Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.26 (invertase)
 4,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activities of intestinal disaccharidases are known to be responsive to changes in the dietary intake of carbohydrates in the adult rat. Little is known, however, regarding the activities of these enzymes in obese subjects and how they are affected by differing carbohydrate intakes. To evaluate the effect of carbohydrate intake on the activity of intestinal disaccharidases in obesity, we used the genetically obese mouse C57BL/6J obob as an experimental model. Representing an example of early-onset obesity and mature-onset diabetes, this animal is characteristically hyperinsulinemic and hyperglycemic. Groups of obese mice and lean littermates were fed for 7 weeks equal amounts of either high-dextrose or low-dextrose isoenergetic diets. Sucrase, maltase, and lactase activities were measured on intestinal homogenates from the proximal and middle portions of the jejunoileum (upper and lower jejunum). Results were expressed as activity per tissue protein as well as total activity. Obese mice were found to have consistently greater total activity of both sucrase and maltase than their lean littermates, mostly as a result of increased intestinal size. Total lactase activity, however, was similar in the upper jejunum in both obese and lean mice, largely related to a decreased specific activity in obese mice. All mice fed the high-dextrose diet had significantly increased total activity of all disaccharidases studied when compared to the low-dextrose-fed animals, except for the lactase activity in the lower jejunum, where no differences were found in either group. Increases in activity related to high carbohydrate intake were a result of increases in specific activity.
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PMID:Effect of a high-dextrose diet on sucrase and lactase activity in jejunum of obese mice (C57BL/6J obob). 309 6

The effect of streptozotocin (SZ) on the development of small intestinal enzymes in postnatal rat pups was studied. SZ was injected ip on Day 10 and, if necessary, again on Day 12. On Days 15, 18, and 21, one pup from each group (including a vehicle-injected control (C) group) was decapitated under conditions which minimized stress. Plasma glucose, insulin (IRI), and corticosterone were measured, as were pancreatic IRI, liver glycogen, and liver membrane binding of IRI. Small intestinal segments were processed and analyzed for sucrase, lactase, maltase, and ileal acid beta-galactosidase activities. Our results indicate that plasma glucocorticoid levels remained virtually constant in both SZ and C groups, while the ontogenic profiles of sucrase and maltase in SZ rats were shifted toward an earlier appearance and a precocious maturation. Circulating levels of IRI were not reduced significantly by SZ despite the fact that pancreatic IRI was decreased 95%. Jejunal lactase, unlike data reported for diabetic rats, was not affected by SZ diabetes. Also, acid beta-galactosidase was unaltered in the SZ rat pups. It is concluded that possibly the elevated disaccharidases seen in diabetic postnatal rat pups are the direct effect of elevated blood glucose. If so, the SZ rat pup model may be a useful tool with which to study effects of glucose on intestinal enzymes in the absence of changes in plasma insulin.
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PMID:Effects of diabetes on development of small intestinal enzymes of infant rats. 312 20

MDL 25,637 is a novel compound designed as a transition-state inhibitor of alpha-glucohydrolases. This compound inhibits rat intestinal sucrase, maltase, isomaltase, glucoamylase and trehalase activities at micromolar concentrations. It is a much weaker inhibitor of alpha-amylase and lactase. Inhibition of sucrase was competitive with sucrose. In mice, MDL 25,637 inhibited the rise in serum glucose after a sucrose or starch load but not after a glucose load. MDL 25,637 also reduced the glycemic response to sucrose in rats. The drug was most effective when administered 0 to 30 min before the sucrose load and was as effective in streptozotocin-treated rats as in normals. The inhibition by MDL 25,637 of intestinal glucohydrolases is an effective means of reducing the hyperglycemic response to an oral sucrose or starch load and, as such, warrants further investigation as a potential drug for the treatment of diabetes mellitus.
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PMID:Inhibition of intestinal disaccharidases and suppression of blood glucose by a new alpha-glucohydrolase inhibitor--MDL 25,637. 329 22

Previous studies have demonstrated enhanced active and passive uptake of many nutrients in animals with experimental diabetes. These changes in absorption cannot be explained by differences in intestinal morphology, although the brush border membrane (BBM) phospholipids do change in diabetes. Manipulation of diet produces alterations in intestinal uptake of lipids and glucose. This study was undertaken to determine the effect of diet and diabetes on jejunal morphology and BBM lipid composition. Rats were rendered hyperglycemic with streptozotocin and were fed for 2 weeks on a diet that was high or low in carbohydrate, essential fatty acids, cholesterol, or protein. In both control and diabetic rats, these diets produced changes in villus height and BBM sucrase and alkaline phosphatase activities. In both control and diabetic rats, BBM phospholipids were unaffected by changes in the dietary content of essential fatty acids, cholesterol, or protein, but total BBM phospholipid content was reduced in animals fed low as compared with high carbohydrate diet. Total BBM phospholipid content was higher in diabetic than in control animals fed the low protein diet, whereas BBM phospholipid content was lower in diabetic than in control animals fed the high carbohydrate diet, and was even lower in diabetic animals fed the low as compared with the high carbohydrate diet. These changes in total phospholipids were due to alterations in the BBM content of phospholipids containing choline. In control animals, BBM cholesterol was higher in rats fed the low as compared with the high cholesterol diet, or the low as compared with the high protein diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diets alter jejunal morphology and brush border membrane composition in streptozotocin-diabetic rats. 356 35

Diabetes was induced in rats by administration of streptozotocin. After 90-120 days, one group of chronic diabetic animals was treated with insulin for chronic diabetic animals was treated with insulin for 10 days. The lipid fluidity and composition of microvillus membranes prepared from ileal enterocytes of control, diabetic, and insulin-treated diabetic animals were determined. Lipid fluidity, as assessed by steady-state fluorescence polarization techniques using the probes 1,6-diphenyl-1,3,5-hexatriene, DL-2-(9-anthroyl)stearic acid and DL-12-(9-anthroyl)stearic acid, was decreased in membranes of diabetic animals compared to membranes of control and insulin-treated diabetic membranes. The differences in fluidity resulted from an increased cholesterol content and cholesterol/phospholipid molar ratio in membranes of diabetic animals. The activities of sucrase and alkaline phosphatase were also found to be higher in membranes of diabetic animals. Insulin treatment, however, failed to significantly influence the enzymatic activities of these membranes. These studies, therefore, demonstrate that alterations in the lipid fluidity, lipid composition, and certain enzymatic activities exist in microvillus membranes of enterocytes prepared from chronic streptozotocin-induced diabetic rats. Administration of insulin for 10 days to these animals restored membrane fluidity and lipid composition but not enzymatic activities to control membrane levels.
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PMID:Correction of abnormal lipid fluidity and composition of rat ileal microvillus membranes in chronic streptozotocin-induced diabetes by insulin therapy. 390 76

The sucrase activity in enterocytes isolated from the villus crypt axis was found to increase in all regions of the villus from day 2 after induction of diabetes, and the increase continued until day 4. In contrast, alkaline phosphatase activity increased mainly in the apical one-third of the villus-crypt column, and the increase occurred abruptly on day 4 with increase in food intake.
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PMID:Changes in brush-border enzyme activities of intestinal epithelial cells isolated from the villus-crypt axis during the early phase of alloxan diabetes in rats. 398 70

The effects of experimental diabetes, hypertonic glucose infusion, and subsequent insulin administration on the sucrase activity of the small intestine were studied using intestinal segments completely excluded from luminal continuity by construction of Thiry-Vella fistulas in rats. Eight weeks after subtotal pancreatectomy, the rats contracted insulin-deficient diabetes mellitus, and sucrase activity was enhanced in both the Thiry-Vella loop and in the proximal jejunum in continuity. Subcutaneous injections of insulin during the last 4 weeks maintained the enzyme activity in the control range in both segments. There was a positive correlation between sucrase activity and blood glucose level in the pancreatectomized rats. Hyperglycemia in normal rats induced by intravenous infusion of 30% glucose solution over 48 hours enhanced the sucrase activity in the jejunum. Furthermore, insulin administration with a glucose solution inhibited the enhancement of enzyme activity. These findings suggest that hyperglycemia itself might play an important role in the diabetic increment of sucrase activity.
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PMID:Hyperglycemia induces intestinal sucrase activity in subtotally pancreatectomized rats. 401 94

The changes of the transmural electrical potential difference (delta PD) evoked by infusion of glucose, maltose and sucrose and the disaccharidase activities in the everted intestine were studied in diabetic rats. After the induction of diabetes by streptozotocin, delta PDs evoked by sugars and the enzyme activities were observed in the jejunum and ileum. delta PDs evoked by glucose, maltose and sucrose markedly increased both in the jejunum and ileum of diabetic rats. The Kt values for these sugars in diabetic rats were the same as those of control rats. The Vmax values were significantly increased in the ileum of diabetic rats. Maltase and sucrase activities in the ileum increased in diabetic rats. Highly significant linear correlations were found between the delta PDs evoked by glucose and the delta PDs evoked by maltose or sucrose both in the jejunum and ileum of control and diabetic rats. However, delta PDs evoked by maltose and sucrose did not correlate with maltase and sucrase activities in the jejunum. In the ileum, delta PDs evoked by sucrose correlated with the sucrase activity which was very low. These results suggest that the increase of transport of glucose derived from disaccharides in the diabetes induced by streptozotocin is mainly due to the increased activity of the glucose transport system, but not due to the increase of disaccharidase activities.
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PMID:Changes of sugar-evoked transmural potential differences in intestine of rats with streptozotocin-induced diabetes. 406 65

Specific and total activities of the disaccharidases, sucrase, maltase, and lactase are increased in mucosa of the small intestine of the streptozotocin diabetic rat. Because disaccharidases are essential for terminal digestion of carbohydrate, and disaccharidase deficiency is a common clinical problem, understanding the mechanisms regulating disaccharidase activity is important. In normal animals, disaccharidase activities are determined by route of feeding and are decreased by parenteral feeding. The indirect exocrine, endocrine, neurocrine, and paracrine functions of the gastrointestinal tract that are dependent on feeding via the gut are greatly decreased in parenteral as compared with enteral feeding. Hormone secretion by the gut and the pattern of response after feeding may be abnormal in diabetes and might be regulatory for disaccharidases. We tested the hypothesis that the elevated intestinal disaccharidases in diabetes are dependent on enteral feeding. Streptozotocin-injected rats (diabetics) and vehicle-injected rats (controls) were fed rat chow ad libitum for 4 days. A subset of control and diabetic animals was then killed to determine disaccharidase activity of the jejunum at the start of pair-feeding the elemental diet. The remaining animals were fed 60 cal/day of glucose, amino acid (Travasol), and electrolyte solution either intragastrically or intravenously for 4 days. Specific and total activities of disaccharidases were greater in diabetics than in controls under all feeding conditions. In controls, the pattern of activity of disaccharidase specific activity was initial greater than intragastric greater than intravenous. In diabetics, disaccharidase specific activities did not differ among groups. In both controls and diabetics, mean mucosal mass was highest initially; intermediate with intragastric feeding; and lowest with intravenous feeding. In both controls and diabetics, total disaccharidases decreased from initial to intragastric to intravenous. We conclude: (1) disaccharidase specific activity in controls is sensitive to feeding route and nature of diet, but is nearly independent of these factors in diabetics; (2) total disaccharidase activities respond to feeding stimuli in parallel with changes in mucosal mass in both controls and diabetics; and (3) the lack of feeding effect on the elevated specific activities of disaccharidases in diabetes suggests that this elevation is a response to the diabetic state and is independent of enteral factors such as luminal nutrition and gastrointestinal hormones.
Diabetes 1983 Mar
PMID:Elevated intestinal disaccharidase activity in the streptozotocin-diabetic rat is independent of enteral feeding. 640 7

In experimental diabetes, a number of intestinal brush-border hydrolases and transport systems are stimulated. In this study, we assessed possible effects of diabetes on the composition and membrane fluidity of rat intestinal brush-border membranes that might correlate with these functional changes. We found similar proportions of lipid and protein in the diabetic and control preparations, although there was a considerable increase in total membrane from the diabetic rats, presumably reflecting mucosal hyperplasia. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of membrane protein revealed an increase in the bands corresponding to sucrase-isomaltase, consistent with an increased enzyme activity of sucrase. Membrane lipid analysis revealed only a decrease in fatty acids of the neutral lipid fraction of diabetics--a change that may well have occurred during membrane preparation. 1-6-Diphenyl-1,3,5-hexatriene fluorescence polarization data, obtained as a function of temperature, was similar for the diabetic and control rats, with a three-phase linear model superior to one- and two-phase linear or quadratic models. The overall composition of the intestinal brush-border membrane, unlike other plasma membranes, appears little affected by experimental diabetes.
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PMID:Intestinal mucosa in diabetic rats: studies of microvillus membrane composition and microviscosity. 662 63


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