Galactose In Urine Research Articles

Awareness about Neonatal Lactose Intolerance among Chinese Neonatologists in Outpatient Settings: A Multi-Center Survey.

This study aimed to identify the specific areas of knowledge gaps regarding lactose intolerance among neonatologists in Chinese outpatient settings as well as to assess the availability of lactose intolerance testing in hospitals. A total of 278 neonatologists in outpatient settings from 144 hospitals were surveyed. To explore the awareness level, diagnosis, and treatment of neonatal lactose intolerance among neonatologists in outpatient settings, a multicenter cross-sectional survey was designed. Descriptive analysis based on frequency and percent distribution was performed for all variables. Most respondents were senior doctors (256, 92.09%) from general hospitals and maternity/maternal and child health hospitals, had over 10 years of experience, and were dominantly associate chief physicians and chief physicians (211, 75.90%). A significant proportion of the participants (236, 84.89%) believed that neonatal lactose intolerance tends to be overlooked during clinical practice. When the most common symptoms of neonatal lactose intolerance were surveyed, diarrhea was selected by 142 (51.08%) respondents, followed by bloating and milk regurgitation or emesis (71, 25.54%). Other symptoms included unexplained crying (36, 12.85%), stool with milk flap or foam (15, 5.40%), and increased venting (14, 5.04%). Furthermore, the survey results indicated that the most common method for diagnosing neonatal lactose intolerance in the respondents' hospitals was qualitative test for urinary galactose (78, 28.06%). Of the respondents, 137 (49.28%) stated that their hospital could not test for lactose intolerance. For treating lactose intolerance, the neonatologists primarily opted for exogenous lactase rather than lactose-free formula milk. This study sheds light on Chinese neonatologists' awareness of neonatal lactose intolerance, revealing some knowledge gaps. The expeditious popularization and conduct of lactose intolerance-related examinations in hospitals will have a positive stimulative effect on the management of lactose intolerance in newborns.

Evaluating the Robustness of Biomarkers of Dairy Food Intake in a Free-Living Population Using Single- and Multi-Marker Approaches.

Studies examining associations between self-reported dairy intake and health are inconclusive, but biomarkers hold promise for elucidating such relationships by offering objective measures of dietary intake. Previous human intervention studies identified several biomarkers for dairy foods in blood and urine using non-targeted metabolomics. We evaluated the robustness of these biomarkers in a free-living cohort in the Netherlands using both single- and multi-marker approaches. Plasma and urine from 246 participants (54 ± 13 years) who completed a food frequency questionnaire were analyzed using liquid and gas chromatography-mass spectrometry. The targeted metabolite panel included 37 previously-identified candidate biomarkers of milk, cheese, and/or yoghurt consumption. Associations between biomarkers and energy-adjusted dairy food intakes were assessed by a ‘single-marker’ generalized linear model, and stepwise regression was used to select the best ‘multi-marker’ panel. Multi-marker models that also accounted for common covariates better captured the subtle differences for milk (urinary galactose, galactitol; sex, body mass index, age) and cheese (plasma pentadecanoic acid, isoleucine, glutamic acid) over single-marker models. No significant associations were observed for yogurt. Further examination of other facets of validity of these biomarkers may improve estimates of dairy food intake in conjunction with self-reported methods, and help reach a clearer consensus on their health impacts.

Evaluation of breath, plasma, and urinary markers of lactose malabsorption to diagnose lactase non-persistence following lactose or milk ingestion

BackgroundAdult lactase non-persistence (LNP) is due to low lactase expression, resulting in lactose malabsorption (LM). LNP is a genetic trait, but is typically determined by LM markers including breath H2, blood glucose, and urinary galactose after a lactose tolerance test. Known validity of these markers using milk is limited, despite being common practice. Compositional variation, such as β-casein variants, in milk may impact diagnostic efficacy. This study aimed to evaluate the diagnostic accuracy to detect LNP using these commonly measured LM markers after both lactose and milk challenges.MethodsFourty healthy young women were challenged with 50 g lactose then randomized for separate cross-over visits to ingest 750 mL milk (37.5 g lactose) as conventional (both A1 and A2 β-casein) and A1 β-casein-free (a2 Milk™) milk. Blood, breath and urine were collected prior to and up to 3 h following each challenge. The presence of C/T13910 and G/A22018 polymorphisms, determined by restriction fragment length polymorphism, was used as the diagnostic reference for LNP.ResultsGenetic testing identified 14 out of 40 subjects as having LNP (C/C13910 and G/G22018). All three LM markers (breath H2, plasma glucose and urinary galactose/creatinine) discriminated between lactase persistence (LP) and LNP following lactose challenge with an area under the receiver operating characteristic (ROC) curve (AUC) of 1.00, 0.75 and 0.73, respectively. Plasma glucose and urinary galactose/creatinine were unreliable (AUC < 0.70) after milk ingestion. The specificity of breath H2 remained high (100%) when milk was used, but sensitivity was reduced with conventional (92.9%) and a2 Milk™ (78.6%) compared to lactose (sensitivities adjusted for lactose content). The breath H2 optimal cut-off value was lower with a2 Milk™ (13 ppm) than conventional milk (21 ppm). Using existing literature cut-off values the sensitivity and specificity of breath H2 was greater than plasma glucose to detect LNP following lactose challenge whereas values obtained for urinary galactose/creatinine were lower than the existing literature cut-offs.ConclusionThis study showed accurate diagnosis of LNP by breath H2 irrespective of the substrate used, although the diagnostic threshold may vary depending on the lactose substrate or the composition of the milk.Trial registrationACTRN12616001694404. Registered prospectively on December 9, 2016.

Clinical characteristics and treatment of infantile lactose intolerance and evaluation of the diagnostic value of fecal pH

Objective To investigate the clinical characteristics, diagnostic approach, and treatment of infantile lactose intolerance, and to evaluate the diagnostic value of fecal pH. Methods The feces and clinical data of all infants(less than 1 year old) diagnosed with simple diarrhea but without signs of infection were collected, who were treated at 4 Grade Ⅲ-Class-A hospitals within the period of June 2012 to June 2015 in Beijing were collected.Lactose intolerance was diagnosed based on urine galactose level, lactose tolerance test, and fecal pH.The clinical characteristics, therapeutic effects and detection methods of lactose tolerance group and intolerance group were analyzed.Then the diagnostic value of fecal pH was evaluated. Results A total of 217 infants were enrolled in the study, consisting of 113 boys and 104 girls.Their age ranged from 3 to 330 days, 174 infants (80.2%) were less than 6 months old.Among them, 156 infants were diagnosed with lactose intolerance (71.9%), their median age 90.0 days (3-330 days), while the median age of the lactose tolerant group was 51.5 days (3-300 days). The incidence of lactose intolerance in infants less than 6 months old was 70.6%, and 76.7% in those older than 6 months.Clinical characteristics showed that more infants in the lactose intolerant group were breastfed compared with the lactose tolerant group [73/156 cases(46.8%) vs.16/61 cases(26.2%), χ2=7.666, P 6 months, between the breastfeeding group and formula-feeding group, or between those with infection and those without infection (all P>0.05). Conclusions Infants with lactose intolerance often manifest foamy feces and tend to be breastfed.Lactose-free treatment efficacy was better than that with lactase.Clinical symptoms when combined with urine galactose level and lactose tolerance test can help diagnosis.However, the decrease of fecal pH proves to be unhelpful in aiding diagnosis. Key words: Lactose intolerance; Clinical characteristics; Treatment; Fecal pH

Arginine does not rescue p.Q188R mutation deleterious effect in classic galactosemia

BackgroundClassic galactosemia is a rare genetic metabolic disease with an unmet treatment need. Current standard of care fails to prevent chronically-debilitating brain and gonadal complications.Many mutations in the GALT gene responsible for classic galactosemia have been described to give rise to variants with conformational abnormalities. This pathogenic mechanism is highly amenable to a therapeutic strategy based on chemical/pharmacological chaperones. Arginine, a chemical chaperone, has shown beneficial effect in other inherited metabolic disorders, as well as in a prokaryotic model of classic galactosemia.The p.Q188R mutation presents a high prevalence in the Caucasian population, making it a very clinically relevant mutation. This mutation gives rise to a protein with lower conformational stability and lower catalytic activity. The aim of this study is to assess the potential therapeutic role of arginine for this mutation.MethodsArginine aspartate administration to four patients with the p.Q188R/p.Q188R mutation, in vitro studies with three fibroblast cell lines derived from classic galactosemia patients as well as recombinant protein experiments were used to evaluate the effect of arginine in galactose metabolism. This study has been registered at https://clinicaltrials.gov (NCT03580122) on 09 July 2018. Retrospectively registered.ResultsFollowing a month of arginine administration, patients did not show a significant improvement of whole-body galactose oxidative capacity (p = 0.22), erythrocyte GALT activity (p = 0.87), urinary galactose (p = 0.52) and urinary galactitol levels (p = 0.41). Patients’ fibroblasts exposed to arginine did not show changes in GALT activity. Thermal shift analysis of recombinant p.Q188R GALT protein in the presence of arginine did not exhibit a positive effect.ConclusionsThis short pilot study in four patients homozygous for the p.Q188R/p.Q188R mutation reveals that arginine has no potential therapeutic role for galactosemia patients homozygous for the p.Q188R mutation.

Effects of cow\u2019s milk beta-casein variants on symptoms of milk intolerance in Chinese adults: a multicentre, randomised controlled study

BackgroundA major protein component of cow’s milk is β-casein. The most frequent variants in dairy herds are A1 and A2. Recent studies showed that milk containing A1 β-casein promoted intestinal inflammation and exacerbated gastrointestinal symptoms. However, the acute gastrointestinal effects of A1 β-casein have not been investigated. This study compared the gastrointestinal effects of milk containing A1 and A2 β-casein versus A2 β-casein alone in Chinese adults with self-reported lactose intolerance.MethodsIn this randomised, crossover, double-blind trial, with a 3-day dairy washout period at baseline, subjects were randomised to consume 300 mL of milk containing A1 and A2 β-casein (ratio 58:42; conventional milk) or A2 β-casein alone; subjects consumed the alternative product after a 7-day washout period. Urine galactose was measured at baseline after a 15 g lactose load. Subjects completed 9-point visual analogue scales for gastrointestinal symptoms (borborygmus, flatulence, bloating, abdominal pain, stool frequency, and stool consistency) at baseline and at 1, 3, and 12 h after milk consumption.ResultsA total of 600 subjects were included. All six symptom scores at 1 and 3 h were significantly lower after consuming A2 β-casein versus conventional milk (all P<0.0001). At 12 h, significant differences remained for bloating, abdominal pain, stool frequency, and stool consistency (all P<0.0001). Symptom scores were consistently lower with A2 β-casein in both lactose absorbers (urinary galactose ≥0.27 mmol/L) and lactose malabsorbers (urinary galactose <0.27 mmol/L).ConclusionMilk containing A2 β-casein attenuated acute gastrointestinal symptoms of milk intolerance, while conventional milk containing A1 β-casein reduced lactase activity and increased gastrointestinal symptoms compared with milk containing A2 β-casein. Thus, milk-related gastrointestinal symptoms may result from the ingestion of A1 β-casein rather than lactose in some individuals.Trial registrationNCT02878876, registered August 16, 2016. Retrospectively registered.

Lactose intolerance in neonates with non-infectious diarrhea

To investigate the development of lactose intolerance in neonates with non-infectious diarrhea and its association with diarrhea, and to evaluate the diagnostic values of fecal pH value and urine galactose determination for neonatal lactase deficiency. Seventy hospitalized neonates who developed non-infectious diarrhea between October 2012 and June 2015 were enrolled as the diarrhea group, and 162 hospitalized neonates without non-infectious diarrhea were enrolled as the non-diarrhea group. Test paper was used to determine fecal pH value. The galactose oxidase method was used to detect urine galactose. The neonates with positive galactose oxidase were diagnosed with lactase deficiency, and those with lactase deficiency and diarrhea were diagnosed with lactose intolerance. According to the results of urine galactose detection, 69 neonates in the diarrhea group who underwent urine galactose detection were classified into lactose intolerance group (45 neonates) and lactose tolerance group (24 neonates), and their conditions after treatment were compared between the two groups. The follow-up visits were performed for neonates with diarrhea at 3 months after discharge. Fecal pH value and positive rate of urine galactose (65% vs 54%) showed no significant differences between the diarrhea and non-diarrhea groups (P>0.05). Fecal pH value showed no significant difference between the lactose intolerance and lactose tolerance groups (P>0.05), while the neonates in the lactose intolerance group had a significantly longer time to recovery of defecation than those in the lactose tolerance group (P<0.05). The incidence of lactase deficiency is high in neonates, and diarrhea due to lactose intolerance tends to occur. Determination of fecal pH value has no significance in the diagnosis of lactose intolerance in neonates with diarrhea.

Early Diet Impacts Infant Rhesus Gut Microbiome, Immunity, and Metabolism

Epidemiological research has indicated a relationship between infant formula feeding and increased risk of chronic diseases later in life including obesity, type-2 diabetes, and cardiovascular disease. The present study used an infant rhesus monkey model to compare the comprehensive metabolic implications of formula- and breast-feeding practices using NMR spectroscopy to characterize metabolite fingerprints from urine and serum, in combination with anthropometric measurements, fecal microbial profiling, and cytokine measurements. Here we show that formula-fed infants are larger than their breast-fed counterparts and have a different gut microbiome that includes higher levels of bacteria from the Ruminococcus genus and lower levels of bacteria from the Lactobacillus genus. In addition, formula-fed infants have higher serum insulin coupled with higher amino acid levels, while amino acid degradation products were higher in breast-fed infants. Increases in serum and urine galactose and urine galactitol were observed in the second month of life in formula-fed infants, along with higher levels of TNFα, IFN-γ, IL-1β, IL-4, and other cytokines and growth factors at week 4. These results demonstrate that metabolic and gut microbiome development of formula-fed infants is different from breast-fed infants and that the choice of infant feeding may hold future health consequences.

Long-term complications in Estonian galactosemia patients with a less strict lactose-free diet and metabolic control

The main aim of our study was to retrospectively evaluate long-term complications and measure urinary galactose and galactitol excretion in classical galactosemia patients in Estonia who have been treated with a less restricted lactose-free diet and metabolic control. Our study group consisted of five classical galactosemia patients aged 7–14 years and diagnosed since 1996 in Estonia. Their diet eliminates lactose present in dairy foods, but we did not restrict the consumption of mature cheeses, fruits and vegetables. All patients had normal growth, except for one patient who was overweight at the last evaluation. In three patients mental and speech development was normal. One patient, number 1, who was diagnosed latest (at 6 weeks of age), had moderate mental retardation, verbal dyspraxia, extrapyramidal signs and bilateral cataracts. In both patients with developmental problems, a brain MRI showed bilateral subcortical changes in the cerebral white matter. Of four females, only patient 4 (p.Q188R homozygote) has premature ovarian insufficiency. Urinary galactose and galactitol content were retrospectively measured using high-performance liquid chromatography and refractive-index detection from urinary samples that were preserved during the years 1996–2009. Galactose ranged from 60 to 600 mmol/mol creatinine (normal = 4–6), and galactitol ranged from 70 to 1200 mmol/mol creatinine (normal = 2–4), which was 10–100 and 17–300 times higher than the respective reference ranges for galactose and galactitol. We conclude that a less strict lactose-free diet and metabolic control performed in Estonian classical galactosemia patients does not change long-term outcome compared to previously published studies.

Features and outcome of galactokinase deficiency in children diagnosed by newborn screening

Galactokinase deficiency (GALK-D), an autosomal recessive disorder in the Leloir pathway, results in accumulation of galactose, galactitol, and galactonate and leads to early onset of juvenile bilateral cataract. Highest incidence of GALK-D is found in Romani populations. The migration wave due to the Yugoslavian civil war has changed the spectrum of inborn errors of metabolism within Europe. Hence, newborn screening (NBS) in the Berlin region, performed from 1991 until 2010 in 683,675 neonates, revealed an increased incidence of GALK-D of 1:40,000, comparable to that of galactose-1-phosphate-uridyltransferase deficiency. A total of 44% of GALK-D patients were of Romani origin. All patients of Bosnian or Serbian origin were homozygous for the Romani founder mutation p.P28T. Detection of GALK-D by NBS and early start of galactose-restricted diet resulted in regression or prevention of cataracts. Slight cataracts without visual impairment occurred in 50% of the patients, 56% of whom were noncompliant. Further clinical symptoms, e.g., hypoglycemia, mental retardation, microcephaly, and failure to thrive, were associated with noncompliance. With treatment, galactose in blood decreased from 8,892 ± 5,243 to 36.5 ± 49.3 μmol/l, galactose in urine from 31,820 ± 32,103 to 30.0 ± 36.1 μmol/mmol creatinine, galactitol in RBC from 1,584 ± 584 to 12.3 ± 9.4 μmol/l, and galactitol in urine from 11,724 ± 4,496 to 236 ± 116 μmol/mmol creatinine. This is the first presentation of outcome and clinical features in GALK-D patients diagnosed by NBS. As our data suggest, GALK-D should be considered for inclusion in NBS in populations expected to have substantial numbers of GALK-D carriers, e.g., Yugoslavian immigrants.

Capillary electrophoresis with laser-induced fluorescence detection for laboratory diagnosis of galactosemia

Galactosemia, a metabolic disorder associated with the intolerance to dietary galactose due to an inherited enzymatic deficiency, is indicated by heightened levels of galactose in urine (galactosuria). In this report, capillary electrophoresis (CE) with laser-induced fluorescence detection was evaluated for its ability to screen urinary carbohydrates, particularly galactose. Neonatal urine samples with normal and abnormal levels of galactose were analyzed with galactose concentrations quantitated relative to urinary creatinine concentrations to account for variable urinary dilution. Analysis of nine samples by CE in a single-blind manner defined four as negative (normal) and five as positive for galactosuria with galactose levels as high as 146.8±5.9 m M. Galactosuria was correlated with clinical galactosemia diagnoses for four of the positive samples, while the remaining positive was associated with a patient diagnosed with Hurler’s syndrome.

Urine screening of five-day-old newborns: metabolic profiling of neonatal galactosuria

We determined urinary galactose and 4-hydroxyphenyllactic acid (4HPLA) in 4338 of 5-day-old newborns using a newly developed GC–MS screening method. Fifty-two infants were chemically diagnosed as having transient galactosuria based upon elevated urinary galactose levels (4.78–30.53 mg/mg creatinine, control 1.10±0.89 mg/mg creatinine). These infants did not excrete galactitol or galactonic acid into the urine, which is typical of hereditary galactosemia. Nearly 40% of the transient galactosuria was associated with immature infants (low birth weight or borne before 37 gestational weeks). Immature hepatic function is one explanation for neonatal transient galactosuria, but heterozygotes or the carriers of galactose degradation enzyme deficiencies were also suspected in some of the newborns, judging from the comparisons of urinary galactose and 4HPLA excretion between neonates and patients with galactosemia.

Comparison of a portable breath hydrogen analyser (Micro H2) with a Quintron MicroLyzer in measuring lactose maldigestion, and the evaluation of a Micro H2 for diagnosing hypolactasia

The measurement of hydrogen in exhaled air and changes in the concentration of blood glucose and urine galactose excretion are indirect methods of diagnosing hypolactasia. The aim of this study was to compare a portable breath hydrogen analyser (Micro H2) with a widely used model (Quintron MicroLyzer) and to compare them with the blood glucose, urine galactose, and gastrointestinal symptoms in the lactose tolerance test. After an overnight fast, 44 volunteers (18-66 y) ingested 50 g lactose in a single oral dose. Changes in exhaled breath hydrogen concentrations were measured with the two analysers, and changes in blood glucose and urinary galactose were assayed for 4 h and used as a reference. Eighteen subjects were diagnosed as maldigesters according to our gold standard of at least two positive tests out of the three: breath hydrogen by Quintron, blood glucose concentration, and urine galactose excretion. The highest increase in the breath hydrogen concentration over the baseline was highly variable: 44-366 ppm (Micro H2) or 27-187 ppm (Quintron MicroLyzer). The sensitivity, specificity, and positive and negative predictive values of the Micro H2 compared to the gold standard were 83%, 96%, 94% and 89%, respectively. Overall agreement was 91% (95% CI 78-97%). Compared to the Quintron, the diagnoses were identical in 100% of the cases (92-100%). Thus, for diagnosing hypolactasia, the Micro H2 appeared as reliable for measuring breath hydrogen concentrations as Quintron MicroLyzer commonly used in oral lactose tolerance tests.

Usefulness of urinary galactose for diagnosis of hypolactasia.

Usefulness of urinary galactose for diagnosis of hypolactasia.

Lactose and galactose intake and metabolism in relation to the risk of epithelial ovarian cancer.

It has been suggested that aspects of lactose consumption and metabolism favoring a relatively high tissue level of galactose-1-phosphate may predispose women to ovarian cancer. The authors sought to examine this hypothesis in a study of 108 18- to 74-year-old Caucasian residents of a three-county area of western Washington who were diagnosed with stage I ovarian cancer during 1989-1991, and 108 age- and race-matched controls. Lactose and galactose intake, measured using a food frequency questionnaire, had been hypothesized to increase risk, but were somewhat lower among the cases than among the controls (75th percentile of lactose intake vs. 25th: odds ratio (OR) = 0.80, 95% confidence interval (Cl) 0.52-1.2; of galactose intake: OR = 0.71, 95% Cl 0.48-1.1). Intestinal lactase activity, also hypothesized to have a positive relation with ovarian cancer occurrence, was measured with an oral lactose challenge followed by determination of urinary galactose; no evidence that it was related to the disease was found (75th percentile of excreted galactose vs. 25th: OR = 0.87, 95% Cl 0.62-1.2). Galactose-1-phosphate uridyltransferase (transferase), the enzyme responsible for the metabolism of galactose-1-phosphate, was measured in erythrocytes; no deficit in cases was observed (75th percentile of transferase activity vs. 25th: OR = 1.3, 95% Cl 0.80-2.1). There was also no excess of cases carrying low-activity genetic variants of the transferase enzyme (lower-activity variants vs. higher-activity variants: OR = 0.61, 95% Cl 0.21-1.7). These results do not support the hypothesis that aspects of lactose and galactose intake and metabolism have a bearing on the etiology of ovarian cancer.

Galactitol in galactosemia.

Urinary galactose and galactitol excretion in controls is age-dependent with the highest concentrations at a younger age. Untreated patients with classical galactosemia excreted highly elevated amounts of galactitol (8000-69,000 mmol/mol creatinine; controls 3-81) which did not correlate with galactose excretion. After treatment, galactose excretion returned to normal in all patients whereas galactitol excretion (45-900 mmol/mol creatinine) remained above the age-matched control range. The excretion of galactitol (96-170 mmol/mol creatinine) in untreated compound heterozygotes was much lower although still above the age-matched control levels, and it returned to normal after treatment. In untreated classical galactosemia patients the galactitol in plasma (120-500 mumol/l) was markedly elevated (controls 0.08-0.86 mumol/l); under treatment, the galactitol concentrations (4.7-20 mumol/l) remained above the control range in all. There was no correlation with age nor with galactose-1-phosphate and UDP-galactose levels. Two untreated compound heterozygotes had elevated plasma galactitol (6.0 and 63 mumol/l) which, when treated, returned to normal.

The frequency distribution of lactose malabsorption among adult populations from the eastern and western Egyptian deserts.

The study consisted of 172 subjects belonging to ethnic groups from Sinai in the Eastern Desert and the New Valley in the Western Desert, with respective mean ages of 36.7 +/- 2.0 and 26.6 +/- 1.0 years. Lactose absorption was assessed by measurement of urinary galactose in pooled 2-hr urine samples following ingestion of an oral lactose dose of 40 g. Mean 2-hr excretion values after ingestion were 32.3 mg galactose in the Sinai and 7.7 mg in the New Valley. In the evaluation of lactose malabsorption, a diagnosis of lactose malabsorption is based upon a cutoff point of 0.075 mg/mg urinary galactose:creatinine ratio. The overall prevalence rate in those populations is 34.3%. The proportion of lactose malabsorbers was 11.1% in Sinai and 51.0% in the New Valley. Highly significant differences (chi 2 = 29.5, P < 0.0001) were found between the two ethnic groups with regard to the frequency distribution of lactose malabsorption. The existence of an east-west gradient of increasing frequencies of lactose malabsorption gene is suggested.

Evaluation of rat intestinal lactase in vivo with 4-galactosylxylose

A deficiency of small intestinal lactase (EC 3.2.1.23) acting in adult type alactasia is the most frequent genetically based syndrome in man, affecting one-third to onehalf of the humans [l]. Its evaluation is important in pediatrics and gastroenterology. This can be carried out directly by mucosal sampling [2], or indirectly from blood glucose determination after a load of lactose [3], administration of lactose and ethanol and determination of galactose in blood [4], determination of 14C02 in the breath after ingestion of a small quantity of 14C-labelled lactose [5], measurement of either breath hydrogen [6,7] or urinary galactose [8] after lactose ingestion and determination of differential urinary excretion of disaccharides [9]. We have reported an entirely different, non-invasive evaluation procedure based on oral administration of 3-methyllactose followed by measurement of 3methylglucose in the urine [ 10,111. 3-Methyllactose proved to be an acceptable

Simple, quantitative enzymic assay of galactose in urine

Journal Article Simple, quantitative enzymic assay of galactose in urine Get access B D Lewis, B D Lewis Search for other works by this author on: Oxford Academic Google Scholar R N Johnson R N Johnson Search for other works by this author on: Oxford Academic Google Scholar Clinical Chemistry, Volume 37, Issue 11, 1 November 1991, Pages 2021–2022, https://doi.org/10.1093/clinchem/37.11.2021a Published: 01 November 1991

Urinary excretion of nitrogenous and non-nitrogenous compounds in the chronic ethanol-fed rat

1. The metabolic consequences of chronic ethanol feeding was investigated by assay of urinary metabolites. Male Wistar rats were fed a liquid diet containing 35% of total energy as ethanol or isovolumetric, isocaloric and isonitrogenous amounts of the same diet in which ethanol was substituted by isocaloric glucose (controls). 2. At 6 weeks the entire skeletal muscle mass was reduced by approximately 20%. The urinary excretion of nitrogen, urea and uric acid increased by between 23 and 128%. Urinary creatinine excretion was not significantly altered. 3. Urinary excretion of magnesium was significantly increased by 43%. Urinary excretion of sodium, potassium, calcium and phosphate was increased slightly (i.e. 5-22%), but this change was not statistically significant. 4. Proton n.m.r. spectroscopic analysis showed that ethanol feeding reduced the urinary excretion of citrate and 2-oxoglutarate (by approximately 50%), suggesting decreased citric acid cycle activity. There was an increased excretion of alanine (44%), but excretion of succinate and acetate was not significantly altered. Ethanol in the urine of ethanol-fed rats comprised approximately 2% of total ethanol intake and less than 1% of total energy intake. 5. Lactose was detectable in urine of ethanol-fed rats, but not in control rats, reflecting the reported decreased intestinal lactase activity and increased gut permeability in alcoholics. Urinary galactose excretion decreased by 41%, but relatively large increases in lactate excretion (50%) did not achieve statistical significance. 6. It was concluded that chronic ethanol feeding causes disturbances in whole-body nitrogen homoeostasis and alterations in intermediary metabolism.