title: Electronegative low density lipoprotein subform (LDL-) is increased in type 2 (non-insulin-dependent) microalbuminuric diabetic patients and is closely associated with LDL susceptibility to oxidation.
abstract: There is increasing evidence that diabetes mellitus is characterized by an enhanced lipoprotein oxidation. We have therefore investigated whether a relationship exists between LDL oxidation and microalbuminuria, which is considered an early marker of vascular involvement in type 2 diabetic patients. We selected 12 microalbuminuric and 12 normoalbuminuric type 2 diabetic patients, and 12 control subjects comparable for age, sex and blood pressure values. Oxidatively modified plasma LDL, referred as LDL-, were measured by ion-exchange HPLC. In vitro susceptibility to oxidation of LDL was evaluated by following the kinetics of conjugated diene formation in the presence of Cu++ ions (lag-phase time). Microalbuminuric diabetic patients had a less satisfactory metabolic control and showed a higher plasma triglyceride concentration than both normoalbuminuric diabetic patients (2.211+/-1.01 vs 1.15+/-0.39 mmol/l, P<0.O1) and controls (1.18+/-0.61 mmol/l, P<0.01 ). The percentage of LDL- in plasma was significantly increased in microalbuminuric diabetic patients in comparison with both normoalbuminuric diabetic patients (5.24+/-1.67 vs 3.13+/-1.22%, P<0.01) and controls (2.34+/-1.03%, P<0.001). LDL isolated from microalbuminuric diabetic patients had a significantly shorter lag-phase time in comparison with normoalbuminuric diabetic patients (79+/-11 vs 97+/-10 min, P<0.05) and controls (120+/-24 min. P<0.001). In diabetic patients a significant linear correlation was observed between the percentage of LDL and amount of fructosamine (r=0.45, P<0.05), HbA1c (r=0.41, P<0.05), and triglycerides (r=0.65, P<0.001). An inverse correlation was found between lag-phase time and fructosamine (r=-0.5, P<0.01) and triglycerides (r=-0.59, P<0.001). This study shows that microalbuminuric type 2 diabetic patients had evidence of increased LDL oxidation, which seems to be mainly due to a poor metabolic control and a more atherogenic lipid profile.
authors.affiliation: Second Department of Internal Medicine and Metabolic Diseases, Regional General Hospital, Venice, Italy.
authors.forename: E
authors.initials: E
authors.lastname: Moro
authors.forename: C
authors.initials: C
authors.lastname: Zambon
authors.forename: S
authors.initials: S
authors.lastname: Pianetti
authors.forename: G
authors.initials: G
authors.lastname: Cazzolato
authors.forename: M
authors.initials: M
authors.lastname: Pais
authors.forename: G
authors.initials: G
authors.lastname: Bittolo Bon
mesh_terms: D000368:Aged; D000419:Albuminuria / Q000097:blood*; D001794:Blood Pressure; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000652:urine*; D005260:Female; D019270:Fructosamine / Q000097:blood; D006801:Humans; D008077:Lipoproteins, LDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction; D012016:Reference Values; D014280:Triglycerides / Q000097:blood
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D008077:Lipoproteins, LDL; D014280:Triglycerides; C099252:oxidized low density lipoprotein; D019270:Fructosamine; D002784:Cholesterol