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. The hypertriglyceridemia in both diabetic animals was solely due to a reduction in the clearance of triglyceride-rich lipoproteins, because the output of triglyceride as determined by the Triton WR1339 method was halved and the fractional catabolic rate of radiolabeled VLDL triglyceride was remarkably decreased. Lipoprotein lipase and hepatic lipase activities in postheparin plasma were lower in hamsters than in rats, and diabetes decreased lipoprotein lipase activity by half in hamsters, but not in rats. These results suggest that hamsters may be a more useful model than rats for delineating the disturbance in lipid metabolism that occurs as a result of insulin-deficient diabetes.
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