, genetics, and lifestyle factors.
METHODS: We performed cross-sectional analysis of 37 163 UK Biobank participants with pancreas imaging data to investigate racial and genetic influences on pancreas volume index (PVI) and pancreatic fat fraction (PFF). We further assessed the influence of prior glycemic status and lifestyle factors on pancreas size and composition after adjusting for sex and age.
RESULTS: White nondiabetic individuals had lower PVI compared to Asian participants (P < .0001), but higher than Black participants (P < .01), whereas PFF was highest in White participants. Similar trends were observed in participants with diagnosed diabetes. When stratified by glycemic status acquired 4 to 14 years before imaging, White and Asian participants exhibited significantly lower PVI and higher PFF with increased hemoglobin A1c. Higher polygenic risk scores for type 2 diabetes and hemoglobin A1c were associated with reduced PVI (ρ = -0.07, P < .0001; and ρ = -0.14, P < .0001, respectively) and elevated PFF (ρ = 0.07, P < .0001 and ρ = 0.18, P < .0001, respectively). In contrast, type 1 diabetes polygenic risk showed no significant association with any pancreas measures. Sedentary lifestyle behaviors associated with type 2 diabetes risk at study baseline correlated with smaller PVI and increased pancreas fat 4 to 14 years later.
CONCLUSION: These findings highlight contributions of race, genetics, and behaviors to pancreatic morphology and fat deposition in glycemic dysregulation.
METHODS: We performed cross-sectional analysis of 37 163 UK Biobank participants with pancreas imaging data to investigate racial and genetic influences on pancreas volume index (PVI) and pancreatic fat fraction (PFF). We further assessed the influence of prior glycemic status and lifestyle factors on pancreas size and composition after adjusting for sex and age.
RESULTS: White nondiabetic individuals had lower PVI compared to Asian participants (P < .0001), but higher than Black participants (P < .01), whereas PFF was highest in White participants. Similar trends were observed in participants with diagnosed diabetes. When stratified by glycemic status acquired 4 to 14 years before imaging, White and Asian participants exhibited significantly lower PVI and higher PFF with increased hemoglobin A1c. Higher polygenic risk scores for type 2 diabetes and hemoglobin A1c were associated with reduced PVI (ρ = -0.07, P < .0001; and ρ = -0.14, P < .0001, respectively) and elevated PFF (ρ = 0.07, P < .0001 and ρ = 0.18, P < .0001, respectively). In contrast, type 1 diabetes polygenic risk showed no significant association with any pancreas measures. Sedentary lifestyle behaviors associated with type 2 diabetes risk at study baseline correlated with smaller PVI and increased pancreas fat 4 to 14 years later.
CONCLUSION: These findings highlight contributions of race, genetics, and behaviors to pancreatic morphology and fat deposition in glycemic dysregulation.