Lipoprotein lipase in plasma after an oral fat load: relation to free fatty acids.
Lipoprotein lipase (LPL) releases fatty acids from triglyceride-rich lipoproteins for use in cellular metabolic reactions. How this hydrolysis, which occurs at the vascular endothelium, is regulated is poorly understood. A fatty acid feedback system has been proposed by which accumulation of fatty a...
| Main Authors: | , , , |
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| Format: | Journal article |
| Language: | English |
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1992
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| _version_ | 1797067647708299264 |
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| author | Karpe, F Olivecrona, T Walldius, G Hamsten, A |
| author_facet | Karpe, F Olivecrona, T Walldius, G Hamsten, A |
| author_sort | Karpe, F |
| collection | OXFORD |
| description | Lipoprotein lipase (LPL) releases fatty acids from triglyceride-rich lipoproteins for use in cellular metabolic reactions. How this hydrolysis, which occurs at the vascular endothelium, is regulated is poorly understood. A fatty acid feedback system has been proposed by which accumulation of fatty acids impedes LPL-catalyzed hydrolysis and dissociates the enzyme from its endothelial binding sites. We examined this hypothesis in humans who were subjected to an oral fat tolerance test of a mixed-meal type. Plasma triglycerides, free fatty acids, and LPL activity were measured before and repeatedly during a 12-h period after intake of the fat load. Since soybean oil with a high content of linoleic fatty acid was the source of triglycerides, a distinction could be made between endogenous free fatty acids (FFA) and FFA derived directly from lipolysis of postprandial triglyceride-rich lipoproteins. Mean LPL activity was almost doubled (P less than 0.01) 6 h after intake of the oral fat load. The rise in LPL activity was accompanied by an increase of plasma triglycerides and linoleic free fatty acids (18:2 FFA), but not of total plasma FFA, which instead displayed a heterogeneous pattern with essentially unchanged mean levels. The postprandial response of LPL activity largely paralleled the postprandial responses of 18:2 FFA and triglycerides. The highest degree of parallelism was seen between postprandial 18:2 FFA and LPL activity levels. Furthermore, the integrated response (area under the curve, AUC) for plasma measurements of LPL correlated with the AUC for 18:2 FFA (r = 0.40, P less than 0.05), but not with the AUC for plasma triglycerides (r = 0.21, ns). The high degree of parallelism and significant correlation between postprandial plasma LPL activity and 18:2 FFA support the hypothesis of fatty acid control of endothelial LPL during physiological conditions in humans. |
| first_indexed | 2024-03-06T21:59:21Z |
| format | Journal article |
| id | oxford-uuid:4e0f7de9-0fa2-4f2c-8090-d418741d3c91 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T21:59:21Z |
| publishDate | 1992 |
| record_format | dspace |
| spelling | oxford-uuid:4e0f7de9-0fa2-4f2c-8090-d418741d3c912022-03-26T15:58:56ZLipoprotein lipase in plasma after an oral fat load: relation to free fatty acids.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:4e0f7de9-0fa2-4f2c-8090-d418741d3c91EnglishSymplectic Elements at Oxford1992Karpe, FOlivecrona, TWalldius, GHamsten, ALipoprotein lipase (LPL) releases fatty acids from triglyceride-rich lipoproteins for use in cellular metabolic reactions. How this hydrolysis, which occurs at the vascular endothelium, is regulated is poorly understood. A fatty acid feedback system has been proposed by which accumulation of fatty acids impedes LPL-catalyzed hydrolysis and dissociates the enzyme from its endothelial binding sites. We examined this hypothesis in humans who were subjected to an oral fat tolerance test of a mixed-meal type. Plasma triglycerides, free fatty acids, and LPL activity were measured before and repeatedly during a 12-h period after intake of the fat load. Since soybean oil with a high content of linoleic fatty acid was the source of triglycerides, a distinction could be made between endogenous free fatty acids (FFA) and FFA derived directly from lipolysis of postprandial triglyceride-rich lipoproteins. Mean LPL activity was almost doubled (P less than 0.01) 6 h after intake of the oral fat load. The rise in LPL activity was accompanied by an increase of plasma triglycerides and linoleic free fatty acids (18:2 FFA), but not of total plasma FFA, which instead displayed a heterogeneous pattern with essentially unchanged mean levels. The postprandial response of LPL activity largely paralleled the postprandial responses of 18:2 FFA and triglycerides. The highest degree of parallelism was seen between postprandial 18:2 FFA and LPL activity levels. Furthermore, the integrated response (area under the curve, AUC) for plasma measurements of LPL correlated with the AUC for 18:2 FFA (r = 0.40, P less than 0.05), but not with the AUC for plasma triglycerides (r = 0.21, ns). The high degree of parallelism and significant correlation between postprandial plasma LPL activity and 18:2 FFA support the hypothesis of fatty acid control of endothelial LPL during physiological conditions in humans. |
| spellingShingle | Karpe, F Olivecrona, T Walldius, G Hamsten, A Lipoprotein lipase in plasma after an oral fat load: relation to free fatty acids. |
| title | Lipoprotein lipase in plasma after an oral fat load: relation to free fatty acids. |
| title_full | Lipoprotein lipase in plasma after an oral fat load: relation to free fatty acids. |
| title_fullStr | Lipoprotein lipase in plasma after an oral fat load: relation to free fatty acids. |
| title_full_unstemmed | Lipoprotein lipase in plasma after an oral fat load: relation to free fatty acids. |
| title_short | Lipoprotein lipase in plasma after an oral fat load: relation to free fatty acids. |
| title_sort | lipoprotein lipase in plasma after an oral fat load relation to free fatty acids |
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