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Research Article Free access | 10.1172/JCI105509
Department of Medicine, University of Washington School of Medicine, Seattle, Wash.
Department of Medicine, New York University School of Medicine, New York, N. Y.
†Established Investigator, American Heart Association. Address requests for reprints to Dr. Peter O. Ways, Dept. of Medicine, University of Washington School of Medicine, Seattle, Wash. 98105.
‡Supported by U. S. Public Health Service Career Development Award K3-HE-14-828.
§Present address: Dept. of Medicine, Veterans Administration Hospital, Richmond, Va.
ǁSupported by an indirect traineeship in gastroenterology (2A-5099) from the National Institute of Arthritis and Metabolic Diseases.
¶Supported by a Career Research Award (K6-3449) from the U. S. Public Health Service.
*Submitted for publication February 21, 1966; accepted September 15, 1966.
This work was supported by funds from the American Heart Association, provided in part by the Washington State Heart Association, and by U. S. Public Health Service grants HE 07326, AM HD 08864, NCI-4320, and 5RO1 HE 06481.
A portion of this work was conducted through the Clinical Research facility of the University of Washington (National Institutes of Health grant FR-37).
Find articles by Ways, P. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Washington School of Medicine, Seattle, Wash.
Department of Medicine, New York University School of Medicine, New York, N. Y.
†Established Investigator, American Heart Association. Address requests for reprints to Dr. Peter O. Ways, Dept. of Medicine, University of Washington School of Medicine, Seattle, Wash. 98105.
‡Supported by U. S. Public Health Service Career Development Award K3-HE-14-828.
§Present address: Dept. of Medicine, Veterans Administration Hospital, Richmond, Va.
ǁSupported by an indirect traineeship in gastroenterology (2A-5099) from the National Institute of Arthritis and Metabolic Diseases.
¶Supported by a Career Research Award (K6-3449) from the U. S. Public Health Service.
*Submitted for publication February 21, 1966; accepted September 15, 1966.
This work was supported by funds from the American Heart Association, provided in part by the Washington State Heart Association, and by U. S. Public Health Service grants HE 07326, AM HD 08864, NCI-4320, and 5RO1 HE 06481.
A portion of this work was conducted through the Clinical Research facility of the University of Washington (National Institutes of Health grant FR-37).
Find articles by Parmentier, C. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Washington School of Medicine, Seattle, Wash.
Department of Medicine, New York University School of Medicine, New York, N. Y.
†Established Investigator, American Heart Association. Address requests for reprints to Dr. Peter O. Ways, Dept. of Medicine, University of Washington School of Medicine, Seattle, Wash. 98105.
‡Supported by U. S. Public Health Service Career Development Award K3-HE-14-828.
§Present address: Dept. of Medicine, Veterans Administration Hospital, Richmond, Va.
ǁSupported by an indirect traineeship in gastroenterology (2A-5099) from the National Institute of Arthritis and Metabolic Diseases.
¶Supported by a Career Research Award (K6-3449) from the U. S. Public Health Service.
*Submitted for publication February 21, 1966; accepted September 15, 1966.
This work was supported by funds from the American Heart Association, provided in part by the Washington State Heart Association, and by U. S. Public Health Service grants HE 07326, AM HD 08864, NCI-4320, and 5RO1 HE 06481.
A portion of this work was conducted through the Clinical Research facility of the University of Washington (National Institutes of Health grant FR-37).
Find articles by Kayden, H. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Washington School of Medicine, Seattle, Wash.
Department of Medicine, New York University School of Medicine, New York, N. Y.
†Established Investigator, American Heart Association. Address requests for reprints to Dr. Peter O. Ways, Dept. of Medicine, University of Washington School of Medicine, Seattle, Wash. 98105.
‡Supported by U. S. Public Health Service Career Development Award K3-HE-14-828.
§Present address: Dept. of Medicine, Veterans Administration Hospital, Richmond, Va.
ǁSupported by an indirect traineeship in gastroenterology (2A-5099) from the National Institute of Arthritis and Metabolic Diseases.
¶Supported by a Career Research Award (K6-3449) from the U. S. Public Health Service.
*Submitted for publication February 21, 1966; accepted September 15, 1966.
This work was supported by funds from the American Heart Association, provided in part by the Washington State Heart Association, and by U. S. Public Health Service grants HE 07326, AM HD 08864, NCI-4320, and 5RO1 HE 06481.
A portion of this work was conducted through the Clinical Research facility of the University of Washington (National Institutes of Health grant FR-37).
Find articles by Jones, J. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Washington School of Medicine, Seattle, Wash.
Department of Medicine, New York University School of Medicine, New York, N. Y.
†Established Investigator, American Heart Association. Address requests for reprints to Dr. Peter O. Ways, Dept. of Medicine, University of Washington School of Medicine, Seattle, Wash. 98105.
‡Supported by U. S. Public Health Service Career Development Award K3-HE-14-828.
§Present address: Dept. of Medicine, Veterans Administration Hospital, Richmond, Va.
ǁSupported by an indirect traineeship in gastroenterology (2A-5099) from the National Institute of Arthritis and Metabolic Diseases.
¶Supported by a Career Research Award (K6-3449) from the U. S. Public Health Service.
*Submitted for publication February 21, 1966; accepted September 15, 1966.
This work was supported by funds from the American Heart Association, provided in part by the Washington State Heart Association, and by U. S. Public Health Service grants HE 07326, AM HD 08864, NCI-4320, and 5RO1 HE 06481.
A portion of this work was conducted through the Clinical Research facility of the University of Washington (National Institutes of Health grant FR-37).
Find articles by Saunders, D. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Washington School of Medicine, Seattle, Wash.
Department of Medicine, New York University School of Medicine, New York, N. Y.
†Established Investigator, American Heart Association. Address requests for reprints to Dr. Peter O. Ways, Dept. of Medicine, University of Washington School of Medicine, Seattle, Wash. 98105.
‡Supported by U. S. Public Health Service Career Development Award K3-HE-14-828.
§Present address: Dept. of Medicine, Veterans Administration Hospital, Richmond, Va.
ǁSupported by an indirect traineeship in gastroenterology (2A-5099) from the National Institute of Arthritis and Metabolic Diseases.
¶Supported by a Career Research Award (K6-3449) from the U. S. Public Health Service.
*Submitted for publication February 21, 1966; accepted September 15, 1966.
This work was supported by funds from the American Heart Association, provided in part by the Washington State Heart Association, and by U. S. Public Health Service grants HE 07326, AM HD 08864, NCI-4320, and 5RO1 HE 06481.
A portion of this work was conducted through the Clinical Research facility of the University of Washington (National Institutes of Health grant FR-37).
Find articles by Rubin, C. in: JCI | PubMed | Google Scholar
Published January 1, 1967 - More info
The nature of the gastrointestinal absorptive defect for triglyceride in three subjects with abetalipoproteinemia has been investigated by studying peroral biopsies of the gastrointestinal mucosa. The following conclusions were reached.
1) In confirmation of other studies, the abnormal vacuoles within the duodenal absorptive cells of these individuals were lipophilic.
2) On chemical analysis there was significantly more mucosal lipid than found in normal fasting specimens, and almost the entire increase was due to triglyceride.
3) This excess mucosal lipid was reduced by a low fat diet, but even after 34 days on such a diet there was still an excess of lipophilic material near the villus tip and increased quantities of total lipid and triglyceride when compared with material from normal subjects similarly treated.
4) Although there are demonstrable qualitative changes in mucosal and plasma lipids after an acute fat load, they are not quantitatively as great as in normal individuals. Fat balance studies and the qualitative changes in plasma and tissue lipids that do occur after more extended periods on different types of dietary fat do indicate that a considerable percentage of the dietary fat is assimilated. The route by which it is absorbed remains to be clarified.
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