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Articles in PresS, published online ahead of print October 22, 2001
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00116.2001
Submitted on March 13, 2001
Accepted on October 3, 2001
1 Medicine, University of Rochester, Rochester, New York, USA
2 Medicine, University of Rochester, Rochester, New York, USA; Physiology and Pharmacology, University of Rochester, Rochester, New York, USA
3 Pediatrics, Baylor College of Medicine, Houston, Texas, USA
* To whom correspondence should be addressed. E-mail: johngerich{at}compuserve.com.
Release of glucose by the kidney in postabsorptive normal humans is generally regarded as being wholly due to gluconeogenesis. Although lactate is the most important systemic gluconeogenic precursor and there is appreciable net renal lactate uptake, renal lactate gluconeogenesis has not as yet been investigated. The present studies were therefore undertaken to quantitate the contribution of lactate to renal gluconeogenesis and the role of the kidney in lactate metabolism. We determined systemic and renal lactate conversion to glucose as well as renal lactate net balance, fractional extraction, uptake and release in 24 postabsorptive humans using a combination of isotopic and renal balance techniques. For comparative purposes accumulated similar data for glutamine, alanine and glycerol are also reported. Systemic lactate gluconeogenesis (1.97 ±0.12 µmol*kg-1*min-1) was about threefold greater than that from glycerol, glutamine and alanine. The sum of gluconeogenesis from these precursors, uncorrected for Krebs cycle carbon exchange, explained 34 % of systemic glucose release. Renal lactate uptake (3.33 ±0.28 µmol*kg-1*min-1) accounted for nearly 30 % of its systemic turnover. Renal gluconeogenesis from lactate (0.78 ±0.10 µmol*kg-1*min-1) was 3.5, 2.5 and 9.6 fold greater than that from glycerol, glutamine and alanine. The sum of renal gluconeogenesis from these precursors equaled about 40 % of the sum of their systemic gluconeogenesis. When the isotopically determined rates of systemic and renal gluconeogenesis were corrected for Krebs cycle carbon exchange, gluconeogenesis from these precursors accounted for 43 % of systemic glucose release and 89 % of renal glucose release. Conclusions: 1) in postabsorptive normal humans lactate is the dominant precursor for both renal and systemic gluconeogenesis; 2) the kidney is an important organ for lactate disposal; 3) under these conditions renal glucose release is predominantly if not exclusively due to gluconeogenesis; and 4) liver and kidney are similarly important for systemic gluconeogenesis.
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