Zhang, Proenca, Maffel, Barone, Leopold, and Friedman state that obesity is a common nutritional disorder in Western societies. Increased body weight or an excess of body fat relative to lean body mass, is found to be associated with type II diabetes, hypertension, hyperlipidemia and some cancers. Obesity is found to be strongly heritable, however predisposing genes have not been identified. Research regarding obesity dating back to 1783 has implied that food intake versus energy output, is physiologically regulated. Evidence shows that body weight appears to be determined by mechanisms that balance food intake and energy expenditure. The site of this regulation is a subject of nearly one hundred years of debate. Early work has identified a causal gene for a dominantly inherited form of obesity, the yellow agouti mutation (intensity of yellow pigmentation correlates positively with extents of obesity). Of the mouse obesity mutations, the ob (obese) and the db (diabetes) genes are the most intensively studied. The obese or ob gene is a molecule that is found to regulate energy balance in the mouse. The obese mutation (ob) was identified in 1950; it is a single gene mutation that results in obesity and type II diabetes (2, 3, 8).
The ob gene in mice is researched in an effort to further understand physiologic pathways that regulate adiposity and body weight, and to understand the pathogenesis of obesity (8). The gene product of the ob locus, OB protein, has been studied regarding its importance in the regulation of body weight (4). Insulin as a possible regulator of ob gene expression has also investigated. Additional factors including glucocorticoids and adipogenic factors other than insulin, need further exploration (6).
Obesity pathogenesis is unknown. Zhang et al. investigated components of the physiological system that control body weight. Positional cloning technologies were applied to isolate mouse obesit...