Determination of [<sup>14</sup>C] Glutamine Specific Activity in Plasma

Jenssen, Trond; Nurjhan, Nurjahan; Perriello, G.; Bucci, A.; Toft, Ingrid; Gerich, John E.

doi:10.1080/10826079408013767

Cited by 15 publications

(3 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The same applies to splanchnic balance studies, where blood flow is equally high and arteriovenous differences similarly small. Use of high-performance liquid chromatography (HPLC), which permits precise determination of arteriovenous differences in plasma concentrations and specific activities [24,25] has helped to minimize this problem.…”

Section: Methodological Considerationsmentioning

confidence: 99%

Renal glucose production and utilization: new aspects in humans

et al. 1997

View full text Add to dashboard Cite

Summary According to current textbook wisdom the liver is the exclusive site of glucose production in humans in the postabsorptive state. Although many animal and in vitro data have documented that the kidney is capable of gluconeogenesis, production of glucose by the human kidney in the postabsorptive state has generally been regarded as negligible. This traditional view is based on net balance measurements which, other than after a prolonged fast or during metabolic acidosis, showed no significant net renal glucose release. However, recent studies have refuted this view by combining isotopic and balance techniques, which have demonstrated that renal glucose production accounts for 25 % of systemic glucose production. Moreover, these studies indicate that glucose production by the human kidney is stimulated by epinephrine, inhibited by insulin and is excessive in diabetes mellitus. Since renal glucose release is largely, if not exclusively, due to gluconeogenesis, it is likely that the kidney is as important a gluconeogenic organ as the liver. The most important renal gluconeogenic precursors appear to be lactate, glutamine and glycerol. The implications of these recent findings on the understanding of the physiology and pathophysiology of human glucose metabolism are discussed. [Diabetologia (1997) 40: 749-757].

show abstract

Section: Methodological Considerationsmentioning

confidence: 99%

Renal glucose production and utilization: new aspects in humans

et al. 1997

View full text Add to dashboard Cite

show abstract

“…Whole blood glucose was immediately determined in triplicate with a glucose analyzer (Yellow Springs Instrument, Yellow Springs, OH). Plasma glutamine, glutamate, alanine, and FFA concentrations, as well as [ 3 H]and [ 14 C]glucose and [ 14 C]glutamine specific activities, were determined by high-performance liquid chromatography (17,28,30). Lactate and glycerol concentrations were measured by microfluorometric methods.…”

Section: Subjectsmentioning

confidence: 99%

Effects of physiological hyperinsulinemia on systemic, renal, and hepatic substrate metabolism

Meyer¹,

Dostou²,

Nadkarni³

et al. 1998

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

To determine the effect of physiological hyperinsulinemia on renal and hepatic substrate metabolism, we assessed systemic and renal glucose release and uptake, systemic and renal gluconeogenesis from glutamine, and certain aspects of systemic and renal glutamine and free fatty acid (FFA) metabolism. These were assessed under basal postabsorptive conditions and during 4-h hyperinsulinemic euglycemic clamp experiments in nine normal volunteers using a combination of isotopic techniques and renal balance measurements. Hepatic glucose release (HGR) and glutamine gluconeogenesis were calculated as the difference between systemic and renal measurements. Infusion of insulin suppressed systemic glucose release and glutamine gluconeogenesis by ∼50% during the last hour of the insulin infusion ( P < 0.001). Renal glucose release and glutamine gluconeogenesis decreased from 2.3 ± 0.4 to 0.9 ± 0.2 ( P < 0.002) and from 0.52 ± 0.07 to 0.14 ± 0.03 μmol ⋅ kg−1 ⋅ min−1( P < 0.001), respectively. HGR and glutamine gluconeogenesis decreased from 8.7 ± 0.4 to 4.5 ± 0.5 ( P < 0.001) and from 0.35 ± 0.02 to 0.27 ± 0.03 μmol ⋅ kg−1 ⋅ min−1( P < 0.002), respectively. Renal glucose uptake (RGU) increased from 1.61 ± 0.19 to 2.18 ± 0.25 μmol ⋅ kg−1 ⋅ min−1( P = 0.029) but accounted for only ∼5% of systemic glucose disposal (40.6 ± 4.3 μmol ⋅ kg−1 ⋅ min−1). Both systemic and renal FFA clearance increased approximately fourfold ( P < 0.001 for both). Nevertheless, renal FFA uptake decreased ( P = 0.024) and was inversely correlated with RGU ( r = −0.582, P = 0.011). Finally, insulin increased systemic glutamine release ( P = 0.007), uptake ( P < 0.005), and clearance ( P < 0.001) but left renal glutamine uptake and release unaffected ( P > 0.4 for both).

show abstract

“…Whole blood glucose was immediately determined in triplicate with a glucose analyzer (Yellow Springs Instrument, Yellow Springs, OH). For high-performance liquid chromatography (HPLC) analysis of plasma alanine and glutamine concentrations as well as [ 14 C]glutamine SA, an internal standard (25 nmol p-fluorophenylalanine) was added to 4.00 ml of plasma; the pH was adjusted to 4.80-5.00, and samples were frozen for later analysis as described previously (29) ]alanine enrichments were determined in duplicate by selected ion monitoring gas chromatography-mass spectroscopy (GC-MS) of the acetylbutylboronate (glucose) or t-butyldimethylsilyl (alanine) ester derivatives (44,51). Some of the […”

Section: Protocolmentioning

confidence: 99%

Renal substrate exchange and gluconeogenesis in normal postabsorptive humans

Meyer¹,

Stümvoll²,

Dostou³

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

125

View full text Add to dashboard Cite

. Renal substrate exchange and gluconeogenesis in normal postabsorptive humans. Am J Physiol Endocrinol Metab 282: E428-E434, 2002. First published October 23, 2001 10.1152/ ajpendo.00116.2001.-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 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 by use of 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 Ϯ 0.12 mol⅐kg Ϫ1 ⅐min Ϫ1) was about threefold greater than that from glycerol, glutamine, and alanine. The sum of gluconeogenesis from these precursors, uncorrected for tricarboxylic acid (TCA) cycle carbon exchange, explained 34% of systemic glucose release. Renal lactate uptake (3.33 Ϯ 0.28 mol⅐kg Ϫ1 ⅐min Ϫ1) accounted for nearly 30% of its systemic turnover. Renal gluconeogenesis from lactate (0.78 Ϯ 0.10 mol⅐kg Ϫ1 ⅐min Ϫ1 ) 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 ϳ40% of the sum of their systemic gluconeogenesis. When the isotopically determined rates of systemic and renal gluconeogenesis were corrected for TCA cycle carbon exchange, gluconeogenesis from these precursors accounted for 43% of systemic glucose release and 89% of renal glucose release. We conclude that 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. glutamine; alanine; glycerol; lactate; kidney RELEASE OF GLUCOSE BY THE KIDNEY has been reported to account on average for ϳ20% of all glucose released into the circulation in postabsorptive healthy humans (7-11, 16, 35-38, 45-47). Because the kidney normally stores little glycogen and its cells that could store glycogen lack glucose-6-phosphatase, renal glucose release is generally thought to be predominantly, if not exclusively, due to gluconeogenesis. At the present time, however, there is relatively little information available on the substrates used for gluconeogenesis by the human kidney. In studies of small numbers of postabsorptive normal volunteers, conversion of glutamine (34, 35, 47), glycerol (7), and alanine (47) to glucose has been found to...

show abstract

Determination of [¹⁴C] Glutamine Specific Activity in Plasma

Cited by 15 publications

References 12 publications

Renal glucose production and utilization: new aspects in humans

Renal glucose production and utilization: new aspects in humans

Effects of physiological hyperinsulinemia on systemic, renal, and hepatic substrate metabolism

Renal substrate exchange and gluconeogenesis in normal postabsorptive humans

Contact Info

Product

Resources

About

Determination of [14C] Glutamine Specific Activity in Plasma

Cited by 15 publications

References 12 publications

Renal glucose production and utilization: new aspects in humans

Renal glucose production and utilization: new aspects in humans

Effects of physiological hyperinsulinemia on systemic, renal, and hepatic substrate metabolism

Renal substrate exchange and gluconeogenesis in normal postabsorptive humans

Contact Info

Product

Resources

About

Determination of [¹⁴C] Glutamine Specific Activity in Plasma