No change in apolipoprotein AI metabolism when subcutaneous insulin infusion is replaced by intraperitoneal insulin infusion in type 1 diabetic patients.

In type 1 diabetic patients, the replacement of subcutaneous insulin infusion by intraperitoneal insulin infusion restores the normal physiological gradient between the portal vein and the peripheral circulation, which is likely to modify HDL metabolism. This stable isotope kinetic study was designed to compare HDL apolipoprotein (apo) AI metabolism in seven type 1 diabetic patients first treated by continuous subcutaneous insulin infusion by an external pump and then 3 months after the beginning of intraperitoneal insulin infusion by an implantable pump. Glycaemic control was comparable under subcutaneous and intraperitoneal insulin infusion (HbA1c=7.34+/-0.94% versus 7.24+/-1.00%, NS). HDL composition was similar under both insulin regimens (esterified cholesterol=20.1+/-2.5% versus 24.0+/-3.0% (NS), free cholesterol=3.4+/-1.1% versus 3.3+/-0.9% (NS), triglycerides=2.4+/-0.9% versus 2.1+/-0.9% (NS), phospholipids=22.7+/-5.3% versus 25.2+/-6.5% (NS) and proteins=51.2+/-6.3% versus 45.5+/-4.7% (NS)). The replacement of subcutaneous insulin infusion by intraperitoneal insulin infusion induced significant changes neither in apoAI fractional catabolic rate, nor in apoAI production rate, nor in apoAI pool size (respectively, 0.199+/-0.051 pool d(-1) versus 0.211+/-0.017 pool d(-1), 12.0+/-3.2 mg kg(-1)d(-1) versus 12.1+/-1.8 mg kg(-1)d(-1), 60.4+/-5.0 mg kg(-1) versus 57.5+/-7.5 mg kg(-1)). In conclusion, HDL metabolism is not modified by the replacement of subcutaneous insulin infusion by intraperitoneal insulin infusion when glycaemia is well controlled under both insulin regimens. As far as HDL metabolism is concerned there is no advantage in favour of one way of insulin administration or another.

Comparison of apolipoprotein B100 metabolism between continuous subcutaneous and intraperitoneal insulin therapy in type 1 diabetes.

OBJECTIVE: In type 1 diabetic patients, the replacement of s.c. insulin infusion with i.p. insulin infusion restores the normal physiological gradient between the portal vein and the peripheral circulation, which is likely to modify lipoprotein metabolism. DESIGN: To check this hypothesis, we performed two apolipoprotein (apo) B100 kinetic studies in seven type 1 diabetic patients, first under s.c. insulin infusion and then 3 months after the beginning of i.p. insulin infusion. RESULTS: Glycemic control was similar under s.c. insulin infusion and i.p. insulin infusion, as assessed by glycated hemoglobin A1c and the capillary glycemic curve determined during the kinetic study. Very low-density and intermediate-density lipoprotein apoB100 pool size, production rate, and fractional catabolic rate (FCR) were similar under s.c. insulin infusion and i.p. insulin infusion. The low-density lipoprotein apoB100 FCR tended to decrease under ip insulin (0.45 +/- 0.06 vs. 0.55 +/- 0.11 pool/d), but the difference did not reach statistical significance (95% confidence interval for the difference, -0.33, 0.11). The low-density lipoprotein apoB100 pool size and production rate remained unchanged under i.p. insulin infusion compared with s.c. insulin infusion. CONCLUSION: In type 1 diabetic patients, the replacement of s.c. insulin infusion with i.p. insulin infusion does not induce profound modifications of apoB100-containing lipoprotein production and FCRs.