There are some studies conducted in the Arab world that have shown a relationship between some genes and obesity. A study on the association of leptin with obesity and metabolic syndrome was conducted in Tunis on 160 obese and 169 non-obese (BMI less than 30 kg/m2). Typing of the leptin G2548A and leptin receptor Q223R genes was performed using the polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) assay. The results of this study showed 262 base pairs for leptin and 416 for the leptin receptor. This study demonstrated the connection of G2548A of the leptin gene and Q223R of the leptin receptor gene polymorphisms with metabolic syndrome and obesity. The leptin receptor {223RR) genotype has been linked to obesity in the obese group of the Tunisian population (Boumaiza et al., 2012). Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essay Another study was conducted in Egypt to detect genetic defects in the Egyptian population and to find the best way to diagnose a genetic defect that can lead to obesity. The study was conducted on thirty obese children and adolescents. DNA was extracted and then amplified by PCR for the coding regions of leptin and the leptin receptor. The results of this study showed that six cases had a monogenic disease with early-onset severe obesity and consanguineous parents, four of the six cases had congenital leptin deficiency while others had congenital leptin receptor deficiency. The high rate of inbreeding in the Egyptian population has led to the discovery of a high incidence of autosomal recessive diseases such as monogenic obesity (El Gammal et al., 2012). Another study on the clinical and molecular genetic spectrum of congenital leptin receptor deficiency demonstrated 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. Of the 300 participants, eight (3%) had missense or nonsense LEPR mutations. Seven were homozygous and one was heterozygous. 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 (IS Farooqi et al., 2007). Another study was conducted in Qatar. Eight hundred and four participants were involved in this study and assigned to three groups based on 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 23 SNPs tested were significantly associated with obesity. This suggests that several unknown loci different from those studied in Western countries play a role in the prevalence of obesity in Qatar (Tomei et al., 2015). Please note: this is just a sample. Get a custom paper from our expert writers now. Get a Custom Essay Finally, a study was conducted in Pakistan on seventy-three children with extreme obesity from consanguineous families. All selected participants were screened for mutations in the leptin receptor (LEP) and melanocortin 4 (MC4R) genes using direct sequencing. The results had studied twenty-two probands and five relatives, with ten different homozygous mutations in the leptin, leptin receptor and MC4R genes, with four.., 2015)