Effects of renal transplantation on apoproteins: decrease in the B/A1 ratio atherogenicity index.
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Adrenal Cortex Hormones↗
Biomedical subjects
M Fénéant-Thibault
Publications and source records attributed to M Fénéant-Thibault.
Interleukin-1 beta-induced changes in the kinetic constants of L-proline uptake in human skin fibroblasts.
The effects of interleukin-1 beta (IL-1) on L-proline uptake in human skin fibroblasts were investigated. Exposure of the fibroblasts to IL-1 (5, 10 or 50 pg/ml) for 2 h did not change L-proline uptake. In contrast, inhibition was observed after 6 h of IL-1 treatment, and only 60% of the control uptake remained after incubation for 24 h with 10 pg of IL-1/ml. IL-1 depressed the activity of both transfer systems; the low-affinity system inhibited by alpha-(methylamino)isobutyric acid (Me-AIB), corresponding to system A, and a high-affinity transfer system which is unaffected by Me-AIB. The inhibitory effect increased as the L-proline concentration decreased. To determine whether IL-1-induced prostaglandin release influences proline uptake, indomethacin (14 microM) was added as a cyclo-oxygenase inhibitor. Indomethacin itself decreased L-proline uptake but to a lesser extent than did IL-1. When IL-1 was tested in the presence of indomethacin, the inhibition of L-proline uptake was still observed, with values between those obtained with each substance in isolation. This suggests that the inhibitory effect of IL-1 on proline uptake by skin fibroblast does not only involve the prostaglandins that accumulate in the medium, but no firm conclusion can be drawn, due to the fact that the inhibition by the two agents was not statistically independent. Kinetic analyses for 1 min combined with inhibition experiments showed that IL-1 induced a decrease in the Km and Vmax, values of the high-affinity transport system, whereas it increased the Km of system A. Therefore the two systems of proline uptake in skin fibroblasts are probably inhibited by IL-1 via different mechanisms.
Biological Transport↗
Isolation and characterization of an abnormal alpha slow-moving high-density lipoprotein subfraction in serum from children with long-standing cholestasis.
An abnormal high-density lipoprotein (HDL) subfraction, detected during periods of mild jaundice in the serum of seven children with chronic cholestasis from birth, was isolated and characterized. This fraction, identified by its slow alpha electrophoretic migration, is present in addition to normal HDL and differs from the abnormal HDL previously described in cholestatic syndromes. It is devoid of apolipoprotein B but is precipitated by phosphotungstate-MgCl2. These properties allowed its isolation by double selective precipitation. This subfraction is undetectable with this procedure in the serum of healthy subjects, is rich in cholesterol, and contains a large amount of apolipoprotein E, which may explain its precipitation by phosphotungstate-MgCl2. These apo E-containing HDL may play a major role in the lipid metabolism of patients with long-standing cholestasis during periods of mild jaundice.
Adolescent↗