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 . 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
F. M. Van't Hooft, G. Ruotolo, S. Boquist, U. De Faire, G. Eggertsen, and A. Hamsten, “Human evidence that the apolipoprotein A-II gene is implicated in visceral fat accumulation and metabolism of triglyceride-rich lipoproteins,” Circulation, vol. 104, no. 11, pp. 1223–1228, 2001.
J. B. Albu, L. Murphy, D. H. Frager, J. A. Johnson, and F. X. Pi-Sunyer, “Visceral fat and race-dependent health risks in obese nondiabetic premenopausal women,” Diabetes, vol. 46, no. 3, pp. 456–462, 1997.
C. Lara-Castro, R. L. Weinsier, G. R. Hunter, and R. Desmond, “Visceral adipose tissue in women: longitudinal study of the effects of fat gain, time, and race,” Obesity Research, vol. 10, no. 9, pp. 868–874, 2002.
I. M. Heid, A. U. Jackson, J. C. Randall et al., “Meta-analysis identifies 13 new loci associated with waist-hip ratio and reveals sexual dimorphism in the genetic basis of fat distribution,” Nature Genetics, vol. 42, pp. 949–960, 2010.
S. A. Cole, N. F. Butte, V. S. Voruganti et al., “Evidence that multiple genetic variants of MC4R play a functional role in the regulation of energy expenditure and appetite in Hispanic children,” American Journal of Clinical Nutrition, vol. 91, no. 1, pp. 191–199, 2010.
D. Corella, D. K. Arnett, M. Y. Tsai et al., “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,” Clinical Chemistry, vol. 53, no. 6, pp. 1144–1152, 2007.
I. Ghalli, N. Salah, F. Hussien et al., “Egyptian growth curves for infants, children and adolescents,” in Crecere nel Mondo, A. Satorio, J. M. H. Buckler, and N. Marazzi, Eds., Ferring Publisher, Milan, Italy, 2008.
J. Hiernaux and J. M. Tanner, “Growth and physical studies,” in Human Biology: A Guide to Field Methods, J. S. Weiner and S. A. Lourie, Eds., IBP, Oxford, UK; Blackwell Scientific Publications, London, UK, 1969.
J. Scott, T. J. Knott, and L. M. Priestley, “High-density lipoprotein composition is altered by a common DNA polymorphism adjacent to apoprotein AII gene in man,” The Lancet, vol. 1, no. 8432, pp. 771–773, 1985.
M.-C. Vohl, B. Lamarche, J. Bergeron et al., “The MspI polymorphism of the apolipoprotein A-II gene as a modulator of the dyslipidemic state found in visceral obesity,” Atherosclerosis, vol. 128, no. 2, pp. 183–190, 1997.
J. M. Martín-Campos, J. C. Escolà-Gil, V. Ribas, and F. Blanco-Vaca, “Apolipoprotein A-II, genetic variation on chromosome 1q21-q24, and disease susceptibility,” Current Opinion in Lipidology, vol. 15, no. 3, pp. 247–253, 2004.
S. M. Fullerton, A. G. Clark, K. M. Weiss et al., “Sequence polymorphism at the human apolipoprotein AII gene (APOA2): unexpected deficit of variation in an African-American sample,” Human Genetics, vol. 111, no. 6, pp. 577–578, 2002.
C. Lara-Castro, G. R. Hunter, J. C. Lovejoy, B. A. Gower, and J. R. Fernández, “Apolipoprotein A-II polymorphism and visceral adiposity in African-American and white women,” Obesity Research, vol. 13, no. 3, pp. 507–512, 2005.
D. Corella, G. Peloso, D. K. Arnett et al., “APOA2, dietary fat, and body mass index: replication of a gene-diet interaction in 3 independent populations,” Archives of Internal Medicine, vol. 169, no. 20, pp. 1897–1906, 2009.
D. Corella, E. S. Tai, J. V. Sorlí et al., “Association between the APOA2 promoter polymorphism and body weight in Mediterranean and Asian populations: replication of a gene-saturated fat interaction,” International Journal of Obesity, vol. 35, no. 5, pp. 666–675, 2011.
C. E. Smith, J. M. Ordovás, C. Sánchez-Moreno, Y. C. Lee, and M. Garaulet, “Apolipoprotein A-II polymorphism: relationships to behavioural and hormonal mediators of obesity,” International Journal of Obesity, vol. 36, no. 1, pp. 130–136, 2012.
M. D. M. Bibiloni, E. Martinez, R. Llull, M. D. Juarez, A. Pons, and J. A. Tur, “Prevalence and risk factors for obesity in Balearic Islands adolescents,” British Journal of Nutrition, vol. 103, no. 1, pp. 99–106, 2010.
D. G. Schlundt, M. K. Hargreaves, and M. S. Buchowski, “The Eating Behavior Patterns Questionnaire predicts dietary fat intake in African American women,” Journal of the American Dietetic Association, vol. 103, no. 3, pp. 338–345, 2003.
K. Fujimoto, J. A. Cardelli, and P. Tso, “Increased apolipoprotein A-IV in rat mesenteric lymph after lipid meal acts as a physiological signal for satiation,” American Journal of Physiology—Gastrointestinal and Liver Physiology, vol. 262, no. 6, pp. G1002–G1006, 1992.
L. Shen, L.-Y. Ma, X.-F. Qin, R. Jandacek, R. Sakai, and M. Liu, “Diurnal changes in intestinal apolipoprotein A-IV and its relation to food intake and corticosterone in rats,” American Journal of Physiology—Gastrointestinal and Liver Physiology, vol. 288, no. 1, pp. G48–G53, 2005.
G. Chiesa, C. Parolini, M. Canavesi et al., “Human apolipoproteins A-I and A-II in cell cholesterol efflux: Studies with transgenic mice,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 18, no. 9, pp. 1417–1423, 1998.
S. Zhong, I. J. Goldberg, C. Bruce, E. Rubin, J. L. Breslow, and A. Tall, “Human ApoA-II inhibits the hydrolysis of HDL triglyceride and the decrease of HDL size induced by hypertriglyceridemia and cholesteryl ester transfer protein in transgenic mice,” Journal of Clinical Investigation, vol. 94, no. 6, pp. 2457–2467, 1994.