Recovery of 13C in breath from NaH13CO3 infused by gut and vein: effect of feeding

Hoerr, Robert; Yu, Yong‐Ming; Wagner, David; Burke, John F.; Young, Vernon R.

doi:10.1152/ajpendo.1989.257.3.e426

Cited by 104 publications

(93 citation statements)

References 24 publications

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“…The estimation of the rate of CO 2 production includes a factor to account for the CO 2 which is produced, but not expired; this factor is based on experimental work done in adults and infants (Spear et al, 1995;Kien & McClead, 1996). This factor has been measured in diverse populations, including critically ill children, and varies between 0.70 and 0.85 (Hoerr et al, 1989;Bresson et al, 1990;Tissot et al, 1993) although most reports have identified values between 0.77 and 0.82 (including those from critically ill infants). We did not measure the amount of CO 2 produced that was then incorporated into other metabolic substrates in our population.…”

Section: Discussionmentioning

confidence: 99%

CO2 production during acute infection in malnourished Malawian children

et al. 2003

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Objective: This study tested the hypotheses that the rate of CO 2 production is less in marasmic children with acute infection when compared to well-nourished children, but greater when compared to uninfected marasmic children. Design: A descriptive comparison of children aged 12-60 months who had their rates of CO 2 production measured using a stable isotope tracer dilution method while receiving feedings. Body mass index (BMI) was the best measure of lean body mass available in this study. Setting: Queen Elizabeth Central Hospital, Blantyre, Malawi. Subjects: A total of 56 children were studied, 28 with marasmus and acute infection, 16 with marasmus, and 12 well nourished with acute infection. Those with acute infection had malaria, pneumonia, or sepsis. Results: Well-nourished children with acute infection produced more CO 2 than marasmic children (344760 vs 225765 mmol CO 2 /h, mean7s.d., Po0.001; 24.274.6 vs 18.475.4 mmol CO 2 /BMI h, P ¼ 0.001). However, the rate of CO 2 production in marasmic children with acute infection was not greater than in uninfected marasmic children (225765 vs 228761 mmol CO 2 /h). The observed rate of CO 2 production was greater than that which could be produced from the dietary intake alone (29.6 vs. 25.8 mmol CO 2 /kg h). Conclusions: Marasmic children do not increase energy expenditure in response to acute infection, as well-nourished children do. Dietary energy provided to marasmic children should be at least 420 kJ/kg day.

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Section: Discussionmentioning

confidence: 99%

CO2 production during acute infection in malnourished Malawian children

et al. 2003

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“…Leucine oxidation (OxLEU; mol ⅐ kg Ϫ1 ⅐ h Ϫ1 ) was calculated on the basis of the excretion of labeled CO2 in expired air: OxLEU ϭ F 14 CO2/(SAKIC ϫ 0.7), where F 14 CO2 is the rate of 14 CO2 excretion in expired air ( mol⅐kg Ϫ1 ⅐h Ϫ1 ) and 0.7 is the assumed fractional recovery of labeled carbon in expired air in the postabsorptive state (22).…”

Section: Methodsmentioning

confidence: 99%

“…Because [ 13 C]glutamine entering systemic plasma is diluted by whole body glutamine turnover rate, the appearance of dietary [ 13 C]glutamine into systemic plasma was estimated as dietary [ 13 Glutamine oxidation. The respiratory excretion of 13 C-labeled carbon dioxide was calculated as (E CO 2 ϫ V CO2)/0.7, where V CO2 is the rate of CO2 excretion ( mol ⅐ kg Ϫ1 ⅐ h Ϫ1 ), E CO 2 is steady-state 13 CO2 enrichment (mole percent excess) in expired air, and 0.7 is the assumed fractional recovery of labeled carbon in expired air in the postabsorptive state (22). The percentage of enterally infused glutamine that underwent oxidation (FoxGLN) was estimated by FoxGLN ϭ 100 ϫ…”

Section: Methodsmentioning

confidence: 99%

Corticosteroids increase glutamine utilization in human splanchnic bed

Thibault

Welch²,

Mauras³

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Thibault R, Welch S, Mauras N, Sager B, Altomare A, Haymond M, Darmaun D. Corticosteroids increase glutamine utilization in human splanchnic bed. Am J Physiol Gastrointest Liver Physiol 294: G548-G553, 2008. First published December 27, 2007 doi:10.1152/ajpgi.00461.2007.-Glutamine is the most abundant amino acid in the body and is extensively taken up in gut and liver in healthy humans. To determine whether glucocorticosteroids alter splanchnic glutamine metabolism, the effect of prednisone was assessed in healthy volunteers using isotope tracer methods. Two groups of healthy adults received 5-h intravenous infusions of L-[1-14 C]leucine and L-[ 2 H5]glutamine, along with q. 20 min oral sips of tracer doses of L-[1-13 C]glutamine in the fasting state, either 1) at baseline (control group; n ϭ 6) or 2) after a 6-day course of 0.8 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 prednisone (prednisone group; n ϭ 8). Leucine and glutamine appearance rates (Ra) were determined from plasma [1-14 C]ketoisocaproate and [ 2 H5]glutamine, respectively, and leucine and glutamine oxidation from breath 14 CO2 and 13 CO2, respectively. Splanchnic glutamine extraction was estimated by the fraction of orally administered [ 13 C]glutamine that failed to appear into systemic blood. Prednisone treatment 1) did not affect leucine Ra or leucine oxidation; 2) increased plasma glutamine Ra, mostly owing to enhanced glutamine de novo synthesis (medians Ϯ interquartiles, 412 Ϯ 61 vs. 280 Ϯ 190 mol ⅐ kg Ϫ1 ⅐ h Ϫ1 , P ϭ 0.003); and 3) increased the fraction of orally administered glutamine undergoing extraction in the splanchnic territory (means Ϯ SE 64 Ϯ 6 vs. 42 Ϯ 12%, P Ͻ 0.05), without any change in the fraction of glutamine oxidized (means Ϯ SE, 75 Ϯ 4 vs. 77 Ϯ 4%, not significant). We conclude that high-dose glucocorticosteroids increase in splanchnic bed the glutamine requirements. The role of such changes in patients receiving chronic corticoid treatment for inflammatory diseases or suffering from severe illness remains to be determined. nutrition; protein metabolism; stable isotopes; stress; gut GLUTAMINE PLAYS AN IMPORTANT role in the maintenance of intestinal function (39,43,46). Glutamine indeed is both a preferred fuel (9, 47) for enterocytes and a precursor for the intestinal synthesis of purines, pyrimidines (9), and glutathione (37), and it may regulate gut protein synthesis (21,30,32). In addition, glutamine is a major donor of carbon for gluconeogenesis (19). This explains why glutamine is extensively extracted in the splanchnic tissues in several animal species (39,47).In humans, the concomitant infusion of two tracers of glutamine (one infused intravenously, the other one enterally) can be used to assess the extraction of glutamine by the splanchnic bed. By using this technique, ϳ50 to 75% of enterally administered glutamine undergoes first-pass extraction within the splanchnic bed, presumably by the gut and liver, in healthy humans (4, 17, 18, 34). Additionally, the major fate of splanchnic glutamine after enteral administration was oxidation, ...

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“…In addition, many studies correct PDR data using the bicarbonate recovery factor to get a true measure of substrate oxidation because a proportion of any 13 C tracer traversing the bicarbonate pool can be irreversibly sequestrated (Irving et al, 1983). Previous studies have shown bicarbonate recovery in breath to approximate 70-80% when subjects are at rest (Hoerr et al, 1989).…”

Section: Methodsmentioning

confidence: 99%

Gastrointestinal handling of glycosyl [13C]ureides

Morrison

Dodson²,

Preston

et al. 2003

Eur J Clin Nutr

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Objectives: Lactose [ 13 C]ureide has been proposed as a noninvasive marker for oro-caecal transit time in adults and children. The present study investigates the handling of lactose [ 13 C]ureide ( 13 C LU) and glucose [ 13 C]ureide ( 13 C GU) by the gastrointestinal tract and describes the metabolic fates of these substrates and describes the extent of tracer excretion by different routes. Study Design and Subjects: Four subjects underwent five studies in which they ingested a test meal plus (1) no substrate, (2) 13 C LU, (3) 13 C GU, (4) 13 C LU after predosing with unlabelled lactose ureide and (5) 13 C LU after predosing with glucose ureide. Subjects were studied at home with at least 1 week between tests and they all completed the study. Breath was analysed for 13 CO 2 recovery and urine was analysed for total 13 C recovery, 13 C urea recovery and 13 C GU recovery. Results: The profiles and extent of tracer recovery in breath and urine were similar when either 13 C GU or 13 C LU was used, suggesting similar handling of these substrates by the gut. 13 C GU was the major 13 C-enriched species recovered in the urine even when 13 C LU was consumed. Predosing with either lactose ureide or glucose ureide increased the rate of appearance of tracer, but did not alter transit times.

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Recovery of 13C in breath from NaH13CO3 infused by gut and vein: effect of feeding

Cited by 104 publications

References 24 publications

CO2 production during acute infection in malnourished Malawian children

CO2 production during acute infection in malnourished Malawian children

Corticosteroids increase glutamine utilization in human splanchnic bed

Gastrointestinal handling of glycosyl [13C]ureides

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