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Research Article Free access | 10.1172/JCI105564
New England Medical Center Hospitals, Boston, Mass.
Department of Medicine, Tufts University School of Medicine, Boston, Mass.
†Fellowship from National Institute of Arthritis and Metabolic Diseases 1965 to 1966, grant AM-29,650.
*Submitted for publication May 5, 1966; accepted December 30, 1966.
Supported by U. S. Public Health Service grants AM-612 and AM 9897.
Part of this work has been reported in abstract form (J. clin. Invest. 1966, 45, 1010).
Find articles by Galton, D. in: JCI | PubMed | Google Scholar
New England Medical Center Hospitals, Boston, Mass.
Department of Medicine, Tufts University School of Medicine, Boston, Mass.
†Fellowship from National Institute of Arthritis and Metabolic Diseases 1965 to 1966, grant AM-29,650.
*Submitted for publication May 5, 1966; accepted December 30, 1966.
Supported by U. S. Public Health Service grants AM-612 and AM 9897.
Part of this work has been reported in abstract form (J. clin. Invest. 1966, 45, 1010).
Find articles by Bray, G. in: JCI | PubMed | Google Scholar
Published April 1, 1967 - More info
Epinephrine stimulated lipolysis and the uptake of oxygen by subcutaneous adipose cells of man. When glucose-14C was present in the medium, its utilization was not increased by epinephrine, although lipolysis was accelerated. Insulin did not reduce the production of fatty acids that had been stimulated by epinephrine.
The combination of human growth hormone and cortisol stimulated the production of fatty acids by isolated human adipose cells to a lesser extent than epinephrine. When human growth hormone or cortisol was used singly, or when bovine growth hormone was added in combination with cortisol, no effect on fatty acid production was observed. Furthermore, an acetone-dried preparation of human pituitary glands, which was shown to stimulate lipolysis in rat adipose cells, had no effect on fatty acid formation in human adipose cells. This suggested that the human pituitary gland contained no more potent lipolytic agents than growth hormone and was supported by the lack of response of human adipose cells to purified corticotropin.