Effects of ethanol on endogenous lipid and lipoprotein metabolism in small intestine
Mistilis, S.P.; Ockner, R.K.
Journal of Laboratory and Clinical Medicine 80(1): 34-46
1972
ISSN/ISBN: 0022-2143 PMID: 5033895 Document Number: 47788
Male Sprague-Dawley rats weighing from 306 to 353 g were maintained on a stock diet. Cannulae were placed in the mesenteric lymphatic duct and the duodenum. Some had catheters inserted into a femoral vein or the common bile duct. After operation the rats were allowed to stabilize overnight during constant infusion of 0.85% NaCl at 3 ml/h into the duodenum. Rats with externally-draining bile fistulae were given constant infusion into the duodenum at 1 ml/h of artificial bile consisting of sodium taurocholate 30 mu moles/ml, lecithin 5 mg/ml and cholesterol 2 mg/ml in 0.85% NaCl. They were then given a constant infusion into the duodenum of 10% w/v ethanol in 0.85% NaCl, a total dose of 5 g ethanol/kg, or isocaloric glucose in 0.85% NaCl, during 8 h. Some rats were given the alcohol solution by intravenous infusion. The infusion of saline into the duodenum was continued for up to 48 h. Rats were killed immediately and at intervals of 8 h up to 48 h. Intestinal mucosal triglycerides increased fourfold after ethanol infusion into the duodenum but only twofold after ethanol infusion by vein. There was a significant increase in mucosal triglycerides even after 48 h in rats given ethanol compared with that in those given glucose. Ethanol and glucose did not differ significantly in their effect on mucosal phospholipid and cholesterol concentrations. From 16 to 24 h after ethanol was given synthesis of intestinal lymph triglycerides increased by 50% compared with amounts up to 8 h and those from 16 to 24 h in rats given glucose. The triglycerides were carried primarily in the very low density lipoprotein fraction. Lymph output of phospholipid and cholesterol rose at same time as triglyceride. Plasma free fatty acids (FFA) in rats given ethanol were significantly higher than basal values and those in rats given glucose. Peak plasma FFA values were reached before the maximum increase in mucosal triglyceride concentration; this in turn preceded peak output of triglyceride in intestinal lymph suggesting that increased availability of plasma FFA after ethanol contributes to the increases in mucosal and lymph triglycerides. The entry of this non-dietary intestinal lipid into plasma may participate, along with other endogenous lipid sources, in the pathogenesis of hyperlipidaemia induced by ethanol.