A retrospective cohort study using the Taiwan National Health Insurance claims database was conducted to examine the risks of HHF among newly diagnosed type 2 diabetic patients who initiated glinide, sulfonylurea, or acarbose therapy during 2006-2012. The outcome of interest was hospitalization due to heart failure after treatment initiation, defined by ICD-9-CM code. A Cox proportional hazard regression model was used to calculate the hazard ratio (HR) and 95% confidence interval (CI) using acarbose as the reference group.
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Glimepiride was associated with a significantly greater responder rate than acarbose (61 vs 34%, p < 0.001), significantly greater decreases in HbA1c (2.5 +/- 2.2% vs 1.8 +/- 2.2%, p = 0.014) and FBG (2.6 +/- 2.6 mmol/l vs 1.4 +/- 2.8 mmo/l, p = 0.004), a decreased glucose response to breakfast compared with acarbose [area under curve (AUC) end: 8.9 +/- 2.7 mmol/l vs 11.3 +/- 3.9 mmol/l, p = 0.0001], and was accompanied by significantly greater compliance (91 < or = 12% vs 66 +/- 26%, p = 0.0001). Weight loss during the study was observed in both the acarbose group (1.9 +/- 3.9 kg, p = 0.001) and glimepiride group [0.4 +/- 5.2 kg, p = 0.8 (NS)].
Acarbose slows progression of IMT in IGT subjects, a high-risk population for diabetes and atherosclerosis. This is the first placebo-controlled prospective subgroup analysis, demonstrating that counterbalancing of postprandial hyperglycemia may be vasoprotective.
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An analytical method for quantifying underivatized amino acids (AAs) in urine samples of rats was developed by using liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS). Classification of type 2 diabetes rats was based on urine amino acids metabolic profiling. LC-MS/MS analysis was applied through chromatographic separation and multiple reactions monitoring (MRM) transitions of MS/MS. Multivariate profile-wide predictive models were constructed using partial least squares discriminant analysis (PLS-DA) by SIMAC-P 11.5 version software package and hierarchical cluster analysis (HCA) by SPSS 18.0 version software. Some amino acids in urine of rats have significant change. The results of the present study prove that this method could perform the quantification of free AAs in urine of rats by using LC-MS/MS. In summary, the PLS-DA and HCA statistical analysis in our research were preferable to differentiate healthy rats and type 2 diabetes rats by the quantification of AAs in their urine samples. In addition, comparing with health group the seven increased amino acids in urine of type 2 rats were returned to normal under the treatment of acarbose.
A model was developed to simulate the course of individuals with IGT under each treatment strategy. Patients remain in the IGT state or transition from IGT to diabetes, to normal glucose tolerance (NGT) or to death. Effectiveness and resource use data were derived from published intervention trials. A comprehensive health-care payer perspective incorporating all major direct costs, reported in 2000 Canadian dollars, was adopted.
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Tendencies in the consumption of antidiabetic agents in Andalusia between 1986-1994 were analysed, with special emphasis on the impact of the introduction of acarbose and mechanized systems for the injection of insulin.
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The use of a single dose of 100 mg acarbose at breakfast time can result in a marked flattening of elevated post-prandial morning blood glucose profiles in both insulin-dependent type II and type I diabetics.
The fermentation of starch in vitro produces a higher proportion of butyrate than the fermentation of most other substrates. The alpha-glucosidase inhibitor acarbose increases the amount of starch entering the colon, and has been shown to increase faecal butyrate in humans. It is generally considered that colonic butyrate is quantitatively removed by the colonic mucosa and liver and does not appear in peripheral blood. However, studies in animals suggest that a small proportion of colonic butyrate reaches peripheral blood. Thus, we hypothesised that an increase in colonic butyrate production would result in a rise in serum butyrate in human subjects. To test this, subjects with impaired glucose tolerance were randomly treated in a double-blind fashion with placebo (n 11) or acarbose (n 11) (100 mg three times per day). Serum short-chain fatty acid concentrations were measured twelve times over 12 h with subjects eating a standard diet before randomization and after 4 months of therapy. At baseline, 12 h mean serum butyrate concentrations were similar in the placebo and acarbose groups (2.8 (SE 0.7) and 3.3 (SE 0.6) microM, respectively). After 4 months on placebo, mean serum butyrate (2.6 (SE 0.5) microM) was no different from baseline. However, after 4 months on acarbose, serum butyrate had increased to 4.2 (SE 1.0) microM, a value which differed significantly from both the baseline value in the acarbose group and the treatment value in the placebo group. We conclude that acarbose increased serum butyrate in subjects with impaired glucose tolerance. These results support the hypothesis that increased colonic butyrate production in human subjects can be detected by an increase in serum butyrate.
Dumping syndrome and postprandial hypoglycemia have been reported after Nissen fundoplication. The physiopathologic mechanisms are poorly understood and a variety of therapies have failed to control the hypoglycemia in these patients. We report a series of 6 infants with postprandial hypoglycemia after Nissen fundoplication who were treated successfully with acarbose.
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Two hundred twelve obese subjects with NIDDM who had not received any diabetic medication for at least 12 weeks were randomized to receive acarbose or placebo. The subjects were stratified by fasting glucose level above or below 11.1 mmol/L (200 mg/dL). Based on the subject's therapeutic response and tolerance, the acarbose dosage was titrated from 50 to 300 mg three times per day. This 36-week study consisted of a 6-week pretreatment period, a 24-week double-blind treatment period, and a 6-week posttreatment period.
To assess the efficacy of acarbose monotherapy during 12-weeks treatment on the fasting glycemic level, lipid and lipoproteins profiles, in patients with type 2 diabetes mellitus.
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Twelve patients with non-insulin-dependent diabetes mellitus (NIDDM) and ten healthy volunteers were studied. Three meal tests with an intake of 90 g of white bread (50 g of carbohydrates) were performed on each subject. In one test, 200 mg of acarbose was given, while 15 g of P. psyllium mucilage was given in another test, and only bread was ingested in the control test. Serum glucose and insulin concentrations were measured every 30 min from 0-180 min. Net area under curve (AUC) concentrations of glucose and insulin, GI and insulinic index were calculated.
Three groups of compounds were isolated in this study (triterpenes, flavonols and dithiolanes). Triterpenes and flavones showed activity in at least one bioassay (antiparasitic or α-glucosidase). In addition, only the pentacyclic triterpenes exhibited a competitive type of inhibition against α-glucosidase.
Glucosidase activity was assayed at PH optima by PNPG substrate. Lobster sauce extracts were prepared by soaking, centrifagation. Polysaccharide were prepared by soaking, centrifagation, separation.
Ascophyllum nodosum is a brown seaweed that grows abundantly in the Northeast coastal region. In this study, the potential of A. nodosum for type 2 diabetes management through antioxidant-mediated alpha-glucosidase and alpha-amylase inhibition was investigated. After the initial screening of 4 locally harvested seaweeds, A. nodosum was chosen for its highest phenolic content and was subjected to water extraction. Among extraction ratios of 50 g to 100 to 1000 mL at room temperature, 50 g/400 mL yielded the highest phenolic content of 4.5 mg/g wet weight. For evaluation of extraction temperature ranging from 20 to 80 degrees C, 50 g/400 mL was chosen as a minimum amount of extractant. Among temperatures studied, extraction at 80 degrees C resulted in the highest total phenolic contents (4.2 mg/g wet weight). All extracts had similar levels of antioxidant activity in the range of 60% to 70% in terms of 1, 1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging activity. The 80 degrees C extract had the highest alpha-glucosidase and alpha-amylase inhibitory activity with IC(50) of 0.24 and 1.34 microg phenolics, respectively, compared to the IC(50) of acarbose, reference inhibitor, being 0.37 and 0.68 microg. The results show that fresh A. nodosum has strong alpha-glucosidase and mild alpha-amylase inhibitory activities that correlated with phenolic contents. This study suggests a nutraceutical potential of A. nodosum based on phytochemical antioxidant and antihyperglycemia activities.
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Since ages, botanical substances are in use for the remedy of diabetes with considerable degree of success. One of the such; an extract of Commelina communis L. (CE-L) after decoction in water has been traditionally used for the treatment of diabetes in Korea. However, its action mechanism has not yet been established. To explore the inside of its action-mechanism, in this study, the effect of the aqueous extract of C. communis L. (CE-L) on the activity of alpha-glucosidase was evaluated in vitro and in vivo. Aqueous extract of CE-L showed inhibitory activity of the alpha-glucosidase in a dose-dependent manner, in vitro. CE-L also seems to be by and large free from exerting any cytotoxic effect at least in CHO-K1 fibroblast and 3T3-L1 adipocyte. CE-L alleviated hyperglycemia caused by maltose or starch loading in normal and Streptozotocin (STZ)-induced diabetic mice with better efficacy than that of acarbose. In addition, prolonged administration of CE-L tends to normalize hyperglycemia in STZ-induced diabetic mice. Such results suggest that inhibitory activity of CE-L on alpha-glucosidase may contribute to delay in carbohydrate digestion and glucose absorption. Thus, CE-L has potential for use in the management of non-insulin-dependent diabetes.
Context 3β-Acetoxyurs-11-en-13β,28-olide (I), a triterpenoid, is found in most plant species. Pharmacologically triterpenes are very effective compounds with potent anticancer, anti-HIV and antimicrobial activities. Objectives Microbial transformation of 3β-acetoxyurs-11-en-13β,28-olide (I) was performed in order to obtain derivatives with improved pharmacological potential. Materials and methods Compound (I, 100 mg) was incubated with Aspergillus niger culture for 12 d. The metabolite formed was purified through column chromatography. Structure elucidation was performed through extensive spectroscopy (IR, MS and NMR). In vitro α- and β-glucosidase inhibitory, and antiglycation potentials of both substrate and metabolite were evaluated. Results Structure of metabolite II was characterized as 3β-acetoxyurs-11,12-epoxy-13β,28-olide (II). Metabolite II was found to be an oxidized product of compound I. In vitro α- and β-glucosidases revealed that metabolite II was a potent and selective inhibitor of α-glucosidase (IC50 value = 3.56 ± 0.38 μM), showing that the inhibitory effect of metabolite II was far better than compound I (IC50 value = 14.7 ± 1.3 μM) as well as acarbose (IC50 value = 545 ± 7.9 μM). Antiglycation potential of compound II was also high with 82.51 ± 1.2% inhibition. Thus, through oxidation, the biological potential of the substrate molecule can be enhanced. Conclusion Biotransformation can be used as a potential tool for the production of biologically potent molecules.
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Many investigations have revealed that a certain concentration of osmolality was indispensable for efficient acarbose production, but little information was available on the response mechanism of acarbose-producing strains to osmotic stress. By using the gas chromatography-mass spectrometry (GC-MS) analysis coupled with the enzyme activity determination of central carbon metabolism, the present work investigated the metabolic characteristics of industrial acarbose-producing Actinoplanes sp. A56 under various osmolality levels. Relatively high osmolality (450-500 mOsm/kg) appeared to favor efficient acarbose production by Actinoplanes sp. A56, although it inhibited cell growth. Further GC-MS analysis showed that fatty acids were the uppermost differential intracellular metabolites under various osmolality levels, and the relatively high osmolality resulted in increases in levels of fatty acids.
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This study describes the derivatization of the pseudooligosaccharide acarbose and its main metabolite, component 2, with 7-aminonaphthalene-1,3-disulfonic acid (ANDS) in human urine. Their efficient separation was possible by means of capillary zone electrophoresis, using a capillary tube of fused-silica containing 100 mM triethylammonium phosphate buffer, pH 1.5. On column laser-induced fluorescence allowed the detection of the pseudooligosaccharides in human urine in the nanomolar range. With this method, acarbose and component 2 were quantified in human urine after application of 300 mg of acarbose.
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Although acarbose-induced hepatotoxicity appears to be uncommon, diabetic patients receiving long-term acarbose therapy should be closely monitored for this adverse effect.
An anonymous questionnaire was used in two centres to assess knowledge about oral agents amongst 261 patients with Type 2 diabetes mellitus (mean age 64 years) and 102 health professionals (including doctors, nurses and pharmacists).
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The study was undertaken to assess the efficacy guargum, Acarbose and their combination in modifying the sucrose absorption in patients of non Insulin dependent diabetes mellitus (NIDDM). Fifty patients of NIDDM were randomly distributed in three groups. Group A had 20 patients who received 20 grams of guargum, Group B had 10 patients who received 100 mg of Acrabose, Group C had 20 patients who received 10 grams of guargum and 50 grams of Acrabose. All the patients underwent 50 grams sucrose tolerance test with and without the trial drugs. Blood glucose levels were determined at 0, 30, 60, 90 and 120 minutes after sucrose loading. With the drugs, there was a significant decrease in the blood glucose levels at all time intervals (p < 001) in all the three groups. In all the three groups the blood glucose levels with the trial drugs was significantly lower (p < 001) than without the drug. It was seen that acarbose alone and guargum alone did not differ significantly in reducing the blood sugar level whereas combination of two produced significantly greater reduction in blood glucose levels than either of the drug used alone. Thus both guargum and acarbose are equally effective in modifying the absorption of sucrose. When combined in half the dosage they have synergistic effect and the reduction in blood glucose level is greater than either of the drug used alone.
Obesity and the onset of diabetes are two closely linked medical complications prevalent globally. Postprandial hyperglycemia is one of the earliest abnormalities of glucose homeostasis associated with type 2 diabetes (T2D). Postprandial glucose levels can be regulated through α-glucosidase inhibition. The present study aims to demonstrate the potent inhibitory role of naringenin against α-glucosidase activity. The mode of inhibition of naringenin was examined by measuring enzyme activity in vitro with different concentrations of substrate using Lineweaver-Burk plot analysis. It shows competitive inhibition towards mammalian α-glucosidase thereby competing with α-limit dextrins and oligosaccharide residues for binding in the active site. Similar results have been obtained from the molecular docking analyses, where naringenin shows preferential binding for the active sites in each of the evaluated human intestinal α-glucosidase enzymes. Post-docking intramolecular hydrogen bonding analysis shows water molecule mediated hydrogen bonding for N-terminal maltase glucoamylase and N-terminal sucrase isomaltase. Naringenin's docked pose in the C-terminal maltase glucoamylase active site does not show any particular water mediated interaction similar to the co-crystallized acarbose. Further, our results suggest that naringenin (25 mg/kg) exerts significant inhibition of intestinal α-glucosidase activity in vivo thereby delaying the absorption of carbohydrates in T2D rats, thus resulting in significant lowering of postprandial blood glucose levels. Both in vitro and in vivo results were compared to the commercially available α-glucosidase inhibitor acarbose. Our findings clearly indicate that naringenin dampens postprandial glycemic response and offers a potential complementary approach in the management of T2D.
Noninsulin-dependent diabetes mellitus is a genetically determined form of diabetes, due to impaired insulin secretion by the B-cells as well as to insulin resistance of the peripheral tissues. According to the glucose toxicity theory hyperglycemia and hyperinsulinemia exist in a vicious circle. Therefore, it is a major therapeutical aim to put the B-cell to rest and improve insulin sensitivity by a strict control of fasting blood glucose and of postprandial hyperglycemia. Furthermore, associated abnormalities within the metabolic syndrome, such as hypertension, dyslipoproteinemia and hemostatic disorders should be corrected to avoid vessel complications. Therefore, it should be started with basic measures as body weight reduction, carbohydrate-rich and fat-poor diet and exercise. If these measures fail to achieve acceptable glycemic control, antihyperglycemic drugs (acarbose, metformin) are indicated, eventually in a combination with small doses of short-acting sulfonylureas. Further impairment of insulin secretion is the indication for sulfonylurea and/or insulin application. HbA1c of 7 to 7.5% should be the goal of antidiabetic therapy, also for patients in advanced age. The main criterion for the choice of antidiabetics is the present insulin secretion capacity. Simple indicators in this respect are changes of body weight, plasma triglycerides and C-Peptide after i.v. glucagon stimulation. Application of insulin in combination with other antidiabetics or in the form of intensified insulin therapy should not be too much postponed.
To investigate the therapeutic effects of methanol extract of Citrus macroptera Montr.fruit in α-amylase inhibitory activity (in vitro) and hypoglycemic activity in normal and glucose induced hyperglycemic rats (in vivo).
Despite abundant research that has been carried out on the potential health benefits of pu-erh tea, no consensus till now, has been reached on which constituent is mainly responsible for its bioactivity. In this work, the aqueous extract (AE) and its fraction enriched with active constituents were prepared from pu-erh tea, and their bioactivities were investigated. It was found that tea polyphenols (TP), tea polysaccharides (TPS), caffeine (Caf), protein (Pro), amino acids (AA) were accumulated in several fractions after solvent extraction despite not being separated completely. Meanwhile, 95% ethanol precipitate (EP) and ethyl acetate fraction (EF) possessed remarkable antioxidant activity and potent inhibitory effects against α-glycosidase in vitro. Furthermore, all the extracts (50 mg/kg BW) showed a significant (p<0.05) effect on postprandial hyperglycemia in diabetic mice as compared with a model group, and the suppression of EP was not significantly (p>0.05) different from that of acarbose at the same dosage (50 mg/kg BW), which indicate that these fractions could be developed as potential anti-diabetic agents.
A cross-sectional and analytic study was conducted in Mexico City.
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Digoxin has a narrow therapeutic margin and potentially life-threatening cardiac adverse effects. Gastrointestinal disorders, neuropsychological disorders and bradycardia are warning signs. Some drug combinations can aggravate the cardiac adverse effects of digoxin, or reduce its efficacy. We reviewed the literature, using the standard Prescrire methodology, in order to examine which drugs are involved in these interactions, and the mechanisms involved. Most relevant data are based on small pharmacokinetic studies or detailed case reports. The adverse effects of digoxin are potentiated by renal impairment, which may be pre-existing or due to nephrotoxic drugs such as nonsteroidal antiinflammatory drugs (NSAIDs), angiotensin-converting-enzyme (ACE) inhibitors, angiotensin II receptor antagonists and ciclosporin. Some coadministered drugs such as macrolides and cardiovascular drugs (especially amiodarone) can cause digoxin overdose through pharmacokinetic interactions. The mechanism most often implicated is inhibition of P-glycoprotein, of which digoxin is a substrate. Hypercalcaemia and hypokalaemia inducing drugs, heart-rate lowering drugs, and drugs that prolong the QT interval or slow cardiac conduction can potentiate the cardiac adverse effects of digoxin. Plasma concentration of digoxin is not affected. Several drugs, including sucralfate, acarbose, cytotoxic agents, and enzyme inducers, can reduce digoxin plasma concentrations. This effect is attributed to decreased gastrointestinal absorption or increased elimination of digoxin. In practice, patients treated with digoxin, and their caregivers, should be aware that digoxin has a narrow therapeutic margin and frequent and potentially severe adverse effects. Close clinical monitoring is necessary to detect early warning signs (bradycardia and gastrointestinal or neurological disorders). Digoxin assay alone is not always sufficient. Special care is required for patients with renal failure, the elderly and patients receiving potentially interacting drugs.
Blood was drawn from 24 subjects (14 male, 10 female, age: 50.7 ± 7.36 years, BMI: 26.64 ± 3.38 kg/m2, GHbA1c: 7.00 ± 0.74%) with drug-naïve T2D at 0 and 120 min following a standard mixed meal for the measurements of active GLP-1, NO and NOS. The CIMT was measured prior to and following 24 weeks of acarbose monotherapy (mean dose: 268 mg daily).