Hajime Yamazaki1, Shinichi Tauchi2, Miho Kimachi3, Mitsuru Dohke4, Nagisa Hanawa4, Yoshihisa Kodama5, Akio Katanuma6, Yosuke Yamamoto3, Shunichi Fukuhara3, Shingo Fukuma7. 1. Department of Healthcare Epidemiology, School of Public Health in the Graduate School of Medicine, Kyoto University, Yoshida Konoe-cho, Sakyo-ku, Kyoto, 606-8501, Japan. yamazaki-myz@umin.ac.jp. 2. Department of Radiology, Keijinkai Maruyama Clinic, 3-16, Odori Nishi 26-chome, Chuo-ku, Sapporo, 064-0820, Japan. 3. Department of Healthcare Epidemiology, School of Public Health in the Graduate School of Medicine, Kyoto University, Yoshida Konoe-cho, Sakyo-ku, Kyoto, 606-8501, Japan. 4. Department of Health Checkup and Promotion, Keijinkai Maruyama Clinic, 3-16, Odori Nishi 26-chome, Chuo-ku, Sapporo, 064-0820, Japan. 5. Department of Radiology, Teine Keijinkai Hospital, 1-40, 1-jo 12-chome, Maeda, Teine-ku, Sapporo, 006-8555, Japan. 6. Center for Gastroenterology, Teine Keijinkai Hospital, 1-40, 1-jo 12-chome, Maeda, Teine-ku, Sapporo, 006-8555, Japan. 7. Human Health Sciences, Kyoto University Graduate School of Medicine, Yoshida Konoe-cho, Sakyo-ku, Kyoto, 606-8501, Japan.
Abstract
BACKGROUND: The association between pancreatic fat and glucose dysmetabolism has been reported in several cross-sectional studies; however, a recent longitudinal study showed that baseline pancreatic fat did not cause subsequent diabetes mellitus. We hypothesized that pancreatic fat is not a cause but a manifestation of glucose dysmetabolism and aimed to investigate the association between baseline prediabetes and future pancreatic fat accumulation. METHODS: Between 2008 and 2015, 198 nondiabetic participants, who underwent a health check-up via unenhanced computed tomography (CT) twice with CT intervals ≥ 5 years, were enrolled as prediabetes (n = 48) and non-prediabetes participants (n = 150). Prediabetes was defined as fasting plasma glucose of 100-125 mg/dl or hemoglobin A1c of 5.7-6.4%. Pancreatic fat was evaluated using a histologically validated method to measure the difference between pancreas and spleen attenuations (P-S) on CT. Pancreatic fat accumulation during follow-up was measured as P-S change from baseline. Multiple linear regression was used to evaluate the association between baseline prediabetes and future pancreatic fat accumulation with adjustment for age, sex, body mass index, physical activity, and liver fat at baseline. RESULTS: Mean pancreatic fat accumulation was 0.30 (SD, 5.8) Hounsfield units during follow-up. On univariate analysis, baseline prediabetes was associated with future pancreatic fat accumulation (β = 3.73; 95% CI 1.91-5.55; P < 0.001). This association remained statistically significant on multivariate analysis (β = 3.14; 95% CI 1.25-5.03; P = 0.001). CONCLUSIONS: Prediabetes is a risk factor for future pancreatic fat accumulation. Pancreatic fat may be a manifestation of glucose dysmetabolism.
BACKGROUND: The association between pancreatic fat and glucose dysmetabolism has been reported in several cross-sectional studies; however, a recent longitudinal study showed that baseline pancreatic fat did not cause subsequent diabetes mellitus. We hypothesized that pancreatic fat is not a cause but a manifestation of glucose dysmetabolism and aimed to investigate the association between baseline prediabetes and future pancreatic fat accumulation. METHODS: Between 2008 and 2015, 198 nondiabetic participants, who underwent a health check-up via unenhanced computed tomography (CT) twice with CT intervals ≥ 5 years, were enrolled as prediabetes (n = 48) and non-prediabetesparticipants (n = 150). Prediabetes was defined as fasting plasma glucose of 100-125 mg/dl or hemoglobin A1c of 5.7-6.4%. Pancreatic fat was evaluated using a histologically validated method to measure the difference between pancreas and spleen attenuations (P-S) on CT. Pancreatic fat accumulation during follow-up was measured as P-S change from baseline. Multiple linear regression was used to evaluate the association between baseline prediabetes and future pancreatic fat accumulation with adjustment for age, sex, body mass index, physical activity, and liver fat at baseline. RESULTS: Mean pancreatic fat accumulation was 0.30 (SD, 5.8) Hounsfield units during follow-up. On univariate analysis, baseline prediabetes was associated with future pancreatic fat accumulation (β = 3.73; 95% CI 1.91-5.55; P < 0.001). This association remained statistically significant on multivariate analysis (β = 3.14; 95% CI 1.25-5.03; P = 0.001). CONCLUSIONS:Prediabetes is a risk factor for future pancreatic fat accumulation. Pancreatic fat may be a manifestation of glucose dysmetabolism.
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