Changes of serum and dialysate leptin levels in continuous ambulatory peritoneal dialysis patients.
- Author:
Kyu Hun CHOI
1
Author Information
1. Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
- Publication Type:Editorial
- Keywords:
Peritoneal dialysis;
Leptin;
Adipokinectic hormone;
VEGF
- MeSH:
Absorption;
Body Composition;
Creatinine;
Cytokines;
Dialysis;
Eating;
Energy Metabolism;
Gene Expression;
Glucose;
Humans;
Hyperinsulinism;
Insulin;
Kidney Failure, Chronic;
Leptin*;
Models, Animal;
Molecular Weight;
Negotiating;
Peritoneal Cavity;
Peritoneal Dialysis;
Peritoneal Dialysis, Continuous Ambulatory*;
Peritoneum;
Vascular Endothelial Growth Factor A
- From:Korean Journal of Medicine
2007;73(2):119-122
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Leptin, the product of the adipose-specific ob gene, regulates food intake and energy expenditure in animal models. It is well known that serum leptin levels are increased in patients with chronic renal failure before start of dialysis or even after dialysis. This disorder is basically mediated by a decrease in the renal clearance of leptin, whereas the potential role of an increased secretion of this hormone awaits further confirmation. In this issue of the Journal, Park and Do investigate the longitudinal changes in body composition, serum(S) and dialysate(D) leptin levels in CAPD patients with time. There are significant increases in fat mass, S and D leptin at the 12th month after initiation of PD, especially in diabetes. Factors associated with the changes of fat mass during the first 1 year are D/Plasma 4-hour creatinine, glucose absorption via peritoneal cavity, and duration of dialysis. The correlation between changes of S or D leptin and %fat mass is significant. Consequently, they conclude that increased leptin levels of serum and dialysate may be associated with fat mass in PD patients with time. They found much further increase of D leptin concentration than S leptin, suggesting the possibility of intraperitoneal production of leptin. The molecular weight of leptin is small enough to pass through the peritoneum. Therefore, the extent of S leptin cleared by PD and/or whether a significant intraperitoneal leptin production occurs during PD with glucose-rich solution should be studied. It is well documented that the continuous glucose load during PD will result in chronic hyperinsulinemia which has been shown to increase leptin level by about 40%. Increased generation of proinflammatory cytokines, which is a common feature of PD, may also be a factor stimulating leptin gene expression. The relationship between insulin or proinflammatory cytokine and leptin concentration in PD patients is worthy of further study. In addition, the finding that the dialysate concentration of vascular endothelial growth factor potentially mediating neovascularization in the peritoneal cavity positively correlate with the increase of D/S leptin during the 1st year deserve consideration.
