Jejunal Sucrase Research Articles

Permissive role of thyroxine in the ontogeny of jejunal sucrase.

The possibility that T4 triggers the appearance of jejunal sucrase in the suckling rat has been studied. When pups were made hypothyroid by administration of n-propylthiouracil (PTU), the timing of the appearance of sucrase was not delayed. However, the rate of the subsequent accumulation of the enzyme (from day 17-day 27) was markedly depressed as compared with euthyroid controls. The PTU regimen had an even greater effect on total weight of the jejunum, there being a complete cessation of growth from day 17 onwards. All reported effects of PTU were prevented by concurrent administration of T4 (0.1 μg/g BW/day) every second day from day 5 onwards. Neither short term (days 9–11) nor long term (days 5–11) periods of physiological hyperthyroidism (0.1 μg T4/g BW/day) caused precocious appearance of sucrase. In contrast, when pups were given hydrocortisone (50 μg/g BW) on day 9 and killed on day 11, they were found to have sucrase activity equivalent to normal 18- to 20-day-old pups. This response to hydroco...

Disaccharide consumption and malabsorption in Canadian Indians

Twenty-eight Sioux and 29 Saluteaux Indians from a southern and an isolated northern Manitoban community were screened for lactose malabsorption; 55 were also screened for sucrose tolerance. Sixty percent of the subjects were lactose malabsorbers; the incidence increased with age. Lactase deficiency appeared, on the average, between 8 and 15 years of age. About 45% of the subjects were lactose intolerant. Malabsorbers who did not regularly drink milk had the highest symptom scores. The northern subjects consumed significantly more lactose and sucrose than the southern subjects. Two Sioux children were sucrose malabsorbers. It was hypothesized that the significantly greater sucrose consumption by the Saulteaux subjects were responsible for their markedly higher blood glucose curve following the sucrose tolerance tests. Dietary sucrose increases jejunal sucrase activity and the intestinal transport of glucose and fructose. Three of eight children less than 4 years were lactose malabsorbers; hence, medical personnel treating noninjective diarrhea in Indian children should examine for lactase deficiency. It was recommended that vitamin D fortified milk supplements to Indian school children be continued and that the milk be treated so as to reduce abdominal symptoms in the intolerant individuals.

DEVELOPMENT OF THE DIURNAL RHYTHM OF JEJUNAL SUCRASE ACTIVITY IN THE WEANLING RAT

In the adult rat, fed ad lib, the activity of jejunal sucrase shows a diurnal rhythm with a peak during the dark period. Onto-genically this enzyme does not appear until approximately the 16th postnatal day; its activity then rises rapidly and reaches adult levels by the 25th day. Our aim was to determine whether the diurnal rhythm is present from the outset or appears only after sucrase has attained adult levels. Rat pups were raised in litters of 9 with a light/dark cycle of 12h. Solid food and water were available to mothers and pups at all times and mothers were normally removed on the 21st postnatal day. Four litters were studied during the 24h period beginning at 8am on the 19th day. One pup from each litter was removed for assay every 3h. Jejunal sucrase showed considerable variation between pups, but there was no discernable pattern with time. In contrast, when the experiment was repeated with pups aged 22 days, there was a distinct peak in sucrase activity during the early part of the dark period. In order to determine whether the rhythm is cued by the process of weaning, two litters were raised on a feeding schedule which ensured that maternal milk was the only food available to the pups. When studied during the 24h period beginning on the 22nd day, the jejunal sucrase activity of these pups exhibited no rhythm. It is concluded that some component of solid food is responsible for the usual appearance of the diurnal rhythm of this enzyme. (supported by NIH Grant No. HD-10042.)

PRECOCIOUS INDUCTION OF RAT JEJUNAL SUCRASE BY TRIIDO THYRONINE (T3): IN FETUSES BY ADMINISTRATION TO THE PREGNANT MOTHER AND IN SUCKLINGS BY ADMINISTRATION TO THE LACTATING MOTHER

Daily application of T3 (20 μg/100 g body wt) to female rats in the last (third) week of pregnancy elicits a precocious appearance of sucrase activity in fetal jejunum. Similarly, administration of T3 in much higher doses (1.25 mg/100 g body wt) from day 11 to 15 postnatally evokes a precocious appearance of jejunal sucrase activity in sucklings. T3 administration to lactating mothers is followed by decrease of TSH and T4 levels in sera of sucklings and by an increase in the T3 levels in the sera and milk of lactating mothers as well as in sera of sucklings.These experiments thus show: (a)sucrase activity is already inducible in fetuses, (b)T3 administration in very high doses to pregnant rats might be transferred to the fetus to the extent of still effective doses, (c)milk may function as an endocrine link between the mother's hormonal and metabolic systems and those of the sucklings.Supported by NIH Research Grant AM 14531)

Prenatal induction of sucrase activity in rat jejunum.

Daily application of cortisone acetate (10mg/100g body wt.) or L-tri-iodothyronine (20 microng/100g body wt.) to female rats in the last (third) week of pregnancy elicits a precocious appearance of jejunal sucrase in their foetuses.

Enzyme activities of jejunal mucosa in experimental blind loop syndrome of rat.

Decreased activities of jejunal mucosal enzymes, i.e. lactase, sucrase, maltase and gamma-glutamyl transpeptidase were found in rats with experimental blind loop syndrome. The peroral administration of Kanamycin induced both reduction in fecal fat excretion and restoration of enzyme activities in rats with the blind loop syndrome. Similar effects of Kanamycin on fecal fat excretion and jejunal mucosal enzyme activities were also recognized in unoperated rats. There was an inverse relationship between fecal fat excretion and activities of those enzymes which are mainly located in the brush border of the enterocyte. From these results, significance of jejunal brush border enzymes in the blind loop syndrome was discussed.

BREATH HYDROGEN IN HYPOSUCRASIA

A simple and reliable test for the diagnosis of hyposucrasia is required, since this may be an unsuspected cause of long-standing gastrointestinal disorder. Furthermore little has been done to define the epidemiology of this condition, possibly because of the limitations of multiple blood-sampling. Breath hydrogen (H 2) production after lactose ingestion is a reliable test for hypolactasia, and has now been measured after sucrose ingestion in eleven patients with various gastrointestinal symptoms. Six who had normal sucrase activity on jejunal biopsy produced no H 2 after taking 50 g of sucrose. No H 2 was produced in three patients with borderline hyposucrasia, either after 50 g sucrose or when retested using 100 g sucrose (two patients). However, the two patients with low jejunal sucrase activity showed rises of breath H 2 after only 25 g sucrose. Breath H 2 measurement is a simple, accurate, and non-invasive test for diagnosing gastrointestinal symptoms due to hyposucrasia.

Development of the small intestine in the hypophysectomized rat: II. Influence of cortisone, thyroxine, growth hormone, and prolactin

The intestinal deficiencies caused by hypophysectomy of rats at 6 days of age can be repaired to varying degrees by thyroxine or cortisone but not by growth hormone or prolactin. Administration of daily doses of thyroxine alone from 19–22 days raises duodenal alkaline phosphatase activity to normal levels at 24 days; it has a strong effect on jejunal sucrase and maltase, although these activities remain below those of controls. Thyroxine causes a marked increase in rough endoplasmic reticulum and restores the Golgi complexes to their normal appearance. It also elicits an intensification of periodic acid-Schiff (PAS) stainability of the brush border. Cortisone acetate given from 19 to 22 days elevates sucrase and maltase to normal levels but does not fully restore phosphatase activity. Like thyroxine, cortisone causes intensification of PAS staining of the brush border and also increases rough endoplasmic reticulum. It seems to stimulate Golgi activity, but results in the appearance of a variety of abnormal forms. The defects in Golgi configuration, brush border carbohydrate content, and activity of glycoprotein enzymes that are bound to the brush border may all reflect impaired glycosylation in the hypophyseoprivic state; the results of thyroxine or cortisone administration suggest that both hormones may affect glycosylation but in different ways.

Studies on Normal and Precocious Appearance of Jejunal Sucrase in Suckling Rats

Some of the cellular and molecular events involved in the normal and precocious appearance of sucrase in jejunum of infant rats have been studied. Actinomycin D has been shown to inhibit (by 79%) the rise in sucrase activity usually seen after administration of hydrocortisone to 9-day-old rats. The precocious appearance of sucrase has also been studied with respect to the cytological localization of enzyme activity in the intestinal mucosa. Tissue was sectioned in a cryostat (transverse to the villi) and sucrase was assayed in homogenates prepared from the sections. By 24 h after administration of hydrocortisone to 9-day-old animals, sucrase was detectable only at the bases of the villi. During the subsequent 72 h the enzyme activity increased and spread along the villi at a rate consistent with that of cell migration. These data have lead to the conclusion that the action of glucocorticoids on enterocytes can occur only when the cells are in their proliferative phase. An ontogenic study of the ability of hydrocortisone to elicit jejunal sucrase showed that the tissue becomes increasingly responsive to the hormone with increasing age through the first and second postnatal weeks. Various hypotheses to explain this increase have been examined.

Thyroxine-evoked precocious decrease of acid hydrolases in the ileum of suckling rats.

SummaryDaily administration of thyrox-ine (200 μg/100g/BW 24 hr s.c.) to intact suckling rats (from 7 to 13 days of postnatal age) and to suckling adrenal-ectomized rats (from 14 to 18 days) caused a precocious decrease of acid-β-galacto-sidase, β-glucuronidase and N-acetyl-β-glucosaminidase in the ileum of the small intestine. Thyroxine treatment evoked also a precocious increase of jejunal sucrase and maltase activities.

Dietary stimulation of sucrase in a patient with sucrase-isomaltase deficiency

A 7-year-old girl with a 6-year history of chronic diarrhea and poor weight gain was found to have jejunal sucrase-isomaltase deficiency. Dietary fructose was used as a form of therapy to increase the sucrase activity to a level that would allow her to ingest small amounts of sucrose without becoming symptomatic. Treatment with isocaloric diets containing fructose caused a concomitant increase in jejunal sucrase activity. The maximal sucrase activity was approximately four times that seen on a fructose free diet (from 0.38 to 1.67 μmoles substrate hydrolyzed/minute/gm mucosa). There was also an improvement in sucrose tolerance tests as measured by a rise in blood sugar and a decrease in urinary and fecal excretion of sucrose. She was subsequently treated with a sucrose-restricted diet which contained approximately 20% of the calories as fructose and has remained asymptomatic for 6 months despite occasional sucrose ingestion.

Alkaline phosphatase and disaccharidase activities in the rat intestine from birth to weaning. I. Effect of diet on enzyme development

Intestinal alkaline phosphatase and disaccharidase activities were determined along the gut in suckling and weaning rats. In normal animals, specific changes occur during this period that concern the enzyme nature, the level of enzymatic activity, and the location of maximum activity in the gut. An attempt was made to influence these intestinal enzymatic properties by changing the nature of food. 1) Lactose-free food (Hyprovit) was used as a weaning inducer in two groups of rats of different age. Of the younger rats (8 days old), the majority died. No change in the levels of the existing enzymes could be observed after 72 hr on Hyprovit and no sucrase activity appeared. 2) The second group (15-day-old rats) adapted well to this artificial feeding, which induced the enzymatic changes associated with weaning 2 days earlier. 3) Lactose-rich food (goat milk, 4.6% lactose) was given to a third group of rats (17 days old) for a period of 5 days. This diet neither prevented nor delayed the natural decrease of the ileal enzymes including lactase. 4) The same diet (goat milk) was given to young adult rats for 5 days. Both jejunal lactase and duodenal phosphatase increased. As sucrase, but not maltase, appeared enhanced also, we explained these results as the sum of two different factors; one of a dietetic nature, lactose acting as a substrate inducer enzyme on lactase, and the second as one of hormonal nature, provoked by the stress of the artificial feeding and responsible for the higher levels of jejunal sucrase and duodenal alkaline phosphatase. It was concluded that from a certain period (approximately the 15th day of life), both diet and hormones are involved in the intestinal enzymatic activities.

Dose Response of Jejunal Sucrase and Maltase Activities to Isocaloric High and Low Carbohydrate Diets in Man

Dose Response of Jejunal Sucrase and Maltase Activities to Isocaloric High and Low Carbohydrate Diets in Man

Time Response of Jejunal Sucrose and Maltase Activity to a High Sucrose Diet in Normal Man

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.

Control of jejunal sucrase and maltase activity by dietary sucrose or fructose in man. A model for the study of enzyme regulation in man.

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.