No abstract

Male rats were given streptozotocin (100 mg/kg) by intraperitoneal injection. Groups of control and streptozotocin-treated animals were sacrificed at daily intervals for 4 days after injection. Over this period, treated rats lost weight continuously while control animals progressively gained weight. Within 24 h of treatment blood glucose and plasma free fatty acids were raised to levels which were sustained for the remainder of the experiment. After 48 h blood ketone bodies, plasma cholesterol and triglycerides were maximally raised and liver glycogen and blood lactate similarly lowered. The percentage composition of major fatty acids in liver lipids was unchanged until 4 days after treatment when there were significant increases in the proportion of oleate and linoleate and reductions in stearate and arachidonate. The data confirm that streptozotocin induces a rapid and sustained diabetes. It is suggested that metabolic experiments, in streptozotocin-diabetic rats, may be performed 48 h after treatment.

1. The work reported was designed to provide quantitative information about the capacity of the extrahepatic tissues of the rat to degrade injected VLD lipoproteins (very-lowdensity lipoproteins, d< 1.006) to LD lipoproteins (low-density lipoproteins, d 1.006-1.063) and to study the fate of the different VLD-lipoprotein apoproteins during the degradative process. 2. Rat liver VLD lipoproteins, radioactively labelled in their protein moieties, were produced by the perfusion of the organ and were either injected into the circulation of the supradiaphragmatic rats or incubated in rat plasma at 370C. At a time (75 min) when approx. 90% of the triacylglycerol of the VLD lipoproteins had been hydrolysed, the supradiaphragmatic rats were bled and VLD lipoproteins, LD lipoproteins and HD lipoproteins (high-density lipoproteins, d 1.063-1.21) were separated from their plasma and from the plasma incubated in vitro. The apoproteins of each of the lipoprotein classes were resolved by gel-filtration chromatography into three main fractions, designated peaks I, II and III. 3. Incubation of the liver VLD lipoproteins in plasma in vitro led to the transfer of about 30 % of the total protein radioactivity to the HD lipoproteins. This transfer mainly involved the peak-II (arginine-rich and/or apo A-I) and peak-Ill (apo C) proteins. There was also a small transfer of radioactivity (about 5 % of the total) to the LD lipoproteins. 4. Injection of the liver VLD lipoproteins into the circulation of the supradiaphragmatic rat resulted in the transfer of about 15 % of the total VLD-lipoprotein radioactivity to the LD lipoproteins. This transfer involved mainly the peak-I (apo B) proteins and accounted for about 20% of the total apo B protein radioactivity of the injected VLD lipoproteins. When the endogenous plasma VLD lipoprotein was taken into account the transfer of apo B protein was about 35 %.5. The transfer of peak-Il protein radioactivity from the VLD to the HD lipoproteins was greater in the plasma of the supradiaphragmatic rat than in the incubated plasma, suggesting that there was a net transfer of peak-II apoproteins during the VLD lipoprotein degradation. The transfer of peak-III protein radioactivity was not greater in the plasma of the supradiaphragmatic rat, but there was a loss of this radioactivity from the circulation.

No abstract

1. Donor perfused rat livers were used to prepare VLD (very-low-density) lipoproteins, labelled in their triacylglycerol and protein components with [1-14C]oleic acid and L-[4,5-3H]leucine respectively. Partially metabolized VLD lipoproteins, similarly labelled, were obtained from supradiaphragmatic rats injected with the parent VLD lipoproteins. 2. The triacylglycerol and protein components of the partially metabolized VLD lipoproteins were removed by recipient perfused rat livers at rates much higher than those of the parent VLD lipoproteins. No degradation of the partially metabolized VLD lipoproteins to LD (low-density) lipoproteins occurred during the perfusions. 3. Removal of hepatic lipase from the livers did not significantly affect the rate of removal of the partially metabolized VLD lipoproteins.