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Alterations of plasma lactate and glucose metabolism in obese children
1Institut National de la Santé et de la Recherche Médicale Unité 342, René Descartes University, Hôpital Saint Vincent de Paul, Paris, France.
Insights
Recently obese children show significantly increased lactate turnover and conversion to glucose, contributing to higher glucose production and potentially driving insulin resistance. This highlights altered glucose metabolism in juvenile obesity.
Area of Science:
- Metabolic Research
- Pediatric Endocrinology
- Obesity Studies
Background:
- Juvenile obesity is a growing health concern.
- Understanding metabolic alterations in obese children is crucial for preventing long-term complications like insulin resistance and glucose intolerance.
Purpose of the Study:
- To quantify plasma glucose and lactate inter-relationships in recently obese children.
- To compare metabolic parameters between obese children and age-matched controls.
Main Methods:
- Utilized a double stable isotope infusion method for precise metabolic quantification.
- Measured total body lactate turnover, lactate conversion to glucose, and glucose production rates.
Main Results:
- Obese children exhibited a 50% increase in total body lactate turnover compared to controls.
- The rate of lactate conversion to glucose was doubled in obese children, with lactate contributing significantly more to glucose production.
- Obese children converted a larger fraction of glucose into lactate, which correlated with increased lipid oxidation.
Conclusions:
- Increased gluconeogenesis from lactate is a key metabolic feature in recently obese children.
- These metabolic shifts, including elevated lipid oxidation, may contribute to the development of insulin resistance and glucose intolerance in juvenile obesity.
Abstract:
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.