ABSTRACT
Leptin, the obese [OB] gene product, is a cytokine-like hormone that plays an important role in energy homeostasis. Mutation of OB in mice results in profound obesity and type II diabetes as part of a syndrome that resembles morbid obesity in humans. This work was done to evaluate the importance of leptin in the pathogenesis of obesity, to study the relationship between serum leptin level and type II diabetes mellitus, and to compare molecular methods versus conventional serum leptin measurements in this respect. The study was done on 34 obese non diabetic patients, 61 non-insulin dependent diabetic patients [NIDDM], and 15 healthy volunteers as controls. Special investigations included serum leptin, insulin, C-peptide, cortisol, and growth hormone. Expression of leptin and leptin receptor were examined by RT-PCR in fat tissues of lipectomy samples from obese subjects. The results of this study revealed that there was significant elevation in leptin level in both obese and diabetic groups compared to controls. There was significant reduction in insulin levels in obese group compared to control group and a significant elevation in C-peptide level in diabetic non-obese group compared to control group. Serum leptin levels showed different patterns in cases of obesity ranging from low or normal to high leptin levels, which cannot by itself explain the cause of obesity. Leptin mRNA was expressed in 66.2% of cases and undetectable in 33.8% of cases. One sample showed longer than expected leptin amplicon. On the other hand, leptin receptor mRNA was detectable in 29.3% and undetectable in 70.7% of samples. This work shows that both NIDDM and obesity are two linked clinical situations in the sense that either of them seems to predispose to the other. Obese have significantly higher mean levels of serum glucose and lower levels of serum insulin and have tendency for developing diabetes. On the other hand, diabetics have higher BMI and have tendency for developing obesity. Serum leptin alone is not enough to explain the pathogenesis of obesity, but molecular methods for measuring both leptin and leptin receptor expressions might be important to explain the pathogenesis of obesity in some cases with hyperleptinemia