title: Marine lipids normalize cholesteryl ester transfer in IDDM.
abstract: Patients with insulin-dependent diabetes mellitus (IDDM) have a pathological increase in cholesteryl ester transfer (CET) that enriches the apolipoprotein B-containing lipoproteins with cholesteryl ester and increases their atherogenicity. Since we have shown earlier that omega-3 (n-3) fatty acids present in marine lipids normalize both CET and lipoprotein composition in non-diabetic patients with hypercholesterolaemia, we sought to determine whether the same beneficial effects could be achieved in nine normolipidaemic (triglycerides 1.10; cholesterol 4.94, high density lipoprotein 1.10 mmol/l) IDDM patients (fructosamine 424 +/- 156; normal 174-286 mumol/l) treated for 2 months with n-3 fatty acids (4.6 g/day). Before treatment, CET measured by both mass and isotopic assays was abnormally accelerated (p < 0.001). While marine lipids modestly decreased triglyceride levels (-14%; p < 0.05 ), CET fell dramatically in all subjects (mass assay: -97% at 1 h; isotopic assay: -58%; p < 0.001) to below control levels with no change in glycaemic control (fructosamine 408 +/- 103 mumol/l). The mass of cholesteryl ester transfer protein paradoxically increased significantly (pre-treatment: 2.04 +/- 0.86 vs post-treatment 2.48 +/- 0.97 micrograms/ml; p < 0.05). Since it is believed that accelerated CET promotes the formation of atherogenic cholesteryl ester-enriched apo B-containing lipoproteins, the capacity of marine lipids to reverse this functional abnormality without altering glycaemic control suggests that these agents may have an adjunctive role to play in the nutritional therapy of IDDM.
authors.affiliation: Section of Endocrinology Rush Medical College, Chicago, IL 60612, USA.
authors.forename: J D
authors.initials: JD
authors.lastname: Bagdade
authors.forename: M
authors.initials: M
authors.lastname: Ritter
authors.forename: P V
authors.initials: PV
authors.lastname: Subbaiah
mesh_terms: D000328:Adult; D001055:Apolipoproteins B / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D002214:Capsules; D002352:Carrier Proteins / Q000097:blood*; D002784:Cholesterol / Q000097:blood; D053480:Cholesterol Ester Transfer Proteins; D002788:Cholesterol Esters / Q000097:blood*; D008076:Cholesterol, HDL / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000097:blood*; D003927:Diet, Diabetic; D015525:Fatty Acids, Omega-3 / Q000008:administration & dosage / Q000494:pharmacology*; D005260:Female; D005395:Fish Oils; D019270:Fructosamine; D006023:Glycoproteins; D006595:Hexosamines / Q000097:blood; D006801:Humans; D008075:Lipoproteins, HDL / Q000097:blood*; D008297:Male; D012016:Reference Values
chemical_list: D001055:Apolipoproteins B; D015415:Biomarkers; D001786:Blood Glucose; C506642:CETP protein, human; D002214:Capsules; D002352:Carrier Proteins; D053480:Cholesterol Ester Transfer Proteins; D002788:Cholesterol Esters; D008076:Cholesterol, HDL; D015525:Fatty Acids, Omega-3; D005395:Fish Oils; D006023:Glycoproteins; D006595:Hexosamines; D008075:Lipoproteins, HDL; D019270:Fructosamine; D002784:Cholesterol