Jejunal Sucrase Activity Research Articles

Effects of soluble dietary fibers on lipid metabolism and activities of intestinal disaccharidases in rats.

The present study was aimed to investigate the effects of indigestible dextrin and polydextrose, soluble dietary fibers with low molecular weight, on lipid metabolism and disaccharidase activities of intestinal mucosa in rats fed a high sucrose diet. Their effects were compared with those of well-known soluble fibers, pectin, and guar gum, and also with an insoluble fiber, cellulose. Dietary fibers added to diets at the 5% (w/w) level were alpha-cellulose, pectin, guar gum, indigestible dextrin, and polydextrose. Male Sprague-Dawley rats were given free access to test diets for 6 weeks. Body weight gain was the lowest in rats fed guar gum, the highest in rats fed cellulose, and in-between in rats fed other diets. Although guar gum, pectin, and indigestible feeding dextrin had lower plasma lipid values than cellulose feeding did, the differences were statistically insignificant. Liver triglyceride of the guar gum-fed group was about a third that of the cellulose-fed group, but although those of rats fed polydextrose, indigestible dextrin, and pectin were lower than that of cellulose, the differences were insignificant. Liver cholesterol and phospholipid concentrations were similar among groups. Daily fecal excretion of total lipid, cholesterol, and bile acids were highest in rats fed guar gum, followed by pectin-fed and cellulose-fed rats, and the lowest in rats fed indigestible dextrin and polydextrose. Jejunal sucrase activity was low in the order of guar-gum, polydextrose, indigestible dextrin, pectin, and cellulose. The results indicate that the hypolipidemic effect of soluble dietary fibers would be lessened with reduction in molecular weight, but that the lower sucrase activity by soluble fibers with low molecular weight might be beneficial for hypoglycemic effect.

The role of 11 β-hydroxysteroid dehydrogenase in maturation of the intestine

Glucocorticoids promote the development of many organs including intestine. At the cellular level, the activity of glucocorticoids is regulated by 11 β-hydroxysteroid dehydrogenase (11 βHSD) which converts active glucocorticoids to inactive metabolites. As 11 βHSD is also expressed in the intestine, this enzyme may be an important regulator of intestinal maturation. To investigate this, we have performed the systematic study of the development of intestinal 11 βHSD activity and its cofactor preference as well as of the effect of 11 βHSD inhibition by carbenoxolone on postnatal development of sucrase, alkaline phosphatase and Na,K-ATPase in the intestine. The activity of 11 βHSD was low in ileum of suckling rats and significantly increased during the weaning period. In colon, the activity was already high in suckling rats and gradually rose during the postnatal development. 11 βHSD activity was undetectable in jejunum both in young and adult rats. At 14.5 nM corticosterone, colonic 11 βHSD utilized predominantly NAD as a cofactor, but displayed significant sensitivity also to NADP. Ileal 11 βHSD had similar sensitivity to both cofactors. With NAD as a cofactor, ileal 11 βHSD had a K m (59±10 nM) compatible with the colonic enzyme (81±14 nM). Carbenoxolone administration to suckling and weanling rats in vivo did not result in any changes of sucrase activity in jejunum and ileum, alkaline phosphatase activity in ileum and distal colon or Na,K-ATPase activity in ileum. However, carbenoxolone significantly increased Na,K-ATPase activity in distal colon. Our results indicate that the high-affinity type of 11 βHSD is expressed not only in colon but also in ileum and that 11 βHSD is an important factor in the regulation of tissue levels of active glucocorticoids in developing colon but not in the small intestine.

Enhanced growth of small bowel in transgenic mice expressing human insulin-like growth factor 1.

Insulin‐like growth factor 1 (IGF‐1) plays an important role in the regulation of intestinal growth and maturation, whereas the direct effects of growth hormone (GH) on intestinal growth are less clear. In this study the authors utilize a transgenic mouse model to assess the extent to which longterm excess of IGF‐1 in a background of GH deficiency stimulates small bowel growth.IGF‐1 transgenic mice that overexpress an IGF‐1 transgene driven by the mouse metallothionein I promotor were compared with wild‐type littermates and GH transgenic mice. The IGF‐1 transgenics showed elevation of circulating IGF‐1, undetectable levels of plasma GH, and a decrease in pituitary GH messenger RNA (mRNA) caused by negative feedback effects of IGF‐1 excess. Growth of small bowel, abundance and localization of mRNAs for the IGF‐1 transgene, and IGF binding protein 3 (IGFBP‐3) were assayed to determine whether enterotrophic effects of excess IGF‐1 correlate with local overexpression of IGF‐1 in small bowel.Small bowel length and mass were greater in IGF‐1 transgenic than in wild‐type mice. Villus height, crypt depth, and crypt cell mitoses were greater in IGF‐1 transgenics than wild‐type mice. Jejunal dissacharidase activities were not different among the IGF‐1 transgenics and wild‐type mice. The IGF‐1 transgene was expressed strongly in villus epithelial cells and at much lower, but significant levels in crypt epithelial cells, lamina propria, and smooth muscle layers. IGFBP‐3 was strongly expressed and localized in the lamina propria.Regional expression of IGF‐1 and IGFBP‐3 correlated with the increase in mucosal mass in IGF‐I transgenics.Effects of IGF‐I overexpression on intestinal length and mucosal mass were similar to effects of GH overexpression, although IGF‐I transgenics showed greater small bowel growth relative to somatic growth compared with GH transgenics. Excess of IGF‐I increased crypt cell proliferation, whereas excess of GH did not increase crypt cell proliferation but did stimulate jejunal sucrase activity. These observations suggest that GH has greater differentiative actions, whereas IGF‐I exerts primarily mitogenic actions in small bowel.

Bolus Versus Continuous Feedings Stimulate Small-Intestinal Growth and Development in the Newborn Pig

Although bolus and continuous tube feedings are common, little is known about their effect on the developing small intestine. To compare their effect on small-intestinal growth and differentiation, six pairs of 3-day-old piglet littermates were randomized to receive similar volumes of sow milk replacer, either by bolus (four times daily, group B) or continuous feedings (over 24 h, group C) for 7 days. The piglets were then killed and small-intestinal length, weight, protein mass, and disaccharidase activities were determined. Small-intestinal mucosal weight and ileal protein mass were greater in group B than in group C (p = 0.0024 and 0.019, respectively). No differences were noted between groups in jejunal mucosal protein mass. Ileal maltase activity also was greater in group B than group C (p = 0.02). Although ileal lactase activity in group B was twice that in group C, the differences did not quite reach statistical significance (p = 0.11). No differences between groups were noted in ileal or jejunal sucrase activity. Our study demonstrated that bolus feedings increased mucosal mass, protein mass, and maltase activity to a greater degree than continuous feedings. These results may have clinical significance for infants receiving long-term tube feedings.

Bolus Versus Continuous Feedings Stimulate Small‐Intestinal Growth and Development in the Newborn Pig

Although bolus and continuous tube feedings are common, little is known about their effect on the developing small intestine. To compare their effect on small‐intestinal growth and differentiation, six pairs of 3‐day‐old piglet littermates were randomized to receive similar volumes of sow milk replacer, either by bolus (four times daily, group B) or continuous feedings (over 24 h, group C) for 7 days. The piglets were then killed and small‐intestinal length, weight, protein mass, and disac‐charidase activities were determined. Small‐intestinal mucosal weight and ileal protein mass were greater in group B than in group C (p = 0.0024 and 0.019, respectively). No differences were noted between groups in jejunal mucosal protein mass. Ileal maltase activity alsc was greater in group B than group C (p = 0.02). Although ileal lactase activity in group B was twice that in group C the differences did not quite reach statistical significance (p = 0.11). No differences between groups were noted in ileal or jejunal sucrase activity. Our study demonstrated that bolus feedings increased mucosal mass, protein mass, and maltase activity to a greater degree than continuous feedings. These results may have clinical significance for infants receiving long‐term tube feedings.

Effects of starvation and refeeding on jejunal disaccharidase activity.

In the rat, starvation lowers jejunal sucrase activity and increases or has no effect upon jejunal lactase activity. The mechanism by which starvation influences these intrinsic microvillus proteins remains unclear. Jejunal sucrase and lactase activities were studied during starvation or refeeding after a three-day fast. Using polyclonal monospecific antibodies, sucrase-isomaltase (SI) and lactase-phlorizin hydrolase (LPH) protein contents were measured in parallel to determine changes in enzyme activation. Sucrase activity and SI protein fell after two and three days of fasting and rose during refeeding. In contrast, lactase activity and jejunal LPH content increased after starvation and decreased after refeeding for 48 hr. For both enzymes, changes in catalytic activity and protein content occurred in parallel. [3H]Leucine incorporation studies in vivo showed more labeling of immunoprecipitable LPH than SI during starvation, but refeeding induced relatively more labeling of SI than of LPH. Therefore, starvation and refeeding produce opposing effects upon jejunal lactase and sucrase activities by modulating LPH and SI protein production and not by modifying enzyme activation.

Dietary-induced increases of disaccharidase activities in rat jejunum

A study was carried out to examine whether the responsiveness of small intestinal epithelial cells to dietary carbohydrate varied during the daily 24 h cycle. The effect of sucrose on disaccharidase activities was compared during a period of decreasing disaccharidase activities, i.e. between 22.00 and 10.00 hours, and increasing disaccharidase activities, i.e. between 10.00 and 22.00 hours, in the jejunum of 7-week-old-rats. Rats were fed on a low-starch, high-fat diet (Lst; starch 5 and fat 73% of gross energy), or a high-starch, low-fat diet (Hst; starch 70 and fat 7% of gross energy). Both dietary groups exhibited typical diurnal variations in jejunal sucrase (EC 3.2.1.48), maltase (EC 3.2.1.20) and lactase (EC 3.2.1.23) activities, exhibiting a peak around 22.00 hours and a trough at approximately 10.00 hours. When rats were fed on diet Lst for 7 d and then force-fed on an isoenergetic sucrose diet (S; sucrose 40 and fat 37% of gross energy) for 6 or 12 h they exhibited increased sucrase, maltase and lactase activities compared with rats fed on diet Lst. The absolute increase in disaccharidase activities was similar regardless of the time diet S was given or whether rats were killed at 10.00 hours or at 22.00 hours. Analyses of sucrase and lactase activities along the villus-crypt columns showed that the distribution of cell cohorts that responded to diet S was not influenced by the time of introduction of diet S. These findings suggest that small intestinal epithelial cells possess the ability to respond to dietary carbohydrate throughout the daily 24 h cycle.

Cortisone and thyroxine modulate intestinal lactase and sucrase mRNA levels and activities in the suckling rat

Glucocorticoids and thyroxine modulate postnatal intestinal sucrase and lactase activities. Whether changes in enzyme activity are accompanied by changes in enzyme mRNA levels were determined in day 6 rats given thyroxine, cortisone, or thyroxine plus cortisone and killed 3 days later. Cortisone induced precocious expression of jejunal sucrase activity which was enhanced when cortisone plus thyroxine was administered; sucrase mRNA changed in parallel. Jejunal lactase activity was unaffected by thyroxine and was increased after cortisone, but not after thyroxine plus cortisone. Jejunal lactase mRNA levels increased equally after cortisone or after cortisone plus thyroxine. Thus, cortisone induces coordinated increases in sucrase and lactase activities and in corresponding mRNA levels. Thyroxine only enhances cortisone induced sucrase expression and antagonizes cortisone by depressing lactase activity post-translationally.

Adaptive response of ileal mucosa to malnutrition in the rat: role of polyamines

Mucosal disaccharidases and ornithine decarboxylase activities were measured in malnourished, preweaning (19 days), post weaning (24 days) and young adult (37 days) rats. Malnutrition resulted in decreased body weight, intestinal weight, DNA and protein content. Mucosal Prot/DNA ratios were elevated in the ileal segments of the 24 and 37 day rats. Preweaned malnourished rats had significantly enhanced lactase specific activity in both jejunal and ileal segments. Adult malnourished rats showed enhanced jejunal lactase and sucrase activities which were not accompanied by elevated ornithine decarboxylase values. Mucosal sucrase and ornithine decarboxylase specific activities were significantly elevated in the ileal segment of the 24 and 37 day old malnourished rats. Studies of adult rats showed that these increased specific activities were located in the mature enterocytes at the villus tip, and persisted during a 24 h diurnal cycle. DFMO administration for 4 days completely inhibited mucosal ornithine decarboxylase and abolished the rise of ileal sucrase activity. We concluded that the intestinal response to reduced food intake is age related and differs in the jejunum and ileum: ornithine decarboxylase and polyamines are involved in ileal adaptation to malnutrition in postweaned and adult rats.

Food Restriction Retards Age-Related Biochemical Changes in Rat Small Intestine

Previous studies have demonstrated that the specific activities of several proximal small intestinal mucosal enzymes fall in the aging rat. This reduction was due to a delay in the full expression of activity of these enzymes during epithelial cell transit from the crypt onto the intestinal villus. We now show in the ad libitum fed Fischer 344 rat that jejunal sucrase, maltase, and alkaline phosphatase specific activities do not fall gradually throughout the life span, but are reduced during senescence. Caloric restriction to 60% of ad libitum intake (DR) abolishes or delays this fall in enzyme activity. Jejunal mucosal immunoprecipitable sucrase-isomaltase (S-I) content also falls with age, but sucrase specific activity per molecule of S-I is less in the older ad libitum fed (approximately 45) than in the DR rats (approximately 60). Jejunal lactase activity falls gradually throughout the life span of ad libitum and DR rats, but lactase activity consistently was higher in DR animals. These observations indicate that DR alters the age-related changes in the activity of several enzymes in the rapidly replicating gut mucosa.

Effect of feeding amaranth (food red no. 2) on the jejunal sucrase and digestion-absorption capacity of the jejunum in rats.

To clarify the effect of feeding 5% amaranth (Food Red No. 2, Am) alone or with 5% dietary fiber on jejunal mucosal integrity, change in jejunal sucrase activity before and after the feeding was compared between rats fed and fasted previously. Digestion-absorption capacity of the jejunum was also examined by perfusing 15 mmol/liter sucrose and 30 mmol/liter glycylglycine through the anesthetized rat jejunum after 14 days of feeding Am. Gobo dietary fiber (GDF) was prepared from the roots of edible burdock (Arctium lappa L.). At the end of 3 days' fasting, rats had 20% less body weight, 30% less mucosal protein and 50% less jejunal sucrase activity per unit length than those before fasting. Although rats fed Am showed severe diarrhea and growth retardation as observed in previous reports, initial sucrase level was not changed by feeding Am for 3 days even in the fasted rats. When sucrase activity on day 3 after feeding was compared among inter-groups, however, rats fed Am showed sucrase activity lower than that of rats fed either the basal diet or the basal diet containing Am plus GDF only when they had been fasted previously. After 14 days of feeding, rats fed Am after 3 days' fasting regained sucrase activity up to that of rats fed the basal diet despite the remarkable growth retardation. Jejunal perfusion in situ showed that digestion-absorption capacity for sucrose and glycylglycine in rats fed 5% Am for 14 days was also the same as that in rats fed the basal diet. These results suggest that feeding Am can reduce neither jejunal sucrase nor digestion-absorption capacity of epithelial cells of the jejunum, but retards the regain of the lowered sucrase level at earlier stage of feeding when rats have been fasted before the feeding, and that concurrent feeding of GDF promotes catch-up of the sucrase level lowered by the fasting.

Induction of intestinal differentiation by systemic and not by luminal corticosterone in adrenalectomized rat pups.

Potential effects of corticosterone (cort) from maternal milk on intestinal differentiation were studied using adrenalectomized (adx) rat pups fed a formula containing differing amounts of cort. Formula cort concentrations in the range found in milk (0.1-0.5 micrograms/ml) increased the survival of adx rats, but did not induce intestinal differentiation. Formulae containing 1.0-50.0 micrograms/ml cort caused a dose-dependent elevation of serum cort concentrations and jejunal maltase activity and precocious jejunal sucrase induction. Adx rats receiving the formula containing 10 micrograms/ml cort showed serum cort concentrations similar to those in day 15 control rats and jejunal sucrase and maltase activities equivalent to those in day 18-20 control rats, suggesting that the rise in serum cort that occurs during postnatal development suffices to modulate intestinal differentiation. To distinguish between direct local and systemic effects of luminal cort on intestinal differentiation, expression of sucrase was determined in jejunal isografts and in host jejunum from adx rats fed luminal cort. Jejunal isografts and host jejunum expressed similar sucrase activities and showed similar immunofluorescent staining. Moreover, administration of cort by continual ip infusion was more effective than continual intragastric infusion in inducing intestinal sucrase and maltase activities. These data imply that luminal cort is absorbed and transported into the systemic circulation before inducing intestinal epithelial cell differentiation through the systemic route.

Differential effects of thyroxine and cortisone on jejunal sucrase expression in suckling rats.

Effects of thyroxine (T4) and cortisone (C) on developmental expression of jejunal immunoreactive sucrase-isomaltase (S-I) and sucrase activity in suckling rats were studied to determine whether these hormones have distinctive actions. Immunoreactive S-I and sucrase activity were absent in infant rats and appeared simultaneously on days 16-18, when cells expressing S-I protein were detected at the villus base. By day 22, the entire jejunal mucosal surface was covered by new cells expressing immunoreactive S-I. Jejunal S-I content surged to adult levels on day 22, whereas the sucrase activity of immunoreactive S-I protein increased continuously until day 32. Administration of 12.5 nmol of T4 or 1.25 mumol of C on day 12 induced precocious expression of jejunal sucrase activity on day 15. T4 also induced sucrase activity in adrenalectomized rats without increasing serum corticosterone concentrations. Both T4 and C appeared to exert their effects in crypt cells, since immunoreactive S-I protein appeared only in villus base cells 24 h after administration. Pulse labeling of [14C]leucine showed that both hormones evoked de novo synthesis of S-I. The S-I induced by C had significantly higher sucrase activity than that induced by T4. We conclude that postnatal development of sucrase activity results from de novo synthesis of S-I with progressively higher catalytic activity until day 32 and these developmental processes are sequentially modulated by thyroid and adrenocortical hormones.

Alterations of intestinal membrane-bound enzymes in three types of hypertensive rats.

Alkaline phosphatase, sucrase, Na+,K+-ATPase and Mg2+-ATPase specific activities of crude membrane fractions, prepared from duodenal, jejunal, ileal and colonic mucosa, have been estimated in three types of hypertensive rats: the spontaneously hypertensive rat (SHR), the DOCA-saline treated rat and the renovascular rat (Goldblatt one-kidney, one-clip rat; 1K-1C). Alkaline phosphatase and sucrase specific activities have been measured in purified jejunal brush-border membranes. When compared with its normotensive age-matched control (WKY rat), the SHR has a lower activity of alkaline phosphatase in duodenal and jejunal crude membrane fractions, whereas a higher activity in colonic Na+,K+-ATPase is recorded. In purified jejunal brush-border membranes, lower alkaline phosphatase activity and higher sucrase activity were found. These differences occur in the young prehypertensive SHR as well as in the adult animal. In the DOCA-treated rat, the only significant alteration in crude membrane fractions is a decreased Mg2+-ATPase activity at all regions of intestinal mucosa. In purified jejunal brush-border membranes both alkaline phosphatase and sucrase activities are increased at 4 or 7 weeks but especially at 13 weeks of hypertension. In the 1K-1C rat, no significant modification appears in crude membrane fractions or in purified jejunal brush-border membranes, but a decrease in alkaline phosphatase and in sucrase activities is probable after 13 weeks of hypertension. Since alterations of the intestinal enzymes are different in the three types of hypertensive rats it is concluded that the changes are not secondary to the hypertension condition. In the SHR, these alterations are present in the young prehypertensive animal.(ABSTRACT TRUNCATED AT 250 WORDS)

Intestinal glucose metabolism during development. II. The role of glucocorticoids and weaning.

Prolonged suckling, until 25 postnatal days, delays the increase in jejunal oxidation of glucose both to lactate and to CO2 that occurs after artificial weaning at 20 days of age. The cortisone-mediated increase in intestinal sucrase activity which normally occurs by 20 days is not effected by prolonged suckling. Following precocious weaning at 16 days, the rate of jejunal glucose oxidation to lactate and to CO2 increases, over a 48-h period, to adult rates. Exogenous cortisone treatment at 10-13 postnatal days, before the endogenous steroid burst, does not change the rate of glucose oxidation in suckling animals. After weaning, both at 20 days of age and precociously at 16 days, the rate of glucose oxidation to lactate and to CO2 increases within 24 h in those animals who received early steroid treatment, in comparison to 48-72 h in untreated controls. After prolonged suckling until 25 days, there is no effect of early steroid treatment. We conclude that neither endogenous glucocorticoid secretion nor exogenous cortisone treatment alters the rate of glucose oxidation in jejunum of suckling animals despite the induction of jejunal sucrase activity. After early cortisone treatment, glucose oxidation increases within 24 h of normal of precocious weaning.

Jejunal mucosal DNA content and maturation. Inverse relation to serum gastrin levels in suckling and weanling rats.

Although pentagastrin has a tropic action on intestinal mucosa in suckling rat pups, and at weaning a rise in gastrin levels coincides with maturation of the intestinal mucosa, direct correlations of serum gastrin levels and intestinal maturation have yet to be made. Ten-day-old rats were subjected either to antrectomy to produce a 43% decrease in serum gastrin levels or to fundectomy to produce a 319% increase over gastrin levels in rumenectomized or normal animals. These changes were not associated with tropic or adaptive changes in jejunal or colonic mucosa as determined by jejunal and colonic DNA content, jejunal sucrase activity, jejunal villous height, or crypt depths in jejunum and colon at the beginning (day 15), middle (day 21), or end (day 27) of the weaning period. To the contrary, an inverse relation was found between serum gastrin levels and both jejunal mucosal DNA content and sucrase activity as an index of maturation.

Effect of somatostatin on small intestine enzyme activities in rat and chick

1. 1. The influence of somatostatin injection on intestinal disaccharidase and alkaline phosphatase activity in rat and chick was investigated. 2. 2. Disaccharidase and alkaline phosphatase activities of rat and chick homogenates were not modified. 3. 3. In rat the activities of mucosal brush-border maltase and sucrase were significantly increased. 4. 4. In chick brush-border a significant increase of duodenal mucosal activity and duodenal and jejunal sucrase activity is observed.

Influence of starvation on sucrase regulation by dietary sucrose in the rat

We have studied the action of sucrose on jejunal sucrase activity. Rats (175 g) were first starved or fed a digestible carbohydrate-free diet for 60 h and then fed a high sucrose diet for varying times up to 84 h. 1) Rats starved for 60 h showed mucosal atrophy with a decrease in protein content/10 cm (18.0 0 ± 1.4 versus 40.1 ± 3 mg (controls p < 0.001) and in villus height (357 ± 18 versus 526 ± 5 µm, p < 0.001) which was fully repaired only after 60 h on the sucrose diet (528 ± 11 µm). Rats on digestible carbohydrate-free diet showed no mucosal atrophy. 2) Starved rats had a delayed (60 h) sucrase activity response to sucrose (53 ± 7 versus 122 ± 4 µm/mg protein, p < 0.001). Maximum activity was obtained after 12 h on sucrose diet in rats maintained on the carbohydrate-free diet : 38 ± 1 versus 108 ± 2.3 µm/mg protein, p < 0.001. 3) Villus and crypt cell analysis after starvation and 12 h on a high sucrose diet localized the increase in sucrase activity to the villus-crypt junction. No change occurred in the upper villus. The increase was complete all along the villus by 36 h. In contrast, after the carbohydratefree diet, sucrase activity increased maximally at all levels of the villus by 12 h on the high sucrose diet. Thus starvation lowers villus height and renders the residual upper villus enterocyte incapable of responding to substrate, while elimination of digestible carbohydrate supports normal morphology and allows enterocytes to maintain their capacity to respond to sucrose by abruptly increasing their sucrase levels.

Role of dietary iron in maturation of rat small intestine at weaning.

The weanling process is characterized by the transition from a liquid diet poor in iron (rat milk) to a solid diet high in iron (chow pellets). To examine the effects of iron content of the weanling diet on terminal maturation of rat small intestine, suckling pups, nursed by iron-sufficient mothers, were weaned by day 16 onto a solid basal diet that was either deficient [low-iron diet (LID): 0.5 mg iron/100 g solid] or high [high-iron diet (HID) controls: 30 mg iron/100 g solid] in iron. The animals were studied during or at the end of the 4th postnatal wk. By day 17 rats weaned onto the LID exhibited an initial rise in jejunal sucrase activity as did their controls, but the activity plateau of the enzyme was reduced to a level 60% of the controls. On day 28 iron-deprived rats were anemic and showed significant decreases (P less than 0.01 compared with HID rats) in the activity of jejunal sucrase (-57%), neutral lactase (-83%), and maltase (-46%), whereas villus height, crypt depth, mucosal mass parameters, ileal acid beta-galactosidase activity, mucosal protein, and DNA synthesis rates were equivalent in LID and HID groups. The concentration of the secretory component, a glycoprotein synthesized by the intestinal crypt cell, was markedly depressed (P less than 0.01 vs. controls) in the jejunum (-54%) and ileum (-79%) of iron-deprived rats. When D-[1-14C]glucosamine was injected intraperitoneally, incorporation of the label into jejunal and ileal brush-border proteins was two to three times lower for iron-deficient rats than for controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Small Intestine of Artificially Reared Rat Pups: Weight Gain and Changes in Alkaline Phosphatase, Lactase and Sucrase Activities during Development

Comparative studies on small intestinal development in artificially reared (AR) and in mother-fed (MF) rats were carried out. When pups at 12 days of age were reared by continuous intragastric infusing of a cow milk formula (CMF), they gained weight equal to MF rats until 20 days; their small intestine weight was approximately 40 and 23% greater than that of MF rats at 16 days and 22 days of age, respectively. Autoradiographic studies indicated that the intestinal DNA synthetic index was 74–85% higher in AR than in MF rats at 16 days; similarly intestinal crypt depth and duodenal villus length were significantly higher in AR rats. The developmental pattern of duodenal alkaline phosphatase activity was similar in both AR and MF rats. In contrast, AR rats showed precocious decrease of lactase activity in the ileum at 16 days and in the jejunum at 18 days; but toal lactase activity in the intestine was not different from MF rats at 16 days. Jejunal sucrase activity in AR rats was precociously induced and elevated. It was concluded that the intestine of AR rats undergoes structural and enzymic modifications. The physiological significance of these changes remains to be elucidated.