[On the etiology of diabetic hyperlipidemia from the aspects of the metabolism of ApoHDL (author's transl)].
Diabetes mellitus was induced in the rats with streptozotocin. Lipoproteins obtained by ultracentrifugation and column chromatography were analyzed. Some groups of rats fed on high cholesterol diet for 3 weeks, others were fed on normal chow. I) In diabetic rats fed on normal chow, the following results were obtained. i) Hypertriglyceridemia, even in fasting state, occurred in the rats whose fasting blood sugar exceeded 270 mg/dl. High density lipoprotein (HDL)-Cholesterol was neither increased, nor decreased. ii) An apoCII peptide, known as the activator of lipoprotein lipase, was decreased in plasma HDL of diabetic rats with hypertriglyceridemia (48% of norm). In diabetic rats without hypertriglyceridemia, the CII peptide was not decreased. iii) An apo E peptide in HDL was decreased significantly (28%-41% of norm). iv) The potency of apoHDL derived from diabetic rats with hypertriglyceridemia for activating lipoprotein lipase was considerably decreased, compared to normal apoHDL. II) In diabetic rats fed on high cholesterol diet (DMC-rats), striking alterations in plasma lipoproteins occurred. i) Compared to normal fed on high cholesterol diet, plasma total cholesterol level rose significantly (7 fold), with an appreciable increase in levels of phospholipids and triglycerides. HDL-cholesterol was decreased. ii) An abnormal peak appeared on agarose column chromatogram. This lipoprotein was estimated to possess an apoE-AII peptide complex, addition to apoB, E, C, AI and AIV, and showed one major band (having a slightly slower mobility than VLDL) and one minor band (alpha mobility) on electrophoresis, and exhibited two types of particles on electronmicroscopy. Diameters of these particles were 40.6 +/- 36.7 A, and 240.3 +/- 47.4 A. iii) The HDL of DMC-rats also had the apoE-AII complex. These results may suggest that the decrease in apoCII in HDL cause the diabetic hypertriglyceridemia, and the apoE-AII complexes observed in cholesterol feeding hinder the incorporation of lipoproteins into the liver.
D000818:Animals; D001053:Apolipoproteins / Q000097:blood*; D002791:Cholesterol, Dietary / Q000008:administration & dosage; D003921:Diabetes Mellitus, Experimental / Q000097:blood*; D004591:Electrophoresis, Polyacrylamide Gel; D006949:Hyperlipidemias / Q000209:etiology*; D008075:Lipoproteins, HDL / Q000097:blood*; D008297:Male; D051381:Rats; D014280:Triglycerides / Q000097:blood
D001053:Apolipoproteins; D002791:Cholesterol, Dietary; D008075:Lipoproteins, HDL; D014280:Triglycerides