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Functional capacity of adipose tissue in human obesity and hyperlipidaemia

Published online by Cambridge University Press:  24 July 2007

J Tremolieres ,
CL Sautier ,
L Carre ,
CL Flament  and
B Plumas
J Tremolieres
Affiliation:
Laboratoire de Nutrition Humaine de I'Inserm, Hospital Bichat, Paris, France
CL Sautier
Affiliation:
Laboratoire de Nutrition Humaine de I'Inserm, Hospital Bichat, Paris, France
L Carre
Affiliation:
Laboratoire de Nutrition Humaine de I'Inserm, Hospital Bichat, Paris, France
CL Flament
Affiliation:
Laboratoire de Nutrition Humaine de I'Inserm, Hospital Bichat, Paris, France
B Plumas
Affiliation:
Laboratoire de Nutrition Humaine de I'Inserm, Hospital Bichat, Paris, France
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Abstract

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1. Fifteen ‘constitutionally’ obese subjects, eleven hyperlipidaemic subjects of mixed-type and fourteen normal subjects were studied.

2. With a reduction in energy intake (range 3.3–4.2 MJ) for 21 d, there was no change in the levels of plasma total cholesterol (TC) and triglyceride (TG) of obese subjects, but the free fatty acid levels increased. However, in hyperlipidaemic subjects there was a reduction in levels of TC and TG with no increase in levels of free fatty acids.

3. There was a significant increase in the serum ketone levels of obese subjects but not in those of hyperlipidaemic subjects. The reduction of the respiratory quotient to a value of 0.7 was more rapid in the obese than in hyperlipidaemic subjects.

4. After administration of a fat load (0.5 g/kg gross body-weight) there was no change in plasma TG levels in obese subjects but there was an increase in those of normal subjects.

5. After administration of a glucose load (1 g/kg ideal body-weight) there was a significant reduction in plasma TG levels in obese subjects but no change in those of hyperlipidaemic subjects.

6. Hyperlipidaemic subjects eating their normal diet were found to have a hydroxybutyrate: acetoacetate ratio three- to fivefold that of obese and normal subjects.

7. These results suggest that obese subjects have an increased ability to store fatty acids, to mobilize them quickly and to generate fatty acid metabolites in the form of ketone bodies, while these same metabolic functions are reduced in hyperlipidaemic subjects.

Type
Clinical and Human Nutrition
Information
British Journal of Nutrition , Volume 32 , Issue 2 , September 1974 , pp. 273 - 282
Copyright
Copyright © The Nutrition Society 1974

References

REFERENCES

Barter, P. J. & Nestel, P. J. (1972). J. Lipid Res. 13, 483.Google Scholar
Barter, P., Nestel, P. & Carrol, K. (1972). Metabolism 21, 117.CrossRefGoogle Scholar
Cahill, G. F. jr, Owen, O. E. & Morgan, A. P. (1968). In Advances in Enzyme Regulation Vol. 6, p. 143 [Weber, J., editor]. London: Pergamon Press.Google Scholar
Debry, G., Laurent, J., Drouin, P., Méjean, L., Gonand, J. & Cherrier, P. (1969). Journées Diabétol., Hotel-Dieu p. 225.Google Scholar
Duncombe, W. G. (1963). Biochem. J. 88, 7.CrossRefGoogle Scholar
Duncombe, W. G. (1964). Clinica chim. Acta 9, 122.CrossRefGoogle Scholar
Geigy, J. R. (1959). Statist. Bull. Metropolitan Life Insurance Co. Vol. 40.Google Scholar
Hohorst, H. J., Kreutz, F. H. & Biicher, Th. (1959). Biochem. 2. 332, 18.Google Scholar
Kekwick, A. & Pawan, G. L. S. (1957). Metabolism 6, 447.Google Scholar
Keston, A. S. (1956). Proc. 129th Meet. Am. Chem. Soc., Dallas, p. 310. Washington, DC: Americand Chemical Society Publications.Google Scholar
Lees, R. S. & Hatch, F. T. (1963). J. Lab. clin. Med. 61, 518.Google Scholar
Lowy, R. & Manchon, Ph. (1968–1969). In Eléments de Statistiqzces Applique's d la Biologie, Vol. 1–3. Paris: Olivetti.Google Scholar
Noble, R. P. (1968). J. Lipid Res. 9, 693.CrossRefGoogle Scholar
Pfleiderer, G. (1965). In Methods of Enzyme Analysis, p. 378 [Bergmeyer, H. U., editor]. Weinheim, W. Germany: Verlag Chemie GmbH.CrossRefGoogle Scholar
Schmidt, F. H. & von Dahl, K. (1968). Z. clin. Chem. 6, 156.Google Scholar
Tamir, I., Grant, D. B., Fosbrooke, A. S., Segall, M. M. & Lloyd, J. K. (1968). J. Lipid Res. 9, 661.CrossRefGoogle Scholar
Trémolières, J. (1973). Proc. Nutr. Soc. 32, 169.CrossRefGoogle Scholar
Trémolières, J., Dontcheff, L. & Huot, A. (1966). J. Physiol., Paris 58, 655.Google Scholar
Waterhouse, C. & Kemperman, J. H. (1966). J. Lab. clin. Med. 68, 250.Google Scholar
Waterhouse, C., Baker, N. & Rostami, H. (1969). J. Lipid Res. 10, 487.CrossRefGoogle Scholar
Williamson, D. H., Mellanby, J. & Krebs, H. A. (1962). Biochem. J. 82, 90.Google Scholar
Zöllner, N. & Kirsch, K. (1962). Z. ges. exp. Med. 135, 545.CrossRefGoogle Scholar