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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The changes in the activity and content of sucrase-isomaltase complex (S-I) in the intestinal mucosa were studied during the development of diabetes induced by streptozotocin in rats. On days 0, 1, 3, 5, and 10 after an intraperitoneal injection of streptozotocin (70 mg/kg), the enzyme activity and the enzyme content were observed in the jejunum and ileum. Sucrase and isomaltase activities markedly increased from the 3rd day both in the jejunum and ileum, and kept increasing till the 10th day especially in the ileum. The enzyme content of S-I also increased in parallel with its activity during the development of diabetes. However, in the early stage of diabetes, sucrase activity per microgram of S-I content increased both in the jejunum and ileum. Isomaltase activity per microgram of S-I content increased temporarily in the ileum. These results suggest that the increase of disaccharidase activities in the early stage of diabetes induced by streptozotocin is not only due to the increase of the enzyme content, but also due to the change of the enzyme catalytic property.
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PMID:Changes of the activity and content of sucrase-isomaltase complex in the intestinal mucosa during the development of streptozotocin-induced diabetes in rats. 666 65

Acarbose, a complex oligosaccharide, is a potent competitive inhibitor of sucrase and decreases postprandial hyperglycemia when administered with food. To evaluate its potential for metabolic control and prevention of diabetic nephropathy, groups of gentically diabetic mice (C57 BLKsJ db/db) were treated with Acarbose for 10 wk. Control mice received normal chow and experimental groups were given Acarbose prepared as a drug-food mixture in doses of 10, 20, and 40 mg/100 g of food. Acarbose did not influence fasting blood glucose, food intake, or the normal development of obesity in the mice. Urinary glucose excretion and glycosylated hemoglobin was significantly reduced in animals receiving high-dose Acarbose (40 mg/100 g food). Immunopathologic examination of the kidneys showed a dose-dependent decrease in glomerular mesangial immunoglobulin deposition. By light microscopy, glomerular mesangial thickening was significantly reduced in the group receiving high-dose Acarbose (40 mg/100 g food). To the extent that Acarbose improves metabolic control in the db/db mouse, chronic treatment with this agent produces a dose-dependent amelioration of diabetic nephropathy. Alphaglycosidase inhibition may be a useful adjunctive therapy for blood glucose control in diabetes mellitus.
Diabetes 1982 Mar
PMID:The effect of chronic alpha-glycosidase inhibition on diabetic nephropathy in the db/db mouse. 675 41

The relation between food intake and enzyme activity of the small intestine and rate of intestinal absorption were studied in rats 15 days after induction of alloxan diabetes. Diabetic rats were given an ad lib. semisynthetic diet or a restricted diet on the basis of either daily intake or body weight. The rates of absorption of 5 mMD-galactose and L-valine were determined in vitro by the everted sac method. The rates of absorption of the substances, expressed per unit weight or per length of intestine, were higher in diabetic rats than in controls, regardless of the amount of food consumed. Maltase and sucrase activities were significantly increased in diabetic rats, regardless of the amount of food consumed. The activity of intestinal alkaline phosphatase was increased in diabetic rats fed ad lib., but not in those on a restricted diet. These findings suggest that in alloxan diabetic rats the increased disaccharidase activity in the small intestine is due to insulin deficiency, and that the increased activity of alkaline phosphatase is only a secondary effect of insulin deficiency, caused by increased food intake resulting from insulin deficiency.
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PMID:Effect of food intake on intestinal absorption and mucosal hydrolases in alloxan diabetic rats. 698 35

Experimentally induced diabetes enhances the specific activity of several microvillus membrane proteins in the rat small intestine. The increase in the specific activity of sucrase-isomaltase has been shown by others to be due to an increase in enzyme protein, raising the possibility that diabetes induces a generalized increase in microvillus membrane proteins. Since intramembrane particles (IMPs) seen on freeze-fracture replicas of microvillus membranes are thought to represent integral membrane proteins, we compared microvillus IMP densities in diabetic rats with those in control rats. In addition, mucosal sucrase, maltase, and alkaline phosphatase specific activities were measured in all animals. Diabetic rats had significantly increased sucrase and maltase but not alkaline phosphatase specific activities compared with control rats. The density of microvillus IMPs on both the protoplasmic and extracellular fracture faces of undifferentiated crypt cells and villus absorptive cells was not increased in experimental diabetes. These data indicate that diabetes does not result in a generalized increase in microvillus membrane proteins. Thus the enhanced activity of microvillus membrane proteins in diabetes appears to be highly selective.
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PMID:Structural features of the rat small intestinal microvillus membrane in acute experimental diabetes. 704 26

The effect of food restriction on the intestinal weight and membrane digestive enzyme activities was observed in rats with diabetes induced by streptozotocin. The specific activities of disaccharidases of food non-restricted diabetic rats were not changed, but total activities were significantly increased due to the increase of intestinal mucosal weight. Restriction of food intake did not increase intestinal mucosal weight, but significantly increased the specific and total activities of disaccharidases in parallel with the increase of sucrase-isomaltase content. On the other hand, experimental diabetes did not influence the activity of alkaline phosphatase and leucine aminopeptidase except for specific and total activities of alkaline phosphatase in food non-restricted rats.
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PMID:Effect of food restriction on intestinal disaccharidases in streptozotocin-induced diabetes of rat. 724 Dec 40

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)
Diabetes 1993 Nov
PMID:Dietary carbohydrate enhances intestinal sugar transport in diabetic mice. 840 98

Rat intestines revealed a significant loss of proteins after seven days of alloxan induced diabetes. The data suggested the presence of two forms of alkaline phosphatase (ALP) in normal rat intestines. Along with the loss of proteins from the intestines during diabetes, a form of ALP which appears to be loosely bound to the intestine is also flushed out. Total brush border membrane (BBM) proteins are relatively preserved from such leaching effect of alloxan induced diabetes. Thus, sucrase and another form of ALP which appears to be strongly bound to the BBM are flushed out at a slower rate as compared to the other intestinal proteins and loosely bound soluble ALP. BBM preparations from diabetic rat intestines showed lower ratios for BBM/intestinal homogenate sucrase or ALP activity/mg proteins as compared to the normal control rats. Such ratios, therefore, misdepict the purity as low for the BBM from diabetic rats which is merely because of the decreased contents of proteins in the intestinal homogenate during alloxan-induced acute experimental diabetes.
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PMID:Alterations in rat intestinal sucrase and alkaline phosphatase activities in alloxan induced experimental diabetes. 840 49

The obese spontaneous hypertensive rat/NIH-corpulent (SHR/N-cp) rat exhibits some of the metabolic and pathologic alterations associated with non-insulin-dependent diabetes mellitus and hypertension. The current study was conducted to investigate the influence of phenotype (ob versus In) and source of dietary carbohydrate (sucrose versus starch) on intestinal sucrase, maltase, lactase, and alkaline phosphatase activity in SHR/N-cp rats. For 3 months, lean and obese male SHR/N-cp rats were fed isocaloric diets containing as the sole source of carbohydrate either 54% cooked corn starch or sucrose. Serum and urine markers for diabetes were observed in obese rats. Wet weight and length of intestines were significantly increased in obese rats compared with lean littermates. Among the intestinal enzymes measured, statistical tests confirmed that sucrase activity was significantly increased (P < 0.01) by both phenotype (ob > In) and feeding a sucrose diet. Diet alone (sucrose > starch) significantly increased (P < 0.05) maltase activity in obese rats, but had no effect on lean rats. Lactase activity was significantly higher (P < 0.05) in obese sucrose-fed rats compared with obese starch-fed and/or lean littermates. Statistical tests revealed that intestinal alkaline phosphatase activity was significantly altered (P < 0.05) by both phenotype and diet. Intestinal alkaline phosphatase was higher in starch-fed lean rats compared with lean littermates fed sucrose and to starch or sucrose-fed obese rats. These results are not indicative of a simple, nonspecific increase in intestinal enzyme activity, since the effects observed in intestinal alkaline phosphatase contrast the effects observed in intestinal sucrase, maltase, and lactase activity. These results indicate that both phenotype and diet alter structural and enzymatic intestinal activities of SHR/N-cp rats. Distinct variations in the observed intestinal enzymatic activities suggest that these enzymes are under the control of genetic, hormonal, and dietary factors. Rationale for these differences are discussed.
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PMID:Effect of dietary carbohydrate and phenotype on sucrase, maltase, lactase, and alkaline phosphatase specific activity in SHR/N-cp rat. 843 90

Antiobesity and antidiabetic actions of the alpha-glucosidase inhibitor AO-128 were examined using genetically obese-diabetic rats, Wistar fatty. Ten-week-old, male fatty rats were kept on CE-2 diet containing 10 or 25 ppm of AO-128 for 4 weeks. The average drug intake was calculated to be 0.74 or 1.78 mg/kg/day from the average food intake, respectively. The intestinal maltase and sucrase activities were decreased by AO-128 in a dose-related fashion. Food intake of fatty rats treated with AO-128 was decreased throughout the experiment. This decrease in food intake could hardly be explained only by diarrhea which occurred for the first 5 days of the administration of AO-128. AO-128 normalized hyperglycemia and markedly reduced hypertriglyceridemia and hyperinsulinemia in fatty rats. In addition, AO-128 decreased body weight gain, food efficiency, epididymal adipose tissue weight, carcass weight, and body fat deposition. These findings indicate that AO-128 may be useful for treating human obesity and diabetes.
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PMID:AO-128, alpha-glucosidase inhibitor: antiobesity and antidiabetic actions in genetically obese-diabetic rats, Wistar fatty. 869 66


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