title: Glucose and Insulin Response to Peritoneal Dialysis Fluid in Diabetic and Nondiabetic Peritoneal Dialysis Patients.
abstract: A postprandial increase in blood glucose in peritoneal dialysis (PD) patients with diabetes was observed in our previous study using continuous blood glucose monitoring. The response was observed in diabetic but not in nondiabetic PD patients. In addition, the response was reduced when patients used icodextrin; glucose absorbed from the peritoneum was responsible for the postprandial increase in blood glucose. Because our PD patients often change their PD fluid before meals, the present study aimed to determine the blood glucose and insulin responses to PD fluid. The 26 patients who agreed to participate in the study protocol [16 with diabetes (12 men, 4 women; 11 receiving insulin; 5 being controlled with oral antidiabetic drugs; average duration from diagnosis with diabetes: 16.4 ± 11 years); 10 without diabetes (4 men, 6 women)] had an average age of 60.5 ± 13.0 years. Average PD vintage was 578.7 ± 352.9 days. Blood samples were taken during a peritoneal equilibration test (PET) with 2.5% glucose solution at baseline and at 0.5, 2, and 4 hours. Levels of blood glucose and insulin were analyzed. A rapid increase in blood glucose (peak at 0.5 hours, 23.5 ± 22.2 mg/dL increase from baseline) was observed in nondiabetic patients. A delayed but higher peak response was observed in diabetic patients (peak at 1 hour, 54.9 ± 38.3 mg/dL increase from baseline). Peak response of insulin occurred at 0.5 hours in nondiabetic patients; in diabetic patients it occurred at 2 hours. No differences in the average insulin level during the PET were observed in the two groups (nondiabetic: 35.3 ± 15.6 μU/mL; diabetic: 38.9 ± 7.6 μU/mL). The study results suggest that a delayed insulin response after a PD fluid exchange could participate in the exaggerated postprandial increase in blood glucose in diabetic PD patients, particularly when the PD fluid exchange is performed before food intake.
authors.forename: Ikuko
authors.initials: I
authors.lastname: Oba
authors.forename: Takefumi
authors.initials: T
authors.lastname: Mori
authors.forename: Makiko
authors.initials: M
authors.lastname: Chida
authors.forename: Naho
authors.initials: N
authors.lastname: Kurasawa
authors.forename: Eri
authors.initials: E
authors.lastname: Naganuma
authors.forename: Emiko
authors.initials: E
authors.lastname: Sato
authors.forename: Kenji
authors.initials: K
authors.lastname: Koizumi
authors.forename: Shinichi
authors.initials: S
authors.lastname: Sato
authors.forename: Mihoko
authors.initials: M
authors.lastname: Tsuchikawa
authors.forename: Sadayoshi
authors.initials: S
authors.lastname: Ito
mesh_terms: D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000378:metabolism*; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D048909:Diabetes Complications / Q000150:complications / Q000188:drug therapy / Q000378:metabolism*; D015314:Dialysis Solutions / Q000378:metabolism; D005260:Female; D005936:Glucans / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D000077607:Icodextrin; D007328:Insulin / Q000627:therapeutic use; D007333:Insulin Resistance / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D010530:Peritoneal Dialysis; D010537:Peritoneum / Q000378:metabolism; D051437:Renal Insufficiency / Q000150:complications / Q000378:metabolism* / Q000628:therapy*
chemical_list: D001786:Blood Glucose; D015314:Dialysis Solutions; D005936:Glucans; D007004:Hypoglycemic Agents; D007328:Insulin; D000077607:Icodextrin; D005947:Glucose