Apoprotein C effect on triglyceride transport in tandem-perfused rat hind end and liver.

The metabolism of double-labeled triglyceride in a synthetic emulsion was defined in an in vitro perfusion system of rat hind end and liver described previously [Am. J. Physiol. 245 (Gastrointest. Liver Physiol. 8): G106-G112, 1983]. The metabolism of [3H]glycerol-[14C]triolein was defined in the absence of added apoproteins and with additions of human CII and both CII and CIII. Without apoprotein, a pronounced lipolysis of the triglyceride was recognized by high concentrations of radiolabeled glycerol and free fatty acid in the perfusate. The removal of an aliquot of hind-end venous effluent 5 min after adding the labeled triglyceride emulsion to the arterial inflow demonstrated a brisk lipolysis of the substrate when incubated outside the perfusion system. The addition of CII protein to the emulsion before its introduction into the tandem system eliminated perfusate lipolysis, both within the perfusion system and in incubations of aliquots withdrawn from the system. Intravascular lipolysis was not seen with triglyceride emulsions containing both CII and CIH or when an aliquot of hind-end venous effluent was incubated with triglycerides that had not been exposed to the perfusion system. The intravascular lipolysis observed for the [14C]triglyceride added to the tandem system without apoproteins was associated with relatively greater recoveries of 14C-fatty acyl in liver, fat, and muscle and relatively greater recoveries of 14CO2 than when CII alone or both CII and CIII were added with the triglyceride. The addition of CIII to CII in a 1:1 molar ratio increased the recovery of 14C-fatty acyl in muscle and the recovery as 14CO2.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of chenodeoxycholic acid on cholesterol and bile acid turnover in humans with cholelithiasis.

The in vivo dynamics of cholesterol were determined in 8 individuals who were part of a national double-blind study testing the efficacy of chenodeoxycholic acid ingestion on the dissolution of gallstones. Despite the ingestion of this bile acid in amounts in excess of its normal endogenous flux, the conversion of neutral sterol to chenodeoxycholic acid continued. The flux of neutral sterol to endogenous chenodeoxycholate was lower for the patients ingesting bile acid than for one of the patients on placebo, but was similar to that of the other control and similar to previously published chenodeoxycholate flux in patients with cholesterol cholelithiasis. The remaining flux was on the basis of the very efficiently absorbed dietary chenodeoxycholate. The total cholesterol fractional catabolic rate and flux were not appreciably diminished by the administration of either high or low dose chenodeoxycholate to these individuals with cholesterol cholelithiasis.