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The Ob gene, which is known to encode the 16 kDa protein hormone leptin, is one of the main genes that has been linked to the obesity phenotype in humans. Examination of Ob gene expression, as well as leptin’s mode of action in the hypothalamus through an intracellular signaling cascade, reveals the complexities of weight regulation (Friedman & Halaas, 1998). Single point mutations in the Ob gene can produce nonfunctional leptin protein due to the disruption of key intramolecular features, resulting in a chronic obesity phenotype (Farooqi et al., 1998; Hager et al., 1998). Current modes of therapy being explored include gene therapy using recombinant adenoviruses, which serve as vectors for leptin cDNA, as well as direct leptin injections (Friedman & Halaas, 1998). While both approaches to correcting leptin deficiency have shortcomings and require further research to improve their effectiveness, they demonstrate potential means of correcting specific metabolic disorders. Such breakthroughs are essential, given the prevalence of obesity in the United States alone and the health threat obesity poses by increasing predisposition to other life threatening conditions (Pi-Sunyer, 2002; Ogden et al., 2008).


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