title: Postprandial triglyceride response in type 1 (insulin-dependent) diabetes mellitus is not altered by short-term deterioration in glycaemic control or level of postprandial insulin replacement.
abstract: The effect of deteriorating glycaemic control on the lipoprotein responses to the ingestion of a high fat meal was investigated in seven normolipidaemic Type 1 (insulin-dependent) diabetic patients and the results were compared with corresponding responses in seven normolipidaemic control subjects. In addition, the importance of insulin in regulating the postprandial lipoprotein responses was examined by comparing the results obtained from the diabetic patients maintained on a basal infusion of insulin throughout the study with those obtained when a step-up, step-down insulin infusion was administered following the meal. Vitamin A was added to the test meal in all subjects to trace the metabolism of the chylomicron (Sf greater than 1000) and non-chylomicron (Sf less than 1000) fractions in the postprandial period. No differences in fasting and postprandial triglyceride levels nor in the concentration of the chylomicron and non-chylomicron fractions were observed between diabetic and control subjects. In the diabetic patients short-term (two-week) deterioration in glycaemic control did not have any adverse influence on the basal and postprandial lipid responses. However, while the amount of insulin administered after the meal in the diabetic patients did not have any effect on the postprandial triglyceride or chylomicron responses, the concentration of non-esterified fatty acids was significantly higher (p less than 0.0005) when only a basal infusion of insulin was administered.
  
  
  CONCLUSIONS
  1) Short-term deterioration in glycaemic control does not adversely affect lipoprotein concentrations in Type 1 diabetes. 2) Non-esterified fatty acids appear to be a more sensitive index of insulinization post-prandially than triglycerides.
authors.affiliation: Department of Medicine, University of Chicago, Pritzker School of Medicine, Illinois.
authors.forename: G F
authors.initials: GF
authors.lastname: Lewis
authors.forename: N M
authors.initials: NM
authors.lastname: O'Meara
authors.forename: V G
authors.initials: VG
authors.lastname: Cabana
authors.forename: J D
authors.initials: JD
authors.lastname: Blackman
authors.forename: W L
authors.initials: WL
authors.lastname: Pugh
authors.forename: A F
authors.initials: AF
authors.lastname: Druetzler
authors.forename: J R
authors.initials: JR
authors.lastname: Lukens
authors.forename: G S
authors.initials: GS
authors.lastname: Getz
authors.forename: K S
authors.initials: KS
authors.lastname: Polonsky
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000188:drug therapy; D004435:Eating; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood / Q000627:therapeutic use*; D007700:Kinetics; D008297:Male; D014280:Triglycerides / Q000097:blood*
chemical_list: D001786:Blood Glucose; D008076:Cholesterol, HDL; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D014280:Triglycerides; D002784:Cholesterol