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Research Article Free access | 10.1172/JCI105503
Division of Metabolism, Department of Medicine, Washington University School of Medicine, St. Louis, Mo.
†Trainee in metabolism, supported by U. S. Public Health Service grant AM 5027. Present address: University of Colorado School of Medicine, Denver, Colo.
‡Address requests for reprints to Dr. William H. Daughaday, Dept. of Medicine, Washington University School of Medicine, St. Louis, Mo. 63110.
*Submitted for publication June 30, 1966; accepted September 28, 1966.
Supported by research grant AM 5105, National Institutes of Arthritis and Metabolic Diseases, and grant 5MO1-FR-36, Division of General Medical Sciences, National Institutes of Health.
Find articles by Beck, P. in: JCI | PubMed | Google Scholar
Division of Metabolism, Department of Medicine, Washington University School of Medicine, St. Louis, Mo.
†Trainee in metabolism, supported by U. S. Public Health Service grant AM 5027. Present address: University of Colorado School of Medicine, Denver, Colo.
‡Address requests for reprints to Dr. William H. Daughaday, Dept. of Medicine, Washington University School of Medicine, St. Louis, Mo. 63110.
*Submitted for publication June 30, 1966; accepted September 28, 1966.
Supported by research grant AM 5105, National Institutes of Arthritis and Metabolic Diseases, and grant 5MO1-FR-36, Division of General Medical Sciences, National Institutes of Health.
Find articles by Daughaday, W. in: JCI | PubMed | Google Scholar
Published January 1, 1967 - More info
The acute metabolic effects and disposition of human placental lactogen (HPL) have been studied in 15 men and 8 women during continuous intravenous infusions. The mean plasma half-life, metabolic pool size, and turnover rate of HPL are comparable to the values previously reported for human growth hormone (HGH). From the data presented, we calculate that the placenta secretes approximately 290 mg HPL daily at term.
After 12-hour infusions of HPL in physiologic amounts, impairment of glucose tolerance despite increased plasma insulin responses to glucose was observed in 7 of 8 subjects tested. However, HPL, unlike HGH, did not produce significant changes in blood glucose, plasma insulin, or plasma free fatty acid concentrations in fasting subjects before glucose administration or in carbohydrate tolerance or plasma insulin responses to glucose during 5-hour infusions. These findings are compatible with the thesis that HPL is a physiologic antagonist to insulin during pregnancy.