Letter: Lactose feeding in lactose-intolerant monkeys.
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Thirty children on a lactose-free diet aged from 2-38 months who had previously been diagnosed as having secondary lactose intolerance were reinvestigated on 32 occasions by an oral lactose tolerance test, small intestinal biopsy, and measurement of disaccharidase activity in order to detect the presence of continuing lactose intolerance before reintroduction of milk. No correlation was found between continuing lactose intolerance, as diagnosed by the development of watery stools containing excess reducing substances after an oral load of lactose, and maximum blood glucose rise during a lactose tolerance test, lactase levels, and small intestinal morphology.
Experiments were conducted to determine the amount of lactose which passed into the large intestine and the lactase activity in the small intestine of rats (200 g) fed a control diet or a diet containing 30% lactose. The fraction of lactose consumed in a single 1-hour meal that escaped hydrolysis in the small intestine was estimated by measuring the area under a smooth curve of a plot of lactose:marker ratio in the terminal ileum expressed as a fraction of intake, against the fraction of the total marker that passed into the large intestine. This amounted to approximately 30% and 31.5% of the lactose consumed for the rats fed the control and 30% lactose diets, respectively. In another experiment in which the rats were fed a diet containing 30% lactose and the Cr-EDTA marker ad libitum for 1 week, approximately 43% of the lactose consumed became available for fermentation in the large intestine. This work suggests that a substantial fraction of the lactose ingested is available for fermentation in the large intestine. The lactase activity of homogenates of the small intestine of rats fed the control or high lactose diet was 106 +/- 5 or 115 +/- 4 mg lactose/30 minutes/rat (P less than 0.05), respectively. The lactase activity in the small intestine homogenate (mucosa + contents) was significantly higher than that actually available in vivo (110 +/- 7 versus 69 +/- 4 mg/30 minutes/rat).
The clinical significance of lactose malabsorption and the individual sensitivity to lactose were investigated in 20 patients with verified lactose malabsorption. Thirteen patients were relieved of all symptoms while seven improved only on a lactose-free dth lactose-free milk but following provocation with increasing amounts of lactose, the tendency to diarrhea and abdominal discomfort increased considerably. Three patients experienced discomfort after provocation with only 5 gl lactose. On provocation with increasing amounts of lactose the seven patients who had not recovered also developed increased abdominal discomfort but none of them developed increased tendency to diarrhea. It is concluded that, in addition to lactose malabsorption, these patients must suffer from ittitable colon with tendency to constipation.
1. Lactose 6'-O-sulphate, N-acetylneuraminyl-(alpha 2 leads to 3)-D-lactose 6'-O-sulphate, N-acetylneuraminyl ?-O-sulphate-(alpha 2 leads to 3)-D-lactose 6'0-O-sulphate, N-acetylneuraminyl ?-O-sulphate-(alpha 2 leads to 6)-D-lactose and N-acetylneuraminyl-(alpha 2 leads to 3)- and -(alpha 2 leads to 6))-lactose 6'-O-sulphate were prepared by chemical sulphation of lactose, N-acetylneuraminyl-lactose and tis isomers by using pyridine-SO3 reagent. 2. Significant kinetic differences were observed in the enzymic hydrolysis of the sulphated derivatives compared with unsubstituted substrates. 3. In the case of reactions catalysed by rat liver lysosomal and Clostridium perfringens neuraminidases (EC 3.2.1.18), the presence of an O-sulphate group in the N-acetylneuraminyl moiety affected the reaction by decreasing the Km and the Vmax, its presence in the galactosyl moiety affected the reaction by decreasing the Km and increasing the Vmax. and its presence in both N-acetylneuraminyl and galactosyl moieties decreased the Km and the Vmax. of the reaction. 4. Mixed-substrate reaction kinetic data indicated competition between the sulphated and unsubstituted substrates for the same active sites on the neuraminidase molecule. 5. Lactose 6'-O-sulphate neither behaved as a substrate nor acted as an inhibitor with respect to unsubstituted lactose and p-nitrophenyl beta-D-galactopyranoside when tested with lactase of suckling rat intestine and Escherichia coli beta-D-galactosidase (EC 3.2.1.23). 6. Preliminary investigation also indicated that, whereas glucose 6-O-sulphate and glucose 3-O-sulphate were were neither substrate nor inhibitor of glucose oxidase (EC 1.1.3.4), galactose 6-O-sulphate was oxidized half as fast as unsubstituted galactose by galactose dehydrogenase (EC 1.1.1.48).
Lactose killing is a peculiar phenomenon in which 80 to 98% of the Escherichia coli cells taken from a lactose-limited chemostat die when plated on standard lactose minimal media. This unique form of suicide is caused by the action of the lactose permease. Since uptake of either lactose or galactose by the lactose permease caused death, the action of rapid transport across the membrane must be the cause of the phenomenon. Alternative causes of lactose killing, such as accumulation of toxic metabolic intermediates or action of the beta-galactosidase, have been eliminated. It is proposed that rapid uptake of sugars by the lactose permease disrupts membrane function, perhaps causing collapse of the membrane potential.
Six lactose absorbers (LA) and 5 lactose malabsorbers (LM) had tests of gastric emptying with 750-ml meals of glucose in water, lactose in water, plain milk, and chocolate milk. The glucose and lactose meals emptied in a similar fashion in LA and LM subjects with a significant decrease in gastric emptying as the osmolarity of the meals was doubled. If the data are normalized by dividing lactose emptying by the emptying of glucose meals of twice the osmolality in each individual, the lactose malabsorbers empty significantly more lactose. Both LA and LM subjects emptied comparable amounts of milk meals having similar osmolarity. Chocolate milk, which had a higher osmolality than plain milk, emptied more slowly than plain milk in both groups, and this difference was significant in the LM group.
The unstable ability to metabolize lactose (lac) via the phosphoenolpyruvate-phosphotransferase system (PTS) was examined in Streptococcus cremoris B1. The presence of functional lactose-specific PTS enzymes was correlated with the presence of a distinct plasmid species. Characterization of deoxyribonucleic acid extracted from lactose-positive (Lac+) S. cremoris B1 revealed two plasmids having molecular weights of 9 X 10(6) and 36 X 10(6). An acriflavine (BC1)-induced, lactose-negative (Lac-) mutant possessed no plasmids and was devoid of all three lac-specific PTS enzymes. A Lac- mutant (DA2) isolated by growing at elevated temperatures only possessed the 9 X 10(6)-dalton plasmid and also lacked the lac PTS enzymes. A spontaneous Lac- mutant possessed both the 9 X 10(6)-and 36 X 10(6)-dalton plasmids. This mutant displayed FIII-lac and phospho-beta-D-galactosidase (P-beta-gal) activity but was deficient in EII-lac activity. The spontaneous Lac- strain reverted to both full and partial lactose-fermenting phenotypes having FIII-lac, EII-lac, and P-beta-gal activities. BC1 and DA2 Lac- mutants reverted only to the partial lactose-fermenting phenotype having P-beta-gal activity; EII-lac and FIII-lac activities were absent. The results indicate that the genetic determinants for EII-lac, FIII-lac, and P-beta-gal are located on the 36 X 10(6)-dalton plasmid in S. cremoris B1. Evidence for a second chromosomally associated P-beta-gal gene operating in the partial lactose-fermenting revertants is also presented.
The breath hydrogen test (BHT) was adapted for use in young infants and children. The diagnostic criterion of sugar malabsorption in the BHT was determined by oral administration of 0.5 g/kg of unabsorbable sugar (lactulose) to 21 healthy infants and children. A maximum increase in breath hydrogen less than 0.05 ml/min per m2 was observed in all subjects. A good correlation between results by the BHT and by the ordinary lactose tolerance test was obtained after oral administration of 2 g/kg lactose to 21 healthy infants and children, 2 congenital lactase-deficient infants, and 7 adults. Using this test, 80 healthy Japanese infants and children (aged between one month and 15 years) and 18 adults were examined for lactose malabsorption after a dose of 1 g/kg lactose. All infants and children under 2-years old absorbed lactose completely. The incidence of lactose malabsorption was 30% in 3-year, 36% in 4-year, 58% in 5-year, and 86% in 6-year-old children, 85% in schoolchildren, and 89% in adults. Thus the incidence of lactase deficiency gradually increases with age from 3 years, and about 90% of all normal Japanese adults are lactase-deficient.
Weight-gain in 35 slightly undernourished Australian Aboriginal infants was studied in hospital (49 admissions) during a blind controlled trial of a pre-hydrolysed low-lactose milk preparation and reconstituted full-cream milk powder. Infants fed the lactose hydrolysed milk gained 70% more weight than those receiving normal milk. Better weight-gains were achieved in those on the lactose hydrolysed milk irrespective of percentage standard weight for age, the presence of diarrhoea on admission to the trial, and stool sugar concentrations. The use of low-lactose milk should be considered in nutritional aid programmes for undernourished children throughout the world.
Milk intolerance was investigated in 87 healthy elderly individuals with a mean age of 77 years who were given 240 ml of a chocolate dairy drink twice in one week with a light lunch. No significant differences in symptomatic responses distinguished the subjects consuming a lactose-free (LF) drink from those consuming a drink containing 4.5% lactose (LC) under double-blind study conditions. Breath hydrogen analysis during lactose tolerance testing identified 23 malabsorbers, none of whom responded exclusively to the LC drink, although five were symptomatic on both days, and two had symptoms only on the day the LF drink was served. A similar percentage of absorbers (72%) and malabsorbers (70%) were asymptomatic on both days. Factors other than lactose malabsorption appeared to be responsible for the symptoms of intolerance reported, and most may have been psychosomatic in origin.
The behaviour of lactose levels in first quarter milk was studied in the context of a large dairy herd in the presence of various udder health defects. The results were related to other criteria generally used in mastitis diagnosis. The lactose level in first quarter milk was found to be a diagnostic criterion which was properly applicable to detecting and identifying clinical and subclinical mastitis. A limit value of 4.6 per cent has been commonly assumed in literature and proved to be a sound basis for udder health assessment, provided that the given phase of lactation is taken into due consideration (exclusion of cows in the first month post partum as well as of aged milking cows from the seventh month of lactation). Also reported in this paper are results regarding milk lactose and its correlations with other criteria for mastitis diagnosis. A close correlation was found to exist between lactose level and electric conductivity of first quarter milk.
A total of 194 publications related to lactose malabsorption or intolerance were reviewed. The poor correlation between lactose malabsorption and intolerance to the amounts of milk ordinarily ingested in a meal, indicates that the assumption of milk tolerance by many populations is exaggerated. The methods for the diagnosis of these conditions were critically evaluated and it is suggested that, a) "physiological" doses of lactose be used; b) milk is the vehicle of choice; c) tests of intolerance be double-blind, and d) analysis of breath hydrogen be used for malabsorption. Most of the evidence indicates that milk consumption allows adequate growth of children, even when they are malnourished and have diarrhea. Nevertheless, it is recommended to substitute temporarily non-human milk by other good sources of dietary protein and energy during episodes of severe diarrhea, and to reintroduce milk to the diet gradually during convalescence. Breast feeding, however, should not be interrupted. These is not enough scientific nor epidemiological support to justify discouraging the use of milk in food supplementation programs, but several aspects that must be considered in such programs are outlined.
A number of specific duplex DNA sequences which correspond to varying lengths of the lactose operator region have been synthesized by a combination of chemical and enzymatic methods. Repressor binding studies on these synthetic duplex operator molecules show that all the nucleotides essential for full lactose operator-repressor interactions are included in a 17-nucleotide-long duplex DNA that constitutes the minimal recognition sequence for this DNA-protein interaction.
Studies were conducted into lactose levels of milk in response to experimentally irritated or artificially infected udder quarters. Milk lactose was found to be suitable as a model parameter by which to objectivate pathophysiological processes in the udder in the context of research, such as experiments on artificial udder infection or testing of udder tolerance of certain medicaments.
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Explore the source record for details and available documents.