title: Total parenteral nutrition and plasma lipoproteins in the rat: evidence for accelerated clearance of apo-A-I-rich HDL.
abstract: The effect of total parenteral nutrition (TPN) containing fat on plasma lipoproteins and apo-A-I-rich HDL catabolism was studied in the rat. TPN rats were intravenously infused for 5 days with a nutritive mixture containing amino acids, lipids (Intralipid 20%) and glucose. In spite of similar plasma levels of total cholesterol in TPN and control orally fed rats, density gradient ultracentrifugation of plasma samples gave evidence of marked differences in the lipoprotein profiles. In the density range 1.010-1.040, were found elevated amounts of apo-B-100 and apo-B-48 containing lipoproteins, as well as an increase in free cholesterol and phospholipids, the latter indicating that the plasma of TPN rats contained abnormal lipoprotein-X-like particles. The level of apo-E-rich HDL (density: 1.040-1.063) was not markedly changed, whereas that of typical HDL (d > 1.063) was lowered, with less apo-A-I and apo-A-IV, and low amounts of cholesterol and phospholipids were found in the most dense HDL3 fractions (d > 1.090) containing the bulk of apo-A-I-rich particles. After intravenous infusion of homologous [14C]sucrose-labelled HDL3, the clearance of these particles was 2-fold faster in TPN than in control rats, with a tissue uptake increased in the liver (+40%) and decreased in the small and large intestines (-60%). Because the pool of apo-A-I-rich HDL was dramatically reduced after 5 days of artificial feeding, the absolute catabolic rate of these lipoproteins was similar in the two groups. These data suggest that, in TPN rats lacking of chylomicron coat components as a source for HDL material, the fall in plasma levels of apo-A-I-rich HDL resulted mainly from accelerated turnover of these particles, mediated by increased uptake by the liver. Conversely, mucosa atrophy was probably involved in the reduced uptake of apo-A-I-rich HDL by the gastrointestinal tract.
authors.affiliation: Laboratoire de Physiologie de la Nutrition, Université Paris-Sud, Orsay, France.
authors.forename: T
authors.initials: T
authors.lastname: Hajri
authors.forename: J
authors.initials: J
authors.lastname: Férézou
authors.forename: P
authors.initials: P
authors.lastname: Steinmetz
authors.forename: C
authors.initials: C
authors.lastname: Lutton
mesh_terms: D000818:Animals; D016632:Apolipoprotein A-I / Q000032:analysis* / Q000302:isolation & purification; D001835:Body Weight; D002499:Centrifugation, Density Gradient; D002784:Cholesterol / Q000097:blood; D002149:Energy Intake; D008074:Lipoproteins / Q000097:blood* / Q000302:isolation & purification; D008075:Lipoproteins, HDL / Q000097:blood / Q000493:pharmacokinetics; D008297:Male; D010289:Parenteral Nutrition, Total; D010743:Phospholipids / Q000097:blood; D051381:Rats; D017208:Rats, Wistar
chemical_list: D016632:Apolipoprotein A-I; D008074:Lipoproteins; D008075:Lipoproteins, HDL; D010743:Phospholipids; D002784:Cholesterol