Relationship between Certain Genes and Obesity in Arab Countries

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There are some studies that have been done in the Arab world, which showed a relationship between certain genes and obesity. A study of the association of leptin with obesity and metabolic syndrome was done in Tunis on 160 obese and 169 non-obese (BMI less than 30 kg/m2). Typing of Leptin G2548A and Leptin receptor Q223R genes was done using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay. The results of this study have shown 262 base pair for leptin and 416 for leptin receptor. This study has shown the connection of G2548A of the leptin gene and Q223R of leptin receptor gene polymorphisms with metabolic syndrome and obesity. The leptin receptor {223RR) genotype was linked with obesity in the obese group of the Tunisian population (Boumaiza et al., 2012).

Another study was done in Egypt to detect genetic defects in Egyptian population and to find the best way to diagnose a gene defect that can lead to obesity. The study was done on thirty obese from both children and adolescents. DNA was extracted then amplified using PCR for the coding regions of the leptin and leptin receptor. The results of this study showed six cases had a monogenic disease with severe early-onset obesity and consanguineous parents, four of the six cases had congenital leptin deficiency while others had a congenital deficiency in the leptin receptor. The high consanguinity rate in Egyptian population had led to the discovery of a high incidence of autosomal recessive disorder such as monogenic obesity (El Gammal et al., 2012).

Another study of Clinical and Molecular Genetic Spectrum of Congenital Deficiency of the Leptin Receptor has shown a relationship between leptin receptor deficiency and obesity. From consanguineous families, 300 were selected to determine the prevalence of leptin-receptor mutations. Genomic DNA was isolated and the coding region of the LEPR gene was amplified. Out of the 300 participants, eight (3%) had missense or nonsense LEPR mutations. Seven were homozygotes, and one was a heterozygote. All missense mutations resulted in a non-signaling receptor. All participants had a history of increased food-seeking behavior in childhood, which did not stop in later life (I. S. Farooqi et al., 2007).

Another study was done in Qatar. Eight hundred and four participants were involved in this study and assigned to three groups according to their body weight. The study aimed to find loci associated with obesity and investigated 23 obesity-related loci in the Qatari population. Only 2 of the 23 SNPs tested were significantly associated with obesity. It suggests that different unknown loci other than the ones studied in Western countries have a role in the prevalence of obesity in Qatar (Tomei et al., 2015).

Lastly, a study was done in Pakistan on seventy-three children with extreme obesity from consanguineous families. All chosen participants were checked for mutations in leptin (LEP) and melanocortin 4 receptor (MC4R) genes using direct sequencing. The results had investigated twenty-two probands and five relatives, with ten different homozygous mutations in leptin, leptin receptor, and MC4R genes, with four new variants. The incidence and prevalence of mutations in genes identified to directly influence leptin-melanocortin signaling is thirty percent in children from consanguineous populations (Sadia Saeed et al., 2015)

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