ponse to glucocorticoids, cytokines, and insulin (Tartaglia, 1997).
The study of leptin and body weight began with research with mice, the ob/ob mouse was deficient in leptin protein and the potency of leptin was highest in this mouse. Higher doses of leptin in normal mice also showed effects on diet-induced obesity. This brought the hope that leptin could be used to treat obesities that were not due to leptin deficiencies. Central administration of leptin in the lateral or third brain ventricle resulted in reduced food intake and weight loss in mice. This implied that leptin acted directly on the receptors in the central nervous system. Studies with mice also showed that this leptin administration resulted in increased energy expenditure. It was hypothesized that a mechanism involved was the activation of brown adipose tissue. Efforts to replicate these studies in humans has met with problems. Leptin deficiencies are not common in human obesity and it has been observed that there is an up-regulation associated with increased body fat. This implies that resistance to normal or elevated leptin levels may be the factor to consider rather than inadequate leptin production in obesity. This theory is parallel to the type II diabetes situation where individuals show insulin resistance while producing increases in insulin. Thus, interest in the db/db mouse, with leptin resistance and elevated leptin levels, became a focal point in an effort to identify the leptin receptor and analyze leptin signal reception (Tartaglia, 1997).
Matsuda, Yokota, Iida, Murakami, Naito, Ito, Shima, and Kuroda (1997) reported on serum leptin concentration in cord blood related to birth weight and gender. For this study the levels of serum leptin levels were measured in the venous cord blood of 43 male and 39 female newborns, with gestational ages of 36 to 42 weeks, and birth weights from 2,306 to 4,128 g. Results showed that males' leptin levels w...