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Research Article Free access | 10.1172/JCI105666

Role of Insulin in Endogenous Hypertriglyceridemia

Gerald M. Reaven, Roger L. Lerner, Michael P. Stern, and John W. Farquhar

Department of Medicine, Stanford University School of Medicine, Palo Alto, California

‡

Postdoctoral Research Fellow, U. S. Public Health Service, currently U. S. Army.

§

Postdoctoral Research Fellow, U. S. Public Health Service, Stanford University School of Medicine, Palo Alto, Calif.

Address requests for reprints to Dr. Gerald M. Reaven, Stanford University School of Medicine, Palo Alto, Calif, 94304.

*

Received for publication 8 May 1967 and in revised form 5 July 1967.

Presented in part at the 48th meeting of the Endocrine Society, 27 June 1966.

Supported in part by the U. S. Public Health Service Research Grants AM 05972 and HE 08506 from the National Institutes of Health, K3-HE 6003 from the Career Development Review Branch, FR-70 from the General Clinical Research Centers Branch, Division of Research Facilities and Resources, and Pfizer Laboratories, Division, Chas. Pfizer and Co., Inc., New York.

Find articles by Reaven, G. in: JCI | PubMed | Google Scholar

Department of Medicine, Stanford University School of Medicine, Palo Alto, California

‡

Postdoctoral Research Fellow, U. S. Public Health Service, currently U. S. Army.

§

Postdoctoral Research Fellow, U. S. Public Health Service, Stanford University School of Medicine, Palo Alto, Calif.

Address requests for reprints to Dr. Gerald M. Reaven, Stanford University School of Medicine, Palo Alto, Calif, 94304.

*

Received for publication 8 May 1967 and in revised form 5 July 1967.

Presented in part at the 48th meeting of the Endocrine Society, 27 June 1966.

Supported in part by the U. S. Public Health Service Research Grants AM 05972 and HE 08506 from the National Institutes of Health, K3-HE 6003 from the Career Development Review Branch, FR-70 from the General Clinical Research Centers Branch, Division of Research Facilities and Resources, and Pfizer Laboratories, Division, Chas. Pfizer and Co., Inc., New York.

Find articles by Lerner, R. in: JCI | PubMed | Google Scholar

Department of Medicine, Stanford University School of Medicine, Palo Alto, California

‡

Postdoctoral Research Fellow, U. S. Public Health Service, currently U. S. Army.

§

Postdoctoral Research Fellow, U. S. Public Health Service, Stanford University School of Medicine, Palo Alto, Calif.

Address requests for reprints to Dr. Gerald M. Reaven, Stanford University School of Medicine, Palo Alto, Calif, 94304.

*

Received for publication 8 May 1967 and in revised form 5 July 1967.

Presented in part at the 48th meeting of the Endocrine Society, 27 June 1966.

Supported in part by the U. S. Public Health Service Research Grants AM 05972 and HE 08506 from the National Institutes of Health, K3-HE 6003 from the Career Development Review Branch, FR-70 from the General Clinical Research Centers Branch, Division of Research Facilities and Resources, and Pfizer Laboratories, Division, Chas. Pfizer and Co., Inc., New York.

Find articles by Stern, M. in: JCI | PubMed | Google Scholar

Department of Medicine, Stanford University School of Medicine, Palo Alto, California

‡

Postdoctoral Research Fellow, U. S. Public Health Service, currently U. S. Army.

§

Postdoctoral Research Fellow, U. S. Public Health Service, Stanford University School of Medicine, Palo Alto, Calif.

Address requests for reprints to Dr. Gerald M. Reaven, Stanford University School of Medicine, Palo Alto, Calif, 94304.

*

Received for publication 8 May 1967 and in revised form 5 July 1967.

Presented in part at the 48th meeting of the Endocrine Society, 27 June 1966.

Supported in part by the U. S. Public Health Service Research Grants AM 05972 and HE 08506 from the National Institutes of Health, K3-HE 6003 from the Career Development Review Branch, FR-70 from the General Clinical Research Centers Branch, Division of Research Facilities and Resources, and Pfizer Laboratories, Division, Chas. Pfizer and Co., Inc., New York.

Find articles by Farquhar, J. in: JCI | PubMed | Google Scholar

Published November 1, 1967 - More info

Published in Volume 46, Issue 11 on November 1, 1967
J Clin Invest. 1967;46(11):1756–1767. https://doi.org/10.1172/JCI105666.
© 1967 The American Society for Clinical Investigation
Published November 1, 1967 - Version history
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Abstract

Dietary carbohydrate accentuation of endogenous triglyceride production has been studied in 33 patients. A broad and relatively continuous spectrum of steady-state plasma triglyceride concentrations was produced in 31 of the 33 subjects during 3 wk of a high carbohydrate (fat-free) liquid formula diet. Two patients developed plasma triglyceride concentrations in excess of 2000 mg/100 ml, and these were the only patients we have studied in which carbohydrate induction of hypertriglyceridemia seemed to be associated with a defect in endogenous plasma triglyceride removal mechanisms. In the remaining 31 patients the degree of hypertriglyceridemia was highly correlated with the insulin response elicited by the ingestion of the high carbohydrate formula (P < 0.005). No significant correlation existed between fasting plasma triglyceride concentration and either plasma glucose or free fatty acid concentrations after the high carbohydrate diet, nor was the degree of hypertriglyceridemia related to degree of obesity. It is suggested that hypertriglyceridemia in most subjects results from an increase in hepatic triglyceride secretion rate secondary to exaggerated postprandial increases in plasma insulin concentration.

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