title: Synthesis and secretion of B-100 and A-I apolipoproteins in response to the changes of intracellular cholesteryl ester content in chick liver.
abstract: We investigated in the chick whether the diet-induced changes of the hepatic content of cholesteryl esters (CE) influence the synthesis and the secretion of apoB- and apoA-I-containing lipoproteins. Control chicks received a low cholesterol diet for 2 (SD-1), 4 (SD-2), or 7 (SD-3) weeks; the chicks in the experimental groups received a cholesterol-rich diet for 2 weeks and were killed at the end of the cholesterol feeding (CH-F), and after 2 (CH-D) or 5 (CH-DD) weeks of a low cholesterol diet. Hepatic CE content in CH-F chicks was 30-fold that observed in controls, but returned to the control level after 5 weeks of cholesterol depletion (CH-DD). The incorporation of 35S-labeled amino acids into cell and medium apoB and apoA-I was measured in liver slices. Intracellular 35S-labeled apoB was similar in all groups whereas medium 35S-labeled apoB was 2-fold higher in CH-F than in controls (SD-1). Pulse-chase experiments showed that radioactive apoB secreted by CH-F chicks at 120 min of chase was 2 times that of SD-1 chicks. This increased secretion of apoB was not found in CH-D chicks. In CH-F chicks, the intracellular and medium 35S-labeled apoA-I were 2-fold the values found in controls (SD-1); apoA-I production returned to the control level only after 5 weeks of cholesterol depletion (CH-DD). The increased secretion of apoB and apoA-I in CH-F chicks was associated with an increased secretion of very low, intermediate, and low density lipoproteins containing newly synthesized apoB and apoA-I and of high density lipoproteins containing predominantly apoA-I. Thus, in response to hepatic CE accumulation induced by cholesterol feeding, a larger proportion of newly synthesized apoB is driven to the secretory pathway and more apoA-I is synthesized. This promotes an increased secretion of plasma lipoproteins that contribute to the removal of CE from the liver.
authors.affiliation: Dipartimento di Scienze Biomediche, Universita di Modena, Italy.
authors.forename: P
authors.initials: P
authors.lastname: Tarugi
authors.forename: S
authors.initials: S
authors.lastname: Nicolini
authors.forename: G
authors.initials: G
authors.lastname: Ballarini
authors.forename: L
authors.initials: L
authors.lastname: Marchi
authors.forename: C
authors.initials: C
authors.lastname: Duvigneau
authors.forename: P
authors.initials: P
authors.lastname: Tartoni
authors.forename: S
authors.initials: S
authors.lastname: Calandra
mesh_terms: D000818:Animals; D016632:Apolipoprotein A-I / Q000096:biosynthesis / Q000378:metabolism*; D053299:Apolipoprotein B-100; D001055:Apolipoproteins B / Q000096:biosynthesis / Q000378:metabolism*; D015152:Blotting, Northern; D001835:Body Weight; D002499:Centrifugation, Density Gradient; D002645:Chickens; D002784:Cholesterol / Q000097:blood; D002788:Cholesterol Esters / Q000378:metabolism*; D002791:Cholesterol, Dietary / Q000008:administration & dosage; D004032:Diet; D008074:Lipoproteins / Q000097:blood; D008099:Liver / Q000737:chemistry / Q000378:metabolism*; D008297:Male; D019301:Oleic Acid / Q000378:metabolism; D009929:Organ Size; D011506:Proteins / Q000378:metabolism; D012313:RNA / Q000378:metabolism; D014280:Triglycerides / Q000097:blood
chemical_list: D016632:Apolipoprotein A-I; D053299:Apolipoprotein B-100; D001055:Apolipoproteins B; D002788:Cholesterol Esters; D002791:Cholesterol, Dietary; D008074:Lipoproteins; D011506:Proteins; D014280:Triglycerides; D019301:Oleic Acid; D012313:RNA; D002784:Cholesterol