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Biomedical subjects

G L Baker

Publications and source records attributed to G L Baker.

At least 55 records · Page 3Linked to original sources
PubMed1983

Effect of aspartame loading on plasma and erythrocyte free amino acid concentrations in one-year-old infants.

Aspartame is a new dipeptide sweetener. It has been suggested that infants metabolize its constituent amino acids (aspartate and phenylalanine) less well than adults. To test this hypothesis, 24 1-year-old infants were administered 34, 50 and 100 mg/kg body weight aspartame in cherry-flavored beverage mix. Plasma amino acid concentrations and the areas under the plasma concentration-time curves (AUC) were determined and were compared with values in adults administered equivalent doses. The doses studied include the 99th percentile of projected ingestion for adults (34 mg/kg), a very high use dose (50 mg/kg body weight), and a potentially abusive dose (100 mg/kg body weight). Plasma aspartate concentrations did not change significantly (P greater than 0.05) at aspartame doses of 34 and 50 mg/kg body weight, but did increase significantly at the 100 mg/kg body weight dose. The change over base line was similar in infants and adults. Aspartame dosing significantly increased both the mean peak plasma phenylalanine concentration and the plasma phenylalanine AUC value in proportion to dose. Mean (+/- SD) peak plasma phenylalanine concentrations in infants were 9.37 +/- 1.44, 11.6 +/- 4.44 and 22.3 +/- 11.5 mumol/100 ml at aspartame doses of 34, 50 and 100 mg/kg body weight, respectively. Values in infants were similar to those noted in adults. The data do not support the suggestion that infants metabolize the amino acids of aspartame less well than adults.

Adult↗
PubMed1983

Blood methanol concentrations in one-year-old infants administered graded doses of aspartame.

Blood methanol concentrations were measured in 24 1-year-old infants administered aspartame, a dipeptide methyl ester sweetener. The doses studied included a dose projected to be the 99th percentile of daily ingestion for adults (34 mg/kg body weight), a very high use dose (50 mg/kg body weight) and a dose considered to be in the abuse range (100 mg/kg body weight). Blood methanol values in infants were compared to values observed previously in adults administered equivalent doses of aspartame. Methanol concentrations were below the level of detection (0.35 mg/dl) in the blood of 10 infants administered aspartame at 34 mg/kg body weight, but were significantly elevated (P less than or equal to 0.05) after ingestion of aspartame at 50 and 100 mg/kg body weight. At the latter doses, mean peak blood methanol concentrations and the area under the blood methanol concentration-time curve increased in proportion to dose. Mean (+/- SEM) peak blood methanol concentration was 0.30 +/- 0.10 mg/100 ml at a 50 mg/kg body weight aspartame dose (n = 6) and 1.02 +/- 0.28 mg/ml at the 100 mg/kg body weight dose (n = 8). Blood methanol values in infants were similar to those observed in normal adults.

Age Factors↗
PubMed1983

Plasma amino acid concentrations in normal adults fed meals with added monosodium L-glutamate and aspartame.

Aspartame is a dipeptide sweetener containing aspartate. It has been suggested that aspartame addition to meals containing large amounts of monosodium L-glutamate (MSG) would result in a rapid rise in plasma glutamate and/or aspartate concentrations and increase the potential for dicarboxylic amino acid--induced toxicity. Sic normal adult subjects were fed three hamburger and milk shake meals providing protein at 1 g/kg body weight in a Latin square design. One meal had no additions, the second provided MSG at 150 mg/kg body weight, and the third provided MSG at 150 mg/kg body weight and aspartame at 23 mg/kg body weight. The addition of MSG alone significantly increased plasma glutamate + aspartate concentration above values noted after ingestion of the meal alone. Aspartame addition to meals already containing MSG did not further significantly increase plasma glutamate + aspartate concentration above values noted when only MSG was added. However, aspartame addition did significantly increase the mean plasma phenylalanine concentration above values noted after ingestion of the meal alone or the meal with added MSG, reflecting aspartame's phenylalanine content. The data do not support the suggestion that aspartame addition to high protein meals already containing large amounts of MSG, will promote a rapid and dangerous rise in plasma glutamate and aspartate concentrations.

Adult↗
PubMed1982

Effect of sampling site on plasma amino acid concentrations of infants: effect of skin amino acids.

Plasma taurine, aspartate, threonine, serine, glycine, alanine, valine, leucine, tyrosine, phenylalanine, tryptophan, lysine, histidine, and ornithine concentrations are significantly greater (p less than 0.05, "Student's" t test) in blood samples obtained by conventional heel skin puncture techniques from 1-yr-old infants than values in venous plasma. Differences in plasma concentrations of taurine, aspartate, serine, glycine, and ornithine were particularly striking, with levels in plasma collected from the heel being 1.6 to 6.7 times higher than levels in venous plasma. These increased plasma amino acid concentrations were shown to result primarily from contamination of the plasma with amino acids present on the skin surface. Thorough washing and stimulation of blood flow to the heel by warming prior to skin puncture reduced observed differences. Plasma amino acid concentrations of blood samples obtained by conventional heel skin puncture procedures can be "normalized" to venous values through the use of data on the amino acid composition of heel skin washings.

Amino Acids↗
PubMed1982

Effect of aspartame plus monosodium L-glutamate ingestion on plasma and erythrocyte amino acid levels in normal adult subjects fed a high protein meal.

It has been suggested that aspartame addition to meals already containing large amounts of monosodium L-glutamate would result in an early rapid rise in plasma glutamate and/or aspartate concentrations and increase the potential for dicarboxylic amino acid-induced toxicity. Six normal adult subjects were fed hamburger and milk shake meals providing protein at 1 g/kg body weight in a randomized cross-over design. One meal had no additions while the other contained added monosodium L-glutamate and aspartame (each present at 34 mg/kg body weight). The addition of aspartame plus glutamate had little effect on either plasma or erythrocyte concentrations of glutamate or aspartate beyond those arising from the meal itself. Plasma phenylalanine concentrations were significantly higher (p less than 0.05, paired t test) after ingestion of meals containing aspartame plus glutamate reflecting the increased phenylalanine load.

Adult↗
PubMed1982

Plasma and erythrocyte amino acid levels in normal adult subjects fed a high protein meal with and without added monosodium glutamate.

It has been suggested that the addition of free glutamate to meals already containing large amounts of protein-bound glutamate would produce an early rapid rise in plasma glutamate and/or aspartate concentrations, increasing the potential for glutamate-induced adverse effects. Normal adult subjects were fed a hamburger and milk shake meal providing protein at 1 g/kg body weight with and without added monosodium L-glutamate (34 mg/kg body weight). The addition of glutamate to the meal at this level had no significant effect on either plasma or erythrocyte concentrations of glutamate or aspartate beyond those arising from the meal itself. Free glutamate added to a hamburger and milk shake meal at this level is rapidly metabolized and does not elevate plasma concentrations of these dicarboxylic amino acids.

Adult↗
PubMed1982

Plasma and urinary methionine levels in one-year-old infants after oral loading with L-methionine and N-acetyl-L-methionine.

N-acetyl-L-methionine has been proposed as a replacement for methionine in supplementing food products low in this amino acid. Previous studies in adult subjects administered equimolar quantities (0.0605 mmoles/kg body weight) of L-methionine and N-acetyl-L-methionine showed equivalent overall release of methionine to the blood as judged by area under the plasma methionine time--absorption curve. In the present study, similar doses (0.0605 mmoles/kg body weight) of L-methionine and N-acetyl-L-methionine were administered to fasting 1-year-old infants in a randomized crossover design. The two compounds produced an equivalent overall release of methionine to the blood as judged by plasma methionine concentrations and by the area under the plasma methionine concentration--time curves. No evidence was obtained that indicated release of N-acetyl-L-methionine to plasma or its excretion in urine after loading. However, peak plasma methionine concentrations, and the areas under the plasma methionine concentration--time curves for infants were approximately one-half the values observed in normal adults administered equimolar doses of each compound on a per kilogram body weight basis. The data suggest more rapid metabolism of methionine and N-acetyl-L-methionine by infants than adults.

Age Factors↗
PubMed1981

Plasma phenylalanine levels in phenylketonuric heterozygous and normal adults administered aspartame at 34 mg/kg body weight.

Following administration of aspartame (34 mg/kg body wt) in orange juice, plasma concentrations of free amino acids were measured in 12 female subjects known to be heterozygous for phenylketonuria and 22 normal subjects (12 male, 10 female). No change in fasting plasma aspartate concentrations were noted after aspartame loading in either group. In normal male subjects, the mean (+/-S.D.) plasma phenylalanine concentration increased from a fasting value of 5.86 +/- 1.25 mumol/dl. Plasma phenylalanine levels in normal female subjects increased from a mean fasting concentration of 4.83 +/- 0.84 mumol/dl to a men peak value of 8.95 +/- 1.49 mumol/dl suggesting a more rapid absorption, metabolism, and/or clearance of phenylalanine by females. In female heterozygous subjects, the mean peak plasma phenylalanine concentration was significantly higher than in normal females. Plasma phenylalanine values increased from a mean fasting value of 5.92 +/- 1.51 mumol/dl to a mean peak value of 15.1 +/- 4.76 mumol/dl. Similarly, the area under the plasma phenylalanine concentration-time curve was significantly greater in heterozygous female subjects (21.36 +/- 5.10 IU) than in normal female subjects (10.84 +/- 2.32 IU). However, peak plasma phenylalanine levels were well below those associated with toxic effects in all cases.

Adult↗
PubMed1981

Blood methanol concentrations in normal adult subjects administered abuse doses of aspartame.

Blood methanol concentrations were measured in 30 normal adult subjects administered aspartame, a dipeptide methyl ester. The doses studied included the 99th percentile of projected daily ingestion (34 mg/kg body weight) and three doses considered to be in the abuse range (100, 150, and 200 mg/kg body weight). Methanol concentrations were below the level of detection (0.4 mg/dl) in the blood of the 12 normal subjects who ingested aspartame at 34 mg/kg. They were significantly elevated (p less than or equal to 0 .001) after ingestion of each abuse dose, with the mean peak blood methanol concentrations and the areas under the blood methanol concentration-time curve increasing in proportion to dose. Mean (+/- SD) peak blood methanol concentrations were 1.27 +/- 0.48 mg/dl at the 100 mg/kg dose, 2.14 +/- 0.35 mg/dl at the 150 mg/kg dose, and 2.58 +/- 0.78 mg/dl at the 200 mg/kg dose. Blood methanol concentrations returned to predosing levels by 8 h after administration of the 100 mg/kg dose. Methanol was still detected in the blood 8 h after the subjects had ingested aspartame at 150 or 200 mg/kg. Blood formate analyses were carried out in the 6 subjects who ingested aspartame at 200 mg/kg, since recent studies indicate that the toxic effects of methanol are due to formate accumulation. No significant increase in blood formate concentrations over predosing concentrations was noted. No changes were noted in any of the blood chemistry profile parameters measured 24 h after aspartame ingestion, compared to values noted before administration. Similarly, no differences were noted in ophthalmologic examinations carried out before and after aspartame loading.

Adult↗
PubMed1981

Plasma and erythrocyte concentrations of free amino acids in adult humans administered abuse doses of aspartame.

Plasma and erythrocyte concentrations of amino acids were measured in 18 fasting adult subjects (9 male, 9 female) administered abuse doses of aspartame (100, 150, and 200 mg/kg body weight) dissolved in 500 ml orange juice. Six subjects were studied at each dose. Plasma aspartate concentrations increased significantly (p less than or equal to 0.05) over baseline values after ingestion of each dose. However, the increase was small in each case, and maximal levels observed were below those noted postprandially in formula-fed infants. No significant changes (p greater than 0.05) were noted in erythrocyte glutamate, or erythrocyte aspartate concentrations after any dose. Plasma phenylalanine concentrations increased significantly over fasting concentrations (p less than 0.01) from 15 min to 6 h after each dose, and the increase was proportional to dose. Mean (+/- SD) peak plasma phenylalanine concentrations were 20.3 +/- 2.03, 35.1 +/- 11.3, and 48.7 +/- 15.5 mumol/dl, respectively, after aspartame doses of 100, 150, and 200 mg/kg. Erythrocyte phenylalanine concentrations showed similar changes. Although these phenylalanine concentrations are considerably above the normal postprandial range (12 +/- 3 mumol/dl), they are below values associated with toxic findings. These data indicate little risk to normal subjects from excessive aspartate or phenylalanine levels after ingestion of single abuse loads of aspartame.

Adult↗
PubMed1981

Effect of aspartame and sucrose loading in glutamate-susceptible subjects.

It has been postulated that individuals reporting an idiosyncratic symptom response after glutamate ingestion might also experience such symptoms after aspartame ingestion. Such sensitive subjects might have been missed in earlier studies of aspartame. In the present study, six subjects reporting various symptoms after glutamate ingestion, but not after placebo, were administered aspartame (34 mg/kg body weight) or sucrose (1 g/kg body weight) dissolved in orange juice in a randomized, cross-over, double-blind study. No subject reported symptoms typical of a glutamate response after either sucrose or aspartame loading. One subject reported slight nausea approximately 1.5 h after aspartame ingestion, but indicated that the symptoms were not those of a glutamate response. Plasma phenylalanine and aspartate levels were similar to those noted in normal subjects administered identical doses of aspartame. The data indicate no effect of aspartame loading in glutamate-susceptible subjects.

Aspartame↗
PubMed1980

Plasma methionine levels in normal adult subjects after oral loading with L-methionine and N-acetyl-L-methionine.

The biological quality of soy protein isolates is limited by methionine content but can be enhanced by methionine addition. Since supplemental methionine may undergo chemical modification during processing, producing objectionable odors, N-acetyl-L-methionine has been proposed as a methionine replacement. Plasma and erythrocyte methionine levels and the area under the plasma and erythrocyte methionine absorption curve were compared in five normal adult subjects administered equimolar quantities (0.0605 mmoles/kg) of L-methionine and N-acetyl-L-methionine. The two compounds produced an equivalent overall release of L-methionine to the blood as judged by the area under the plasma and erythrocyte methionine time-absorption curves. There was a difference in the early part of both absorption curves (15 to 45 minutes), with plasma and erythrocyte levels higher after L-methionine administration than after N-acetyl-L-methionine administration. However, this difference was only statistically significant at 15 minutes (P = 0.03). Gastric emptying did not account for this difference apparently reflecting a slower rate of absorption of N-acetyl-L-methionine by mucosal cells. No evidence was obtained that indicated release of N-acetyl-L-methionine to the plasma or its excretion in urine after loading. The data are consistent with previous data showing L-methionine and N-acetyl-L-methionine to be equivalent sources of methionine.

Adult↗
PubMed1980

Effect of an abuse dose of aspartame upon plasma and erythrocyte levels of amino acids in phenylketonuric heterozygous and normal adults.

Plasma and erythrocyte levels of free amino acids were measured in five female subjects known to be heterozygous for phenylketonuria and six subjects assumed to be normal (three male, three female) who were administered an abuse dose of aspartame (100 mg/kg) in orange juice. Small increases in plasma aspartate levels were noted 30 minutes after aspartame loading in both groups, with mean (+/- SD) levels increasing from 0.15 +/- 0.05 mumoles/100 ml to 0.43 +/- 0.23 mumoles/100 ml in normal subjects (P = 0.02), and from 0.49 +/- 0.23 mumoles/100 ml to 0.80 +/- 0.56 mumoles/100 ml in heterozygous subjects (P > 0.05). However, plasma aspartate levels remained within normal postprandial levels in each case. Erythrocyte aspartate levels were unchanged in both groups. In normal subjects, plasma phenylalanine levels (mean +/- SD) increased from fasting levels (5.40 +/- 1.05 mumoles/100 ml) to mean peak values of 20.2 +/- 6.77 mumoles/100 ml. In heterozygous subjects, mean peak plasma phenylalanine levels were approximately twice as high (41.7 +/- 2.33 mumoles/100 ml), and the area under the plasma concentration-time curve twice as large. Peak plasma phenylalanine levels, however, were below those associated with toxic effects. The data indicate slower, but adequate metabolism and clearance of an abuse dose of aspartame by the phenylketonuric heterozygote.

Amino Acids↗