ApoA-IV metabolism in the rat: role of lipoprotein lipase and apolipoprotein transfer
| Autor: | Michael Lefevre, Mei-Yu Chuang, Paul S. Roheim |
|---|---|
| Rok vydání: | 1990 |
| Předmět: |
Apolipoprotein E
medicine.medical_specialty Lipoprotein lipase Apolipoprotein B biology Cholesterol nutritional and metabolic diseases QD415-436 Cell Biology Metabolism Apolipoproteins A Biochemistry chemistry.chemical_compound Endocrinology chemistry Internal medicine polycyclic compounds medicine biology.protein lipids (amino acids peptides and proteins) Perfusion Incubation |
| Zdroj: | Journal of Lipid Research, Vol 27, Iss 11, Pp 1163-1173 (1990) |
| ISSN: | 0022-2275 |
| DOI: | 10.1016/s0022-2275(20)38752-6 |
| Popis: | Factors influencing the association of apoA-IV with high density lipoproteins (HDL) were investigated by employing a crossed immunoelectrophoresis assay to estimate the distribution of rat plasma apoA-IV between the lipoprotein-free and HDL fractions. Incubation of rat plasma at 37 degrees C resulted in the complete transfer of lipoprotein-free apoA-IV to HDL within 45 min. When plasma obtained from fat-fed rats was incubated at 37 degrees C in the presence of postheparin plasma as a source of lipolytic activity, there was a complete transfer of HDL apoA-IV to the lipoprotein-free fraction within 30 min. With extended incubation (120 min), lipoprotein-free apoA-IV began to transfer back to HDL. Similar patterns of apoA-IV redistribution were seen when plasma from fat-fed rats was incubated with postheparin heart perfusate or was perfused through a beating heart. Incubations conducted with plasma obtained from fasted rats showed similar but markedly attenuated apoA-IV responses. Similar observations were found in vivo following intravenous heparin administration. To determine whether the transfer of apolipoproteins from triglyceride-rich lipoproteins to HDL was partially responsible for the lipolysis-induced redistribution of apoA-IV, purified apoA-I, apoE, and C apolipoproteins were added to plasma from fasted rats. When added to plasma, all of the apolipoproteins tested displaced apoA-IV from HDL in a dose-dependent manner. Conversely, apolipoproteins were removed from HDL by adding Intralipid to plasma from fasted rats. With increasing concentrations of Intralipid, there was a progressive loss of HDL apoC-III and a progressive increase in HDL apoA-IV. Intravenous injection of a bolus of Intralipid to fasted rats resulted in a transient decrease of HDL apoC-III and concomitant increase in HDL apoA-IV. From these studies, we conclude that the binding of apoA-IV to HDL is favored under conditions that result in a relative deficit of HDL surface components, such as following cholesterol esterification by LCAT or transfer of apolipoproteins to nascent triglyceride-rich lipoproteins. |
| Databáze: | OpenAIRE |
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