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Obesity, which is present predominantly in the industrialized world, is a significant risk factor for diabetes, hypertension, cardiovascular diseases, lipid abnormalities and certain types of cancer and is associated with increased mortality and morbidity. Although genetic, socioeconomical and psychosomatic factors influence the development of obesity, it is the net result of a prolonged positive energy balance. Several single gene recessive mutations including the obese (ob) mutation cause obesity in genetic models (1). Since the discovery of the ob gene (2), significant progress has been made in defining the role of leptin in body weight regulation (reviewed in 3, 4). Except for ob/ob mice, adipose ob mRNA is increased in all other genetic and experimental models of obesity and in obese humans. Unlike ob/ob mice, no significant mutations have been found in the coding region of the adipose ob gene in human obesity, although some linkage studies have indicated the ob
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