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The changes in serum leptin, body fat mass and insulin resistance after renal transplantation
S Mehmet Kayacan1, Alaattin Yildiz, Rumeyza Kazancioglu
1Division of Nephrology, Department of Internal Medicine, Istanbul School of Medicine, Istanbul University, Turkey.
Background:
In this prospective-controlled study, we aimed to investigate the effect of changes in insulin resistance and anthropometrical parameters on serum leptin levels (SLL) after renal transplantation (Tx).
Patients And Methods:
Thirty-four patients (M/F: 19/15, mean age: 29 +/- 9 yr) and 30 age and sex-matched healthy controls (C) were included. Body weight, subscapular, suprailiac, periumbilical, biceps and triceps skinfold thicknesses, neck, wrist, hip and waist circumferences, as well as body mass index and body fat mass were measured as anthropometrical parameters. In order to measure the serum glucose, insulin and SLL, blood samples were obtained before and 1 wk, 1 and 6 months after Tx. Homeostasis Model Assessment (HOMA) values were calculated as an index of insulin resistance.
Results:
Serum leptin levels (SLL) of the patients at pre-Tx were significantly higher than C (21.5 +/- 3.5 vs. 7.8 +/- 0.9 ng/mL, p = 0.002) and decreased at first week after Tx (from 21.5 +/- 3.5 to 8.4 +/- 1.5 ng/mL, p < 0.001). Thereafter, it gradually increased to 12.8 +/- 2.1 ng/mL in the first month and to 14.4 +/- 2.1 ng/mL in the sixth month after Tx. Serum leptin levels at sixth month were significantly higher than C (p = 0.005). Serum insulin and HOMA values changed similar to SLL after Tx. Correlations between SLL and HOMA persisted during the study period [pre-Tx (r: 0.40) and at first (r: 0.38) and sixth (r: 0.47) months]. In linear regression analysis, HOMA and fat mass were found as independent variables for predicting SLL at the sixth month after Tx.
Conclusion:
Serum leptin levels dramatically decreased immediately after Tx and significantly correlated with serum insulin levels and HOMA during the entire study. Increase in SLL at sixth months was probably because of increase in fat mass, insulin resistance and steroid use in renal transplant recipients.
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