The interaction of Apolipoprotein A5 gene promoter region T-1131C polymorphism (rs12286037) and lifestyle modification on plasma triglyceride levels in Japanese
2
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
BACKGROUND/OBJECTIVE: Apolipoprotein A5 gene promoter region T-1131C polymorphism (APOA5 T-1131C) is known to be associated with elevated plasma TG levels, although little is known of the influence of the interaction between APOA5 T-1131C and lifestyle modification on TG levels. To investigate this matter, we studied APOA5 T-1131C and plasma TG levels of subjects participating in a three-month lifestyle modification program. SUBJECTS/METHODS: A three-month lifestyle modification program was conducted with 297 participants (Age: 57 ± 8 years) in Izumo City, Japan, from 2001-2007. Changes in energy balance (the difference between energy intake and energy expenditure) and BMI were used to evaluate the participants’ responses to the lifestyle modification. RESULTS: Even after adjusting for confounding factors, plasma TG levels were significantly different at baseline among three genotype subgroups: TT, 126 ± 68 mg/dl; TC, 134 ± 74 mg/dl; and CC, 172 ± 101 mg/dl. Lifestyle modification resulted in significant reductions in plasma TG levels in the TT, TC, and CC genotype subgroups: -21.9 ± 61.0 mg/dl, -20.9 ± 51.0 mg/dl, and -42.6 ± 78.5 mg/dl, respectively, with no significant differences between them. In a stepwise regression analysis, age, APOA5 T-1131C, body mass index (BMI), homeostasis model assessment-insulin resistance (HOMA-IR), and the 18:1/18:0 ratio showed independent association with plasma TG levels at baseline. In a general linear model analysis, APOA5 T-1131C C-allele carriers showed significantly greater TG reduction with decreased energy balance than wild type carriers after adjustment for age, gender, and baseline plasma TG levels. CONCLUSIONS: The genetic effects of APOA5 T-1131C independently affected plasma TG levels. However, lifestyle modification was effective in significantly reducing plasma TG levels despite the APOA5 T-1131C genotype background.
Abstract
BACKGROUND/OBJECTIVE: Apolipoprotein A5 gene promoter region T-1131C polymorphism (APOA5 T-1131C) is known to be associated with elevated plasma TG levels, although little is known of the influence of the interaction between APOA5 T-1131C and lifestyle modification on TG levels. To investigate this matter, we studied APOA5 T-1131C and plasma TG levels of subjects participating in a three-month lifestyle modification program. SUBJECTS/METHODS: A three-month lifestyle modification program was conducted with 297 participants (Age: 57 ± 8 years) in Izumo City, Japan, from 2001-2007. Changes in energy balance (the difference between energy intake and energy expenditure) and BMI were used to evaluate the participants’ responses to the lifestyle modification. RESULTS: Even after adjusting for confounding factors, plasma TG levels were significantly different at baseline among three genotype subgroups: TT, 126 ± 68 mg/dl; TC, 134 ± 74 mg/dl; and CC, 172 ± 101 mg/dl. Lifestyle modification resulted in significant reductions in plasma TG levels in the TT, TC, and CC genotype subgroups: -21.9 ± 61.0 mg/dl, -20.9 ± 51.0 mg/dl, and -42.6 ± 78.5 mg/dl, respectively, with no significant differences between them. In a stepwise regression analysis, age, APOA5 T-1131C, body mass index (BMI), homeostasis model assessment-insulin resistance (HOMA-IR), and the 18:1/18:0 ratio showed independent association with plasma TG levels at baseline. In a general linear model analysis, APOA5 T-1131C C-allele carriers showed significantly greater TG reduction with decreased energy balance than wild type carriers after adjustment for age, gender, and baseline plasma TG levels. CONCLUSIONS: The genetic effects of APOA5 T-1131C independently affected plasma TG levels. However, lifestyle modification was effective in significantly reducing plasma TG levels despite the APOA5 T-1131C genotype background.
참고문헌 (30)
- Ho JS, "Relation of the number of metabolic syndrome risk factors with all-cause and cardiovascular mortality", Am J Cardiol, 102, pp.689~692 (2008)
- Patel A, "Serum triglycerides as a risk factor for cardiovascular diseases in the Asia-Pacific region", Circulation, 110, pp.2678~2686 (2004)
- Sarwar N, "Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies", Circulation, 115, pp.450~458 (2007)
- Yuan G, "Hypertriglyceridemia: its etiology, effects and treatment", CMAJ, 176, pp.1113~1120 (2007)
- Shiwaku K, "Triglyceride levels are ethnic-specifically associated with an index of stearoyl-CoA desaturase activity and n-3 PUFA levels in Asians", J Lipid Res, 45, pp.914~922 (2004)
- Parzianello L, "Increased triglyceride levels in a Japanese population living in southern Brazil", Arch Med Res, 36, pp.59~64 (2005)
- Ordovas JM, "Gene-diet interaction and plasma lipid responses to dietary intervention", Biochem Soc Trans, 30, pp.68~73 (2002)
- Willer CJ, "Newly identified loci that influence lipid concentrations and risk of coronary artery disease", Nat Genet, 40, pp.161~169 (2008)
- Kathiresan S, "Six new loci associated with blood low-density lipoprotein cholesterol, high-density lipoprotein cholesterol or triglycerides in humans", Nat Genet, 40, pp.189~197 (2008)
- Maraki M, "Effects of energy balance on postprandial triacylglycerol metabolism", Curr Opin Clin Nutr Metab Care, 13, pp.608~617 (2010)
- Perez-Martinez P, "Influence of genetic factors in the modulation of postprandial lipemia", Atheroscler Suppl, 9, pp.49~55 (2008)
- Kolovou GD, "Familial hypercholesterolemia and triglyceride metabolism", Int J Cardiol, 147, pp.349~358 (2011)
- Tamasawa N, "Influence of apolipoprotein E genotype on the response to caloric restriction in type 2 diabetic patients with hyperlipidaemia", Diabetes Obes Metab, 5, pp.345~348 (2003)
- Ordovas JM, "Why study gene-environment interactions?", Curr Opin Lipidol, 19, pp.158~167 (2008)
- Nabika T, "The genetic effect of the apoprotein AV gene on the serum triglyceride level in Japanese", Atherosclerosis, 165, pp.201~204 (2002)
- Wong K, "Characterization of apolipoprotein A-V structure and mode of plasma triacylglycerol regulation", Curr Opin Lipidol, 18, pp.319~324 (2007)
- Aberle J, "A polymorphism in the apolipoprotein A5 gene is associated with weight loss after short-term diet", Clin Genet, 68, pp.152~154 (2005)
- McCormack G, "An update of recent evidence of the relationship between objective and self-report measures of the physical environment and physical activity behaviours", J Sci Med Sport, 7, pp.81~92 (2004)
- Resources Council of the Science and Technology Agency of Japan, "Standard Tables of Food Composition in Japan. 5th rev" (2000), Resources Council of the Science and Technology Agency of Japan
- Ministry of Health, Labour and Welfare (JP), "Exercise and Physical Activity Guide for Health Promotion 2006: To Prevent Lifestyle-Related Diseases" (2006), Ministry of Health, Labour and Welfare
- VINE Corp, "The Instruction Manual of Non-Dispersive Infrared Analysis" (2000), VINE Corp
- Pennacchio LA, "An apolipoprotein influencing triglycerides in humans and mice revealed by comparative sequencing", Science, 294, pp.169~173 (2001)
- Suchanek P, "Changes of plasma lipids during weight reduction in females depends on APOA5 variants", Ann Nutr Metab, 53, pp.104~108 (2008)
- Zhang X, "APOA5 genotype modulates 2-y changes in lipid profile in response to weight-loss diet intervention: the Pounds Lost Trial", Am J Clin Nutr, 96, pp.917~922 (2012)
- St George A, "Effect of a lifestyle intervention in patients with abnormal liver enzymes and metabolic risk factors", J Gastroenterol Hepatol, 24, pp.399~407 (2009)
- Stone NJ, "Successful control of dyslipidemia in patients with metabolic syndrome: focus on lifestyle changes", Clin Cornerstone, 8(Suppl 1), pp.S15~S20 (2006)
- Wang H, "Lipoprotein lipase: from gene to obesity", Am J Physiol Endocrinol Metab, 297, pp.E271~E288 (2009)
- Merkel M, "Apolipoprotein AV accelerates plasma hydrolysis of triglyceride-rich lipoproteins by interaction with proteoglycan-bound lipoprotein lipase", J Biol Chem, 280, pp.21553~21560 (2005)
- Seip RL, "Induction of human skeletal muscle lipoprotein lipase gene expression by short-term exercise is transient", Am J Physiol, 272, pp.E255~E261 (1997)
- Miyashita M, "Twelve-week jogging training increases pre-heparin serum lipoprotein lipase concentrations in overweight", obese middle-aged men, 2010, pp.17, 21~29