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Research Article Free access | 10.1172/JCI105526
Department of Medicine, Medical College of Virginia, Richmond, Va.
†Address requests for reprints to Dr. William R. Harlan, Medical College of Virginia, Richmond 19, Va.
‡Recipient of a summer fellowship from the Richmond Area Heart Association.
*Submitted for publication June 20, 1966; accepted October 27, 1966.
Supported by U. S. Public Health Service grants HO 7364 and FR 0065 from the General Clinical Research Center.
A partial report of this work was read before the Southern Society for Clinical Investigation, January 28, 1966.
Find articles by Harlan, W. in: JCI | PubMed | Google Scholar
Department of Medicine, Medical College of Virginia, Richmond, Va.
†Address requests for reprints to Dr. William R. Harlan, Medical College of Virginia, Richmond 19, Va.
‡Recipient of a summer fellowship from the Richmond Area Heart Association.
*Submitted for publication June 20, 1966; accepted October 27, 1966.
Supported by U. S. Public Health Service grants HO 7364 and FR 0065 from the General Clinical Research Center.
A partial report of this work was read before the Southern Society for Clinical Investigation, January 28, 1966.
Find articles by Winesett, P. in: JCI | PubMed | Google Scholar
Department of Medicine, Medical College of Virginia, Richmond, Va.
†Address requests for reprints to Dr. William R. Harlan, Medical College of Virginia, Richmond 19, Va.
‡Recipient of a summer fellowship from the Richmond Area Heart Association.
*Submitted for publication June 20, 1966; accepted October 27, 1966.
Supported by U. S. Public Health Service grants HO 7364 and FR 0065 from the General Clinical Research Center.
A partial report of this work was read before the Southern Society for Clinical Investigation, January 28, 1966.
Find articles by Wasserman, A. in: JCI | PubMed | Google Scholar
Published February 1, 1967 - More info
Lipoprotein lipase activity (LLA) was measured in the adipose tissue of six healthy subjects and five members of a family in whom the trait for familial exogenous hypertriglyceridemia was segregating. The lipase activity measured was characteristic of lipoprotein lipase: increased by feeding, dependent on the presence of serum, and inhibited by sodium chloride and protamine sulfate. When compared with lipase activity in healthy individuals, LLA was grossly deficient in two siblings with postabsorptive chylomicronemia and was intermediate in both parents and one sibling, who had normal postabsorptive triglycerides. These findings are compatible with autosomal recessive inheritance. The hormone-sensitive lipolytic enzyme responsible for mobilization of free fatty acids from adipose storage was normal in the hyperlipemic subjects.
After a 104-g fat meal, the serum triglyceride increased more in subjects heterozygotic for LLA deficiency than in the healthy subjects, and there was a relatively greater increase in chylomicrons and very low density lipoproteins in the affected individuals. These observations demonstrate the physiologic importance of lipoprotein lipase in removal of these lipoprotein groups and further clarify the differences between endogenous and exogenous hypertriglyceridemia.