SP492
METABOLIC EFFECTS OF GLUCOSE BASED PERITONEAL DIALYSIS SOLUTIONS IN A RAT MODEL OF CKD

INTRODUCTION AND AIMS: Peritoneal dialysis is a treatment option for end stage renal disease using the peritoneum as a membrane and glucose-based solutions as osmotic agents to remove toxins from the blood. The effects of glucose and its metabolites are well known on peritoneum function but there is no data on its consequences on adipose tissue biology. Indeed, adipose tissue (AT) is present in all peritoneal tissues and is one of the largest endocrine organs playing a central role in energy and vascular homeostasis. The aim of the present study is to decipher the effect of glucose-based solutions on white adipose tissue in control and uremic rats.

METHODS: Seventy-two rats were randomly assigned to three different peritoneal fluids: Ringer Lactate (control solution), Glucose-based solutions (low glucose i.e.1.36% w/v, high glucose i.e. 3.86% w/v). Experimental chronic kidney disease (CKD) was induced by a three weeks of adenine diet (adenine 0.75% w/v) and the control rats were pair fed with a regular diet (n=12 per group). The peritoneal dialysis solutions (PDS) were infused three times a week for four weeks. Metabolic profiles and kidney function were evaluated. Retroperitoneal, subcutaneous and epididymal adipose tissues were collected and weighed to study the potential effects of glucose exposure. Isolated adipocytes were incubated with the different solutions to explore the effect of glucose based solution on lipolytic activity.

RESULTS: No difference was observed between the six groups for the body weight and the white adipose tissue accretion. As expected, the plasma urea concentration was significantly higher in the CKD group (P<0.001). High glucose based PDS induce a transient increase of blood glucose and insulin without altering insulin tolerance and lipid profile which were not significantly different from the low glucose infusion group. Total cholesterol and triacylycerols were significantly higher and non esterified fatty acids were lower in the CKD group (P<0.05). Retroperitoneal and epididymal (directly exposed to PDS) and sub cutaneous AT cellularity was not affected by the nature of PDS. In vitro, basal lipolytic activity was increased by 3.86% with the high glucose solution while no difference was noticed for lipolytic sensitivity for catecholamines.

CONCLUSIONS: We didn’t find any difference in body composition and adipose tissue weight and cellularity but lipolytic activity was increased when adipocytes were incubated with high glucose solution in vitro. An exposure to glucose based peritoneal dialysis solution does not impact adipose tissue accretion and systemic glycoregulation in our model. Whether protein and mRNA expression of adipokines or local AT inflammation is differentially impacted needs to be further investigated.