Biomedical subjects

J Wahren

Publications and source records attributed to J Wahren.

At least 55 records · Page 3Linked to original sources

PubMed1997

Long-term use of smokeless tobacco and physical performance in middle-aged men.

To determine the influence of prolonged nicotine exposure on maximal physical working capacity, a study of clinical measures of physical fitness and cardiovascular response to exercise was performed in 144 healthy men, 35-60 years old, subdivided into smokeless tobacco users, smokers and non-users of tobacco. Regular users of smokeless tobacco, with exposures of more than 20 years, showed similar maximal oxygen uptake (mean 3.48 L min-1, SD 0.49, n = 48) to non-users (mean 3.51 L min-1, SD 0.51, n = 65). In smokeless tobacco users, higher blood pressure and heart rate values were observed at rest and at submaximal work, after exposure to tobacco shortly before the exercise test, but not at maximal work. However, significantly lower maximal oxygen uptake was found for smokers (mean 2.88 L min-1, SD 0.49, n = 31) compared with non-users (P < 0.001). Plasma concentration of continine, the main metabolite of nicotine, was significantly higher in smokeless tobacco users (mean 347 ng mL-1, SD 175, n = 48) than in smokers (mean 253 ng mL-1, SD 153, n = 31, P < 0.001). The findings indicate that long-term use of smokeless tobacco does not significantly influence exercise capacity in healthy, physically well-trained subjects.

Adult↗

PubMed1997

Whole body and splanchnic metabolic and circulatory effects of glucose during beta-adrenergic receptor inhibition.

The aim of the study was to assess the possible contribution of adrenergic mechanisms to the thermogenic and circulatory effects of glucose ingestion. With the use of indirect calorimetry and arterial, pulmonary arterial, and hepatic venous catheterization, whole body and splanchnic oxygen uptake and blood flow were examined in nine propranolol-treated healthy male volunteers before and during 2 h after oral ingestion of 75 g of glucose. The glucose effects were compared with those in nine untreated controls. After propranolol, the glucose-induced rise in splanchnic blood flow was reduced by approximately 60%, and the hepatic venous glucose release to the systemic circulation was significantly delayed. Glucose-induced increments in pulmonary and splanchnic oxygen uptake and cardiac output were similar in the two groups. It is concluded that adrenergic mechanisms contribute to the glucose-induced rise in splanchnic blood flow and thereby probably to the time course for intestinal absorption of nutrients. It is suggested that the magnitude of glucose-induced thermogenesis is independent of adrenergic stimulation.

Adrenergic beta-Antagonists↗

PubMed1997

Glucose production and gluconeogenesis in adults with uncomplicated falciparum malaria.

Although glucose production is increased in severe malaria, the influence of uncomplicated malaria on glucose production is unknown. Therefore, we measured in eight adult Vietnamese patients with uncomplicated falciparum malaria and eight healthy Vietnamese controls glucose production (by infusion of [6,6-2H2]glucose) and the fractional contribution of gluconeogenesis (by oral ingestion of 2H2O); glycogenolysis was calculated as the difference between the two. After 20 h of fasting, plasma glucose was 4.7 +/- 0.2 mmol/l in the patients and 4.3 +/- 0.2 mmol/l in the controls (not significant). Glucose production was approximately 25% higher in the patients (16.9 +/- 1.3 vs. 13.4 +/- 0.3 mumol.kg-1.min-1, P = 0.01). Fractional and absolute gluconeogenesis were increased in the patients (approximately 87 vs. approximately 59%, P < 0.001; and 14.6 +/- 1.3 vs. 7.9 +/- 0.2 mumol.kg-1.min-1, P < 0.001, respectively). The contribution of glycogenolysis to total glucose production was decreased in the patients: 2.3 +/- 0.5 vs. 5.5 +/- 0.4 mumol.kg-1.min-1 (P < 0.002). In conclusion, in adult patients with uncomplicated falciparum malaria, glucose production is increased by approximately 25% due to an increased rate of gluconeogenesis, whereas glycogenolysis is decreased. The mechanism by which these changes occur is uncertain. However, counterregulatory hormone and cytokine concentrations were increased in the patients.

Adult↗

PubMed1997

Quantifying gluconeogenesis during fasting.

The use of 2H2O in estimating gluconeogenesis' contribution to glucose production (%GNG) was examined during progressive fasting in three groups of healthy subjects. One group (n = 3) ingested 2H2O to a body water enrichment of approximately 0.35% 5 h into the fast. %GNG was determined at 2-h intervals from the ratio of the enrichments of the hydrogens at C-5 and C-2 of blood glucose, assayed in hexamethylenetetramine. %GNG increased from 40 +/- 8% at 10 h to 93 +/- 6% at 42 h. Another group ingested 2H2O over 2.25 h, beginning at 11 h (n = 7) and 19 h (n = 7) to achieve approximately 0.5% water enrichment. Enrichment in plasma water and at C-2 reached steady state approximately 1 h after completion of 2H2O ingestion. The C-5-to-C-2 ratio reached steady state by the completion of 2H2O ingestion. %GNG was 54 +/- 2% at 14 h and 64 +/- 2% at 22 h. A 3-h [6,6-2H2]glucose infusion was also begun to estimate glucose production from enrichments at C-6, again in hexamethylenetetramine. Glucose produced by gluconeogenesis was 0.99 +/- 0.06 mg.kg-1.min-1 at both 14 and 22 h. In a third group (n = 3) %GNG reached steady state approximately 2 h after 2H2O ingestion to only approximately 0.25% enrichment. In conclusion, %GNG by 2 h after 2H2O ingestion and glucose production using [6,6-2H2]glucose infusion, begun together, can be determined from hydrogen enrichments at blood glucose C-2, C-5, and C-6. %GNG increases gradually from the postabsorptive state to 42 h of fasting, without apparent change in the quantity of glucose produced by gluconeogenesis at 14 and 22 h.

Adult↗

PubMed1997

Effect of C-peptide on insulin and glucagon release by isolated perfused rat pancreas.

Administration of rat C-peptide (0.1 mumol/l) to isolated rat pancrease failed to inhibit insulin release induced by a high concentration of D-glucose (11.1 mmol/l) but prevented the progressive increase in insulin output otherwise observed during prolonged perfusion in the presence of 3.3 mmol/l glucose and 5.0 mmol/l L-arginine. In these experiments, C-peptide failed to affect glucagon output. The findings suggest that in suitable conditions C-peptide can inhibit insulin release.

Animals↗

PubMed1996

Contributions of gluconeogenesis to glucose production in the fasted state.

Healthy subjects ingested 2H2O and after 14, 22, and 42 h of fasting the enrichments of deuterium in the hydrogens bound to carbons 2, 5, and 6 of blood glucose and in body water were determined. The hydrogens bound to the carbons were isolated in formaldehyde which was converted to hexamethylenetetramine for assay. Enrichment of the deuterium bound to carbon 5 of glucose to that in water or to carbon 2 directly equals the fraction of glucose formed by gluconeogenesis. The contribution of gluconeogenesis to glucose production was 47 +/- 49% after 14 h, 67 +/- 41% after 22 h, and 93 +/- 2% after 42 h of fasting. Glycerol's conversion to glucose is included in estimates using the enrichment at carbon 5, but not carbon 6. Equilibrations with water of the hydrogens bound to carbon 3 of pyruvate that become those bound to carbon 6 of glucose and of the hydrogen at carbon 2 of glucose produced via glycogenolysis are estimated from the enrichments to be approximately 80% complete. Thus, rates of gluconeogenesis can be determined without corrections required in other tracer methodologies. After an overnight fast gluconeogenesis accounts for approximately 50% and after 42 h of fasting for almost all of glucose production in healthy subjects.

Adult↗

PubMed1996

C-peptide stimulates rat renal tubular Na+, K(+)-ATPase activity in synergism with neuropeptide Y.

This study was performed in order to test the hypothesis that the connecting peptide of proinsulin, C-peptide, might in itself possess biological activity. Renal tubular Na+, K(+)-ATPase, which is a well-established target for many peptide hormones, was chosen as a model. Rat C-peptide (I) was found to stimulate Na+, K(+)-ATPase activity in single, proximal convoluted tubules dissected from rat kidneys. C-peptide increased the Na+ affinity of the enzyme and all subsequent studies were performed at non-saturating Na+ concentrations. C-peptide stimulation of Na+, K(+)-ATPase activity occurred in a concentration-dependent manner in the dose range 10(-8)-10(-6) mol/l. The presence of neuropeptide Y, 5 x 10(-9) mol/l, enhanced this effect and stimulation of Na+, K(+)-ATPase activity then occurred in the C-peptide dose range 10(-11)-10(-8) mol/l. C-peptide stimulation of Na+, K(+)-ATPase activity was abolished in tubules pretreated with pertussis toxin. It was also abolished in the presence of FK 506, a specific inhibitor of the Ca2(+)-calmodulin-dependent protein phosphatase 2B. These results indicate that C-peptide stimulates Na+, K(+)-ATPase activity, probably by activating a receptor coupled to a pertussis toxin-sensitive G-protein with subsequent activation of Ca2(+)-dependent intracellular signalling pathways.

Animals↗

PubMed1996

C-peptide improves autonomic nerve function in IDDM patients.

In order to determine the possible influence of C-peptide on nerve function, 12 insulin-dependent diabetic (IDDM) patients with symptoms of diabetic polyneuropathy were studied twice under euglycaemic conditions. Tests of autonomic nerve function (respiratory heart rate variability, acceleration and brake index during tilting), quantitative sensory threshold determinations, nerve conduction studies and clinical neurological examination were carried out before and during a 3-h i.v. infusion of either C-peptide (6 pmol.kg-1.min-1) or physiological saline solution in a double-blind study. Plasma C-peptide concentrations increased from 0.11 +/- 0.02 to 1.73 +/- 0.04 nmol/l during C-peptide infusion. Clinical neurological examination quantitative sensory threshold evaluations and nerve conduction measurements failed to detect significant changes between C-peptide and saline study periods. Respiratory heart rate variability increased significantly from 13 +/- 1 to 20 +/- 2% during C-peptide infusion (p < 0.001), reaching normal values in five of the subjects; control studies with saline infusion did not alter the heart rate variability (basal, 14 +/- 2; saline, 15 +/- 2%). A reduced brake index value was found in seven patients and increased significantly during the C-peptide infusion period (4.6 +/- 1.0 to 10.3 +/- 2.2%, p < 0.05) but not during saline infusion (5.9 +/- 2 to 4.1 +/- 1.1%, NS). It is concluded that short-term (3-h) infusion of C-peptide in physiological amounts may improve autonomic nerve function in patients with IDDM.

Adult↗

PubMed1996

Effect of C-peptide administration on whole body glucose utilization in STZ-induced diabetic rats.

Recent studies suggest that C-peptide stimulates glucose transport in isolated skeletal muscle. In order to determine the effect of C-peptide on whole body glucose utilization, streptozotocin (60 mg kg-1) (STZ)-induced diabetic and normal rats were studied using the euglycaemic clamp procedure and continuous infusion of somatostatin (1.0 micrograms kg-1 min-1) in pentobarbital-anaesthetized rats. Plasma insulin levels during the 6.0- and 30.0-mU kg-1 min-1 insulin infusions rose to 70-90 microU mL-1 and 500-700 microU mL-1, respectively. Blood glucose concentrations were clamped at 7.5-7.9 mmol L-1 in the diabetic rats and at basal levels or 7.7 mmol L-1 in the non-diabetic (normal) rats. Biosynthetic human C-peptide (0.5 nmol kg-1 min-1) was infused in 12 diabetic and 11 normal rats, resulting in concentrations of 26-41 nmol L-1. The metabolic clearance rate of glucose (MCR) for the diabetic rats receiving C-peptide (12.0 +/- 1.0 mL kg-1 min-1) was significantly (P < 0.01) higher than that in the diabetic rats given saline (6.3 +/- 0.7 mL kg-1 min-1) or a randomly scrambled C-peptide (7.8 +/- 1.3 mL kg-1 min-1) at low-dose insulin infusion but not at the high-dose insulin infusion. In normal rats C-peptide did not significantly increase the MCR for glucose. These results thus demonstrate that C-peptide has the capacity to increase glucose utilization in STZ-induced diabetic rats.

Animals↗

PubMed1996

C-peptide revisited--new physiological effects and therapeutic implications.

Recent studies have demonstrated that replacement of C-peptide to normal physiological concentrations in insulin-dependent diabetic (IDDM) patients on a short-term basis (1-3 h) results in decreased glomerular hyperfiltration, augmented glucose utilization and improved autonomic nervous function. More prolonged administration (1-3 months) of C-peptide to IDDM patients is accompanied by improvements in both renal and autonomic nervous function. Moreover, both in-vitro and in-vivo studies indicate that C-peptide may have a role in the regulation of insulin secretion. The effects of C-peptide may in part be explained by its ability to stimulate Na+,K(+)-ATPase activity. In conclusion, the combined findings indicate that C-peptide is a biologically active hormone. The possibility that C-peptide therapy in IDDM patients may be beneficial should be considered.

Animals↗

PubMed1996

Effects of oral vs. i.v. glucose administration on splanchnic and extrasplanchnic O2 uptake and blood flow.

The metabolic and circulatory responses to intravenous or oral administration of glucose (75 g) were studied in healthy subjects. Pulmonary oxygen uptake increased promptly after oral but not during intravenous glucose infusion. The average 2-h rise above basal in whole body oxygen uptake was 8 +/- 1% (P < 0.001) after oral glucose and 3 +/- 1% (P < 0.05) during intravenous glucose infusion. After oral glucose, splanchnic oxygen uptake rose initially by approximately 15% (P < 0.01) and then declined; its average 2-h postprandial level was not significantly higher than that in the basal state. During intravenous glucose, splanchnic oxygen uptake decreased gradually during the first 75 min, reaching a level approximately 25% below basal (P < 0.05). Oxygen consumption by extrasplanchnic tissues rose significantly and to a similar extent (8%, 2 h average) with both intravenous and oral glucose. Splanchnic blood flow increased significantly after oral but not during intravenous glucose. It is concluded that 1) intravenous infusion and oral glucose administration elicit extrasplanchnic thermogenic effects of similar magnitude, 2) during intravenous glucose infusion, the extrasplanchnic thermogenic effect is counterbalanced by a simultaneous reduction in splanchnic oxygen uptake, resulting in a minimal (3%) net rise in whole body oxygen uptake, and 3) oral glucose ingestion but not intravenous glucose infusion increases the splanchnic blood flow.

Administration, Oral↗

PubMed1996

Glycerol production and utilization in humans: sites and quantitation.

Liver is assumed to be the major site of glycerol uptake and fatty acid reesterification. [U-13C]glycerol was infused into ten 60 h-fasted healthy subjects. Measured were 1) blood glycerol concentrations and 13C enrichments in brachial and pulmonary arteries and in hepatic, renal, superficial, and deep forearm veins; 2) glycerol appearance rates in systemic circulation; and 3) splanchnic bed and kidney glycerol uptakes with use of balance and tracer methodology. Glycerol concentrations were one-fifth in hepatic, one-half in renal, 40% more in superficial, and the same in deep vein and pulmonary artery as in brachial artery blood. Glycerol enrichments were one-fifth in hepatic, two-thirds to three-quarters in renal and superficial veins, and the same in pulmonary as in brachial artery blood. Splanchnic glycerol uptake was 29% and kidney glycerol uptake was 17% of glycerol's rate of appearance, 5.11 mumol.min-1.kg-1. Splanchnic fatty acid uptake was 25% of calculated fatty acid release. Glycerol contributed 15% to glucose production. Most of the [13C]glycerol uptake by splanchnic bed and kidneys was incorporated into glucose. Thus, in 60 h-fasted individuals, most glycerol uptake does not occur in liver, and the extent of fatty acid reesterification in liver is in doubt.

Adult↗

PubMed1995

Gluconeogenesis and glucuronidation in liver in vivo and the heterogeneity of hepatocyte function.

In order to examine metabolic zonation in human liver, [2-14C]glycerol, which labels carbons 2 and 5 of glucose-6-P, and [1-14C]lactate, which labels carbons 3 and 4 of glucose-6-P, in the process of gluconeogenesis, were infused intravenously into healthy subjects who ingested acetaminophen and had fasted 36 h. Distributions of 14C were determined in glucose in blood and in the glucuronic acid moiety of acetaminophen glucuronide excreted in urine. Ratios of 14C in carbons 2 and 5 to 14C in carbons 3 and 4 were significantly higher in blood glucose than in glucuronide. Since glucose and glucuronic acid are formed from glucose-6-P in liver without randomization of carbon, the differences in the ratios indicate that the pool of glucose-6-P in liver is not homogeneous. The glucuronide sampled glucose-6-P with more label from lactate than glycerol compared to the glucose-6-P sampled by the glucose. The apparent explanation is the greater decrease in glycerol compared with lactate concentration as blood streams from the periportal to the perivenous zones of the liver lobule. Glucuronidation is then expressed in humans relatively more in the perivenous than periportal zones and gluconeogenesis from glycerol more in the periportal than perivenous zones.

Acetaminophen↗

PubMed1995

Estimates of Krebs cycle activity and contributions of gluconeogenesis to hepatic glucose production in fasting healthy subjects and IDDM patients.

Normal subjects, fasted 60 h, and patients with insulin-dependent diabetes mellitus (IDDM), withdrawn from insulin and fasted overnight, were given phenylacetate orally and intravenously infused with [3-14C]lactate and 13C-bicarbonate. Rates of hepatic gluconeogenesis relative to Krebs cycle rates were estimated from the 14C distribution in glutamate from urinary phenylacetylglutamine. Assuming the 13C enrichment of breath CO2 was that of the CO2 fixed by pyruvate, the enrichment to be expected in blood glucose, if all hepatic glucose production had been by gluconeogenesis, was then estimated. That estimate was compared with the actual enrichment in blood glucose, yielding the fraction of glucose production due to gluconeogenesis. Relative rates were similar in the 60-h fasted healthy subjects and the diabetic patients. Conversion of oxaloacetate to phosphoenolpyruvate was two to eight times Krebs cycle flux and decarboxylation of pyruvate to acetyl-CoA, oxidized in the cycle, was less than one-30th the fixation by pyruvate of CO2. Thus, in estimating the contribution of a gluconeogenic substrate to glucose production by measuring the incorporation of label from the labelled substrate into glucose, dilution of label at the level of oxaloacetate is relatively small. Pyruvate cycling was as much as one-half the rate of conversion of pyruvate to oxaloacetate. Glucose and glutamate carbons were derived from oxaloacetate formed by similar pathways if not from a common pool. In the 60-h fasted subjects, over 80% of glucose production was via gluconeogenesis. In the diabetic subjects the percentages averaged about 45%.

Adult↗

PubMed1995

Metabolic, thermal and circulatory effects of intravenous infusion of amino acids in tetraplegic patients.

Metabolic, circulatory and thermal effects of intravenously (i.v.) administered amino acids were studied in eight patients with complete cervical spinal cord injuries, and compared with the effects in eight healthy subjects. Using indirect calorimetry and catheter techniques, whole-body and splanchnic oxygen consumption, blood flow and blood temperatures were measured before and at timed intervals during 2.5 h of i.v. infusion of 600 kJ of a mixture of 19 amino acids. Pulmonary oxygen uptake increased from 209 +/- 11 to 267 +/- 13 ml min-1 in the patients and from 268 +/- 5 to 320 +/- 8 ml min-1 in the controls. The thermic effect of amino acids was 21 +/- 3% and 16 +/- 2% in patients and controls, respectively. In both groups the splanchnic tissues accounted for approximately half of the rise in whole-body oxygen consumption. Cardiac output rose by, on average, 0.5 +/- 0.1 and 0.8 +/- 0.2 1 min-1 in patients and controls, respectively, while the hepatic blood flow remained unchanged in both groups. Pulmonary arterial blood temperature increased by 0.647 +/- 0.100 degrees C in the patients and by 0.244 +/- 0.174 degrees C in the controls (P < 0.05). The whole-body specific heat was low in the patients, its calculated maximum value being approximately 20% below the normal level. During the amino acid infusion the arterial blood concentration of amino acids rose by approximately 170% and 112% of its basal levels in patients and controls, respectively, indicating a significantly reduced capacity for cellular uptake of amino acids in tetraplegic patients. It is concluded that, in tetraplegic patients, i.v. infused amino acids induce prompt thermogenesis of normal magnitude accompanied by supranormal temperatures and amino acid concentrations in the blood, and that low whole-body specific heat contributes to the well-known thermoregulatory instability in tetraplegia.

Adult↗

PubMed1995

A limitation in the use of mass isotopomer distributions to measure gluconeogenesis in fasting humans.

The use of distributions of mass isotopomers in glucose from [U-13C]glycerol to estimate fractional rates of gluconeogenesis was examined. [U-13C]glycerol was infused into normal subjects who ingested acetaminophen and fasted for 60 h. Isotopomer distributions were measured by mass spectrometry in blood glucose and in glucuronic acid from urinary acetaminophen glucuronide. The distributions are incompatible with glucose production solely via gluconeogenesis from a single pool of triose phosphates. Rather, with the assumption of a single enriched triose phosphate pool, the distributions indicate, despite the 60 h of fasting, about as much glucose formation from an unlabeled glucose source as from that pool. Therefore the data indicate cellular heterogeneity in glycerol's metabolism, so that two or more pools with significantly different enrichments were the source of the glucose and glucuronic acid. This heterogeneity is related to much greater concentrations of glycerol in periportal than in pericentral zones of the liver lobule. Beyond evidence for heterogeneity, the findings emphasize a limitation in applying analyses of mass isotopomer distributions to measure polymer biosynthesis in the presence of heterogeneity in the precursor pool.

Acetaminophen↗

PubMed1995

Splanchnic and muscle metabolism during exercise in NIDDM patients.

To characterize splanchnic and muscle metabolism during exercise in non-insulin-dependent diabetes mellitus (NIDDM), eight male nonobese patients and seven healthy control subjects (CON) were studied during 40 min of bicycle exercise at 60% of maximal oxygen uptake. Biopsies were obtained from the quadriceps femoris muscle at rest and immediately after exercise. Arterial glucose concentration in NIDDM had declined by 10% (P < 0.01) at the end of exercise, whereas in CON it had risen by 21% (P < 0.05). Leg glucose uptake rose from 0.19 +/- 0.06 mmol/min at rest to 2.25 +/- 0.61 mmol/min at the end of exercise in NIDDM and from 0.13 +/- 0.05 to 1.17 +/- 0.34 mmol/min in CON. Splanchnic glucose output increased from 0.52 +/- 0.06 to 2.37 +/- 0.26 mmol/min in NIDDM and from 0.79 +/- 0.12 to 2.44 +/- 0.38 mmol/min in CON. Leg lactate output during exercise was twofold higher in NIDDM. Muscle contents of lactate and glycogen were similar in both groups at rest, whereas after exercise lactate tended to be higher (19.5 +/- 1.7 vs. 12.7 +/- 5.9 mmol/kg dry wt) and glycogen lower (154 +/- 35 vs. 251 +/- 41 mmol glucosyl units/kg dry wt) in NIDDM. Whole body respiratory exchange ratio during exercise was higher in NIDDM (0.84 +/- 0.02 vs. 0.78 +/- 0.02, P < 0.05). Exercise-induced changes in other muscle metabolites were similar in NIDDM and CON. These data indicate that the decline in blood glucose during exercise in nonobese NIDDM is due to enhanced peripheral glucose utilization rather than to an attenuated increase in splanchnic glucose output.

Adult↗

PubMed1995

Use of 2H2O for estimating rates of gluconeogenesis. Application to the fasted state.

A method is introduced for estimating the contribution of gluconeogenesis to glucose production. 2H2O is administered orally to achieve 0.5% deuterium enrichment in body water. Enrichments are determined in the hydrogens bound to carbons 2 and 6 of blood glucose and in urinary water. Enrichment at carbon 6 of glucose is assayed in hexamethylenetetramine, formed from formaldehyde produced by periodate oxidation of the glucose. Enrichment at carbon 2 is assayed in lactate formed by enzymatic transfer of the hydrogen from glucose via sorbitol to pyruvate. The fraction gluconeogenesis contributes to glucose production equals the ratio of the enrichment at carbon 6 to that at carbon 2 or in urinary water. Applying the method, the contribution of gluconeogenesis in healthy subjects was 23-42% after fasting 14 h, increasing to 59-84% after fasting 42 h. Enrichment at carbon 2 to that in urinary water was 1.12 +/- 0.13. Therefore, the assumption that hydrogen equilibrated during hexose-6-P isomerization was fulfilled. The 3H/14C ratio in glucose formed from [3-3H,3-14C]lactate given to healthy subjects was 0.1 to 0.2 of that in the lactate. Therefore equilibration during gluconeogenesis of the hydrogen bound to carbon 6 with that in body water was 80-90% complete, so that gluconeogenesis is underestimated by 10-20%. Glycerol's contribution to gluconeogenesis is not included in these estimates. The method is applicable to studies in humans of gluconeogenesis at safe doses of 2H2O.

Adult↗