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At least 595 records · Page 33Linked to original sources
PubMed1993

[Lactose-free formula versus adapted formula in acute infantile diarrhea].

We have studied a population of 60 children with acute diarrhea. In order to evaluate the benefit of lactose suppression from the diet on the clinical course of the disease, these children were randomly assigned to either the control group or the experimental group. No differences were found in respects to the duration of the illness (lactose containing formula 4.8 +/- 2 days vs lactose free formula 4.4 +/- 3.1 days). Similarly, body weight change did not change significantly (12.5 +/- 235.8 gr vs 55.9 +/- 238.0 gr, t-test non-significant). Children fed with the lactose free diet voided less frequently than did children in the control group (12.8 +/- 10.5 vs 19.8 +/- 9.5 times; p < 0.01). This difference disappeared when only invasive diarrheas were considered (26.6 +/- 12 vs 21.5 +/- 9.5 voidings; t-test nonsignificant). Finally, only 2 of the 32 cases fed with lactose containing formula showed clinical intolerance to lactose. Therefore, we conclude that in patients with mild-to-moderate acute diarrhea, the resumption of feeding should be undertaken with the same formula that they were previously fed, restricting the use of lactose free formulas to selected cases and to those children in whom a standard milk made symptoms reappear.

Acute Disease↗
PubMed1993

[Lactulose fermentation and lactose absorption in Chilean patients with liver cirrhosis: importance for hepatic encephalopathy therapy].

BACKGROUND: Non-absorbable carbohydrates are widely used in the therapy of hepatic encephalopathy. It has been argued that their effects depend on intestinal fermentation. In some geographic areas other than Chile up to 27% of healthy inhabitants are not able to increase breath hydrogen after a lactulose load, a parameter of intestinal fermentation of carbohydrate. Lactose has been proposed as an alternative to non-absorbable disaccharides in patients with lactase deficiency. AIM: To investigate intestinal fermentation of lactulose and lactose malabsorption in Chilean patients with liver cirrhosis. PATIENTS AND METHODS: 22 healthy controls and 52 patients with liver cirrhosis (16 with hepatic encephalopathy) were prospectively studied by means of lactulose or lactose hydrogen breath tests and lactose tolerance test. MAIN RESULTS: In the control group, 19% were non-hydrogen excretors after lactulose, meanwhile a significant rise in breath hydrogen concentration was observed in all cirrhotic patients (p < 0.01). Lactose tolerance test was indicative of lactase persistance in 37% of cirrhotics and in 43% of controls (NS). Finally, 41% of cirrhotics and 50% of controls had a normal lactose hydrogen breath test (NS). These results were not significantly modified by the presence of hepatic encephalopathy. CONCLUSION: Our data suggest that a lack in bacterial fermentation is not a cause of lactulose therapy failure in Chilean patients with hepatic encephalopathy. Lactose might be an inappropriate substitute to lactulose treating a significant proportion of patients with this condition in our country.

Adolescent↗
PubMed1993

[Prevalence of lactose malabsorption in Roman school children. A H2 breath test study using a cow's milk].

The aim of this study was to evaluate the prevalence of lactose malabsorption in a population of 75 (43 males, 32 females) apparently healthy school-children using the H2 breath test with cow's milk. The children, ranging in age from 8 years and 6 months to 15 years and 2 months (mean: 11 years, 7 months) were divided into 2 age groups: Group I (no. = 26): age < 11 years and Group II (no. = 49): age > 11 years. After on overnight fasting, lasting at least 8 hours, samples of expired air were collected at 0 time and at 30-min intervals following the administration of 250 ml cow's milk for a total time of 3 hours. The H2 breath concentration was then measured by gas chromatography (Micro-Lyzer Quintron Instruments Company mod. 12). A net rise of more than 20 ppm H2 was considered as lactose malabsorption. Subjects with symptoms such as excessive flatulence, abdominal pain, or diarrhoea, were considered as lactose intolerant. Two-hundred and 50 ml of cow's milk (12 g of lactose) was considered a more physiological vehicle than the traditional lactose aqueous solution. The examined children, all on free diet, showed a fasting alveolar from 0 to 43 ppm (mean +/- SD = 7.9 +/- 7.6). Sixty-six children out of 70 (93.3%), who completed the test had a total absorption of lactose. Two out of 4 children with lactose malabsorption originated from areas (East Africa and Central America), where a high incidence of this metabolic disorder is a characteristic findings.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

[Uses of microbial beta-galactosidases to reduce lactose content in milk and dairy products].

The commercial sources of microbial beta-galactosidases (lactases) include the yeasts species Kluyveromyces marxianus, Kluyveromyces lactis and Candida kefyr which are used to hydrolyse lactose in milk due to their optimum pH. On the other hand, lactases obtained from the moulds Aspergillus niger and Aspergillus oryzae have an acid optimum pH and therefore are used to hydrolyse lactose in whey to obtain whey syrups to be used as raw materials in the food industry. The lactose intolerance problem has led to many studies concerning lactose hydrolysis by means of these microbial enzymes to obtain milk suitable for people with lactose maldigestion and special diets for ill persons, elderly population and intolerant babies due to secondary deficiency of lactose. Most industries obtain hydrolyzed lactose milk with free enzyme; however, there are some developments of immobilized lactase catalysts which are being used mainly in whey.

Animals↗
PubMed1999

Association of Clostridium difficile with enterocolitis and lactose intolerance in a foal.

Diagnoses of Clostridium difficile enterocolitis and lactose intolerance were made in a neonatal foal with persistent diarrhea. It was determined that the foal had lactose intolerance on the basis of the results of a lactose tolerance test, and a diagnosis of C difficile enterocolitis was subsequently made. The foal responded to oral administration of metronidazole and lactase. Lactose intolerance is a secondary problem most commonly associated with rotavirus infection, but it can be caused by any condition affecting the small intestine. Because C difficile can affect the small intestine in foals, it was presumably the cause of the lactose intolerance in this foal with persistent diarrhea. Oral administration of lactase was not initially successful in this foal, most likely because of ongoing C difficile enterocolitis. Presumably, metronidazole was an effective treatment for C difficile enterocolitis and administration of lactase allowed for normal digestion of milk until endogenous lactose production returned. Clostridium difficile enterocolitis and lactose intolerance should be considered as differential diagnoses in neonatal foals with diarrhea, especially when the foal is bright and alert.

Animals↗
PubMed2004

Lactose malabsorption in a population with irritable bowel syndrome: prevalence and symptoms. A case-control study.

BACKGROUND: Symptoms after intake of milk are common in persons with irritable bowel syndrome (IBS). The aims of this study were to compare the prevalence of lactose malabsorption (LM) and symptoms related to intake of milk and lactose in subjects with IBS with that of healthy volunteers, and to search for symptoms that are characteristic of LM. METHODS: A case-control study in a Norwegian population was initiated. Subjects with IBS were asked for symptoms related to intake of milk and lactose, tested for LM, and compared with a group of healthy volunteers. RESULTS: The study comprised a total of 187 persons (82 with IBS and 105 volunteers), females/males: 138/49, mean age 47 years. In subjects with IBS and in healthy volunteers, LM was present in 3/74 (4.1%) and 4/105 (3.8%), respectively (ns), milk-related symptoms in 32/79 (40%) and 13/105 (12%), respectively (P < 0.001) and symptoms after intake of lactose in 28/74 (38%) and 21/104 (20%), respectively (P=0.01). Borborygmi starting within 5 h after intake of lactose and lasting for more than 2 h indicated LM (OR 61 (95% CI: 8-475), P < 0.001). CONCLUSIONS: IBS and LM are unrelated disorders in a Norwegian population. Milk-related symptoms and symptoms after intake of lactose are unreliable predictors for LM. Precise symptom-based criteria might enhance the diagnostic accuracy for LM.

Adult↗
PubMed2006

Low lactase activity in a small-bowel biopsy specimen: should dietary lactose intake be restricted in children with small intestinal mucosal damage?

OBJECTIVE: Small intestinal mucosal damage can result in decreased lactase activity (LA). When LA is low in a small-bowel biopsy (SBB) specimen, a reduction of dietary lactose intake is usually advised. This is often done by reducing dietary dairy products, which also reduces the intake of calcium, protein and vitamins. Since intestinal damage can have a patchy character and LA varies along the horizontal axis of the small intestine, the relevance of SBB measurement for intestinal LA could be questioned. We compared LA in the SBB with the in vivo capacity to digest lactose using the Lactose Digestion Index (LDI). MATERIAL AND METHODS: LA was measured in 18 children aged 0.8-10.9 years (mean 3.9, SD 2.4) undergoing SBB for various indications. In all children the LDI was determined using the (13)C-lactose/(2)H-glucose test. RESULTS: In 9/18 biopsy specimens LA was low (<10 U/g protein). LDI was normal in 14/18 patients. In 8 out of 9 patients with normal lactase activity, LDI was also normal, while in 6 out of 9 patients LDI was normal despite low LA in the biopsy. In patients with normal LDI, histology was normal in 6/14, in 4/14 mild histological changes (Marsh II) were seen and in 4 patients histological damage was severe (grade III). CONCLUSIONS: In children with small-bowel mucosal damage, lactose digestive capacity can remain high despite low LA and histological changes in an SBB. Extrapolation of LA in SBB specimens to overall lactose digestive capacity may not be reliable. The advice concerning the restriction of intake of dairy products cannot be based on the data of the SBB only.

Biopsy↗
PubMed1975

Relationship of milk consumption to blood glucose rise in lactose intolerant individuals.

Lactose intolerant populations are heterogeneous with respect to their milk-drinking habits. A gradation of lactase activity in the intolerant population may result in sufficient lactose hydrolysis to obviate symptoms and lead to continued milk consumption. This paper reports on differences in maximum blood sugar rise in lactose intolerant children who are observed to consume or reject milk. Of the 89 black elementary school children, 48 (54 per cent) evidenced a flat lactose tolerance curve. Twenty-eight of these 48 children (58 per cent) were defined as nonmilk drinkers. The maximum blood sugar rise was 12.3 mg/100 in the 20 lactose malabsorbers who were defined as milk drinkers. It appears that some lactose malabsorbing children may have sufficient, albeit lower, levels of lactase to hydrolyze moderate amounts of milk.

Adolescent↗
PubMed1977

Lactose malabsorption in preschool black children.

One hundred sixteen healthy black children ages 13 to 59 months, representing high and low socioeconomic deciles, were studied for lactose malabsorption. A fasting lactose tolerance test using 2 g of lactose/kg of body weight was carried out. Glucose was determined at 0, 15, 30, and 60 min. Of the 116 preschoolers 34 (29%) evidenced lactose malabsorption as determined by a blood glucose rise of less than 26 mg/100 ml. Clinical signs of diarrhea, gas, and cramps were noted singly or in combination in 18% of the 34 lactose-malabsorbing children. Of the 82 lactose absorbers, 12% demonstrated similar signs. The nature and length of the initial infant milk feeding failed to show any relationship to the onset of malabsorption. Current milk drinking patterns were reported as being similar. Eight-seven percent of the malabsorbers and 92% of the absorbers report drinking 240 ml or more of milk/day. Socioeconomic status, education, marital status, and medical assistance of the parent is similarly distributed between lactose absorbers and malabsorbers.

Absorption↗
PubMed1988

Reduced intolerance symptoms from lactose consumed during a meal.

Lactose digestion from and tolerance to lactose-containing beverages consumed with food was evaluated in 12 lactase-deficient subjects by breath-hydrogen techniques. Peak hydrogen production after a milk-based food supplement was delayed 2 h as compared with a lactose solution. Addition of a breakfast meal further delayed peak hydrogen production by 1 h. Hydrogen production was significantly lower (p less than 0.03) for the first 4 h after ingestion of the supplement plus meal compared with the supplement alone. Nine subjects experienced intolerance symptoms after consumption of the supplement alone but only three experienced them after consumption of the meal plus supplement. Severity of symptoms was significantly reduced with the ingestion of the supplement compared with an equal lactose load and was further reduced with the consumption of food, presumably due to delayed gastric emptying. Thus, lactose malabsorbers should consume food simultaneously with lactose-containing beverages to reduce intolerance symptoms.

Adult↗
PubMed1989

Enzyme replacement for lactose malabsorption using a beta-D-galactosidase.

We evaluated 10 healthy symptomatic lactose malabsorbers for effect of an oral beta-D-galactosidase derived from Aspergillus oryzae (Lactrase, Kremers Urban Company, Milwaukee, WI, U.S.A.) on symptom and breath hydrogen response to challenge with 50 g lactose. Basally and at 30-min intervals for 8 h after lactose challenge, end-alveolar breath samples were collected and analyzed for hydrogen using gas chromatography. Symptoms were scored at 30 min and hourly for 8 h, rating bloating, cramps, nausea, pain, diarrhea, and flatulence. Four challenges were performed on 4 separate days with at least 3 days between challenges. The first two challenges served as baselines. Just before ingestion of 50 g powdered lactose dissolved in 200 ml water, beta-D-galactosidase capsules were given orally as a 250-mg dose for the third challenge and a 500-mg dose for challenge 4. Hydrogen excretion, quantified by using a trapezoidal method for computing area under the discontinuous curve of breath hydrogen concentration, was decreased in subjects receiving beta-D-galactosidase (base-line I, 346.0 ppm/h; baseline II, 367.2 ppm/h; 250-mg galactosidase 208.2 ppm/h; 500-mg galactosidase, 178.0 ppm/h; p less than or equal to 0.05). Other analyzed parameters of H2 excretion were also decreased. Analysis of symptom response scores showed a dose-related decrease for bloating and flatus (p less than or equal to 0.05) and no statistical difference in the other assessed symptoms. We conclude that beta-D-galactosidase from Aspergillus oryzae, when given just before ingestion of lactose by lactose malabsorbers, can produce a dose-dependent reduction (statistically significant for the 500-mg dose) in breath hydrogen excretion, bloating, and flatus.

Adult↗
PubMedDate not supplied

Gastric emptying of lactose and glucose-galactose in patients with low intestinal lactase activity.

To test the hypothesis that in subjects with low intestinal lactase activity (LLA) lactose solutions leaves the stomach at an abnormally fast rate, we have measured the gastric emptying rate of solutions of lactose and glucose-galactose in patients with LLA (n = 9) and in control subjects with high intestinal lactase levels (n = 7) as proved by the assay of disaccharidases in specimens of intestinal mucosa. The volume of the test meals was 300 ml. Lactose solutions contain 50 g of disaccharide and glucose-galactose solutions contain 25 g of each monosaccharide. The volumes remaining in the stomach at different times after the intragastric instillation of the test meals were estimated by the double sampling test meal. In the control group, minor differences between lactose and glucose-galactose gastric emptying rates was found. By contrast, in LLA patients, the lactose meal left the stomach at a significantly faster rate than the glucose-galactose test meal. These findings support previous evidence obtained in patients with putatively low intestinal lactase activity and are consistent with the view that duodenal osmoreceptors, whose excitation results in inhibition of gastric emptying, lie deeper than the disaccharidases in intestinal mucosa. Thus, incomplete hydrolysis of lactose results in a faster than normal gastric emptying rate of the sugar and this may contribute to the symptoms found in LLA patients after milk ingestion.

Adult↗
PubMedDate not supplied

[Lactose malabsorption in adult patients at the Hospital das Clínicas de Ribeirão Preto].

A standard oral lactose tolerance test (LTT) was performed in 32 white and 18 non-white hospitalized Brazilian adults. A flat LTT was found in 22 (68,75%) white and in 17 (97,45%) non-white patients indicating a 78% overall rate of lactose malabsorption, Both lactose absorbers and malabsorbers showed a modal milk ingestion of less than a 1 glass/day. Symptoms related to milk consumption or lactose administration were more common among lactose malabsorbers. Estimations of disaccharidase activity in intestinal mucosa specimens obtained by peroral biopsy in 28 patients confirmed a high prevalence of lactose deficiency, and disclosed only one false result, in the patient with a flat LTT and high intestinal lactase levels.

Adolescent↗
PubMed1998

The diversion of lactose carbon through the tagatose pathway reduces the intracellular fructose 1,6-bisphosphate and growth rate of Streptococcus bovis.

Twenty strains of Streptococcus bovis grew more slowly on lactose (1.21 +/- 0.12 h-1) then than on glucose (1.67 +/- 0.12 h-1), and repeated transfers or prolonged growth in continuous culture (more than 200 generations each) did not enhance the growth rate on lactose. Lactose transport activity was poorly correlated with growth rate, and slow growth could not be explained by the ATP production rate (catabolic rate). Batch cultures growing on lactose always had less intracellular fructose 1,6-bisphosphate (Frul,6P2) than cells growing on glucose (6.6 mM compared to 16.7 mM), and this difference could be explained by the pathway of carbon metabolism. Glucose and the glucose moiety of lactose were metabolized by the Embden-Meyerhoff-Parnas (EMP) pathway, but the galactose moiety of lactose was catabolized by the tagatose pathway, a scheme that by-passed Frul,6P2. A mutant capable of co-metabolizing lactose and glucose grew more rapidly when glucose was added, even though the total rate of hexose fermentation did not change. Wild-type S. bovis grew rapidly with galactose and melibiose, but these galactose-containing sugars were activated by galactokinase and catabolized via EMP. On the basis of these results, rapid glycolytic flux through the EMP pathway is needed for the rapid growth (more than 1.2 h-1) of S. bovis.

Adenosine Triphosphate↗
PubMed2004

Toxicological studies on Lactose Oxidase from Microdochium nivale expressed in Fusarium venenatum.

A new carbohydrate oxidase, Lactose Oxidase, with high specificity of oxidizing the disaccharide lactose to lactobionic acid has been found. This enzyme opens up for a variety of applications. A programme of toxicological studies was conducted to establish the safety of Lactose Oxidase to be used as a processing aid in the food industry. The enzyme used in this study was produced by a submerged fermentation of Fusarium venenatum and contained a gene code from Microdochium nivale. Oral administration to rats of up to 10 mL/kg bodyweight (bw)/day (equivalent to a total organic solids dosage of 900 mg/kg bw/day or a Lactose Oxidase dosage of 344 LOXU/kg bw/day) for 13 weeks did not cause any adverse effect. Lactose Oxidase was not found to be mutagenic in the bacterial reverse mutation assay, nor did it cause chromosomal aberrations in cultured human lymphocytes. The maximum recommended dosage of Lactose Oxidase is 50 LOXU/kg liquid whey protein concentrate. The safety margin for exposure is estimated to be at least 6.2 x 10(4) for daily diary product consumption. In conclusion Lactose Oxidase can be considered as safe for use in the food industry.

Administration, Oral↗
PubMed2000

Topography of the surface of the Escherichia coli phosphotransferase system protein enzyme IIAglc that interacts with lactose permease.

The unphosphorylated form of enzyme IIAglc of the Escherichia coli phosphoenolpyruvate:sugar phosphotransferase system inhibits transport catalyzed by lactose permease. We (Seok et al. (1997) Proc. Natl. Acad. Sci. U.S.A. 94, 13515-13519) previously characterized the area on the cytoplasmic face of lactose permease that interacts with enzyme IIAglc, using radioactive enzyme IIAglc. Subsequent studies (Sondej et al. (1999) Proc. Natl. Acad. Sci. U.S.A. 96, 3525-3530) suggested consensus binding sequences on proteins that interact with enzyme IIAglc. The present study characterizes a region on the surface of enzyme IIAglc that interfaces with lactose permease. Acetylation of lysine residues by sulfosuccinimidyl acetate treatment of enzyme IIAglc, but not lactose permease, reduced the degree of interaction between the two proteins. To localize the lysine residue(s) on enzyme IIAglc that is(are) involved in the regulatory interaction, selected lysine residues were mutagenized. Conversion of nine separate lysines to glutamic acid resulted in proteins that were still capable of phosphoryl acceptance from HPr. Except for Lys69, all the modified proteins were as effective as the wild-type enzyme IIAglc in a test for binding to lactose permease. The Lys69 mutant was also defective in phosphoryl transfer to glucose permease. To derive further information concerning the contact surface, additional selected residues in the vicinity of Lys69 were mutagenized and tested for binding to lactose permease. On the basis of these studies, a model for the region of the surface of enzyme IIAglc that interacts with lactose permease is proposed.

Acetates↗
PubMed1968

The lactose synthetase particles of lactating bovine mammary gland. Characteristics of the particles.

1. The conditions that promoted the solubilization of particulate lactose synthetase were effective for solubilizing the thiamine pyrophosphatase of the Golgi apparatus but differed from those effective for beta-glucuronidase or acid phosphatase of lysosomes. 2. Lactose synthetase-containing particles did not bind Mg(2+) or Cs(+) ions, suggesting that they are not related to endoplasmic reticulum membranes. 3. Intact lactose synthetase and thiamine pyrophosphatase particles banded isopycnically at a density of 1.143 in a sucrose gradient. The dissociated ;A' sub-unit of lactose synthetase, UDP-galactose hydrolase, p-nitrophenyl phosphate acid phosphatase, alkaline phosphatase and phosphodiesterase I were associated with particles of a broad density range from 1.12 to 1.20. Lysosomal enzymes beta-glucuronidase, arylsulphatase and beta-glycerophosphate acid phosphatase were associated with particles of density 1.20, 1.175 and 1.15 respectively. 4. Rate-zonal sedimentation studies indicated that lactose synthetase particles have S(20,w) values exceeding 24000s, corresponding to spherical particles of diameter exceeding 5.4x10(-5)cm. 5. Electron micrographs of lactose synthetase particles purified over 20-fold revealed small spherical bodies (0.1-0.5mu) resembling lysosomes, the smaller of which were attached to membranes, and larger heterogeneous spherical or oval bodies (0.7-1.8mu) resembling lipofuscin secretory granules. 6. The relationship between lactose synthetase particles and the Golgi origin of secretion granules is discussed.

Acid Phosphatase↗
PubMed2000

A revised model for the structure and function of the lactose permease. Evidence that a face on transmembrane segment 2 is important for conformational changes.

The lactose permease is an integral membrane protein that cotransports H(+) and lactose into the bacterial cytoplasm. Previous work has shown that bulky substitutions at glycine 64, which is found on the cytoplasmic edge of transmembrane segment 2 (TMS-2), cause a substantial decrease in the maximal velocity of lactose uptake without significantly affecting the K(m) values (Jessen-Marshall, A. E., Parker, N. J., and Brooker, R. J. (1997) J. Bacteriol. 179, 2616-2622). In the current study, mutagenesis was conducted along the face of TMS-2 that contains glycine-64. Single amino acid substitutions that substantially changed side-chain volume at codons 52, 57, 59, 63, and 66 had little or no effect on transport activity, whereas substitutions at codons 49, 53, 56, and 60 were markedly defective and/or had lower levels of expression. According to helical wheel plots, Phe-49, Ser-53, Ser-56, Gln-60, and Gly-64 form a continuous stripe along one face of TMS-2. Several of the TMS-2 mutants (S56Y, S56L, S56Q, Q60A, and Q60V) were used as parental strains to isolate mutants that restore transport activity. These mutations were either first-site mutations or second-site suppressors in TMS-1, TMS-2, TMS-7 or TMS-11. A kinetic analysis showed that the suppressors had a higher rate of lactose transport compared with the corresponding parental strains. Overall, the results of this study are consistent with the notion that a face on TMS-2, containing Phe-49, Ser-53, Ser-56, Gln-60, and Gly-64, plays a critical role in conformational changes associated with lactose transport. We hypothesize that TMS-2 slides across TMS-7 and TMS-11 when the lactose permease interconverts between the C1 and C2 conformations. This idea is discussed within the context of a revised model for the structure of the lactose permease.

Biological Transport↗