Apoprotein A-I synthesis in normal intestinal mucosa and in Tangier disease.
To determine whether human small intestine synthesizes apoA-I, the major apoprotein of plasma high-density lipoproteins, we used immunofluorescence technics and monospecific antiserums to visualize apoA-I within intestinal epithelial cells from four normal subjects and one patient with Tangier disease. Biopsies from all subjects during fasting showed limited fluorescence. After lipid feeding intracellular apoA-I markedly increased in both normal subjects and the patient. During alimentary lipemia, mean plasma apoA-I levels (milligrams per deciliter) increased in four normal subjects from 161 +/- 12 (+/- S.E.M.) to 180 +/- 15 (P less than 0.05) and in the patient from 1.9 to 6.8. Normal plasma chylomicrons contained apoB, apoE and the C peptides but not apoA-I. The patient's chylomicrons contained ap0A-I. Normal and Tangier-disease intestinal-mucosa cells increase their content of apoA-I during chylomicron formation and subsequently contribute to plasma apoA-I levels. The low levels of apoA-I in Tangier disease are not due to a failure of intestinal synthesis but might be due to abnormal metabolism of chylomicron apoproteins.
D001053:Apolipoproteins / Q000096:biosynthesis* / Q000097:blood; D001706:Biopsy; D002096:C-Peptide / Q000097:blood; D002914:Chylomicrons / Q000097:blood / Q000378:metabolism; D004041:Dietary Fats / Q000008:administration & dosage; D005455:Fluorescent Antibody Technique; D006801:Humans; D007009:Hypolipoproteinemias / Q000378:metabolism*; D007122:Immunoelectrophoresis; D007413:Intestinal Mucosa / Q000378:metabolism*; D007583:Jejunum / Q000378:metabolism; D008075:Lipoproteins, HDL / Q000097:blood; D008297:Male; D013631:Tangier Disease / Q000097:blood / Q000378:metabolism*
D001053:Apolipoproteins; D002096:C-Peptide; D002914:Chylomicrons; D004041:Dietary Fats; D008075:Lipoproteins, HDL