title: Leptin kinetics during peritoneal dialysis in acutely uraemic rats.
abstract: BACKGROUND
  Leptin has been shown to function as an inhibitor of appetite and energy expenditure accelerator. However, it was recently reported that leptin has other important functions as a fibrogenetic factor and a novel, independent risk factor for coronary heart disease. The present study aimed to assess the blood concentration of leptin in acute uraemic rats by using various peritoneal dialysis (PD) solutions.
  
  
  METHODS
  To induce acute renal failure, the bilateral renal arteries were ligated via a mid-abdominal incision 1 h before starting PD. Rats were divided into four groups: 13.6 g/L glucose-containing dialysate (group L); 38.6 g/L glucose-containing dialysate (group H); 13.6 g/L glucose and 25 g/L mannitol-containing dialysate with equal osmotic pressure to the dialysate of group H (group M); and renal failure without PD (group F). The concentrations of glucose, urea nitrogen (UN), leptin and insulin were measured at 0, 2 and 4 h after starting PD.
  
  
  RESULTS
  We observed significant blood UN suppression in all dialysed groups. Blood glucose was significantly higher in rats treated with the high glucose solution than in those treated with the low glucose solution. Insulin and leptin significantly increased in the high glucose solution group. There was a strong correlation between the blood glucose and insulin levels. We also found a strong correlation between the percentage changes in blood glucose and leptin. The relationship between the percentage changes in insulin and leptin were weak but significant.
  
  
  CONCLUSIONS
  The high glucose PD solution resulted in increased circulating levels of leptin, glucose, and insulin, suggesting that these changes are linked with PD performed with glucose-based dialysis fluid.
authors.affiliation: The Second Department of Internal Medicine, Faculty of Medicine, Kagawa University, Kagawa, Japan.
authors.forename: Keisuke
authors.initials: K
authors.lastname: Matsubara
authors.forename: Hideyasu
authors.initials: H
authors.lastname: Kiyomoto
authors.forename: Kumiko
authors.initials: K
authors.lastname: Moriwaki
authors.forename: Taiga
authors.initials: T
authors.lastname: Hara
authors.forename: Naoki
authors.initials: N
authors.lastname: Kondo
authors.forename: Takatomi
authors.initials: T
authors.lastname: Shokoji
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Hitomi
authors.forename: Yasuharu
authors.initials: Y
authors.lastname: Aki
authors.forename: Masaki
authors.initials: M
authors.lastname: Aono
authors.forename: Akira
authors.initials: A
authors.lastname: Nishiyama
authors.forename: Koji
authors.initials: K
authors.lastname: Ohmori
authors.forename: Masakazu
authors.initials: M
authors.lastname: Kohno
mesh_terms: D058186:Acute Kidney Injury / Q000097:blood* / Q000150:complications; D000818:Animals; D005950:Glucose Solution, Hypertonic / Q000494:pharmacology*; D015312:Hemodialysis Solutions / Q000494:pharmacology*; D020738:Leptin / Q000097:blood*; D008297:Male; D010530:Peritoneal Dialysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D014511:Uremia / Q000097:blood* / Q000209:etiology
chemical_list: D005950:Glucose Solution, Hypertonic; D015312:Hemodialysis Solutions; D020738:Leptin