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Journal of Clinical Endocrinology & Metabolism Vol. 27, No. 11 1573-1580
doi:10.1210/jcem-27-11-1573
Copyright © 1967 by the Endocrine Society.
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Metabolism of {alpha}-Glycerol Phosphate in Human Adipose Tissue in Obesity1

DAVID J. GALTON and GEORGE A. BRAY2

New England Medical Center Hospitals and the Department of Medicine, Tufts University School of Medicine Boston, Massachusetts 02111

  1. 1. Experiments were carried out to examine the possibility that a metabolic defect underlies the development of some types of obesity in man. Glycerol phosphate, which is an obligatory acyl acceptor for lipogenesis in human adipose tissue, is formed by a cytoplasmic L-aglycerophosphate dehydrogenase whose activity in adipose tissue of lean and obese patients was, respectively: 36 ± 4 (7)3 and 20 ± 2 (7) mµxmoles NADH/min/mg protein (p <.01).
  2. 2. {alpha}-Glycerol phosphate can be oxidized by mitochondria of human adipose tissue at a rate of: 14.2 ± 2.2 (8) and 6.9 ± 1.8 (7) µl O2/30 min/mg protein in lean and obese patients, respectively (p < 0.02). Since {alpha}-glycerol phosphate is present oxidation of {alpha}-glycerol phosphate by mitochondria contributes in part to the development of obesity by increasing the supply of {alpha}-glycerol phosphate for lipogenesis.
  3. 3. Not all obese patients displayed this mitochondrial deficiency. Three patients were studied in whom an intracranial lesion was possibly responsible for the weight gain. Comparisons of the rates of mitochondrial oxidation of {alpha}-glycerol phosphate between this group and 3 obese controls adjacent in the series were: 6.5 ± 2.1 (3) and 2.7 ± 1.5 (3) (p > 0.1). These values suggest that the metabolism of {alpha}-glycerol phosphate may be different in the former type of obesity.

1 Part of this work has been presented in a preliminary communication (29).

2 Send reprint requests to George Bray, 171 Harrison Ave., Boston, Mass. 02111.

Received April 27, 1967.

Accepted July 24, 1967.






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Copyright © 1967 by The Endocrine Society