When I-14C oleic acid at 120 micron Eq/hr was infused into the duodenum in normal rats in a micellar solution with mono-olein (60 mu moles/hr) in 15 mM taurocholate over 6 hr uptake was nearly complete (97%). However, when this same solution was infused into the mid small bowel in control animals uptake was incomplete (88.9 +/- 2.6%, mean +/- SEM, P < 0.01). After 4 weeks on a high fat diet, containing 45% vegetable oil by weight, oleic acid uptake increased to 98.1 +/- 0.1% (P < 0.01 compared to controls). The improved uptake of oleic acid was associated with increased dry weight of mucosa in the proximal half of the ileum from 109 +/- 8.8/20 cm in controls to 135.6 +/- 7.3 mg/20 cm in high fat diet fed rats (P < 0.05), while protein increased from 107.4 +/- 6.5 to 124.9 +/- 4.8 mg/20 cm (P < 0.05). There was no increase in DNA expressed as mg/g wet weight of mucosa or in number of cells per villus. Lipid content of the mucosa and degree of esterification of absorbed oleic also were unaltered. These results indicate that the mucosa of the proximal ileum responds to high fat feeding by hypertrophy (increased mass and protein, with no change in DNA content or cell number) and that this change is associated with more complete uptake of oleic acid reaching this part of the small bowel.

Triglyceride release by livers isolated from normal fed animals has been shown previously to be stimulated by the addition of palmitate to the perfusate. It may be concluded from the data reported herein that the output of cholesterol and phospholipid into the d < 1.006 lipoprotein class is proportional to release of triglyceride into this fraction. Triglyceride, cholesterol, and phospholipid may be secreted in constant proportion in order to maintain a physical-chemical stability and solubility of the very low density lipoprotein whose primary function is transport of triglyceride from liver to extrahepatic tissues. CCl4, which inhibits triglyceride release by the liver, also inhibits output of cholesterol and phospholipid into the d < 1.006 lipoprotein. Release of cholesterol into the d < 1.063 lipoprotein is not clearly related to non-esterified fatty acid levels in the medium, to triglyceride release by the liver, or to other lipids present in this fraction. The serum lipoprotein class containing the largest initial concentration of any lipid is not necessarily identical with the fraction having the major net hepatic release of that lipid. Thus, each lipoprotein class released may have specific and different lipid carrier functions.

No abstract