Lipoprotein Kinetics in Patients With Analbuminemia

Author:

Maugeais C.1,Braschi S.1,Ouguerram K.1,Maugeais P.1,Mahot P.1,Jacotot B.1,Darmaun D.1,Magot T.1,Krempf M.1

Affiliation:

1. From the Centre de Recherche en Nutrition Humaine, Hôpital G. & R. Laënnec, Nantes, France (C.M., K.O., P.M., D.D., T.M., M.K.); Service de Médecine Interne, Hôpital Henri Mondor, Créteil, France (S.B., B.J.); and Clinique d’Endocrinologie, Maladies Métaboliques et Nutrition, Hôtel Dieu, Nantes, France (P.M., M.K.).

Abstract

Abstract In vitro data suggested that albumin is a key factor controlling apolipoprotein (apo) synthesis by hepatocytes. Studies in analbuminemic rats have shown an increase in secretion of apoB-containing lipoprotein from the liver. We studied the kinetic aspects of apoB- and apoAI-containing lipoprotein metabolism in two sisters with analbuminemia using a constant 14-hour infusion of leucine labeled with stable isotopes. Compared with control subjects, total cholesterol was higher in the two patients (432 and 461 versus 155±14 mg/dL), as was apoB (257 and 230 versus 72±7 mg/dL). Triglycerides were slightly increased (134 and 105 versus 89±9 mg/dL), whereas apoAI was lower (109 and 105 versus 124±6 mg/dL). VLDL–apoB production was higher, as was the production of IDL–apoB and LDL–apoB (32.8 and 36.0 versus 24.8±5.9, 32.1 and 27.2 versus 16.4±2.3, and 14.1 and 17.6 versus 10.3±1.2 mg · kg −1 · d −1 , respectively). The fractional catabolic rate of all the apoB-containing lipoproteins was decreased (0.23 and 0.37 versus 0.48±0.05, 0.27 and 0.28 versus 0.62±0.08, and 0.012 and 0.009 versus 0.022±0.002 · h −1 , respectively). A similar mechanism could explain the dyslipidemia observed in other conditions associated with low albumin levels, such as nephrotic syndrome.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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