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PubMed1984

A quantitative cytochemical assay of beta-galactosidase in single cultured human skin fibroblasts.

A quantitative cytochemical method for the measurement of beta-galactosidase activity in cultured human skin fibroblasts has been developed using 5-bromo-4-chloro-3-indolyl-beta-D-galactopyranoside as the indigogenic substrate. The method relies upon the oxidation of the primary reaction product by ferro/ferricyanide during which an insoluble indigo dye is generated as the final reaction product. The reaction was linear with time up to 60 min using the final cytochemical standard procedure. The enzyme showed maximum activity at pH 4.0 to 4.1. The concentration optima of indigogenic substrate and potassium ferro/ferricyanide were 3.67 mM and 3.13 mM respectively. The presence of sodium chloride activated beta-galactosidase up to 100 mM, but was inhibitory above that concentration. The enzyme was inhibited by N-ethylmaleimide, N-acetyl-D-galactosamine and heparin. The enzyme molecules were shown to diffuse out of the cells using media without a suitable inert colloid stabilizer. However, diffusion was completely prevented by using polyvinyl alcohol (PVA) grade G18/140. Air-drying of cells was essential to make the cell membrane permeabel to the substrate and, thereby, to avoid a pronounced lag phase. However, in a biochemical analysis, air-drying itself caused a decrease in enzyme activity to 43% of the control. Even after air-drying lysosomal latency could still be demonstrated by using PVA grade G04/140. Control persons, one carrier of and two patients with beta-galactosidase deficiency were easily identified as belonging to three separate groups by using the cytochemical assay. It is proposed that the quantitative cytochemical approach may also be applied to cultured human amniotic fluid cells or chorion biopsies giving a rapid prenatal diagnosis of beta-galactosidase deficiency due to the small number of cells needed in the analysis.

Cells, Cultured↗
PubMed1982

Human beta-galactosidase and alpha-neuraminidase deficient mucolipidosis: genetic complementation analysis of the neuraminidase deficiency.

Human beta-galactosidase and alpha-neuraminidase deficient mucolipidosis [ML(gal-neur-)] is an inherited lysosomal enzymopathy which recently was designated as a sialidosis. We analyzed the neuraminidase deficiency of this disorder with genetic complementation analyses using a heterokaryon enrichment procedure. The genetic defects of two apparent variants of this disorder complemented the defects of the neuraminidase deficiency diseases, sialidosis I and mucolipidosis I, resulting in the restoration of neuraminidase activity in heterokaryons. The neuraminidase deficiency, therefore, may not be the primary defect in ML(gal-neur-) and is not an appropriate test for determining carrier status. The clinical and biochemical characteristics of this disorder suggest that a post-translational or processing event for these enzymes may be defective. The defect, however, is different from I-cell disease and pseudo-Hurler polydystrophy, two disorders of post-translational lysosomal enzyme biosynthesis, since complementation studies demonstrated recovery of intracellular beta-galactosidase and alpha-neuraminidase levels in heterokaryons. The lack of human beta-galactosidase expression in man-mouse somatic cell hybrids formed from fibroblasts of the infantile onset type disorder suggests that the defect is not corrected by the mouse genome. The ML(gal-neur-) disorder therefore appears to be a distinct subtype of the inherited neuraminidase deficiencies in which the defect mat occur in a post-translational or regulatory step which coordinately affects the expression of lysosomal beta-galactosidase and alpha-neuraminidase.

Animals↗
PubMed1983

Neuropathological findings of an autopsy case of adult beta-galactosidase and neuraminidase deficiency.

An autopsy case of a Japanese male with familial beta-galactosidase and neuraminidase deficiency is reported. The clinical picture was characterized by adult onset, a gargoyle-like face, cerebellar ataxia, myoclonus, convulsions, retinal degeneration and cortical blindness. Histopathologically, most neurons seemed to have become degenerated in the whole cerebral cortex. Moreover, the calcarine cortex appeared spongy with depopulation of nerve cells. Stuffed neurons or neuronal storage changes were found throughout the brain, especially in the motor nuclei of the spinal cord and brain stem. The inclusions in the stuffed neurons revealed various profiles on the electron microscope. They were composed of membranous lamellar and/or multilamellar structures, often accompanying vacuoles and reminiscent of lipofuscin-like profiles.

Age Factors↗
PubMed1981

A family study of lactose tolerance.

Survey data from 38 families consisting of both parents and at least one biological offspring provided no support for the belief that lactose tolerance resulted from having at least one dominant gene on an autosomal gene pair and did not support the belief that Caucasians are more frequently tolerant of lactose than are persons of Oriental or of mixed Caucasian-Oriental ancestry.

Adult↗
PubMed1976

Sugar absorption by small bowel biopsy samples from patients with primary lactase deficiency and with adult celiac disease.

The present study was undertaken to compare the 3-O-methyl-D-glucose (3MG) absorption by jejunal biopsies from normal human subjects (N = 3) with that by the jejunum of the rat (N = 8) and of the hamster (N = 8), and to examine whether jejunal biopsies from normal subjects (N = 3), patients with primary lactase deficiency (N = 5) and from patients with celiac sprue (N = 5) follow the same pattern of sugar absorption as usually observed in vivo. The results indicate that under the conditions of our experiments the estimated affinity of carrier for 3MG (ie, apparent Km) in the biopsies from normal subjects did not differ significantly from that in rat or hamster jejunum. The estimated capacity of carriers for 3MG absorption (ie, Vmax) appeared to be similar in biopsies from normal subjects and in hamster jejunum, but significantly lower in rat jejunum. There was no difference in apparent Km between the biopsies from normal subjects and those from the patients with lactase deficiency. Although the Vmax for the lactase deficient patients was substantially higher than that for the normal subjects, the difference was not statistically significant. The absorption of 3MG by the biopsies from patients with celiac sprue did not follow Michaelis-Menten kinetics and was compatible with that of passive diffusion or low saturation conditions. Since the intracellular concentration of 3MG in all biopsies from celiac patients exceeded the concentration of the media, sugar transport could not have occurred by diffusion, and it is concluded that the absence of Michaelis-Menten kinetics was the result of low saturation conditions. This active transport with low saturation kinetics in patients with celiac disease suggests that in these patients not only the number of functioning carrier molecules is diminished but also the affinity of the existing carrier for sugar molecule is reduced. This situation, at least in some patients, seems to improve after treatment with gluten-free diet.

Adult↗
PubMed1977

Gastric emptying of lactose and milk in subjects with lactose malabsorption.

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.

Adult↗
PubMed1977

Effects of age on lactose malabsorption in Oklahoma Native Americans as determined by breath H2 analysis.

Breath H2 excretion was used to determine lactose malabsorption in 30 health females and 30 healthy males between the ages of 3 and 64 yr who were at least 7/8 Native American. The test meal consisted of 5 ml reconstituted nonfat dry milk (0.25 g lactose) per kg of body weight. On the basis of breath H2 tests in 15 control subjects with normal oral lactose tolerance tests, a response factor of 20 ppm was selected as the upper limit for lactose absorbers. Of the 60 subjects in the study group, 36 (60%) were classified as lactose malabsorbers since they had a response factor of 20 ppm or greater of breath H2. Only 3 of 20 children (15%) who were under the age of 12 yr were nondigesters of the small lactose dose used in this study. Approximately 82 percent (82.5%) of subjects who were 13 yr and older were lactose malabsorbers. Adolescence appears to be the period in which malabsorption of lactose becomes evident in Native North Americans.

Adolescent↗
PubMed1978

The geographic hypothesis and lactose malabsorption. A weighing of the evidence.

Reviewed in this article is evidence bearing on the geographic hypothesis advanced eight years ago to explain the striking ethnic or racial differences in prevalence of primary adult lactose malabsorption that are found around the world. Most evidence is found to support the hypothesis and the likelihood that some human groups came to have low prevalences of such lactose malabsorption because of selective pressures over a long historical period that favored the adult lactose absorber under particular ecological conditions.

Adult↗
PubMed1993

Comparative effects of exogenous lactase (beta-galactosidase) preparations on in vivo lactose digestion.

Microbial-derived beta-galactosidase (beta-gal) enzyme preparations improve in vivo lactose digestion and tolerance through enhanced gastrointestinal digestion of lactose. Three different beta-gal preparations, Lactogest (soft gel capsule), Lactaid (caplet), and DairyEase (chewable tablet) and placebo were fed to lactose maldigesters with either 20 g or 50 g of lactose to compare the efficacy of these products and to further establish a dose-response relationship for use. All enzyme preparations dramatically reduced both the peak and total breath hydrogen production when fed with milk containing 20 g of lactose. Four capsules of Lactogest, two caplets of Lactaid, or two tablets of DairyEase (each treatment containing approx 6000 IU) reduced total hydrogen production significantly (P < 0.05) below that observed with two capsules of Lactogest (containing approx 3000 IU) in a stoichiometric manner. Symptoms were significantly (P < 0.05) less severe with all the beta-gal products. In contrast, with 50 g of lactose in water, peak and total hydrogen production was modestly, but not significantly reduced by the enzyme treatment. Furthermore, symptom scores for bloating, cramping, nausea, pain, diarrhea, and flatus were not different between treatments and the control. The 50-g lactose dose appeared to overwhelm the ability of either 3000 or 6000 IU of beta-gal to assist significantly with lactose digestion. Results from these studies demonstrate the relative equivalency of chewable, caplet, and soft-gel beta-gal products, based on IUs of enzyme fed.

Administration, Oral↗
PubMed1980

Treatment of chronic portal-systemic encephalopathy with lactose in lactase-deficient patients.

A controlled cross-over clinical comparison of lactose (50 g twice a day) versus neomycin (3 g/day) plus milk of magnesia, was carried out in ten cirrhotic patients with chronic portal-systemic encephalopathy and documented lactase deficiency. Serial semiquantitative assessments were done including: mental state, asterixis, number connection test, electroencephalogram, and blood ammonia levels. No patient developed deep coma while ingesting either lactose or neomycin plus milk of magnesia. However, a significant improvement of mental state, asterixis, number connection tests, and electroencephalograms was evident during lactose therapy. apart from mild diarrhea and bloating, no severe side effects were noticeable during lactose treatment. Based on these results, we propose lactose as a valuable alternate treatment of portal-systemic encephalopathy in lactase-deficient populations.

Chronic Disease↗
PubMed1979

Absorption of nutrients in lactase deficiency.

The influence of malabsorption of lactose, as a result of primary lactase deficiency, on the absorption of the nutrients in milk was tested in four healthy controls and four subjects with lactase deficiency. An ileal perfusion technique was used to quantify arrival in the ileum of nutrients and a nonabsorbable marker (polyethylene glycol, PEG 4000) ingested as a test meal of milk. The meal was 250 ml of whole milk or milk in which the lactose had been hydrolyzed to glucose and galactose. In the fasting state, ileal flow of volume, protein, carbohydrate, and electrolytes was small and not different in controls and lactase-deficient subjects. Ileal flow increased in all subjects after the test meal of milk; more fluid and nutrient was recovered from the ileum in lactase-deficient subjects after whole milk than in control subjects or in lactase deficiency after hydrolyzed milk. Two deficient subjects showed marked malabsorption of lactose (35 and 50%); two did not. Protein, calcium, magnesium, and phosphorus were also recovered from the ileum in greater quantities in lactase deficients after whole milk. However, apart from decreased absorption of lactose, the nutritional consequences of malabsorption in association with primary lactase deficiency in adults are probably minimal.

Adult↗
PubMed1986

Calcium absorption from milk in lactase-deficient and lactase-sufficient adults.

To determine whether lactose influences the absorption of calcium, the uptake of calcium from lactose-hydrolyzed milk and from unhydrolyzed milk was measured in 20 adults: 10 were lactase-deficient and 10 were lactase-sufficient as defined by breath hydrogen test, plasma glucose determination after oral lactose dose, and presence or absence of symptoms after lactose ingestion. On different days, each subject received either lactose-hydrolyzed or unhydrolyzed milk. Calcium absorption was measured by a double-isotope technique. In the lactase-deficient group, the mean absorptions were 33.5% from hydrolyzed milk and 36.2% from the same volume of unhydrolyzed milk (P greater than 0.30). In the lactase-sufficient group, mean absorptions were 24.2% from hydrolyzed milk and 25.7% from unhydrolyzed milk. The mean calcium absorption from both lactose-hydrolyzed milk and unhydrolyzed milk was significantly greater (P less than 0.01) in the lactase-deficient group compared to the lactase-sufficient group, presumably reflecting lower dietary calcium intake in the former. These data indicate that, in lactase-deficient subjects, malabsorption of lactose does not affect calcium absorption.

Adult↗
PubMed1993

Relationship between methane production and breath hydrogen excretion in lactose-malabsorbing individuals.

Recent studies have shown reduced breath hydrogen (H2) excretion in methane (CH4)-producing healthy individuals following ingestion of lactulose. This questions the reliability of the breath hydrogen test (BHT) in CH4 excretors, but the relationship between CH4 and H2 excretion in other clinical applications of the BHT is not known. We reviewed BHT results in two groups of subjects: (1) 385 children tested for lactose malabsorption in a hospital setting, and (2) 109 lactose-malabsorbing patients tested with a home kit. The percentage of lactose malabsorbers in group 1 (51%) was the same regardless of CH4-producing status (P = 0.97). The BHT data from group 2 showed a positive correlation (r = 0.6, P < 0.000001) between the magnitude of the rise in CH4 and H2 concentrations, and the H2 excretion curves were significantly higher in the CH4-producing individuals. We conclude that attention to CH4-producing status is not necessary in the interpretation of the lactose BHT.

Adolescent↗