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AJP - Endocrinology and Metabolism, Vol 271, Issue 5 E814-E820, Copyright © 1996 by American Physiological Society
ARTICLES |
C. L. Stunff and P. F. Bougneres
Institut National de la Sante et de la Recherche Medicale Unite 342, Rene Descartes University, Hopital Saint Vincent de Paul, Paris, France.
Using a double stable isotope infusion method, we quantified plasma glucose and lactate inter-relationships in five recently obese children. Compared with five age-matched controls, obese children had an approximately 50% increase of total body lactate turnover [167 +/- 20 vs. 111 +/- 20 (SE) mg/min, P < 0.05]. The rate of lactate conversion to glucose was double the normal rate (96 +/- 21 vs. 46 +/- 10 mg/min, P < 0.05). Increased gluconeogenesis from plasma lactate correlated with total glucose production (r = 0.74), with plasma lactate contributing to 58% of glucose production in obese children vs. 38% in normal children (P < 0.05). Conversion into glucose correlated with the rate of lactate release in the circulation (r = 0.76). In turn, the obese children converted a larger fraction (35 +/- 2 vs. 27 +/- 2%, P < 0.02) and amount (58 +/- 10 vs. 34 +/- 5 mg/min, P < 0.05) of glucose into plasma lactate. The amount of lactate originating from plasma glucose correlated (r = 0.70) with lipid oxidation, which was increased in the obese children (58 +/- 4 vs. 23 +/- 5 mg/min, P < 0.02). Our data suggest that increased gluconeogenesis from lactate is associated with increased lipid oxidation and could contribute to the progressive development of insulin resistance and glucose intolerance in juvenile obesity.
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