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At least 19 recordsLinked to original sources
PubMed2004

Lactose surface modification by decantation: are drug-fine lactose ratios the key to better dispersion of salmeterol xinafoate from lactose-interactive mixtures?

PURPOSE: The role of fine lactose in the dispersion of salmeterol xinafoate (SX) from lactose mixtures was studied by modifying the fine lactose concentration on the surface of the lactose carriers using wet decantation. METHODS: Fine lactose was removed from lactose carriers by wet decantation using ethanol saturated with lactose. Particle sizing was achieved by laser diffraction. Fine particle fractions (FPFs) were determined by Twin Stage Impinger using a 2.5% SX mixture, and SX was analyzed by a validated high-performance liquid chromatography method. Adhesion forces between probes of SX and silica and the lactose surfaces were determined by atomic force microscopy. RESULTS: FPFs of SX were related to fine lactose concentration in the mixture for inhalation grade lactose samples. Reductions in FPF (2-tp 4-fold) of Aeroflo 95 and 65 were observed after removing fine lactose by wet decantation; FPFs reverted to original values after addition of micronized lactose to decanted mixtures. FPFs of SX of sieved and decanted fractions of Aeroflo carriers were significantly different (p < 0.001). The relationship between FPF and fine lactose concentration was linear. Decanted lactose demonstrated surface modification through increased SX-lactose adhesion forces; however, any surface modification other than removal of fine lactose only slightly influenced FPF. CONCLUSIONS: Fine lactose played a key and dominating role in controlling FPF. SX to fine lactose ratios influenced dispersion of SX with maximum dispersion occurring as the ratio approached unity.

Administration, Inhalation↗
PubMed1996

Colonic adaptation to daily lactose feeding in lactose maldigesters reduces lactose intolerance.

We conducted blinded, controlled crossover studies to determine the effect of daily lactose feeding on colonic adaptation and intolerance symptoms. The initial study with nine lactose maldigesters showed a threefold increase in fecal beta-galactosidase activity after 16 d of lactose feeding. To determine the effects of this adaptation on breath hydrogen and intolerance symptoms, 20 lactose-maldigesting adults were randomly assigned to lactose or dextrose supplementation for 10 d (days 1-10), crossing over to the other period for days 12-21. The sugar dosage was increased from 0.6 to 1.0 g.kg-1.d-1, subdivided into three equal doses, by adjusting the dose every other day. Symptoms during lactose supplementation and comparison of symptoms during the lactose and dextrose feeding periods showed no significant differences. On days 11 and 22, challenge doses of lactose (0.35 g/kg) were administered after an overnight fast, and breath hydrogen and intolerance symptoms (abdominal pain, flatulence, and diarrhea) were carefully monitored for 8 h. Frequency of flatus passage and flatus severity ratings after the lactose challenge decreased 50% when studied at the end of the lactose period compared with the dextrose period. The sum of hourly breath-hydrogen concentrations (1-8 h) was significantly reduced after the lactose feeding period (9 +/- 38 ppm.h) compared with after the dextrose period (385 +/- 52 ppm.h, P < 0.001). We conclude that there is colonic adaptation to regular lactose ingestion and this adaptation reduces lactose intolerance symptoms.

Abdominal Pain↗
PubMed1982

[Effect of prolonged consumption of lactose or hydrolyzed lactose in the rat. 2. Digestibility, retention and utilization of lactose components].

Nutritional balances are made with groups of 12 rats Wistar receiving well-balanced diets with 40 p. 100 of sucrose (T), or 40 p. 100 of lactose (L and P), or hydrolyzed lactose (LH and PH). Whey (L) and ultrafiltration permeate (P) are used in crude state or after enzymic industrial lactase hydrolysis (LH and PH). The animals consume diets during eight months. Faeces contain neither lactose nor galactose, but glucose in small quantities. In all urines occurs about 0,5 mg/day of glucose. The lactose diets (L and P) provoke a week lactosury (0,36 p. 100 of ingestion). Galactose and galactitol are abundant in urines: with lactose diets (L and P), the urinary excretion is equal to 4 p. 100 of ingested galactose. In urines of hydrolyzed lactose diets (LH and PH) the excretion reaches 26 p. 100 of ingestion. In this case the excretion is remarkably invariable from third day of eighth month: the urinary galactose corresponds to 23 p. 100 and galactitol to 3 p. 100 of consumed galactose. The urines of lactose diets (L and P) and hydrolyzed lactose diets (LH and PH) contain 100 and 300 mg/day of non sugar reducing substances respectively, i.e. 40 p. 100 of total urinary reducing power. The apparent retention of lactose (L and P) is 95,5 p. 100 and that of the hydrolyzed lactose (LH and PH) is 86 p. 100 after 8 months of experiment but it is estimated that digestive flora consumes 40 p. 100 of dietary lactose (L and P).

Animals↗
PubMed1997

Raising milk energy content retards gastric emptying of lactose in lactose-intolerant humans with little effect on lactose digestion.

Lactose digestion improves when the energy content of a meal is raised, perhaps due to delayed gastric emptying; however, this has not been demonstrated directly. It is not known whether lactose-intolerant subjects should consume full-fat or high energy milk instead of half-skimmed milk. In this study, breath 13CO2 and hydrogen (H2) measurements were combined to assess simultaneously the effect of increasing milk energy content on gastric emptying, digestion, and tolerance of lactose. On two separate days, 11 adult lactose maldigesters ingested, in the fasting state, a single dose of 710 kJ half-skimmed milk or 1970 kJ high energy milk. Both contained 18 g lactose and were supplemented with 100 mg 13C-glycine for breath 13CO2 measurement. For 6 h after milk ingestion, samples of expired breath were collected, and subjects scored their symptoms on a four-grade questionnaire. Gastric emptying was measured from excretion of breath 13CO2. The mean gastric emptying half-time was significantly longer after ingestion of high energy milk than after half-skimmed milk (84 +/- 4 vs. 64 +/- 4 min, P = 0.004). The mean area under the breath H2 excretion curve measured for 6 h was 330 +/- 61 microL/L after subjects consumed high energy milk vs. 470 +/- 82 microL/L after they consumed half-skimmed milk (P = 0.07). Mean symptom scores did not differ after ingestion of the two milks, but only two subjects experienced disturbing symptoms after high energy milk ingestion compared with five subjects after ingestion of half-skimmed milk (P = 0.56). Although ingestion of high energy milk delayed the gastric emptying of lactose for significantly longer than the ingestion of half-skimmed milk (P < 0.01), it did not lead to significant improvement in symptoms and reflected only a trend toward improved lactose digestion (P = 0.07), as measured by the area under the breath H2 excretion curve. These results indicate that it is not beneficial for most lactose-intolerant subjects to replace consumption of half-skimmed milk by milk with a higher energy content.

Adult↗
PubMed1977

Reinvestigation of lactose intolerant children: lack of correlation between continuing lactose intolerance and small intestinal morphology, disaccharidase activity, and lactose tolerance tests.

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.

Child, Preschool↗
PubMed1992

Lactose digestion from unmodified, low-fat and lactose-hydrolyzed yogurt in adult lactose-maldigesters.

The efficiency of carbohydrate absorption from two unmodified plain yogurts, a low-fat yogurt and a yogurt produced from lactose-hydrolyzed milk, was compared using the breath hydrogen response in 14 lactose-maldigesters. The maldigesters showed symptoms of intolerance to a standard 360 ml glass of milk containing 18 g lactose. Compared to intact milk, the breath hydrogen response to two varieties of unmodified yogurt and the lactose hydrolyzed yogurt was severely attenuated while the hydrogen response to low-fat yogurt was intermediate. Intolerance symptoms were significantly and equally reduced with all four yogurt products compared to milk. Ten lactose-digesters had a significantly greater efficiency of lactose digestion with 360 ml of milk than the 14 maldigesters; however, except for the magnitude of the maximum rise in breath H2, no inter-group differences were observed in response to unmodified yogurt. We conclude that lactose prehydrolysis adds nothing to the ability to tolerate and digest plain, full-fat yogurts, but it may be useful with low-fat or pasteurized varieties.

Adult↗
PubMed1991

Evidence that the asparagine 322 mutant of the lactose permease transports protons and lactose with a normal stoichiometry and accumulates lactose against a concentration gradient.

The single asparagine 322 mutant of the lactose permease was made by constructing a hybrid plasmid which contained the amino-terminal coding sequence from the wild-type permease gene and the carboxyl-terminal coding sequence from a previously characterized double mutant permease which contained an asparagine residue at position 322. Since histidine at position 322 has been postulated to be critically involved with H+ transport and the active accumulation of sugars, the ability of the Asn-322 mutant to couple H+ and sugar transport was carefully examined. Measurements of proton/lactose stoichiometries gave very similar values for the wild-type (0.78) and the Asn-322 strain (0.82). Moreover, the Asn-322 mutant was able to effectively accumulate lactose against a concentration gradient although the levels of accumulation in the Asn-322 mutant (approximately 5-7-fold) were significantly less than that of the wild-type strain (approximately 30-40-fold). Overall, these results are inconsistent with the notion that an ionizable histidine residue at position 322 is obligatorily required for H+ transport or the active accumulation of galactosides against a concentration gradient. The ability of the Asn-322 mutant to recognize a variety of sugars was compared with wild-type, Val-177, and Val-177/Asn-322 strains. The Asn-322 mutant exhibited an ability to recognize and transport maltose (an alpha-glucoside) which was significantly better than the wild-type strain but not as good as either the single Val-177 mutant or the double Val-177/Asn-322 mutant. Both the Asn-322 and the Val-177/Asn-322 strain showed a relatively poor recognition for alpha-galactosides (i.e. melibiose), beta-galactosides (lactose and thiodigalactoside), and beta-glucosides (cellobiose). In contrast, the single Val-177 strain exhibited a normal recognition for these sugars.

Asparagine↗
PubMed1996

Lactose handling by women with lactose malabsorption is improved during pregnancy.

OBJECTIVE: To evaluate lactose handling among women in late pregnancy and post partum to determine whether lactose handling is altered in pregnancy. DESIGN: Prospective study of lactose intolerance among pregnant women with and without lactose malabsorption. SETTING: Gastroenterology service of the Sir Mortimer B. Davis-Jewish General Hospital, Montreal. PATIENTS: Thirty-three pregnant women, of whom 18 had lactose malabsorption, 12 did not and 3 were excluded. OUTCOME MEASURES: Lactose breath hydrogen (BH2) concentration after ingestion of lactose or lactulose; comparison before and after delivery of area under the curve (AUC) for lactose, oral-cecal transit time (OCTT) for lactulose, lactose-BH2-derived transit time and estimated dietary lactose consumption. RESULTS: After weaning (at a median time of 9 months after delivery), 28 of the women returned for follow-up. Of the 12 who could absorb lactose before delivery, 4 could no longer absorb lactose. Of the other 16 women, lactose intolerance worsened in 12, remained the same in 2 and improved in 2. The AUC was greater (p < 0.005), the maximal BH2 concentration was higher (p = 0.004) and the number of women whose BH2 concentration peaked was fewer (p < 0.025) post partum than before delivery. The women's symptoms during and after lactose BH2 tests were also greater post partum. The OCTT (based on the lactulose BH2 test) was shorter post partum (p = 0.001). Transit time derived from lactose BH2 tests was also shorter, but not significantly so. The OCTT was not inversely correlated with the change in AUC before and after delivery, but the lactose-BH2-derived transit time was inversely correlated. Pregnant women consumed more lactose before delivery than afterward (p < 0.004). CONCLUSIONS: Women with lactose malabsorption handle lactose better than usual in late pregnancy. Slow intestinal transit and bacterial adaptation to increased lactose intake may be primarily responsible.

Breath Tests↗
PubMed1999

Fructooligosaccharides and lactulose cause more symptoms in lactose maldigesters and subjects with pseudohypolactasia than in control lactose digesters.

BACKGROUND: Many lactose maldigesters tolerate more lactose in experimental studies than in everyday life, in which their symptoms may result from other carbohydrates as well. OBJECTIVE: The question of whether the symptoms caused by large quantities of carbohydrates are more severe in lactose maldigesters than in control lactose digesters or in lactose digesters who report milk to be the cause of their gastrointestinal symptoms (pseudohypolactasic subjects) was studied in a randomized, double-blind, crossover study. Comparisons between commonly used diagnostic methods for lactose maldigestion were also made. DESIGN: The subjects were 40 women aged 20-63 y from 3 groups: lactose maldigesters (n = 12), pseudohypolactasic subjects (n = 15), and control lactose digesters (n = 13). The subjects were given either 50 g lactose, 50 g sucrose, 25 g lactulose, or 25 g fructooligosaccharides. After carbohydrate ingestion, urine was collected and the breath-hydrogen concentration was measured every 30 min for 3 h. Blood glucose was measured every 20 min for 1 h and subjective gastrointestinal symptoms were monitored for 8 h with a questionnaire. RESULTS: When lactulose and fructooligosaccharides were ingested, the lactose maldigesters (P = 0.04 and 0.09, respectively) and the pseudohypolactasic subjects (P = 0.006 and 0.01, respectively) reported more symptoms than did the control lactose digesters. Sucrose caused more symptoms in the lactose maldigesters than in the control lactose digesters (P = 0.05). CONCLUSIONS: Lactose maldigesters and lactose digesters with pseudohypolactasia experience more symptoms than control lactose digesters after a single intake of large amounts of indigestible carbohydrates. Lactose maldigesters also experience more symptoms after ingesting sucrose.

Adult↗
PubMed2001

The effect of a lactose-restricted diet in patients with a positive lactose tolerance test, earlier diagnosed as irritable bowel syndrome: a 5-year follow-up study.

DESIGN AND METHODS: Prospectively, the effect of a lactose-restricted diet was evaluated among irritable bowel syndrome patients with lactose malabsorption. Lactose malabsorption was defined by a positive hydrogen breath test and a positive blood-glucose test. An analysis of symptoms was completed before, during, 6 weeks after and 5 years after starting the diet. In addition, the number of visits made by the patients to the outpatient clinic was scored during 6 years. RESULTS: In 17 out of 70 irritable bowel syndrome patients (24.3%), lactose malabsorption was detected. There was no difference in the symptom score between patients with a positive lactose tolerance test and patients with a negative lactose tolerance test. After 6 weeks of the lactose-restricted diet, symptoms were markedly improved in lactose malabsorption-positive patients (P < 0.001). After 5 years, one patient was lost for follow-up, and 14 out of the remaining 16 lactose malabsorption patients (87.5%) still had no complaints during the lactose-restricted diet. Two patients chose not to follow the diet continuously and accepted the discomfort caused by lactose intake. Only two out of 16 patients (12.5%) no longer experienced any benefit from lactose restriction. In the 5 years before their diagnosis of lactose malabsorption, these 16 patients visited the outpatient clinic a total of 192 times (mean 2.4 visits per year per person; range 1-7 visits). In the 5 years after diagnosis, they visited the outpatient clinic a total of 45 times (mean 0.6 visits per year per person; range 0-6 visits; P < 0.0001). CONCLUSIONS: In a large majority of irritable bowel syndrome patients with lactose malabsorption, which was previously clinically unrecognized, a lactose-restricted diet improved symptoms markedly both in the short term and the long term. Furthermore, visits by all patients to the outpatient clinic were reduced by 75%. We conclude that diet therapy is extremely cost- and time-saving. Therefore, it is strongly recommended that lactose malabsorption, which is easily treatable, is excluded before diagnosing irritable bowel syndrome.

Adolescent↗
PubMed1995

A comparison of symptoms after the consumption of milk or lactose-hydrolyzed milk by people with self-reported severe lactose intolerance.

BACKGROUND: Ingestion of a large dose of the milk sugar lactose--for example, the 50-g load in 1 liter of milk--causes symptoms such as abdominal pain, diarrhea, bloating, and flatulence in the majority of people with lactose malabsorption. It is uncertain whether the ingestion of more common doses of lactose, such as the amount in 240 ml (8 oz) of milk, causes symptoms. Some people insist that even smaller quantities of milk, such as the amount used with cereal or coffee, cause severe gastrointestinal distress. METHODS: In a randomized, double-blind, crossover trial, we evaluated gastrointestinal symptoms in 30 people (mean age, 29.4 years; range, 18 to 50) who reported severe lactose intolerance and said they consistently had symptoms after ingesting less than 240 ml of milk. The ability to digest lactose was assessed by measuring the subjects' end-alveolar hydrogen concentration after they ingested 15 g of lactose in 250 ml of water. Subjects then received either 240 ml of lactose-hydrolyzed milk containing 2 percent fat or 240 ml of milk containing 2 percent fat and sweetened with aspartame to approximate the taste of lactose-hydrolyzed milk; each type of milk was administered daily with breakfast for a one-week period. Using a standardized scale, subjects rated the occurrence and severity of bloating, abdominal pain, diarrhea, and flatus and recorded each passage of flatus. RESULTS: Twenty-one participants were classified as having lactose malabsorption and nine as being able to absorb lactose. During the study periods, gastrointestinal symptoms were minimal (mean symptom-severity scores for bloating, abdominal pain, diarrhea, and flatus between 0.1 and 1.2 [1 indicated trivial symptoms; and 2, mild symptoms]). When the periods were compared, there were no statistically significant differences in the severity of these four gastrointestinal symptoms. For the lactose-malabsorption group, the mean (+/- SEM) difference in episodes of flatus per day was 2.5 +/- 1.1 (95 percent confidence interval, 0.2 to 4.8). Daily dietary records indicated a high degree of compliance, with no additional sources of lactose reported. CONCLUSIONS: People who identify themselves as severely lactose-intolerant may mistakenly attribute a variety of abdominal symptoms to lactose intolerance. When lactose intake is limited to the equivalent of 240 ml of milk or less a day, symptoms are likely to be negligible and the use of lactose-digestive aids unnecessary.

Abdominal Pain↗
PubMed1995

Prospective study of lactose absorption during cancer chemotherapy: feasibility of a yogurt-supplemented diet in lactose malabsorbers.

Chemotherapy is a recognized cause of morphological alterations to the proximal intestine. Lactose malabsorption, the functional consequence of a small intestinal enzymatic derangement, has been shown to play an important role in causing gastrointestinal symptoms in subjects receiving chemotherapy. To establish a rational basis for the exclusion of lactose from the diet and to reduce the risk of developing gastrointestinal symptoms, we conducted a study of lactose absorption in 20 children during cancer chemotherapy. Because lactose is an important nutritional sugar, the tolerance of lactose provided by yogurt was examined. Lactose absorption was investigated by a hydrogen breath test (BT) after oral ingestion of milk (250 ml) containing physiological doses of lactose (12 g). The effect of yogurt supplementation was also tested by BT after meals of yogurt (450 g) also containing physiological doses of lactose (12.1 g). In 11 children, lactose malabsorption was detected by BT during the study before any gastrointestinal symptom revealed this status. Of these 11 children, no gastrointestinal discomfort developed in five receiving a lactose-excluded diet. In contrast, in the six children not restricted in lactose intake, gastrointestinal symptoms were observed 4 to 13 weeks after lactose malabsorption was detected by BT. The findings of our study suggested the usefulness of dietary supplementation with yogurt, a lactose-containing food, in children who developed lactose malabsorption. In fact, all lactose-malabsorbent children showed good lactose absorption and tolerance when tested by yogurt BT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1998

Lactose intolerance and self-reported milk intolerance: relationship with lactose maldigestion and nutrient intake. Lactase Deficiency Study Group.

BACKGROUND: The relationship between lactose-maldigestion, self-reported milk intolerance and gastrointestinal symptoms has not been clearly defined. OBJECTIVES: To evaluate: a) the prevalence of lactose maldigestion and lactose intolerance in a sample of the general population taken from a rural center; b) the frequency of self-reported milk-intolerance and its correlation with lactose-maldigestion; c) the influence of lactose maldigestion, lactose intolerance and self-reported milk intolerance on dietary habits and consumption of total calories, protein, and calcium. SUBJECTS: We studied a randomized sample of the general population in a small center in Sicily. 323 subjects (150 males, 173 females), age range 5 to 85 years (median 44) were included and underwent H2-breath test after 25 g lactose load. The preliminary dietary investigation spanned 7 consecutive days using a printed dietary form and was under the daily control of a team of dietitians. METHODS: The dietary investigation was completed in the first part of the study and the results were analyzed for nutrient composition by a computerized database. The subjects were then divided into self-reported milk-intolerants and self-reported milk-tolerants and they underwent H2 breath testing; subjects with H2 concentration >20 ppm over the baseline concentration were considered maldigesters and those with one or more symptoms were classified as intolerants. RESULTS: 104/323 subjects (32.2%) were lactose maldigesters but tolerants, while 13/323 (4%) were lactose maldigesters and intolerants. In each age-class group (pediatric, adult, and elderly subjects) only the lactose maldigester and intolerant subjects showed differences in nutrient intake with a significantly lower daily consumption of milk and a lower calcium intake. 49/323 subjects were self-reported milk-intolerants; of these, 26 (53%) were lactose maldigesters but tolerants, 18 (37%) were lactose digesters and tolerants and only 5 (10%) were lactose maldigesters and intolerants. In the whole group of self-reported milk-intolerants, dietary milk consumption was significantly reduced and calcium intake was lower than in all the other subjects studied (320 mg/day vs. 585 mg/day, p<0.05). CONCLUSIONS: In studies of the general population, the frequency of lactose intolerance is much lower than that of lactose maldigestion. Gastrointestinal symptoms after lactose load in self-reported milk-intolerants are found in only a very low number of these subjects. Furthermore, in these subjects we observed an unnecessary reduction in milk consumption and an insufficient dietary calcium intake.

Adolescent↗
PubMed1976

Symptom response to lactose-reduced milk in lactose-intolerant adults.

The possible usefulness of low-lactose milk for those lactose-intolerant subjects who develop symptoms from milk consumption was investigated. In the first part of the study, 16 intolerant subjects (blood glucose rise less than 25 mg/100 ml) received low-lactose skim milk containing 15 g lactose (2.5 cups) and 7.5 g lactose (2.5 cups), regular skim milk containing 30 g lactose (2.5 cups), and all three milks plus a small breakfast. The low lactose milks produced significantly fewer symptoms. The food given with the milk had no significant effect on symptomatic response. The second group of 17 subjects received 25 g lactose in water (250 ml), skim milk (500 ml) and whole milk (500 ml); 10 g lactose in lactose-reduced skim (500 ml) and whole milk (500 ml) and whole milk (500 ml); and a placebo (250 ml). There was a significant positive relationship between amount of lactose consumed and symptom response. The form in which the lactose was administered (e.g., whole versus skim milk) was not significantly related to symptoms. It is concluded that in a symptomatic subjects a significantly greater quantity of low-lactose milk than regular milks can be consumed.

Adult↗
PubMed1996

Tolerance to small amounts of lactose in lactose maldigesters.

In this study we examined whether small doses of lactose induced symptoms in 39 lactose maldigesters and 15 lactose digesters in a randomized, crossover, double-blind design. The test doses were 200 mL fat-free, lactose-free milk to which 0, 0.5, 1.5, and 7 g lactose was added. Every third day of a lactose-free diet, after an overnight fast, the subjects drank one of the test milks in random order and registered the occurrence and severity of gastrointestinal symptoms in the next 12 h. During the study, the maldigesters reported significantly more abdominal bloating (P = 0.0003) and abdominal pain (P = 0.006) than the digesters. There was no difference in the mean severity of the reported symptoms between the test milks and the lactose-free milk in the group of lactose maldigesters, of whom one-third did not experience any symptoms from any of the test doses. The same proportion (64%) of the maldigesters experienced symptoms after both the lactose-free milk and the milk with 7 g lactose. However, the symptoms occurred inconsistently with the different test doses in 59% of the maldigesters. Thus, it can be concluded that the gastrointestinal symptoms in most lactose maldigesters are not induced by lactose when small amounts (0.5-7.0 g) of lactose are included in the diet.

Abdominal Pain↗
PubMed1991

[Lactose--a potential dietary fiber. The regulation of its microecological effect in the intestinal tract. 2. The nutrient effect of lactose].

In the small intestine lactose is subjected to the hydrolytic impact of beta-galactosidase originating mainly from the mucosa. In rats about two thirds of the enzyme activity are located in the first part of the small intestine, and one third in the second one. A part of the mucosal enzyme does not remain in the mucosa. It becomes detached and can be determined in the chymus. The ratio of the transient to the resident proportion amounts to 1.8: 1 in germfree and 0.23: 1 in conventional rats. Bacterial settlement causes an increase in the mucosal mass resulting in higher total activity whereas the specific activity of the mucosal enzyme remains unchanged. Microorganisms occurring close to the small intestine mucosa take part in lactose degradation. Lactose-containing diet leads to an increase in both the bacterial and the mucosal activity, the latter one to varying degrees. Lactose concentration in the ileal chymus rises with increasing intake of lactose and decreasing protein and phosphate intake. Following a saturation kinetics the velocity of lactose hydrolysis is correlated with the lactose concentration of the diet. alpha-lactose is hydrolysed more rapidly in the small intestine of both human sucklings and rats than beta-lactose. As the results of a mathematical model show lactose mutarotation does not effect on the degree of lactose degradation in the small intestine. Depending on the intake of lactose and the food composition the rate of lactose hydrolysis amounts to: --max. 50% after small intestine perfusion in human sucklings, --max. 80% after small intestine perfusion in rats, --max. 60% in rats with ileostomata.

Animals↗
PubMed2003

Breath testing to evaluate lactose intolerance in irritable bowel syndrome correlates with lactulose testing and may not reflect true lactose malabsorption.

OBJECTIVES: An increased prevalence of lactose intolerance is seen in irritable bowel syndrome (IBS). Recently, we demonstrated a high prevalence of abnormal lactulose breath test results in IBS suggesting bacterial overgrowth. Because symptoms of lactose intolerance result from bacterial fermentation, the purpose of this study was to determine whether an abnormal lactose breath test is reflective of malabsorption or early presentation to bacteria. METHODS: Subjects with diarrhea-predominant IBS were enrolled. On day 1, subjects underwent a lactulose breath test after an overnight fast. Within 1 wk, subjects returned after fasting for a lactose breath test with simultaneous blood glucose measurements every 15 min to complete a lactose tolerance test (LTT). Symptoms were evaluated 3 h after lactose administration. RESULTS: Twenty subjects completed the study. One subject inadvertently received dextrose through the intravenous and was excluded. Of the remaining 19 subjects, three (16%) had an abnormal LTT suggesting malabsorption. In all, 10 subjects (53%) had an abnormal lactose breath test, 14 (74%) had an abnormal lactulose breath test, and 11 (58%) had symptoms after lactose administration. The agreement with symptoms was moderate (kappa = 0.47) and fair (kappa = 0.24) when compared to the lactose breath test and LTT, respectively. There was a fair correlation between lactose breath test and LTT (kappa = 0.29). However, lactose breath test hydrogen levels >166 ppm were universally predictive of abnormal LTT. Finally, a significant correlation was seen between the hydrogen production on lactose and lactulose breath test (r = 0.56, p = 0.01). CONCLUSIONS: Lactose breath testing in IBS subjects does not seem to reflect malabsorption; it may be an indicator of abnormal lactulose breath test, suggesting bacterial overgrowth.

Adult↗