|SMITH, CAREN E. - Jean Mayer Human Nutrition Research Center On Aging At Tufts University|
|ORDOVAS, JOSE M. - Jean Mayer Human Nutrition Research Center On Aging At Tufts University|
|SANCHEZ-MORENO, CARMEN - Non ARS Employee|
|LEE, YU-CHI - Jean Mayer Human Nutrition Research Center On Aging At Tufts University|
|GARAULET, MARTA S. - Non ARS Employee|
Submitted to: International Journal of Obesity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/8/2011
Publication Date: 3/8/2011
Citation: Smith, C., Ordovas, J., Sanchez-Moreno, C., Lee, Y., Garaulet, M. 2011. Apolipoprotein A-II polymorphism: relationships to behavioural and hormonal mediators of obesity. International Journal of Obesity. DOI: 10.1038/ijo.2011.24.
Interpretive Summary: The prevalence of obesity and overweight continues to increase; currently, an estimated 66 percent of adult Americans fit within these categories. This trend is unprecedented in U.S. history and is an important underlying cause of many related disorders, including cardiovascular disease, Type 2 diabetes and several cancers, as well as escalating health care costs. Reduction of excess weight is difficult to achieve and even harder to sustain, and there is critical need for effective, proven methods for the primary prevention of weight gain. More tailored recommendations should increase the chance of success, but we don’t have the tools to predict the individual risk as well as responses to therapeutic recommendations. Moreover, behavioral and hormonal factors need to be considered in the equation. Therefore, we have conducted a weight loss study to investigate the role of a functional genetic variant, known as APOA2 -265T>C, in the regulation of food intake and body weight taking into consideration behavior and hormones. Those subjects who were homozygous for this polymorphism were more likely to exhibit behaviors that impede weight loss and less likely to exhibit the protective behavior. Thereefore, APOA2 m265 genotype may be associated with eating behaviors and dietary modulation of plasma ghrelin (an appetite hormone). Expansion of knowledge of APOA2 and obesity to include modulation of specific behaviors and hormonal mediators not only broadens understanding of gene-diet interactions, but also facilitates the pragmatic, future goal of developing dietary guidelines based on genotype.
Technical Abstract: Background: The interaction between apolipoprotein A-II (APOA2) m265 genotype and saturated fat for obesity traits has been more extensively demonstrated than for any other locus, but behavioural and hormonal mechanisms underlying this relationship are unexplored. In this study, we evaluated relationships between APOA2 and obesity risk with particular focus on patterns of eating and ghrelin, a hormonal regulator of food intake. Design: Cross-sectional study. Subjects: Overweight and obese subjects (n 1/4 1225) were evaluated at baseline in five weight loss clinics in southeastern Spain. Methods: Behavioural data were assessed using a checklist of weight loss obstacles. Logistic regression models were fitted to estimate the risk of a specific behaviour associated with APOA2 genotype. Relationships between APOA2 genotype and saturated fat intakes for anthropometric traits and plasma ghrelin were evaluated by analysis of variance. To construct categorical variables to evaluate interactions, saturated fat intake was dichotomized into high and low according to the population median intake or as tertiles. Results: Homozygous minor (CC) subjects were more likely to exhibit behaviours that impede weight loss (‘Do you skip meals’, odds ratio (OR)1/4 2.09, P 1/4 0.008) and less likely to exhibit the protective behaviour of ‘Do you plan meals in advance’ (OR 1/4 0.64, P 1/4 0.034). Plasma ghrelin for CC subjects consuming low saturated fat was lower compared with (1) CC subjects consuming high saturated fat, (2) TT beta TC carriers consuming low saturated fat and (3) TT beta TC carriers consuming high saturated fat (all Po0.05). Conclusions: APOA2 m265 genotype may be associated with eating behaviours and dietary modulation of plasma ghrelin. Expansion of knowledge of APOA2 and obesity to include modulation of specific behaviours and hormonal mediators not only broadens understanding of gene–diet interactions, but also facilitates the pragmatic, future goal of developing dietary guidelines based on genotype.