| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
American Journal of Clinical Nutrition, Vol 20, 1070-1083, Copyright © 1967 by The American Society for Clinical Nutrition, Inc.
1 From Department of Biochemistry and Nutrition, Graduate School of Public Health, and the Department of Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania
Diets containing linoleate at either 4 or 18% of calories were fed to four male volunteers, two of whom were normolipemic subjects and two of whom were hyperlipemic subjects. After 3 weeks, each subject was fed 100 µc of linoleic acid-l-14C as the free acid, and blood and expired air samples were collected at intervals for 120 hr. Expired air was analyzed for 14CO2 and comparative rates of the conversion of linoleate-l-14C to 14CO2 were calculated. The specific activities and total incorporation of linoleate-l-14C into triglyceride, cholesterol, and phospholipid linoleate were determined at various times. Chylomicrons were excluded by centrifugation.
The total amount of radioactivity from linoleate-l-14C incorporated into lipids of the plasma lipoproteins was greater in the hyperlipemic subjects than in normolipemic subjects. This difference was most evident in the triglyceride fraction and less so in phospholipids and cholesterol esters. These results suggest that in the hyperlipemic individuals studied, the primary metabolic abnormality is an overproduction of hepatic triglycerides. This observation correlated with the high concentration of low-density liproproteins present in the plasma of such individuals.
The oxidation of linoleate-l-14C to carbon dioxide in subjects subsisting on diets containing 4% of calories from linoleate was depressed in the hyperlipemic subjects as compared to the normal controls. Diets high in linoleate stimulated the conversion of linoleic acid to carbon dioxide in both normo- and hyperlipemic subjects. The data suggest that high linoleate feeding may contribute to the control of hyperlipemia by diverting more dietary fatty acid toward oxidative pathways, thus leaving less for hepatic biosynthesis of low-density lipoproteins.
This article has been cited by other articles:
|
|
 |
|
  A. E. Millen, M. A. Tucker, P. Hartge, A. Halpern, D. E. Elder, D. Guerry IV, E. A. Holly, R. W. Sagebiel, and N. Potischman Diet and Melanoma in a Case-Control Study Cancer Epidemiol. Biomarkers Prev., June 1, 2004; 13(6): 1042 - 1051. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 U. McCloy, M. A. Ryan, P. B. Pencharz, R. J. Ross, and S. C. Cunnane A comparison of the metabolism of eighteen-carbon 13C-unsaturated fatty acids in healthy women J. Lipid Res., March 1, 2004; 45(3): 474 - 485. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. E Olson Nutrition and genetics: an expanding frontier: Robert H Herman Memorial Award in Clinical Nutrition Lecture, 2002 Am. J. Clinical Nutrition, August 1, 2003; 78(2): 201 - 208. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. E. Olson The Key to an Enigma: How Do Dietary Polyunsaturated Fatty Acids Lower Serum Cholesterol? J. Nutr., January 1, 2002; 132(1): 134 - 135. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
