Article citations

    T. Rankinen, L. Pérusse, S. J. Weisnagel, E. E. Snyder, Y. C. Chagnon, and C. Bouchard, “The human obesity gene map: the 2001 update,” Obesity Research, vol. 10, no. 3, pp. 196–243, 2002.

has been cited by the following article:

  • TITLE: APOA2 Polymorphism in Relation to Obesity and Lipid Metabolism
  • AUTHORS: Moushira Erfan Zaki,Khalda Sayed Amr,Mohamed Abdel-Hamid
  • JOURNAL NAME: Cholesterol DOI: 10.1155/2013/289481 Sep 16, 2014
  • ABSTRACT: Objectives. This study aims to analysis the relationship between c.-492T>C polymorphism in APOA2 gene and the risk for obesity in a sample of Egyptian adolescents and investigates its effect on body fat distribution and lipid metabolism. Material and Methods. A descriptive, cross-sectional study was conducted on 303 adolescents. They were 196 obese and 107 nonobese, aged 16–19 years old. Variables examined included body mass index (BMI), waist circumference (WC), waist to hip ratio (WHR), systolic and diastolic blood pressure (BP), body fat percentage (BF%), abdominal visceral fat layer, and dietary intake. Abdominal visceral fat thickness was determined by ultrasonography. The polymorphism in the APOA2 c.-492T>C was analyzed by PCR amplification. Results. Genotype frequencies were in Hardy-Weinberg equilibrium. The frequency of the mutant C allele was significantly higher in obese cases compared to nonobese. After multivariate adjustment, waist, BF% and visceral adipose layer, food consumption, and HDL-C were significantly higher in homozygous allele CC carriers than TT+TC carriers. Conclusions. Homozygous individuals for the C allele had higher obesity risk than carriers of the T allele and had elevated levels of visceral adipose tissue and serum HDL-C. Moreover, the study shows association between the APOA2 c.-492T>C polymorphism and food consumption. 1. Introduction Obesity-linked genetic variations in the presence of other routine habits such as smoking, physical inactivity, and unhealthy food intake may greatly raise the risk of a person developing heart diseases (cardiovascular diseases, CVD). Excess body fat, obesity, is one of the most common disorders in clinical practice. The location of the body fat is a major determinant of the degree of excess morbidity and mortality due to obesity [1]. At least two components of body fat are associated with obesity-related adverse health outcomes. These are the amount of subcutaneous truncal or abdominal fat, and the amount of visceral fat located in the abdominal cavity. Each of these components of body fat is associated with varying degrees of metabolic abnormalities and independently predicts adverse health outcomes. Many complex traits are thought to be inherited since they often run in families. However, these complex traits do not show typical mendelian pedigree patterns. These nonmendelian diseases may depend on several susceptibility loci, with a variable contribution from environmental factors. Discovering the major susceptibility locus may be the key to advances in understanding the