Associations of apolipoprotein A5 (APOA5), glucokinase (GCK) and glucokinase regulatory protein (GCKR) polymorphisms and lifestyle factors with the risk of dyslipidemia and dysglycemia in Japanese — a cross-sectional data from the J-MICC Study

Asahi Hishida; Emi Morita; Mariko Naito; Rieko Okada; Kenji Wakai; Keitaro Matsuo; Kazuyo Nakamura; Naoyuki Takashima; Sadao Suzuki; Toshiro Takezaki; Haruo Mikami; Keizo Ohnaka; Yoshiyuki Watanabe; Hirokazu Uemura; Michiaki Kubo; Hideo Tanaka; Nobuyuki Hamajima

doi:10.1507/endocrj.EJ11-0310

ORIGINALS

Associations of apolipoprotein A5 (APOA5), glucokinase (GCK) and glucokinase regulatory protein (GCKR) polymorphisms and lifestyle factors with the risk of dyslipidemia and dysglycemia in Japanese — a cross-sectional data from the J-MICC Study

Asahi Hishida, Emi Morita, Mariko Naito, Rieko Okada, Kenji Wakai, Keitaro Matsuo, Kazuyo Nakamura, Naoyuki Takashima, Sadao Suzuki, Toshiro Takezaki, Haruo Mikami, Keizo Ohnaka, Yoshiyuki Watanabe, Hirokazu Uemura, Michiaki Kubo, Hideo Tanaka, Nobuyuki Hamajima

Author information

Asahi Hishida
Department of Preventive Medicine, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan
Emi Morita
Department of Preventive Medicine, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan
Mariko Naito
Department of Preventive Medicine, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan
Rieko Okada
Department of Preventive Medicine, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan
Kenji Wakai
Department of Preventive Medicine, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan
Keitaro Matsuo
Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan
Kazuyo Nakamura
Department of Preventive Medicine, Faculty of Medicine, Saga University, Saga 849-8501, Japan
Naoyuki Takashima
Department of Health Science, Shiga University of Medical Science, Otsu 520-2192, Japan
Sadao Suzuki
Department of Public Health, Nagoya City University Graduate School of Medical Sciences, Nagoya 467-8601, Japan
Toshiro Takezaki
Department of International Island and Community Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima 890-8544, Japan
Haruo Mikami
Division of Epidemiology, Chiba Cancer Center Research Institute, Chiba 260-8717, Japan
Keizo Ohnaka
Department of Geriatric Medicine, Kyushu University Graduate School of Medical Sciences, Fukuoka 812-8582, Japan
Yoshiyuki Watanabe
Department of Social Medicine and Cultural Sciences, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan
Hirokazu Uemura
Department of Preventive Medicine, Institute of Health Biosciences, the University of Tokushima Graduate School, Tokushima 770-8503, Japan
Michiaki Kubo
Center for Genomic Medicine, RIKEN, Yokohama 230-0045, Japan.
Hideo Tanaka
Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan
Nobuyuki Hamajima
Department of Preventive Medicine, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan

Keywords: APOA5 , GCK, Single nucleotide polymorphisms, Dyslipidemia, Dysglycemia

JOURNAL FREE ACCESS

2012 Volume 59 Issue 7 Pages 589-599

DOI https://doi.org/10.1507/endocrj.EJ11-0310

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Abstract

This study examined the associations of the APOA5 T-1131C (rs662799), G553T (Cys185Gly, rs2075291), GCK G-30A (rs1799884), GCKR A/G at intron 16 (rs780094) and T1403C (Leu446Pro, rs1260326) polymorphisms with serum lipid and glucose levels in Japanese, considering lifestyle factors. Study subjects were 2,191 participants (aged 35-69 years, 1,159 males) enrolled in the Japan Multi-Institutional Collaborative Cohort (J-MICC) Study. Dyslipidemia was defined as fasting serum triglycerides (FTG) ≥ 150 mg/dL and/or HDL-cholesterol (HDL-C) < 40 mg/dL, while dysglycemia was as fasting blood sugar (FBS) ≥ 110 mg/dL. When those with APOA5 -1131 T/T or 553 G/G were defined as references, those with APOA5 -1131 T/C, C/C or 553 G/T, T/T demonstrated significantly elevated risk of dyslipidemia (age- and sex-adjusted odds ratio: 1.77 [95% confidence interval:1.39-2.27], 3.35 [2.41-4.65], 2.23 [1.64-3.02] and 13.78 [3.44-55.18], respectively). Evaluation of FTG, HDL-C or FBS levels according to the genotype revealed that FTG and HDL-C levels were significantly associated with the APOA5 T-1131C and G553T polymorphisms, FTG with the GCKR rs780094 and rs1260326 polymorphisms, and FBS with the GCKR rs780094 and rs1260326 polymorphisms. Moreover, a significant positive interaction between APOA5 553 G/T+T/T genotypes and fat intake ≥ 25% of total energy for the risk of dyslipidemia was observed. Our cross-sectional study confirmed the essential roles of the polymorphisms of the APOA5, GCK and GCKR in the lipid or glucose metabolism disorders, and suggested the importance of fat intake control in the individualized prevention of dyslipidemia.

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