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Carbohydrate utilization in obese subjects after an oral load of 100 g naturally-labelled [13C] glucose

Published online by Cambridge University Press:  25 February 2008

E. Ravussin ,
Annelise Doerner ,
K. J. Acheson ,
P. Pahud ,
M. J. Arnaud  and
E. Jéquier
E. Ravussin
Affiliation:
Institute of Clinical Physiology, 7 Rue du Bugnon, 1011 Lausanne, Switzerland and Nestlé Laboratory, 1814 La Tour-de-Peilz, Switzerland
Annelise Doerner
Affiliation:
Institute of Clinical Physiology, 7 Rue du Bugnon, 1011 Lausanne, Switzerland and Nestlé Laboratory, 1814 La Tour-de-Peilz, Switzerland
K. J. Acheson
Affiliation:
Institute of Clinical Physiology, 7 Rue du Bugnon, 1011 Lausanne, Switzerland and Nestlé Laboratory, 1814 La Tour-de-Peilz, Switzerland
P. Pahud
Affiliation:
Institute of Clinical Physiology, 7 Rue du Bugnon, 1011 Lausanne, Switzerland and Nestlé Laboratory, 1814 La Tour-de-Peilz, Switzerland
M. J. Arnaud
Affiliation:
Institute of Clinical Physiology, 7 Rue du Bugnon, 1011 Lausanne, Switzerland and Nestlé Laboratory, 1814 La Tour-de-Peilz, Switzerland
E. Jéquier
Affiliation:
Institute of Clinical Physiology, 7 Rue du Bugnon, 1011 Lausanne, Switzerland and Nestlé Laboratory, 1814 La Tour-de-Peilz, Switzerland
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Abstract

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1. Total carbohydrate (CHO) and ingested glucose oxidation was measured in five obese subjects with normal glucose tolerance after an oral load of 100g naturally-labelled [13C]glucose using indirect calorimetry and mass spectrometry respectively.

2. CHO utilization rate (107 ± 14 mg/min in the post-absorptive state) increased 30 min after the glucose load to reach a plateau (245±25 mg/min) between 90 and 120 min. It then decreased to basal values at 330 min. Cumulative CHO oxidation over 480 min was 66±7 g and the CHO oxidized above basal levels was 26 ± 7g.

3. Enrichment of expired carbon dioxide with 13c began at 45 min and maximum values were observed between 210 and 300 min. At 480 min, cumulative oxidation of the ingested glucose was 24± 2 g.

4. Compared with controls, the obese subjects exhibit an impairment of CHO utilization which precedes glucose intolerance. This impairment can be explained by an increased availability of free fatty acids which favours lipid oxidation at the expense of ingested [13C]glucose oxidation.

Type
Papers of direct relevance to Clinical and Human Nutrition
Information
British Journal of Nutrition , Volume 43 , Issue 2 , March 1980 , pp. 281 - 288
Copyright
Copyright © The Nutrition Society 1980

References

Acheson, K. J., Flatt, J. P. & Jéquier, E. (1979). Proceedings of the Fifth international Meeting of Endocrinology: Diabetes and Obesity, Marseille, 06 1978. Amsterdam: Excerpta Media.Google Scholar
Björntorp, P. & Sjöström, L. (1978). Metabolism 27, 1853.CrossRefGoogle Scholar
Ebiner, J. R., Acheson, K. J., Doemer, A., Maeder, E., Amaud, M. J., Jéuier, E. & Felber, J. P. (1979). Br. J. Nutr. 41, 419.CrossRefGoogle Scholar
Fajans, S. S. & Conn, J. W. (1965). In On the Nature and Treatment of Diabetes, p. 641 [Leibel, B. S. and Wrenshall, G. A., editors]. Amsterdam: Excerpta Media Foundation.Google Scholar
Felber, J. P., Magnenat, G., Casthelaz, M., Geser, C. A., Miiller-Has, R., de Kalbermatten, N., Ebiner, J. R., Curchod, B., Pittet, Ph. & Jéuier, E. (1977). Diabetes 26, 693.CrossRefGoogle Scholar
Felig, P., Wahren, J. & Hendler, R. (1975). Diabetes 24, 468.CrossRefGoogle Scholar
Gomez, F., Jéuier, E., Chabot, V., Büber, V. & Felber, J. P. (1972). Metabolism 21, 381.CrossRefGoogle Scholar
Goodman, M. N., Berger, M. & Ruderman, N. B. (1974). Diabetes 23, 881.CrossRefGoogle ScholarPubMed
Hales, C. N. & Randle, P. J. (1963). Biochem. J. 88, 137.CrossRefGoogle Scholar
Heindel, J. J., Cushman, S. W. & Jeanrenaud, B. (1974). Am. J. Physiol. 226, 16.CrossRefGoogle Scholar
Jefferson, L. S., Koehler, J. O. & Morgan, H. E. (1972). Proc. Natl Acad. Sci. U.S.A. 69, 816.CrossRefGoogle Scholar
Krebs, H. A., Hems, R., Weidmann, M. J. & Speake, R. N. (1966). Biochem. J. 101, 242.CrossRefGoogle Scholar
Lefébvre, P., Mosora, F., Lacroix, M., Luyckx, A., Lopez-Habib, G. & Duchesne, J. (1975). Diabetes 24, 185.CrossRefGoogle ScholarPubMed
Lusk, G. (1924). J. biol. Chem. 59, 41.CrossRefGoogle Scholar
Metropolitan Life Insurance Company (1959). Stat. Bull. 4, 40.Google Scholar
Morse, W. I., Sidorov, J. J., Soeldner, J. S. & Dickson, C. (1960). Metabolism 9, 666.Google ScholarPubMed
Ogilvie, R. F. (1935). Q. Jl Med. 3, 345.Google Scholar
Passmore, R. & Swindells, E. (1963). Br. J. Nutr. 17, 331.CrossRefGoogle Scholar
Pittet, Ph., Chappuis, P., Acheson, K. J., de Techtermann, F. & Jéuier, E. (1976). Br. J. Nutr. 35, 281.CrossRefGoogle Scholar
Randle, P. J., Garland, P. B., Hales, C. N. & Newsholme, E. A. (1963). Lancet i, 785.CrossRefGoogle Scholar
Ravussin, E., Pahud, P., Doerner, A., Amaud, M. & Jéquier, E. (1979). Pflügers Arch. 382, 197.CrossRefGoogle Scholar
Rennie, M. J. & Holloszy, J. O. (1979). Biochem. J. 168, 161.CrossRefGoogle Scholar
Shreeve, W. W. (1965). Ann. N.Y. Acad. Sci. 131, 464.CrossRefGoogle Scholar
Shreeve, W. W., Hoshi, M., Oji, N., Shigeta, Y. & Abe, H. (1968). Am. J. clin. Nutr. 21, 1404.CrossRefGoogle Scholar
Slein, M. W. (1965). In Methods of Enzymatic Analysis, 2nd ed., p. 117 [Bergmeyer, H. W., editor]. Weinheim: Verlag Chemie.CrossRefGoogle Scholar
Smith, B. N. & Epstein, S. (1971). Plant Physiol. 47, 380.CrossRefGoogle Scholar
Streja, D. A., Steiner, G., Marliss, E. B. & Vranic, M. (1977). Metabolism 26, 1089.CrossRefGoogle Scholar
Vranic, M. (1973). Fedn Proc. Fedn Am. Socs exp. Biol. 33, 1837.Google Scholar