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)

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.
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PMID:Elevated intestinal disaccharidase activity in the streptozotocin-diabetic rat is independent of enteral feeding. 640 7

The rate of intestinal absorption of sugars and their site of absorption determine postprandial plasma glucose concentrations. Does chronic consumption of high-carbohydrate, high-fiber, low-fat diets of the type recommended by many diabetes associations induce adaptive changes in transport and metabolism of sugars in the small intestine? Control and STZ-induced diabetic (> 60 days diabetic) mice were fed high-carbohydrate or no-carbohydrate rations for 7 days. Brush-border glucose and fructose uptake per milligram increased 2 times with dietary carbohydrate in both diabetic and control mice; uptake, however, did not differ between diabetic and control mice. Compared with the distal small intestine, glucose uptake per milligram was 2 to 6 times higher in the proximal and middle regions, and enhancement of uptake by diet was limited to these regions. Changes in site density of intestinal glucose transporters as determined by specific phlorizin binding were tightly correlated with changes in brush-border glucose uptake per milligram. There were neither diabetes- nor diet-induced changes in the Kd of specific phlorizin binding, in the amount of glucose absorbed per transporting site, or in passive glucose permeability. Intestinal weights, wt/cm, intestinal length, and mucosal mass increased significantly with diabetes, and sugar transport per centimeter and per small intestine was up to 60% greater in diabetic mice. Dietary carbohydrate stimulated specific sucrase activity in the proximal small intestine of both diabetic and control mice. Chronic diabetes enhances sugar transport by nonspecific increases in intestinal mass.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dietary carbohydrate enhances intestinal sugar transport in diabetic mice. 840 98

Summary. Many studies have shown that experimental type 1 diabetes causes morphological, functional, and metabolic alterations in the small intestine. The more frequent form of the disease, type 2 diabetes, however, has been less studied. Here the influence of diabetes on the functionality of the small intestine was studied in an experimental diabetes model, with a certain degree of residual insulin secretion, specifically in the n0-STZ model. - The diabetic rats in this model were found to have glycaemia levels higher than in the controls (8.82 +/- 0.27 and 6.18 +/- 0.18 mmol/L; p < 0.01), while their plasma insulin levels were lower than in the control rats (2.65 +/- 0.32 and 3.60 +/- 0.25 ng/ml; p < 0.05). Although there were no significant variations in body weight between the two groups, both the weight and the length of the intestine were significantly greater (p < 0.05) in the diabetic rats than in the controls. The sucrase and maltase activities were greater (p < 0.01) in the proximal intestine of the diabetic rats (94 +/- 8 and 234 +/- 12 mU/mg protein, respectively) than in the control rats (50 +/- 2 and 149 +/- 20 mU/mg protein, respectively). The 6-phosphofructo-1-kinase activity (mU/mg proteins) was less (p < 0.05) in the proximal and distal intestine of the diabetic rats (160 +/- 40 and 80 +/- 20, respectively) than in the controls (280 +/- 30 and 230 +/- 30, respectively). No significant differences were observed in the lactate dehydrogenase or active and total pyruvate dehydrogenase measured in the distal and proximal intestine of control and diabetic rats. In conclusion, our results show that experimental diabetes (n0-STZ model) similar to human type 2 diabetes produces certain morphological and enzymatic alterations which affect the digestion and absorption of carbohydrates and the intestinal metabolism of glucose. These alterations may contribute to producing the post-prandial hyperglycaemia which characterizes diabetes.
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PMID:Morphological and enzymatic changes of the small intestine in an n0-STZ diabetes rat model. 1201 71

A purified pancreatic alpha-amylase inhibitor (alpha-AI) from white beans (Phaseolus vulgaris) was administered orally (100 mg/kg body weight dissolved in 9 g NaCl/l) for 22 d to non-diabetic (ND) and type 2 diabetic (neonatal diabetes models n0-STZ and n5-STZ) male Wistar rats. Mean glycaemia (mmol/l) declined from day 4 of the alpha-AI administration in ND rats (5.48 (sem 0.08) v. 4.39 (sem 0.13); P<0.05), n0-STZ diabetic rats (7.94 (sem 0.42) v. 5.56 (sem 0.32); P<0.01) and n5-STZ diabetic rats (17.34 (sem 2.58) v. 11.93 (sem 1.96)), until the end of treatment: ND (5.22 (sem 0.21) v. 3.97 (sem 0.06); P<0.01); n0-STZ (8.10 (sem 0.19) v. 5.21 (sem 0.30); P<0.01); and n5-STZ (16.36 (sem 2.14) v. 7.69 (sem 1.34); P<0.01). There was a decrease in water intake (ml/d) in the alpha-AI-treated diabetic rats: n0-STZ (30 (sem 0.10) v. 22 (sem 1.50); P<0.01) and n5-STZ (76 (sem 5.04) v. 57 (sem 4.85); P<0.01). Food intake (g/d) decreased in all three groups: ND (23 (sem 0.31) v. 20 (sem 0.03); P<0.05); n0-STZ (22 (sem 0.55) v. 16 (sem 0.98); P<0.01); and n5-STZ (31 (sem 0.58) v. 23 (sem 1.20); P<0.01). The enterocyte sucrase and maltase activities (U/g proteins) were high (P<0.01) in the untreated diabetic rats, n0-STZ (45 (sem 4) and 152 (sem 10), respectively) and n5-STZ (67 (sem 12) and 151 (sem 10), respectively) with respect to the ND rats (24 (sem 2) and 74 (sem 10), respectively). After alpha-AI treatment, enzyme activities declined in both diabetic rats, n0-STZ (21 (sem 2) and 85 (sem 11); P<0.01) and n5-STZ (28 (sem 7) and 75 (sem 19); P<0.05), to values close to those in the ND rats. In conclusion, alpha-AI significantly reduced glycaemia in both the ND and diabetic animals and reduced the intake of food and water, and normalized the elevated disaccharidase levels of the diabetic rats.
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PMID:White bean amylase inhibitor administered orally reduces glycaemia in type 2 diabetic rats. 1692 60

A screening of 5 plants used for making drinks in Vietnam revealed a Cleistocalyx operculatus (Roxb.) Merr and Perry flower bud extract to have the highest inhibitory activity against the alpha-glucosidase enzyme. The anti-hyperglycemic effects of an aqueous extract from flower buds of Cleistocalyx operculatus (CO), a commonly used material for drink preparation in Vietnam, were therefore investigated in vitro and in vivo. In vitro, the CO extract inhibited the rat-intestinal maltase and sucrase activities, with IC50 values of 0.70 and 0.47 mg/ml, respectively. These values are lower than those for a guava leaf extract (GE; IC50 0.97 and 1.28 mg/ml, respectively). Postprandial blood glucose testing of normal mice and STZ-induced diabetic rats by maltose loading (2 g/kg body weight (bw)) showed that the blood glucose reduction with CO (500 mg/kg bw) was slightly less than that with acarbose (25 mg/kg bw) but was more potent than that with GE (500 mg/kg bw). In an 8-week experiment, the blood glucose level of STZ diabetic rats treated with 500 mg of CO/kg bw/day was markedly decreased in comparison with that of non-treated diabetic rats. Consequently, CO is considered to be a promising material for preventing and treating diabetes.
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PMID:Anti-hyperglycemic activity of an aqueous extract from flower buds of Cleistocalyx operculatus (Roxb.) Merr and Perry. 1721 65