生物谷报道：来自塔夫茨大学人类营养学研究中心的研究者发现，人体内的一种名为APOA2的基因的某一个位置在不同个体之间存在差异，而正是这种差异导致了不同人对脂肪、碳水化合物和蛋白质有不同的偏好。该基因在人群中有三个类型，其中1和2类型占大约85%，3类型占大约15%。与1、2相比，3类型的人群更偏好脂肪和蛋白质的摄入，而对碳水化合物的摄入量较少。而且3类型个体血液中含有较高的低密度脂蛋白（该蛋白含量过高易引起心血管疾病）。
我们都知道，肥胖不只与饮食有关，还和基因有着密切的联系。即便两个人吃得一样多、运动的一样多，拥有“肥胖基因”的个体可能还是会有更显著的增重。而本研究表明饮食的偏好也与基因有关，那么是不是意味着一个人生下来，他的基因就决定了他以后会吃什么？吃了东西以后会不会发胖？那么对这些基因的进一步研究和探讨会给我们什么样的启示？让我们拭目以待。(原文参考自《临床化学》杂志)（引自新闻晨报）
原始出处:
Clinical Chemistry 53: 1144-1152, 2007. First published April 19, 2007; 10.1373/clinchem.2006.084863
The –256T>C Polymorphism in the Apolipoprotein A-II Gene Promoter Is Associated with Body Mass Index and Food Intake in the Genetics of Lipid Lowering Drugs and Diet Network Study
Dolores Corella1,2, Donna K. Arnett3, Michael Y. Tsai4, Edmond K. Kabagambe3, James M. Peacock5, James E. Hixson6, Robert J. Straka7, Michael Province8, Chao-Qiang Lai1, Laurence D. Parnell1, Ingrid Borecki8 and Jose M. Ordovas1,a
1 Nutrition and Genomics Laboratory, Jean Mayer-US Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, MA.
2 Genetic and Molecular Epidemiology Unit and CIBER Fisiopatología de la Obesidad y Nutrición, School of Medicine, University of Valencia, Valencia, Spain.
3 Department of Epidemiology, School of Public Health, and Clinical Nutrition Research Center, University of Alabama at Birmingham, AL.
4 Laboratory of Medicine and Pathology, University of Minnesota, Minneapolis, MN.
5 Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, MN.
6 Human Genetics Center, University of Texas Health Science Center, Houston, TX.
7 Experimental and Clinical Pharmacology Department, College of Pharmacy, University of Minnesota, Minneapolis, MN.
8 Division of Biostatistics, Washington University School of Medicine, St. Louis, MO.
aAddress correspondence to this author at: Nutrition and Genomics Laboratory, JM-USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington St., Boston, MA 02111-1524. Fax 617-556-3211; e-mail jose.ordovas@tufts.edu .
Background: Apolipoprotein A-II (APOA2) plays an ambiguous role in lipid metabolism, obesity, and atherosclerosis.
Methods: We studied the association between a functional APOA2 promoter polymorphism (–265T>C) and plasma lipids (fasting and postprandial), anthropometric variables, and food intake in 514 men and 564 women who participated in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study. We obtained fasting and postprandial (after consuming a high-fat meal) measures. We measured lipoprotein particle concentrations by proton nuclear magnetic resonance spectroscopy and estimated dietary intake by use of a validated questionnaire.
Results: We observed recessive effects for this polymorphism that were homogeneous by sex. Individuals homozygous for the –265C allele had statistically higher body mass index (BMI) than did carriers of the T allele. Consistently, after multivariate adjustment, the odds ratio for obesity in CC individuals compared with T allele carriers was 1.70 (95% CI 1.02–2.80, P = 0.039). Interestingly, total energy intake in CC individuals was statistically higher [mean (SE) 9371 (497) vs 8456 (413) kJ/d, P = 0.005] than in T allele carriers. Likewise, total fat and protein intakes (expressed in grams per day) were statistically higher in CC individuals (P = 0.002 and P = 0.005, respectively). After adjustment for energy, percentage of carbohydrate intake was statistically lower in CC individuals. These associations remained statistically significant even after adjustment for BMI. We found no associations with fasting lipids and only some associations with HDL subfraction distribution in the postprandial state.
Conclusions: The –265T>C polymorphism is consistently associated with food consumption and obesity, suggesting a new role for APOA2 in regulating dietary intake.
