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This study was conducted to investigate the effects of in ovo feeding (IOF) of Arg solution on the hatchability, growth performance, gastrointestinal hormones, serum AA, activities of digestive enzymes, and mRNA expressions of sensing receptors and nutrient transporters in the jejunum of posthatch broilers. One thousand two hundred embryonated eggs with similar weight were randomly allocated to 5 groups consisting of 8 replicates of 40 eggs each. The 5 treatments were arranged as a noninjected control, a diluent-injected (0.75% NaCl solution) group, and Arg solution-injected groups with 0.5%, 1.0%, and 2.0% Arg, all dissolved in diluent. At 17.5 d of incubation, 0.6 mL of IOF solution was injected into the amniotic fluid of each egg of the injected groups. Results showed the hatchability of the 2% Arg group was lower (linear, = 0.025) than that of the other groups, and the BW of 21-d-old broilers increased (linear, = 0.008; quadratic, = 0.003) with increasing IOF concentration of Arg. The ADFI (linear, = 0.005; quadratic, = 0.001) and ADG (linear, = 0.010; quadratic, = 0.004) increased during d 1 to 21 with increasing IOF concentration of Arg. For 7- and 21-d-old broilers, the weights of digestive organs increased (linear, < 0.05) with increasing IOF concentrations of Arg; the greatest values were observed in the 1% Arg group. For 21-d-old broilers, IOF of the 1% Arg solution increased ( < 0.05) the concentrations of ghrelin and glucagon-like peptide 2; the activities of digestive enzymes, alkaline phosphatase, maltase, and sucrase in the jejunum; and the concentrations of serum AA of Val, Met, Ile, Leu, Arg, and Pro compared with those of the noninjected control and diluent-injected group. In ovo feeding of the 1% Arg solution also increased ( < 0.05) the mRNA expressions of jejunal sensing receptors of taste receptor type 1 members 1 and 3; the G protein-coupled receptor, class C, group 6, subtype A; nutrient transporters of solute carrier family 7, members 4, 6, and 7; sodium-glucose transporter 1; and fatty acid-binding protein 1. In conclusion, the 1% Arg solution was the appropriate injection level. In ovo feeding of the 1% Arg solution did not affect the hatchability but facilitated the release of gastrointestinal hormones, increasing the digestive and absorptive capacity and finally improving the growth performance of 21-d-old broilers. Therefore, IOF of the appropriate Arg solution could be an effective technology for regulating early nutrition supply and subsequent growth development in the poultry industry.

BACKGROUND Prebiotics selectively stimulate the growth of beneficial bacteria within the gastrointestinal tract, and have been investigated in human and animal studies for their capacity to improve intestinal health. OBJECTIVE We investigated the prebiotics fructo-oligosaccharide (FOS), galacto-oligosaccharide (GOS), and mannan-oligosaccharide (MOS) for their potential to alleviate intestinal damage in rats. METHODS Female Dark Agouti rats (6-8 wk old, 110-150 g) were allocated to 1 of the following treatment groups (n = 8/group): saline/water, saline/FOS, saline/GOS, saline/MOS, 5-fluorouracil (5FU)/water, 5FU/FOS, 5FU/GOS, and 5FU/MOS. Rats were pretreated with either 5% GOS, MOS, or FOS or vehicle (water) from day -12 to day 0. On day 0, rats received a single intraperitoneal injection of saline or 5FU. Metabolic data were recorded daily and all rats were killed on day 3. Histopathology was quantified in hematoxylin and eosin-stained sections. Intestinal sucrase and myeloperoxidase activity were quantified by biochemical assay. Fecal SCFAs-acetic, propionic, and butyric acid-were also measured. Statistical analysis was by repeated-measures, 2-factor ANOVA or Kruskal-Wallis and Mann-Whitney U test; P

Intestinal epithelial cells undergo rapid renewal along the crypt-villus axis (CVA), which ensures intestinal functions. Weaning stress differentially effects intestinal epithelial cell metabolism and physiological states along the CVA. Sulfur amino acids (SAA) play a key role in intestinal epithelial cell functioning. This study evaluated the effects of SAA dietary supplementation on weaning pig jejunal epithelial cells along the CVA. Sixteen Duroc × Landrace × Yorkshire piglets (6.16 ± 0.22 kg BW) were weaned at 21 d of age and were blocked by BW and gender and the randomly assigned to 1 of 2 groups fed diets consisting of low (0.53%) or high (0.85%) levels of SAA for a 7-d period. All piglets were euthanized for tissue sampling on day 7 postweaning. Jejunal epithelial cells were isolated along the CVA to yield 3 "cell fractions" (upper villus, middle villus, and crypt cells). The number of proliferating cells per crypt of piglets fed the high SAA diet was lower (P < 0.05) than that for low SAA diet. High SAA diet piglets tended to have decreased (P = 0.059) sucrase activities compared low SAA diet piglets. A high SAA diet increased (P < 0.05) total antioxidant capacity, catalase, and superoxide dismutase activities compared with a low SAA diet. mRNA expression levels of claudin-1, Slc5a1, and Slc7a9 in high SAA diet piglets were lower (P < 0.05) than for low SAA diet piglets. There were no interactions between dietary SAA and cell sections along the CVA for enzyme activities and mRNA expression in any of the weaned piglets. Protein amounts and phosphorylation levels related to Wnt/β-catenin and mechanistic targeting of rapamycin (mTOR) signaling pathways were affected by SAA in weaning piglets. These findings indicate that dietary SAA affects jejunal cell proliferation and functions in weaning piglets. There appears to be no interactions between dietary SAA and cell sections along the CVA. The effects of SAA may be partly through affecting antioxidant capacity, and Wnt/β-catenin and mTOR signaling pathway.

During diabetes, structural and functional changes in the alimentary tract are known to take place resulting in an increased absorption of intestinal glucose and alterations in the activities of brush-border disaccharidases. To elucidate the effect of administrating polysaccharide fromGynura divaricata(PGD) on disaccharidase activities, the specific activities of intestinal disaccharidases, namely sucrase, maltase and lactase, were measured in streptozotocin-induced diabetic rats. Normal control and diabetic rats were treated by oral administration with PGD. Specific activities of intestinal disaccharidases were increased significantly during diabetes, and amelioration of the activities of sucrase and maltase during diabetes was clearly visible by the treatment with PGD. However, the increased activity of lactase during diabetes mellitus was remarkably alleviated by the administration of PGD only in the duodenum. Meanwhile, oral sucrose tolerance tests demonstrated that PGD alleviated the hyperglycaemia during diabetes mellitus, resulting from the amelioration in the activities of intestinal disaccharidases. The present investigation suggests that PGD exerted an anti-diabetic effect partly via inhibiting the increased intestinal disaccharidase activities of diabetic rats. This beneficial influence of administration of PGD on intestinal disaccharidases clearly indicates their helpful role in the management of diabetes.

Castrated male Iberian (n = 12) and Landrace × Large White (n = 12) pigs were used to study histological structure and enzymatic activity in the small intestine at 3 points of the productive cycle (BW = 15, 50, and 115 kg). Both strains were fed the same cereal-based diets (DE = 2,799 kcal·kg −1 , and CP = 15%) throughout the entire experimental period. Dif- ferences (P < 0.05) in histometrical variables (villus height, width and surface, crypt depth, villus height/ crypt depth relationship, mucosal thickness, muscular layer thickness, and number of goblet cells) were found among samples of small intestinal sections (duodenum, jejunum, and ileum) at the 3 productive stages studied. Also, differences (P < 0.05) in histometrical variables of small intestinal samples were found between Iberian and lean pigs at all productive stages, although these differences tended to disappear with age. Differences (P < 0.05) in enzymatic activities (lactase, sucrase, maltase, isomaltase, aminopeptidase, and alkaline phosphatase) of small intestinal samples were found be- tween the different intestinal sections at all productive stages studied. Although differences (P < 0.05) in enzy- matic activities of small intestinal samples were found between Iberian and lean pigs at all productive stages, values tended to equalize with pig age. We concluded that differences previously found in dietary nutritional utilization between Iberian and lean strains are likely not due to differences in intestinal absorption or hydro- lytic capacity.

1. The objective of the present study was to examine the effect of in ovo injection of disaccharides (DS), disaccharides and glutamine (DS + Gln) or disaccharides and β-hydroxy-β-methylbutyrate (DS + HMB) at d 23 of incubation on the development of the small intestine. 2. In DS + Gln-injected ducks, the greatest relative small intestine mass and muscularis layer thickness among 4 treatments was observed from d 25 of incubation to 7 d of age. 3. Jejunal sucrase activity in DS-injected ducks was significantly greater than in controls at hatch and on d 7. 4. In DS + HMB-treated ducks, a tendency toward slightly higher jejunal DNA concentration was observed throughout the experiment. 5. Greater body weight was found in DS + Gln and DS + HMB treated ducks in the first two weeks. However, there was no significant difference in the market weight (35 d) of ducks among the 4 treatments. 6. The results of present study suggest that administering disaccharides and Gln, or disaccharides and HMB, to the duck embryos exerted a beneficial effect on the early development of small intestine and on growth performance.

To evaluate the effects of dietary hemi- cellulose from corn on growth and metabolic measures, female pigs (n = 48; initial BW 30.8 kg) were fed di- ets containing 0 to 38.6% solvent-extracted corn germ meal for 28 d. Increasing the hemicellulose level had no impact on ADG or ADFI, but resulted in a quadratic response (P < 0.03) on G:F. To investigate physiologi- cal changes that occur with increased dietary hemicel- lulose, blood, colon contents, and tissue samples from the liver and intestine were obtained from a subset (n = 16; 8 pigs/treatment) of pigs fed the least and great- est hemicellulose levels. The abundance of phospho- adenosine monophosphate-activated protein kinase (AMPK) and the mitochondrial respiratory protein, cytochrome C oxidase II (COXII) were determined in liver, jejunum, ileum, and colon by Western blotting. The mRNA expression levels of AMPKα1, AMPKα2, PPAR coactivator 1α (PGC1-α), PPARγ2, and sirtuin 1 (Sirt1) were determined in liver and intestinal tis- sues. When compared with pigs fed the control diet, pigs fed the high hemicellulose diet had increased (P < 0.02) plasma triglycerides, but there was no differ- ence in plasma cholesterol, glucose, or insulin. Absolute and relative liver weights were decreased (P < 0.03) in pigs consuming the high hemicellulose diet. The high- fiber diet led to a tendency (P < 0.12) for decreased liver triglyceride content. In pigs fed the high hemicel- lulose diet, ileal mucosal alkaline phosphatase activity was increased (P < 0.08) and sucrase activity tended (P < 0.12) to be increased. The high hemicellulose diet had no effect on phospho-AMPK, AMPK mRNA, or colonic VFA, but in pigs consuming the high fiber diet there was a greater (P < 0.05) abundance of COXII in colon tissue. The expression of PGC1-α, PPARγ, or Sirt1 mRNA was not altered by dietary fiber in liver, jejunum, or ileum tissue. In colon tissue from pigs fed the high fiber diet there was an increase (P < 0.09) in Sirt1 mRNA and a trend (P < 0.12) toward increased of PGC1-α mRNA. These data suggest that alterations in metabolism involved in adaptation to a diet high in hemicellulose are associated with increased colonic Sirt1 mRNA and COXII expression, indicating an increased propensity for oxidative metabolism by the intestine.

Galacto-oligosaccharides (GOS) are non-digestible oligosaccharides with short galactosyl chain units produced by lactose fermentation which are considered as prebiotics. Only few studies have investigated the effects of GOS medium-term ingestion on the small intestinal epithelium characteristics. In this study, we evaluated the consequences of GOS ingestion on small intestinal mucosal morphology, on brush-border membrane enzyme activities and on mucin content in BALB/c mice. Mice received the experimental diets for 4 weeks and then the small intestine was collected to measure sucrase, lactase and alkaline phosphatase activities, to study the villus heights in the jejunum mucosa and to determine mucosal mucin content as well as MUC-2 and MUC-4 mRNAs expression by qRT-PCR. Our results showed that GOS has no detectable effect on the intestine villus height but increased the total protein content by twofold. Sucrase activity was significantly increased in the intestinal mucosa recovered from animals fed the GOS diet without any detectable modification of lactase and phosphatase activities. Interestingly, GOS was also able to increase sucrase activity in cultured Caco-2 cells raising the view that they likely act directly on these cells. Furthermore, GOS was found to markedly increase O-linked glycoproteins associated with the intestinal mucosa without modifying MUC-2, MUC-4 mRNAs expression. Lastly, TNF-α mRNA expression was also not modified after GOS ingestion. These results suggest that, in BALB/c mice, 4-week GOS ingestion is able to increase the small intestinal mucosa-associated mucin content and enterocyte-associated sucrase activity without modifying villus height.

The aim of our study was to investigate the possible effects of the removal of different parts of the stomach (fundectomy, antrectomy, gastrectomy) on the total protein content and enzyme activity in the pancreas and the brush border of the intestinal mucosa. Twenty-four 2.5-month-old male Wistar rats were divided into four groups: sham-operated animals (SHO) and those subjected to gastrectomy (Gx), fundectomy (Fx), and antrectomy (ANT). After a six-week experiment, the rats were sacrificed, and blood was collected for further gastrin analysis in serum. Samples of the pancreas, duodenum, and jejunum (proximal part in 25% of length, middle part in 50% of length, and distal part in 75% of length) were collected to determine the total protein content and enzyme activity. The rats subjected to fundectomy, antrectomy and gastrectomy showed an increased total protein content and enzyme activity (amylase, trypsin) in pancreatic tissue. They exhibited an increase in the total protein content in the homogenates of the mucosa of the proximal, middle and distal jejunum, compared to the control, and a statistical increase in maltase activity. Compared with the control group, the rats subjected to Fx and ANT showed a decreased sucrase activity in the homogenates of the mucosa of the duodenum and of the proximal, middle and distal jejunum. In the gastrectomized rats, there was a statistically significant increase in the total protein content in the homogenates of the mucosa of the jejunum, compared to the control, while the activities of lactase and sucrase were decreased. There was a statistically significant increase in the gastrin level in all experimental groups (Fx, ANT, Gx). We suggest that surgical removal of a part of the stomach radically changes the level of hormones that determine many functions of the organism. Hormonal changes may have an impact on the pancreas and the activity of brush border enzymes. .

Diabetes was induced in rats with streptozotocin. They were fed either with wheat bran as a source of insoluble dietary fibre or guar gum as soluble dietary fibre. The effect of these fibres on intestinal and renal disaccharidases in diabetic rats was studied. Activities of intestinal maltase, sucrase and lactase increased during diabetes, which was ameliorated to a considerable extent in fibre fed groups. The activities of disaccharidases in renal tissue was decreased in diabetic rats and there was an improvement in fibre fed group.

1. Effects of early feeding with a diet containing added putrescine on duck intestinal development and growth performance were examined by a 2 x 2 factorial arrangement with two different feeding times (6 and 48 h) and two levels of putrescine (0 and 025%). 2. A significant main effect of early feeding on increasing body weight (BW) was observed from hatch to 35 d, whereas dietary putrescine had no significant effect on BW. 3. In the first week posthatch, enhanced small intestinal weight and intestinal density (weight of intestinal tissue/unit length of intestine), increased villus length and reduced crypt depth were observed in the early feeding group, while no effect was observed when putrescine was added to the diet. 4. Maltase and sucrase activity and protein/DNA ratio in jejunum were increased by early feeding in the first week, while decreased by putrescine supplementation. 5. In conclusion, early feeding methods have great potential for small intestine development and thereafter enhanced the growth performance of ducks, but dietary putrescine used during this period should be used cautiously to avoid toxicity.

Congenital sucrase-isomaltase deficiency (CSID) is characterized by absence or deficiency of the mucosal sucrase-isomaltase enzyme. Specific diagnosis requires upper gastrointestinal biopsy with evidence of low to absent sucrase enzyme activity and normal histology. The hydrogen breath test (BT) is useful, but is not specific for confirmation of CSID. We investigated a more specific 13C-sucrose labeled BT.Determine whether CSID can be detected with the 13C-sucrose BT without duodenal biopsy sucrase assay, and if the 13C-sucrose BT can document restoration of sucrose digestion by CSID patients after oral supplementation with sacrosidase (Sucraid).Ten CSID patients were diagnosed by low biopsy sucrase activity. Ten controls were children who underwent endoscopy and biopsy because of dyspepsia or chronic diarrhea with normal mucosal enzymes activity and histology. Uniformly labeled 13C-glucose and 13C-sucrose loads were orally administered. 13CO2 breath enrichments were assayed using an infrared spectrophotometer. In CSID patients, the 13C-sucrose load was repeated adding Sucraid. Sucrose digestion and oxidation were calculated as a mean percent coefficient of glucose oxidation averaged between 30 and 90 minutes.Classification of patients by 13C-sucrose BT percent coefficient of glucose oxidation agreed with biopsy sucrase activity. The breath test also documented the return to normal of sucrose digestion and oxidation after supplementation of CSID patients with Sucraid.13C-sucrose BT is an accurate and specific noninvasive confirmatory test for CSID and for enzyme replacement management.

The effects of a cafeteria diet on the small intestine were investigated in adult Wistar rats under sedentary conditions and after physical training.Parameters including morphometry, enzyme activities, and total myenteric populations in the jejunum were evaluated.The cafeteria diet, characterized as hyperlipidic, produced obese rats, corroborated by increases in the Lee index and the weights of the periepididymal and retroperitoneal adipose tissues (P0.01). Obesity caused increases in the length of the small intestine, villi height, crypt depth, whole-wall thickness (P0.05), and the enzymatic activities of alkaline phosphatase, lipase, and sucrase (P0.01), in addition to a reduction in the number of goblet cells (P0.05). With reference to the jejunal intrinsic innervations, the total number and area of myenteric neurons was unchanged regardless of the group. Physical training promoted 1) a reduction of the weight in the retroperitoneal and periepididymal adipose tissues (P0.05) and 2) an increase in the thickness of the muscular layer (P0.05).The cafeteria diet promoted obesity in rodents, leading to alterations in morphometry and enzymatic intestinal parameters, which were partily attenuated by physical training.

The ontogenetic development of intestinal digestive functions for avian species other than the domesticated chicken are not well documented. Therefore, this study was conducted to resolve the developmental patterns of some intestinal digestive functions in White Pekin ducks. The ducks were killed and their intestines harvested when they were 1, 3, 5 and 7 wk old. Several small intestinal tissue characteristics, sucrase and alkaline phosphatase (ALP) activities of homogenates from the small intestine mucosa were measured, and the small intestinal L-threonine uptake capacities were estimated with brush border membrane vesicles prepared from the corresponding age groups. Between 1 wk (0.37 +/- 0.04 kg) and 7 wk (3.79 +/- 0.06), posthatch ducks exhibited relative body growth rates of 352, 77 and 28% from 1 to 3, 3 to 5 and 5 to 7 wk, respectively. Allometric changes in small intestine weight indicated that the small intestine grew in direct proportion to the duck's metabolic body weight. Total homogenate sucrase activity per unit body weight did not differ (P0.05) among the age groups studied. Total homogenate ALP activity per body weight was lower at 3 wk than at 1 wk (P0.05) but did not differ (P0.05) among 3, 5 and 7 wk-old ducks. The development pattern of L-threonine uptake capacities normalized to body weights paralleled the course of relative body growth rates.

Factors, such as insulin, found in human and pig colostrum and mature milk likely influence small intestinal growth and development. Although pharmacologic doses of insulin injected parenterally may accelerate small intestinal development in altricial animals such as the rodent, the effects of oral insulin on intestinal development have not been studied. In the first of two studies, we randomized 2-d-old miniature piglets to receive bottle-feedings of a swine weaning milk formula with (group F + I) or without (group F) the addition of insulin. Serum glucose, insulin, and cortisol were measured before and 1 h after the first feeding the piglets received at our facility. In the second study, piglets were randomized (groups F and F + I) and fed for 6 d, after which blood samples were obtained as in the first experiment. The piglets were then killed and the small intestine removed for analysis. We found no differences between groups in serum glucose, insulin, and cortisol at both 2 and 8 d of age, both before and after feeding. In the second experiment, small intestinal weight was greater in the F + I than in the F group. Although no differences were noted between groups in the jejunum, values were greater for group F + I versus group F for ileal mucosal weight, protein, RNA, lactase, and maltase activities. No differences were found between groups in ileal DNA or sucrase activity. We conclude that the administration of oral insulin stimulated an increase in ileal mass and disaccharidase activity in the newborn miniature pig without apparent concomitant changes in serum glucose, insulin, or cortisol.

Lactase and sucrase are two disaccharidases that differ not only in their substrate specificity and developmental patterns, but also in their resistance to mucosal insult. In this experiment, we tested the hypothesis that there might be a dichotomy in expression of enzyme activity along the jejunal villuscrypt unit. Sectioning of the villus-crypt unit in a cryostat enabled direct comparison of the distribution of lactase and sucrase enzyme activities in the adult rat. There is a stepwise increase in mean lactase/sucrase ratio going from crypt to villus. The data indicate that unlike sucrase activity, which is expressed maximally in enterocytes along the entire villus, maximal lactase activity is not attained until midvillus. The delay in expression of maximal lactase activity might help to explain the vulnerability of this enzyme to acute mucosal insult such as occurs in viral gastroenteritis.

1. The effects of low-protein and protein-free diets on the levels of disaccharidase, peptidase and aldolase activities in the jejunal mucosa of rats were studied.2. Maltase, palatinase and sucrase activities increased significantly after both types of feeding, although there was an initial fall with the protein-free diet.3. The rise in lactase levels was, however, not so marked.4. Glycyl-glycine and glycyl-leucine dipeptidase levels fell consistently with both diets.5. Aldolase activities were generally unaltered, but tended to fall if the period of low-protein feeding was prolonged.6. Enzyme levels rapidly returned to normal when the rats were given a normal diet after a period on a protein-deficient one.7. It is suggested that the rise in disaccharidase and fall in peptidase levels are adaptive changes to the high-carbohydrate, low-protein diet, with diminished enzyme synthesis, due to lack of nitrogen, contributing to the lowered peptidase activities. The relevance of these results to disaccharide intolerance in chronic malnutrition, kwashiorkor and gastro-intestinal infection is discussed.

Intestinal sucrase activity of the rat varies with the age, but not the sex, of the animal. Sucrase activity of rats 23 days of age was approximately two-thirds that of adults.Sucrase activity of adult rats was significantly decreased by several days of fasting. The decrease was rapid during the first 2 to 4 days of the fast, but became negligible thereafter.Diets containing large (70%) amounts of sucrose, galactose, melizitose, or α-methyl-D-glucoside produced highly significant increases in intestinal sucrase levels (compared with a carbohydrate-free, high-casein control diet) when fed ad libitum for 24 hours to adult male rats previously fasted for 3 days. Similar diets containing fructose, fructose plus glucose in equimolar amounts, or maltose significantly increased sucrase activity, but diets containing glucose, mannose, xylose, or lactose were not stimulatory. A 70% raffinose diet significantly decreased sucrase activity. Normal male rats which were fed the 70% sucrose diet for 4 weeks had sucrase activities similar to those of controls fed Purina fox checkers, but animals fed the carbohydrate-free, high-casein diet for 1 day or longer had sucrase activities significantly lower than those of controls. The significance of these observations in regard to enzyme "adaptation" is discussed.

This study determined the time required for the adaptive changes in human jejunal sucrase and maltase activities when dietary carbohydrate was changed from glucose to sucrose, sucrose to carbohydrate-free, and glucose to fructose. Four volunteer subjects were studied. The time for the increases and decreases in activity was 2 to 5 days and there was no further change for 9 weeks thereafter. This time response is similar to the estimated time for intestinal epithelial cell turnover in the small intestine of man. It is proposed that the changes in disaccharidase activity produced by changes in dietary sugar content are due primarily to an effect on the crypt cell. The effect becomes increasingly manifest as these crypt cells divide and migrate up the villus.

Intestinal dipeptidases (eight substrates) and disaccharidases (five substrates) were studied in 18 subjects with the flat intestinal mucosa pattern seen in celiac disease. On a gluten-free diet, 12 patients improved; the other 6 showed no improvement or an uncertain effect. Thirty-seven persons with histologically verified normal intestinal mucosa served as control subjects for the enzymatic determinations. All enzyme activities were reduced in both the gluten responsive and the nonresponsive celiac group. Peptidyl-proline dipeptidase activities were reduced to about 30% of the mean activities in the control group, the other dipeptidase activities to about 50%. No specific deficiency of any particular dipeptidase activity could be demonstrated. The disaccharidase activities corresponded to 10 to 20% of these in the control group. After gluten-free diet the responsive group showed only slight improvement in the peptidyl-proline dipeptidase, maltase, isomaltase, and sucrase activities, whereas the other dipeptidase activities increased considerably. Trehalase and lactase were unchanged during the observation period.

A deficiency of the intestinal enzyme sucrase was found in tropical sprue. This deficiency persists even after therapy and is probably responsible for the sucrosuria characteristic of the disease.

OSTEOPOROSIS (senile and postmenopausal) is a common disorder of the elderly, with an estimated morbidity of at least 20 per cent of persons over the age of fifty years.1 2 3 Despite this high prev...

Two experiments were carried out with laying hens to determine the effect of overcrowding stress on reproductive performance and on certain other parameters that might be expected to be affected and thus be useful indices of this type of stress. The first experiment consisted of eight treatments in a factorial arrangement with four bird densities of one, two, three, or four birds in 30.5 × 45.7-cm (12 × 18″) cages and two levels of dietary energy. The second experiment involved three bird densities of one, three, and five birds in 30.5 × 45.7-cm cages fed a single diet. There were four replicate cages per treatment in both experiments. Feed consumption, weight gain, and egg production were not significantly affected by the population densities employed in experiment 1. In experiment 2, increasing bird density significantly reduced egg production, and hens maintained at five per cage suffered a net loss of body weight. In neither experiment was energy utilization affected by crowding since the dietary metabolizable energy values remained constant. In both experiments mucosal maltase and sucrase activities were significantly increased with increasing bird density when birds were fed diets of relatively normal starch content. Plasma-free fatty acids, total fatty acids, and triglyceride levels were not significantly affected by population density, nor were the oleic–linoleic–arachidonic acid levels expressed as percentages of total fatty acids. It would thus appear that lipid metabolism remained relatively normal in hens subjected to overcrowding stress. The levels of peripheral plasma corticosterone and adrenal corticosterone increased in a linear fashion in both experiments with increasing bird density. It would appear that plasma and adrenal corticosterone levels might be useful indices of overcrowding stress in hens.

1. Forty Large White pigs varying in age from birth to 5 weeks were slaughtered and their carbohydrate digesting enzymes studied for any change in activity with increase in age.2. Pancreatic amylase, sucrase and maltase increased from low levels at birth to high levels at 5 weeks of age.3. The total amount of lactase present at birth and of small intestine amylase at 1-week-old was maintained at a constant level up to 5 weeks of age. The increased weight of the intestine with the growth of the pig made the quantity of these enzymes appear to decrease with age when the values were expressed per kg. body weight or per g. dry tissue.4. Anaemia had no marked effect on the activity of the enzymes though the rate of enzyme development appeared to be retarded in the case of maltase.5. The quantity of pancreatic amylase present in the pancreas was sufficient at all ages to digest the amounts of starch likely to be included in a synthetic diet. Maltase, on the other hand, appeared to be limiting in early life.

Thoughtheamylase ofduodenal juice hydrolyses thepolysaccharides ofthediettooligosaccharides anddisaccharides, thefinal cleavage ofthelatter to themonosaccharides, whichisessential forabsorption, isalmost entirely effected byspecific enzymes located intheintestinal mucosa.An inherited deficiency ofintestinal lactase wasfirst suggested as apossible causeofchronic diarrhoea andfailure to thrive ina 13-month-old infant, byDurand(1958) andlater byHolzel, Schwarz, andSutcliffe (1959) for asimilar condition intwosibs.Since thenanumber ofcases, notonlyoflactase deficiency butalsoof sucrase deficiency, havebeenreported. Thediagnosishasalmost always rested uponsevere diarrhoea following ingestion ofthecarbohydrate, aninability tometabolize thesugarasshownbythepresence of thecarbohydrate intheurine andfaeces andthe failure ofthebloodglucose toriseafter oral administration ofthedisaccharide. Ithaslongbeenknownthatextracts ofthe intestinal mucosaof mammalshaveinvertase activity. Following hischaracterization ofseveral specific disaccharidases inhogintestinal mucosa, Dahlqvist (1961) hasdemonstrated thespecific character ofthedisaccharidases inhumanintestinal mucosaaswellastheoverlapping specificities of someofthem.He hasshowninparticular that human intestinal sucrase(invertase), likethe corresponding enzymeinthepig, hasalsosome maltase activity. Anderson, Messer,Townley, Freeman,and Robinson (1962) andAnderson, Messer, Townley, andFreeman(1963) havedemonstrated theabsence ofsucrase inbiopsy specimens ofduodenal mucosa intwo sibswithsucrose intolerance. Mucosal homogenates wereincubated withsucrose andthe incubation mixture wassubsequently examined by paperchromatography. Onlyavisual estimate of theenzymeactivity asjudged bytheamountof monosaccharide produced byhydrolysis waspossible bythis method. Inthepresent article, wepresent 7further cases of aninherited absence ofintestinal sucrase, including 2 inonefamily. Theinitial diagnosis wasmadeon clinical grounds, and confirmed by theusual laboratory findings. Ineachcase, abiopsy specimen ofthejejunal mucosahasbeenobtained andthe enzymeactivities to a numberofcarbohydrate substrates, including sucrose, determined quantitatively. Onlyonthis basis isitpossible todiagnose withcertainty thespecific sucrase defect, andto differentiate itfromtheacquired carbohydrate intolerance thatmayoccurindisease involving the small intestine. Itislikely thatcasesofhereditary sucrose intolerance arenotuncommon, asthese now described weredetected within a relatively short period. Thoughtheultimate prognosis maybegoodeven

The activities of intestinal lactase, sucrase, and maltase in rats receiving food of normal composition but in restricted amounts were compared with those of younger, normally fed control rats of equal weight. The activities of all three disaccharidases were increased in the nutritionally abnormal animals, on the basis of both fresh weight and mucosal protein content. Total intestinal lactase activity was also increased in the nutritionally abnormal rats, although total intestinal sucrase and maltase activity were not.

SYNOPSIS Refractory diarrhoea occurring in young babies subsided following exclusion of lactose from the diet. In most patients investigated, small bowel biopsy demonstrated abnormal histology and depression of lactase activity. However, the intestinal mucosa eventually returned to normal and the ingestion of lactose no longer produced symptoms. The clinical value of the observations leading to decreased morbidity in babies with persistent gastroenteritis and the simple management of these patients, without the need for special investigations, is discussed.

IN the absorption of disaccharides from the intestine, hydrolysis of the sugars into their component monosaccharides is necessary. Largely through the elegant studies of Crane and his associates,1 , 2 it is now recognized that this hydrolysis occurs not primarily in the lumen of the intestine as previously believed but more probably just within the epithelial cells of the mucosa. It has been demonstrated that the various specific hydrolytic enzymes (disaccharidases) are localized predominantly in the brush-border region (microvilli) of the mucosal cells. Over the past five years reports from a number of laboratories have shown the occurrence of primary or hereditary . . .

The specific effect of dietary sugars on jejunal disaccharidase activity in seven normal nonfasted male volunteers was studied. The sugars tested were sucrose, maltose, lactose, glucose, fructose, and galactose. Comparisons were made of the effects of each sugar in an isocaloric liquid diet. In all subjects, sucrose feeding, as compared to glucose feeding, significantly increased jejunal sucrase (S) and maltase (M) activities, but not lactase (L) activity. The S/L and M/L ratios increased to a significant degree. Fructose feeding, in two subjects, gave results similar to sucrose when comparing fructose and glucose diets. One subject was fed lactose, galactose, and maltose. These sugars, compared to glucose, did not increase disaccharidase activity. Fructose appears to be the active principle in the sucrose molecule. These results demonstrate that specific dietary sugars can alter enzyme activity in the small intestine of man in a specific fashion. Sucrose and fructose are able to regulate sucrase and maltase activity. Dietary alteration of intestinal enzymes may represent a suitable system for studying the regulation of enzyme activity in man.

1. 1. The hydrolysis of disaccharides by homogenates of small intestinal mucosa from five carnivorous mammals was investigated. Maltase, sucrase and lactase activities were present in the small intestine of the domestic cat, lion, ferret, dog and polar bear. Trehalase activity was absent from the intestine of the domestic cat and lion, but was present in the other carnivores. 2. 2. A detailed investigation was made of intestinal lactase levels in cats of various ages. Lactase activity was high at birth and decreased to relatively low levels in the adult animal. The decline in activity occurred most rapidly during 4–7 weeks of age, which coincides with the weaning period. 3. 3. Evidence for the existence of at least two intestinal β-galactosidases in the domestic cat was obtained. One is a soluble enzyme which hydrolyses ortho-nitrophenyl β-galactoside but not lactose; the other is a particulate enzyme which catalyses the hydrolysis of both substrates.

Intestinal disaccharide enzyme deficiencies of either lactase, maltase, or sucrase with concomitant isomaltase deficiency have recently been recognized. These deficiency states have not usually been associated with steatorrhea. Evidence is here presented for the association of lactase, sucrase, and isomaltase deficiency with steatorrhea and failure to thrive in a young infant. Restriction of disaccharide intake resulted in improvement in weight gain and disappearance of the steatorrhea. At present the child is gaining weight slowly.

Summary The effect of iron deficiency anaemia, protein deficiency and worm infestation upon intestinal disaccharidase activity in the rat was assessed following the observation that these factors may have contributed to the premature onset of lactase deficiency in man. Adaptation of intestinal lactase occurred between eight and ten weeks of age in young rats fed a 10% lactose diet. Iron deficiency anaemia depressed jejunal and ileal lactase activity. Sucrase and maltase activities were not significantly affected by iron deficiency. Adaptation of intestinal lactase was prevented by both protein deficiency and combined iron/protein deficiency. Sucrase activity was not significantly depressed by either of these and in many instances activity was higher than the control group. Similar changes were noted with maltase. Worm infestation with Nippostrongylus brasi-liensis consistently depressed jejunal lactase and maltase activities, but had little effect on sucrase activity. It was concluded that intestinal lactase in particular was depressed by a number of environmental factors and adaptation of lactase thereby prevented.

The administration of a carbohydrate-containing diet for 24 hours to rats previously fasted for 3 days led to a twofold increase in total intestinal sucrase and sucrase specific activity. The specific activity of maltase was similarly increased, but lactase activity was unaffected. The sucrose-containing diet led to a greater increase in sucrase than maltase activity, whereas the converse was true of the maltose-containing diet. A carbohydrate-free isocaloric diet led to a slight increase in the total intestinal sucrase, but sucrase specific activity was unchanged. Assay of sucrase activity of mixed homogenates from casein-fed and sucrose-fed rats or fasted and sucrose-fed animals yielded activities that were additive. The Michaelis constant (Km) of the enzyme hydrolyzing sucrose was similar in the fasted, casein-fed, and sucrose-fed rats. The maximal velocity (Vmax) was twice greater in sucrose-fed as compared to casein-fed or fasted rats, suggesting an increased quantity of enzyme subsequent to sucrose feeding. Adrenalectomized rats maintained on 1.0% salt intake had sucrase and maltase levels comparable to those of controls. Steroid administration did not significantly increase their activities. The response to sucrose feeding was similar in both control and adrenalectomized rats, indicative of the absence of steroidal control on sucrase and maltase activity in the adult animal. Studies using intestinal ring preparations indicated that sucrose hydrolysis by the intact cells proceeded more rapidly when animals were fed sucrose. Additional corroboration of the physiologic significance of the increased enzyme levels in homogenates was afforded by intestinal perfusion studies. Sucrose hydrolysis increased twofold and fructose absorption fourfold in animals fed sucrose when compared to either fasted or casein-fed rats.

Jejunal lactase activities have been determined in 41 patients who had consulted general practitioners on account of “unspecific abdominal complaints”. Twelve of these patients had low jejunal lactase activity and they all had selective lactase deficiency. A lactose-free diet for two weeks had a beneficial effect on all the patients with low lactase activity, and the effect was not temporary, as could be noted on inquiry about six months later. It is remarkable that only two of the twelve patients with low lactase activity had a history of milk intolerance. Determination of small-intestinal lactase activity or a peroral lactose tolerance test is recommended as a routine test for milk-drinking patients with “unspecific abdominal complaints”.

A breastfed female infant is described who developed from the third day of life a severe watery diarrhoea, with weight loss. This ceased when lactose was omitted from the feeds and returned when it was resumed. Intolerance to this carbohydrate was confirmed by a lactose tolerance test which showed inability to hydrolyse the disaccharide. Absorption of glucose and sucrose was normal. No other cause for the diarrhoea was established. Congenital lactose malabsorption (alactasia) was confirmed by examination of the duodenal mucosa. The lactase activity was virtually absent, and the maltase, isomaltase, and sucrase activities were normal. The differential diagnosis of the congenital and acquired forms is discussed, and the importance of intestinal mucosal enzyme assays for final confirmation of the diagnosis is stressed.