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

The effect of long-term (6 months) administration of voglibose in a dietary mixture (10 ppm) on intestinal disaccharidase activity was examined in non obese type 2 diabetes model Goto-Kakizaki (GK) rats. The postprandial blood glucose level in voglibose-treated GK rats was significantly lower than in untreated GK rats (190+/-19 vs. 250+/-25 mg/dl, P<0.01; 1 h, 212+/-23 vs. 256+/-20, P<0.05; 2 h), and the activities of maltase, sucrase, and isomaltase remained significantly lower throughout the 6 months of voglibose treatment. The expressions of protein and mRNA of sucrase-isomaltase (SI) complex were significantly higher in voglibose-treated GK rats. Voglibose administration then was stopped after 6 months of treatment. The mRNA level and protein level of the SI complex became normalized during the interruption of drug administration, and disaccharidase activities increased almost to the level of the untreated group 1 month after treatment was stopped. After 1 day of re-administration of the drug, however, disaccharidase activities again became significantly inhibited. These results indicate that voglibose may improve glucose tolerance since it inhibits activities of disaccharidases in spite of increasing the expression of them on intestine, furthermore voglibose may be reversible and reproducible through interruption and re-administration.
Diabetes Res Clin Pract 2003 Feb
PMID:Long-term therapeutic effects of voglibose, a potent intestinal alpha-glucosidase inhibitor, in spontaneous diabetic GK rats. 1256 Jan 60

The purpose of this study was to examine the short-term effects of 75, 100 and 150 mg of acarbose mixed in 100 g standard laboratory chow on specific intestinal disaccharidase activities and on hyperglycaemia in diabetic CBA strain mice on standard diet. The small intestine was excised and divided into three segments, from pylorus to duodenum, and two equal lengths of the jejunum and ileum of control and diabetic mice with or without added acarbose. Specific maltase and sucrase activities were determined using maltose and sucrose as substrates respectively. Increased specific activities of maltase and sucrase were detected in the intestines of CBA mice on standard laboratory diet seven days after alloxan-induced diabetes. Feeding for 7 days with 75, 100 or 150 mg acarbose uniformly mixed in 100 g standard laboratory chow, induced a decrease in the specific maltase and sucrase activities, compared with diabetic mice on standard laboratory diet. Feeding with 75 mg acarbose mixed in 100 g standard laboratory chow caused a statistically significant decrease of maltase in the duodenum and of sucrase in duodenum and jejunum, without a antihyperglycaemic effect. Feeding with 100 or 150 mg caused statistically significant decreases in specific maltase and sucrase activities in duodenum, jejunum and ileum. An antihyperglycaemic effect was observed only in the group of diabetic mice fed with 100 mg acarbose. This indicates that the antihyperglycaemic effect of acarbose involves factors other than these, related only to its inhibitory effect on disaccharidase activities.
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PMID:Short-term effect of acarbose on specific intestinal disaccharidase activities and hyperglycaemia in CBA diabetic mice. 1286 6

The small intestine plays an important role in the digestion and absorption of many nutrients. To investigate the contribution of carbohydrate digestion to diabetes mellitus, we examined the morphological changes of the small intestine, and the expression of sucrase-isomaltase, which is one of the intestinal disaccharidases, in diabetic model rat, that is the streptozotocin-induced (STZ) diabetic rat (insulin-deficient model), and the Otsuka Long-Evans Tokushima Fatty (OLETF) rats and the Goto-Kakizaki (GK) rats (type 2 diabetic models). Intestinal hyperplasia was observed in STZ, OLETF, and GK rats. Moreover, in the small intestine of each diabetic strain, the proliferating cell nuclear antigen (PCNA)-labeling index, which is a marker of proliferation, was higher than in the respective control. Cdx1 and Cdx2, known to be transcriptional factors related to intestinal proliferation and differentiation, were more highly expressed in STZ, OLETF and GK rats than in the respective controls. These findings indicate that small intestinal hyperplasia, and thereby the resultant increase of total activity of disaccharidases such as sucrase and isomaltase in the entire small intestine, might be one of the reasons for postprandial hyperglycemia in diabetes mellitus.
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PMID:Morphological changes and increased sucrase and isomaltase activity in small intestines of insulin-deficient and type 2 diabetic rats. 1294 Apr 55

Diabetes in humans and in experimental animals produces changes in the function and structure of the small intestine. The authors determined the activity of intestinal disaccharidases (maltase and sucrase) and of 6-phosphofructo-1-kinase (PFK-1) in enterocytes isolated from the small intestine of male Wistar rats (2.5 to 3 months old) with experimental nonobese type 2 diabetes, induced by streptozotocin (STZ) injection on the day of birth (n0-STZ) or on the 5th day of life (n5-STZ), with different degrees of hyperglycemia and insulinemia (n0-STZ and n5-STZ models). The glycemia (mmol/L) of the diabetic rats (n0-STZ: 8.77 +/- 0.47; n5-STZ: 20.83 +/- 0.63) was higher (P <.01) than that of the nondiabetic (ND) rats (5.99 +/- 0.63); on the contrary, the insulinemia (ng/mL) was significantly lower in both n0-STZ (1.74 +/- 0.53; P <.05) and n5-STZ (1.12 +/- 0.44; P <.01) diabetic rats than in normal rats (3.77 +/- 0.22). The sucrase and maltase activities (U/g protein) in diabetic rats (n0-STZ: 89 +/- 9 and 266 +/- 12; n5-STZ: 142 +/- 23 and 451 +/- 57) were significantly higher than those in the ND group (66 +/- 5 and 228 +/- 22). The PFK-1 activities (mU/mg protein) in the diabetic models (n0-STZ: 14.89 +/- 1.51; n5-STZ: 13.35 +/- 3.12) were significantly lower (P <.05) than in ND rats (20.54 +/- 2.83). The data demonstrated enzymatic alterations in enterocytes isolated from the small intestine of n0-STZ rats that are greater (P <.05) than in the more hyperglycemic and hypoinsulinemic n5-STZ animals. The results also show that nonobese type 2-like diabetes in the rat produces modifications that favor an increase in glucose absorption rates.
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PMID:Experimental type 2 diabetes induces enzymatic changes in isolated rat enterocytes. 1463 May 73

We investigated whether dietary supplementation with L-arginine, the endogenous precursor of nitric oxide, might affect serum lipid levels and activities of intestinal mucosa enzymes in animals, in which diabetes was induced by administration of streptozotocin. Control and diabetic rats were fed diets with or without 2% L-arginine supplementation for 4 weeks. Diabetic rats had significantly higher concentrations of serum triglycerides and LDL-cholesterol than control rats. These alterations were partially reduced by L-arginine supplementation. Experimental diabetes did not influence the lactase and leucine aminopeptidase activity in the intestine, but the activity of alkaline phosphatase was increased. Furthermore, activities of maltase and sucrase in the intestinal mucosa were elevated in streptozotocin-induced diabetic rats and were restored to control levels after dietary L-arginine supplementation. On the basis of the present experimental evidence, dietary L-arginine supplementation appears to affect the metabolism of lipoproteins and might alleviate some gastrointestinal dysfunctions, commonly seen in diabetes mellitus.
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PMID:Effects of dietary L-arginine supplementation on serum lipids and intestinal enzyme activities in diabetic rats. 1535 82

Mutations in transcription factors hepatocyte nuclear factors (HNF)-1alpha and HNF-1beta cause maturity-onset diabetes of the young (MODY) types 3 and 5, respectively. HNF-1alpha and HNF-1beta mutations are well studied in some tissues, but the mechanism by which HNF-1alpha and HNF-1beta mutations affect sucrase-isomaltase (SI) transcription in the small intestine is unclear. We studied the effects of 13 HNF-1alpha mutants and 2 HNF-1beta mutants on human SI gene transcription, which were identified in subjects with MODY3 and MODY5, respectively. Transactivation activity of 11 HNF-1alpha and 2 HNF-1beta mutants was significantly lower than that of wild (wt)-HNF-1alpha and wt-HNF-1beta. Furthermore, in co-expression studies with mutant (mu)-HNF-1alpha/ wt-HNF-1beta and wt-HNF-1alpha/mu-HNF-1beta, the combination of mu-HNF-1alpha (P379fsdelCT and T539fsdelC)/wt-HNF-1beta impaired SI transcription, but the others were not remarkably different from wt-HNF-1alpha/wt-HNF-1beta. Although wt-HNF-1beta inhibited the transactivation activity of wt-HNF-1alpha on SI transcription, the inhibitory effect was reduced by 2 HNF-1beta mutants. These results suggest that SI transcription might tend to be unchanged or lower in MODY3, while occurring more in MODY5.
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PMID:Effect of mutations in HNF-1alpha and HNF-1beta on the transcriptional regulation of human sucrase-isomaltase in Caco-2 cells. 1552 34

Intravenous immunoglobulin infusion induces acute renal failure via a mechanism of osmotic nephrosis. Most reported cases are related to the use of sucrose-based intravenous immunoglobulin. Maltose-based intravenous immunoglobulin is thought to be a safer alternative and have a lower risk of renal toxicity than sucrose-based preparations. Maltase, but not sucrase, is present in the brush border of proximal convoluted renal tubules, where the maltose is metabolised. We report a case of maltose-based intravenous immunoglobulin-induced acute renal failure in an elderly diabetic woman. In this case, the risk factors included advanced age, hypovolaemia, sepsis, diabetes mellitus, and the high infusion rate of the intravenous immunoglobulin. Maltase is readily inhibited by hyperglycaemia; therefore, poor glycaemic control may predispose patients to develop acute renal failure even with the better-tolerated maltose-based intravenous immunoglobulin.
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PMID:Acute renal failure related to intravenous immunoglobulin infusion in an elderly woman. 1568 16

During diabetes, structural and functional changes in the alimentary tract are known to take place resulting in increased absorption of intestinal glucose and alterations in the activities of brush border disaccharidases. Similar observations are also reported in the renal cortex. In the present investigation, we examined the effect of feeding bitter gourd fruit devoid of seeds on activities of intestinal and renal disaccharidases, viz., maltase, sucrase, and lactase in streptozotocin-induced diabetic rats. Normal and diabetic rats were fed either with basal diet or a diet containing 10% bitter gourd powder. Specific activities of intestinal disaccharidases were significantly increased during diabetes, and supplementing bitter gourd in the diet clearly indicated amelioration in the activities of maltase and lactase during diabetes. However, a significant change was not observed with sucrase activity by feeding of bitter gourd. During diabetes, renal disaccharidase activities were significantly lower than those in the control rats. Bitter gourd supplementation was beneficial in alleviating the reduction in maltase activity during diabetes. However, not much change in the activities of sucrase and lactase was observed upon feeding. This positive influence of feeding bitter gourd on intestinal and renal disaccharidases clearly indicates their beneficial role in the management of diabetes, thus making diabetic animals more tolerant to hyperglycemia.
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PMID:Bitter gourd (Momordica charantia) modulates activities of intestinal and renal disaccharidases in streptozotocin-induced diabetic rats. 1600 24

To elucidate the effect of feeding fenugreek seed mucilage and spent turmeric (10%) on disaccharidases activities, the specific activities of intestinal and renal disaccharidases viz., sucrase, maltase and lactase were measured in streptozotocin induced diabetic rats. Specific activities of intestinal disaccharidases were increased significantly during diabetes and amelioration of these activities during diabetes was clearly visible by supplementing fenugreek seed mucilage and spent turmeric in the diet. However during diabetes renal disaccharidases activities were significantly lower than those in the control rats. Fenugreek seed mucilage and spent turmeric supplementations were beneficial in alleviating the reduction in maltase activity during diabetes, however not much change in the activities of sucrase and lactase was observed upon feeding. This positive influence of feeding fenugreek seed mucilage and spent turmeric on intestinal and renal disaccharidases clearly indicates their beneficial role in the management of diabetes.
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PMID:Modulatory effect of fenugreek seed mucilage and spent turmeric on intestinal and renal disaccharidases in streptozotocin induced diabetic rats. 1602 36

Intakes of some macronutrients can comprise risk factors for life-style-related diseases such as obesity, hyperlipidemia, diabetes, hypertension, and atherosclerosis. In this study, we examined the effects in C57BL/6J mice of consuming excess fat or sucrose for a long period of time (55 wk). Another group of mice consumed a low-fat, low-sucrose (LL) diet. Mice fed the high-fat (HF) diet gained weight and developed hyperlipidemia and hyperleptinemia. At 25 wk, but not at 55 wk, hepatic glucose-6-phosphatase (G6Pase) activity of the mice fed the high sucrose (HS) diet was greater than that of mice fed the LL or HF diet. Those fed the HS diet were not obese and had greater hepatic lipogenic and gluconeogenic enzyme activities. The HF and HS diets resulted in different types of glucose intolerance. In an oral glucose tolerance test, mice fed the HF diet had a delay in the clearance of glucose compared with those fed the LL diet, perhaps due to the peripheral insulin resistance that resulted from higher levels of circulating free fatty acids. Feeding the HS diet for 55 wk induced hyperglycemia 10 min after oral glucose administration, although blood glucose declined rapidly after i.p. insulin injection. This finding suggests that the effects of chronic HS diet intake may be due to the reduction in early insulin secretion from pancreatic islets and the increase in sucrase activity in the small intestine. It is important to consider the effects of macronutrients in lean as well as obese mice to clarify the pathogenesis of the metabolic disorders.
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PMID:Chronic intake of high-fat and high-sucrose diets differentially affects glucose intolerance in mice. 1648 28


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