Alterations of plasma lactate and glucose metabolism in obese children

• Published in: The American journal of physiology Vol. 271; no. 5; pp. E814 - E820
• Main Authors: Le Stunff, C, Bougneres, P.F
• Format: Journal Article
• Language: English
• Published: United States 01-11-1996
• Subjects: 3-Hydroxybutyric Acid; Blood Glucose - metabolism; Calorimetry, Indirect; Carbon Isotopes; Child; Child, Preschool; Citric Acid Cycle; Deuterium; diet-related diseases; Fatty Acids, Nonesterified - blood; Gluconeogenesis; Glucose - metabolism; human nutrition; Humans; Hydroxybutyrates - blood; Insulin - blood; Lactates - blood; Lactates - metabolism; Lipolysis; Models, Biological; nutrition physiology; Obesity - blood; Obesity - metabolism; Reference Values; Weight Gain
• ISSN: 0002-9513; 2163-5773
• DOI: 10.1152/ajpendo.1996.271.5.E814

Using a double stable isotope infusion method, we quantified plasma glucose and lactate interrelationships 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.