生物谷報道：來自塔夫茨大學(xué)人類營養(yǎng)學(xué)研究中心的研究者發(fā)現(xiàn),，人體內(nèi)的一種名為APOA2的基因的某一個位置在不同個體之間存在差異，而正是這種差異導(dǎo)致了不同人對脂肪,、碳水化合物和蛋白質(zhì)有不同的偏好,。該基因在人群中有三個類型,，其中1和2類型占大約85%,，3類型占大約15%。與1,、2相比,，3類型的人群更偏好脂肪和蛋白質(zhì)的攝入，而對碳水化合物的攝入量較少,。而且3類型個體血液中含有較高的低密度脂蛋白（該蛋白含量過高易引起心血管疾?。?/p>
我們都知道,，肥胖不只與飲食有關(guān),，還和基因有著密切的聯(lián)系。即便兩個人吃得一樣多,、運(yùn)動的一樣多,，擁有“肥胖基因”的個體可能還是會有更顯著的增重。而本研究表明飲食的偏好也與基因有關(guān),，那么是不是意味著一個人生下來,，他的基因就決定了他以后會吃什么？吃了東西以后會不會發(fā)胖,？那么對這些基因的進(jìn)一步研究和探討會給我們什么樣的啟示,？讓我們拭目以待。(原文參考自《臨床化學(xué)》雜志)（引自新聞晨報）
原始出處:
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 [email protected] .
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.
