Alex Aregbesola1, Vanessa D F de Mello2, Jaana Lindström3, Sari Voutilainen2, Jyrki K Virtanen2, Sirkka Keinänen-Kiukaanniemi4, Tomi-Pekka Tuomainen2, Jaakko Tuomilehto5, Matti Uusitupa2. 1. Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Yliopistonranta 1C, P.O. Box 1627, FI70211 Kuopio, Finland. Electronic address: alex.aregbesola@uef.fi. 2. Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Yliopistonranta 1C, P.O. Box 1627, FI70211 Kuopio, Finland. 3. Diabetes Prevention Unit, National Institute for Health and Welfare, Helsinki, Finland. 4. Center for Life Course Health Research, University of Oulu, Finland; Medical Research Center and Unit of General Practice, Oulu University Hospital and Oulu Health Center, Oulu, Finland. 5. Centre for Vascular Prevention, Danube-University Krems, Krems, Austria; Dasman Diabetes Institute, Dasman, Kuwait; Diabetes Research Group, King Abdulaziz University, Jeddah, Saudi Arabia.
Abstract
AIMS: Body iron inhibits the metabolism of adiponectin, an insulin sensitizing adipokine. We investigated the relationships of baseline and average of 4-year change in values of serum adiponectin (sA), serum ferritin (sF) and sA/sF ratio on type 2 diabetes (T2D) risk and insulin sensitivity (Matsuda ISI) and secretion (disposition index; DI30). METHODS: Prospective analyses were conducted in participants with impaired glucose tolerance of the Finnish Diabetes Prevention Study (n = 516) recruited in 1993-1998. Cox and linear regression analyses were used to investigate the associations of sA, sF and sA/sF ratio, as continuous variables, with incident T2D, Matsuda ISI, and DI30. RESULTS: During the mean follow-up of 8.2 years, 157 incident T2D cases occurred (intervention group, n = 65 and control group, n = 92). In adjusted models, baseline sA and sA/sF ratio were inversely associated with T2D risk (HR = 0.49, 95% CI 0.31-0.76, P = 0.002 and HR = 0.83, 95% CI 0.70-0.99, P = 0.044, respectively). Furthermore, a direct association was observed with Matsuda ISI (β=0.13, 95% CI 0.03-0.22, P = 0.009, for sA and β=0.04, 95% CI 0.01-0.07, P = 0.035, for sA/sF ratio) during the average 4-year follow-up. The changes in sA and sA/sF ratio were also inversely associated with T2D risk (HR = 0.36, 95% CI 0.20-0.63, P < 0.001 and HR = 0.76, 95% CI 0.62-0.92, P = 0.006, respectively), and directly with Matsuda ISI (β=0.27, 95% CI 0.17-0.38, P < 0.001, for sA and β=0.07, 95% CI 0.03-0.11, P < 0.001, for sA/sF ratio). No consistent associations were found with DI30. CONCLUSIONS: Baseline levels and changes during the follow-up in sA and sA/sF ratio are related to T2D risk and insulin sensitivity.
AIMS: Body iron inhibits the metabolism of adiponectin, an insulin sensitizing adipokine. We investigated the relationships of baseline and average of 4-year change in values of serum adiponectin (sA), serum ferritin (sF) and sA/sF ratio on type 2 diabetes (T2D) risk and insulin sensitivity (Matsuda ISI) and secretion (disposition index; DI30). METHODS: Prospective analyses were conducted in participants with impaired glucose tolerance of the Finnish Diabetes Prevention Study (n = 516) recruited in 1993-1998. Cox and linear regression analyses were used to investigate the associations of sA, sF and sA/sF ratio, as continuous variables, with incident T2D, Matsuda ISI, and DI30. RESULTS: During the mean follow-up of 8.2 years, 157 incident T2D cases occurred (intervention group, n = 65 and control group, n = 92). In adjusted models, baseline sA and sA/sF ratio were inversely associated with T2D risk (HR = 0.49, 95% CI 0.31-0.76, P = 0.002 and HR = 0.83, 95% CI 0.70-0.99, P = 0.044, respectively). Furthermore, a direct association was observed with Matsuda ISI (β=0.13, 95% CI 0.03-0.22, P = 0.009, for sA and β=0.04, 95% CI 0.01-0.07, P = 0.035, for sA/sF ratio) during the average 4-year follow-up. The changes in sA and sA/sF ratio were also inversely associated with T2D risk (HR = 0.36, 95% CI 0.20-0.63, P < 0.001 and HR = 0.76, 95% CI 0.62-0.92, P = 0.006, respectively), and directly with Matsuda ISI (β=0.27, 95% CI 0.17-0.38, P < 0.001, for sA and β=0.07, 95% CI 0.03-0.11, P < 0.001, for sA/sF ratio). No consistent associations were found with DI30. CONCLUSIONS: Baseline levels and changes during the follow-up in sA and sA/sF ratio are related to T2D risk and insulin sensitivity.