title: Hyperlipidemia in streptozocin-diabetic hamsters as a model for human insulin-deficient diabetes: comparison to streptozocin-diabetic rats.
abstract: Characteristics of the lipoprotein profile and metabolism of triglyceride-rich lipoproteins in diabetic hamsters were investigated to assess their suitability as a model for human diabetic hyperlipidemia. Diabetes was induced in the hamsters by intraperitoneal injection of streptozocin (30 mg/kg) for 3 days and compared with the results in streptozocin-diabetic rats (50 mg/kg intravenously). Similar degrees of hyperglycemia and hypoinsulinemia were observed 8 to 10 days after the final streptozocin injection in both groups. Fasting plasma lipid concentrations were about 2.5 times greater in hamsters than in rats. Plasma cholesterol was principally associated with high-density lipoprotein (HDL) in both rodents, although the distribution in very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) was significantly greater in hamsters (44%) than in rats (13%). Diabetes increased the concentrations of triglyceride, cholesterol, and phospholipid 5.6- to 7.8-fold in hamsters, whereas it increased them only 1.3- to 1.6-fold in rats. Diabetic hamsters have a plasma lipoprotein profile similar to that of diabetic man, ie, triglyceride-rich lipoproteins are increased and HDL cholesterol is decreased. The concentration of HDL cholesterol was inversely correlated with the severity of hypertriglyceridemia (r = .76, P < .005). This combination of events does not occur in diabetic rats. Hamsters had a low level of apoprotein B-48-containing triglyceride-rich lipoproteins, although diabetes increased the estimated concentration by fourfold. In rats apoprotein B-48 is the predominant form, but diabetes did not alter the relative proportion of apoprotein B isoforms.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Ebara
authors.forename: T
authors.initials: T
authors.lastname: Hirano
authors.forename: J C
authors.initials: JC
authors.lastname: Mamo
authors.forename: R
authors.initials: R
authors.lastname: Sakamaki
authors.forename: S
authors.initials: S
authors.lastname: Furukawa
authors.forename: S
authors.initials: S
authors.lastname: Nagano
authors.forename: T
authors.initials: T
authors.lastname: Takahashi
mesh_terms: D000818:Animals; D001055:Apolipoproteins B / Q000032:analysis; D006224:Cricetinae; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000150:complications*; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000150:complications*; D004195:Disease Models, Animal; D006949:Hyperlipidemias / Q000097:blood / Q000150:complications*; D015228:Hypertriglyceridemia / Q000097:blood; D007536:Isomerism; D008049:Lipase / Q000032:analysis / Q000378:metabolism; D008055:Lipids / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood; D008099:Liver / Q000201:enzymology; D008297:Male; D008647:Mesocricetus / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar / Q000502:physiology*; D013311:Streptozocin; D013997:Time Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D001055:Apolipoproteins B; D008055:Lipids; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D014280:Triglycerides; D013311:Streptozocin; D008049:Lipase