Toshiaki Ohkuma1,2, Masanori Iwase1,3, Hiroki Fujii1,4, Hitoshi Ide1, Shinako Kaizu1, Tamaki Jodai1, Yohei Kikuchi1, Yasuhiro Idewaki3, Akiko Sumi1, Udai Nakamura1, Takanari Kitazono1. 1. 1Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582 Japan. 2. 2Center for Cohort Studies, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582 Japan. 3. Diabetes Center, Hakujyuji Hospital, Ishimaru 3-2-1, Nishi-ku, Fukuoka, 819-8511 Japan. 4. 4Division of General Internal Medicine, School of Oral Health Science, Kyushu Dental University, Manazuru 2-6-1, Kokurakita-ku, Kitakyushu, 803-8580 Japan.
Abstract
AIMS: Little is known about the combined effects of unhealthy lifestyle behaviors on glycemia. The objective of this study was to examine the association between combined modifiable lifestyle and glycemic control, as well as markers of insulin resistance and secretion. PATIENTS AND METHODS: In total, 4,870 patients with type 2 diabetes were sorted by lifestyle scores. Scores were determined by summing the number of unhealthy lifestyle factors that showed a significant association with hemoglobin A1c (HbA1c) (current smoking, decreased dietary fiber intake, eating quickly, inadequate sleep duration, and obesity). The associations between lifestyle score and hemoglobin A1c (HbA1c), homeostasis model assessment of insulin resistance (HOMA2-IR), and β-cell function (HOMA2-%B) were cross-sectionally analyzed. RESULTS: HbA1c increased progressively with increases in lifestyle score (p for trend <0.001). Mean HbA1c was 0.48% (95% confidence intervals 0.34-0.63) higher in patients with scores of four to five than in those with zero scores. HOMA2-IR and high-sensitivity C-reactive protein also revealed a similar tendency, but adiponectin showed an inverse association. However, these graded tendencies were not observed for HOMA2-%B. Additionally, lower HOMA2-%B levels enhanced the effects of lifestyle score on glycemia. Increases in HbA1c per point in the lifestyle score in patients with the lowest and highest quartiles of HOMA2-%B were 0.25% (0.18-0.32) and 0.10% (0.06-0.15), respectively (p for interaction <0.001). CONCLUSIONS: Accumulation of unhealthy lifestyle factors was dose-dependently associated with poor glycemic control, which may be modified by insulin secretory capacity.
AIMS: Little is known about the combined effects of unhealthy lifestyle behaviors on glycemia. The objective of this study was to examine the association between combined modifiable lifestyle and glycemic control, as well as markers of insulin resistance and secretion. PATIENTS AND METHODS: In total, 4,870 patients with type 2 diabetes were sorted by lifestyle scores. Scores were determined by summing the number of unhealthy lifestyle factors that showed a significant association with hemoglobin A1c (HbA1c) (current smoking, decreased dietary fiber intake, eating quickly, inadequate sleep duration, and obesity). The associations between lifestyle score and hemoglobin A1c (HbA1c), homeostasis model assessment of insulin resistance (HOMA2-IR), and β-cell function (HOMA2-%B) were cross-sectionally analyzed. RESULTS: HbA1c increased progressively with increases in lifestyle score (p for trend <0.001). Mean HbA1c was 0.48% (95% confidence intervals 0.34-0.63) higher in patients with scores of four to five than in those with zero scores. HOMA2-IR and high-sensitivity C-reactive protein also revealed a similar tendency, but adiponectin showed an inverse association. However, these graded tendencies were not observed for HOMA2-%B. Additionally, lower HOMA2-%B levels enhanced the effects of lifestyle score on glycemia. Increases in HbA1c per point in the lifestyle score in patients with the lowest and highest quartiles of HOMA2-%B were 0.25% (0.18-0.32) and 0.10% (0.06-0.15), respectively (p for interaction <0.001). CONCLUSIONS: Accumulation of unhealthy lifestyle factors was dose-dependently associated with poor glycemic control, which may be modified by insulin secretory capacity.
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