Among these are the genes encoding leptin, tumor necrosis factor-alpha and adiptonectin. These genes may be involved in the development of insulin resistance. Therefore, to address the potential genetic association between resistance to type 2 diabetes, it is important to assess whether individuals whose phenotype shows resistance to the disorder are genetically screened to see if differences exist between the structure and/or activity of adipocytokine genes in groups women with similar risk factors (viz. obesity) and markedly different incidence rates for diabetes. A subpopulation of Saudi Arabian women has been identified that is resistant to the development of type 2 diabetes, despite incidence rates of obesity at the same level as the entire population of women in Saudi Arabia. The purpose of this research was to identify whether or not there was a genetic basis to this phenotypic observation.
The present study involves a genetic assessment of the gene called resistin, previously identified in mice on chromosome 8 (Steppan et al, 2001). To study this gene in humans it was necessary to clone the gene. This process is initiated by a technique called fluorescent in situ hybridization (FISH). The mouse gene is used as a probe to identify the chromosomal location of its human gene counterpart. Since gene sequences are frequently homologous among different species, the related genes or orthologues can be used to identify similar genes in different species (Gregory & Hebert, 1999). The mouse gene is attached to a fluorescent probe and mixed with human chromosomal DNA that has been denatured (connverted to single stranded form). The fluorescent band identifies the chromosomal location of the gene in humans. The chromosome segment can then be cut with restriction enzymes and linked to an expression vector to generate a recombinant