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Eighty five patients were recruited for the study but 64 complied with the treatment protocol. The age of these patients was 56 +/- 8.8 years old, their diabetes duration was 7.8 +/- 8.8 years and their body mass index was 27.6 +/- 3.6 kg/m2. During acarbose treatment, glycosilated hemoglobin decreased from 8.36 +/- 1.33 to 7.71+ 1.7% (p < 0.001), fasting blood glucose decreased from 173 +/- 48 to 159 +/- 59 mg/dl (p < 0.03) and post-prandial blood glucose decreased from 254 +/- 80 to 241 +/- 80 mg/dl (NS). After discontinuing acarbose glycosilated hemoglobin and blood glucose levels returned to basal levels. Body weight and blood pressure did not change during the treatment period. Fifty nine patients had gastrointestinal symptoms (meteorism, flatulence and abdominal distention) that were mild in 59% and moderate in 39%. Episodes of hypoglycemia were not observed.
To investigate the effect of combined use of insulin and acarbose on glucose excursion in type 1 diabetic patients.
Type 2 diabetes plays a major role in public health, affecting about 400 million adults. One of the used strategies to control type 2 diabetes is the inhibition of α-amylase activity to reduce post-prandial blood glucose levels. Therefore, in past decades, the search of new α-amylase inhibitors has led to the evaluation of natural products as a source of these compounds. Pouteria torta (Sapotaceae) is widespread in Brazil and bears edible fruits. Epicarp and pulp crude extracts of fresh fruits were studied for in vitro α-amylase inhibition activity. The pulp did not present activity while epicarp, usually considered as waste, showed a high α-amylase inhibitory capacity when compared with acarbose and Triticum aestivum. Therefore, an assay-guided fractionation study of epicarp crude extract was performed. Fraction VI shows very high inhibitory activity with IC50 of 9 μg/mL. However, subsequent fractionation led to lower inhibition potential (IC50 of 22.1 μg/mL). The qualitative characterization of fraction VI were performed by chromatographic and spectrometric analysis and showed the presence of epicatechin, catechin, sucrose, glucose, and fructose. Total phenolic and flavonoid contents and antioxidant capacity were also assessed and there seemed to be no correlation between phenolic or flavonoids-rich fractions and antioxidant capacity or α-amylase inhibitory activity.
We aimed to evaluate the effects of gliclazide, metformin, and acarbose monotherapy on body composition, fat distribution, and other cardiometabolic risk factors in patients with newly diagnosed type 2 diabetes.
The addition of ASE inhibited α-glucosidase activity but not α-amylase activity. The α-glucosidase inhibitory activity of ASE was approximately 1/13 of that of acarbose. The addition of ASE inhibited 2'-deoxy-D-glucose (DG) uptake in human intestinal Caco-2 cells, and the inhibitory activity of ASE was approximately 1/40 of that of phloretin. Kinetic analysis of glucose uptake indicated that ASE has no effects on DG uptake through passive diffusion, but that ASE inhibits intracellular DG uptake chiefly by inhibiting transport via a glucose transporter. In the glucose tolerance study, db/db mice orally administered ASE for 3 days showed significantly lower plasma glucose level than the control group 30 min after sucrose loading, without affecting plasma insulin levels. In addition, ASE oral administration significantly inhibited α-glucosidase activity in the small intestine mucosa extirpated from the mice.
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Impaired glucose tolerance (IGT) is determined by measuring plasma glucose levels 2 hours after glucose loading in the oral glucose tolerance test. There is good evidence from epidemiologic and prospective trials [e.g. Diabetes Epidemiology: Collaborative Analysis of Diagnostic Criteria in Europe (DECODE)] linking IGT with the development of type 2 diabetes mellitus and cardiovascular disease (CVD). IGT is characterized by an increase in postprandial glucose levels, which is considered the earliest metabolic abnormality in type 2 diabetes mellitus. It is one of a series of risk factors for CVD (hypertension, high triglyceride levels, low high-density lipoprotein-cholesterol and central obesity), known as the metabolic syndrome. The different factors making up this syndrome are intimately related. An impaired lipid profile can contribute to insulin resistance, as IGT may play a pathogenic role on other cardiovascular risk factors. IGT is the first easily identifiable step in the pathophysiology of type 2 diabetes mellitus. It is associated with high risk for type 2 diabetes mellitus and subsequent vascular morbidity and mortality. It is currently unknown whether treating IGT will reduce the incidence of macrovascular complications, as studies addressing this issue have yet to be conducted. Therefore, the main reason to identify and treat IGT is to prevent or delay the onset of type 2 diabetes mellitus. It has been demonstrated that lifestyle intervention with diet and exercise can reduce the incidence of type 2 diabetes mellitus. Pharmacologic intervention with metformin and acarbose is also effective. Other drugs, such as those indicated to treat other parameters of the metabolic syndrome, may also be useful. We can now be assured that prevention or delay of onset of type 2 diabetes mellitus is possible in individuals with IGT, either by changes in lifestyle or by pharmacotherapy.
Fitness cost is usually associated with insecticide resistance and may be mitigated by increased energy accumulation and mobilization. Preliminary evidence in the maize weevil (Coleoptera: Curculionidae) suggested possible involvement of amylases in such phenomenon. Therefore, alpha-amylases were purified from an insecticide-susceptible and two insecticide-resistant strains (one with fitness cost [resistant cost strain], and the other without it [resistant no-cost strain]). The main alpha-amylase of each strain was purified by glycogen precipitation and ion-exchange chromatography (>or=70-fold purification,
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This was a 1-year, prospective, randomized, open-label, parallel-group study in patients with established CAD (≥50% stenosis on quantitative coronary angiography) who were newly diagnosed with IGT or mild T2DM. IGT was defined as 2-hour glucose concentrations of 140 to 199 mg/dL on the 75-g oral glucose tolerance test (OGTT). Mild T2DM was defined as a fasting plasma glucose concentration <126 mg/dL, 2-hour plasma glucose concentration on OGTT >200 mg/dL, and glycosylated hemoglobin (HbA(1c)) <6.5%. On the day after undergoing coronary angiography, patients were randomly allocated to receive either acarbose 150 mg/d or control (no treatment). Carotid IMT was measured by ultrasonography at baseline and at 12 months of follow-up. The changes in glucose profiles (75-g OGTT), HbA(1c), and lipid profiles were also compared between baseline and follow-up. At visits every 2 months, data on adverse events, drug adherence, and changes in medication were collected. Adverse events were recorded based on spontaneous reports and questioning by the investigator. Clinical follow-up data on outcomes of interest were obtained from patients' hospital charts or from telephone interviews; these outcomes were the incidence of mortality, nonfatal myocardial infarction, repeat percutaneous coronary intervention for a treated coronary artery, and stroke.
Enzyme assay using acarbose as an inhibitor, can be performed in isolated lymphocytes for rapid diagnosis of infantile Pompe disease.
The aim of this study was to evaluate whether treatment with acarbose, an alpha-glucosidase inhibitor, improved hyperandrogenic symptoms, insulin and androgen serum concentrations in hyperinsulinaemic patients with polycystic ovary syndrome (PCOS).
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MEDLINE (January 1966-August 1997) and Current Contents database searches identified applicable English-language experimental trials, epidemiologic studies, reviews, and editorials.
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(1) There are few clinical trials comparing combination therapy with a sulphonylurea and metformin after oral antidiabetic monotherapy fails to provide adequate glycaemic control. The UKPDS study suggested that this combination had a negative impact on mortality. (2) The assessment of insulin therapy in patients in whom oral antidiabetic therapy fails is based solely on surrogate endpoints: mainly HbA1c (glycated haemoglobin), bodyweight, and the frequency of hypoglycaemia. (3) In a comparative randomised trial involving patients whose glucose levels were no longer controlled by a sulphonylurea, the addition of metformin or a daily injection of insulin isophane (NPH) was similarly effective in reducing HbA1c levels. However, metformin caused less weight gain. (4) There are no randomised controlled trials comparing the addition of insulin versus a sulphonylurea when ongoing metformin monotherapy is inadequate. (5) Randomised comparative trials show that, when glycaemia is no longer controlled by a sulphonylurea plus metformin, adding a daily insulin injection is more effective in lowering HbA1c levels than the addition of acarbose and as effective as adding a glitazone. The adjunction of insulin appears to have a better risk-benefit balance than an oral three-drug regimen. (6) Several randomised controlled trials have shown that the addition of an oral antidiabetic to ongoing insulin therapy reduces HbA1c levels in patients with type 2 diabetes. The addition of metformin is also beneficial in terms of body weight changes. (7) Nine randomised controlled trials involving patients whose glycaemia was inadequately controlled by a sulphonylurea, alone or in combination with metformin, have compared the addition of a bedtime injection of insulin isophane versus replacement of the oral antidiabetics by several daily insulin injections. The two strategies had a similar impact on HbA1c (-1.5% to -2.5%), but patients experienced less weight gain when the oral antidiabetics were continued and a single insulin injection was added. (8) The few available comparative trials fail to show which oral treatment (a sulphonylurea, metformin, or a combination of the two) has the best risk-benefit balance when combined with a bedtime injection of insulin isophane. (9) Insulin isophane is the first-choice insulin for combination therapy with an oral antidiabetic. In comparative trials, when combined with an oral antidiabetic, insulin glargine was no more effective than insulin isophane in terms of HbA1c levels or weight gain. Insulin glargine seems to provoke less hypoglycaemia but, in the absence of adequate follow-up, its long-term adverse effects are not known. (10) When a bedtime insulin injection plus an oral antidiabetic fail to control hyperglycaemia, indirect comparisons support the use of several daily insulin injections plus metformin, or three injections of an ultrarapid insulin analogue plus a sulphonylurea.
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Turmeric (Curcuma longa L) rhizome extracts were evaluated for their antidiabetic, antihypertensive and antioxidant potentials. α-Glucosidase (0.4 μg/mL) and α-amylase (0.4 μg/mL) inhibitory potential of turmeric ethyl acetate extract was significantly higher than those of the reference drug acarbose (17.1 μg/mL and 290.6 μg/mL respectively). Protein glycation inhibitory potential of ethyl acetate extract was 800 times higher than that of ascorbic acid. High potential of ethyl acetate extract to scavenge free radicals and to reduce LDL oxidation and cellular oxidative stress was also revealed. The positive correlation obtained between the free radical scavenging capacity of the extracts and their antiglycation potential further confirmed the role of antioxidants in controlling glycation reactions. Ethyl acetate extract was also found as effective in reducing hypertension by inhibiting angiotensin converting enzyme (ACE). Antidiabetic, ACE inhibitory and antioxidant capacities of the extracts were in the order of their curcumin contents.
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Current approach against type 2 diabetes involves α-glucosidase inhibitors like acarbose associated with many side effects. Therefore, as an alternative to the existing drug, many natural products mainly from plant sources have been investigated which inhibit α-glucosidase. Here, we have selected medicinally important Alpinia nigra to explore its α-glucosidase inhibitory activity. Organic extracts of seeds and two purified natural diterpenes I: (E)-labda-8(17), 12-diene-15, 16-dial and II: (E)-8β, 17-epoxylabd-12-ene-15, 16-dial from A. nigra were investigated towards inhibition of α-glucosidase activity. Dose-dependent inhibition pattern were observed for seed extracts and both the compounds. Further, inhibition kinetics studies of the diterpenes indicated a non-competitive type of inhibition against α-glucosidase. Docking studies were carried out which revealed that both the diterpenes interacted within the active site of N-terminal and C-terminal domain of human maltase-glucoamylase enzyme, respectively. This is the first report of α-glucosidase inhibitory activity of these isolated diterpenes and their higher inhibitory potential than any terpenoids studied till date against α-glucosidase.
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Hepatotoxicity is a rare complication following the use of propofol and can be potentially serious if an early diagnosis is not made. Propofol is being increasingly used in daily practice, not only in surgery, but also in outpatient sedation procedures, such as endoscopy. Acarbose is a well-known drug used in type 2 diabetes treatment, particularly in the early phase. A case is reported on a patient who suffered an acute hepatitis secondary to the use of propofol in ophthalmology surgery, a hepatitis probably enhanced by prior use of acarbose, a drug that also can cause hepatotoxicity. An early diagnosis and it was resolved without complications. This case could contribute to improve pre-anesthetic evaluation of patients who will be undergoing sedation with propofol in order to avoid the possible appearance of hepatitis.
A series of bisbenzimidazole derivatives starting from o-phenylenediamine and 4-nitro-o-phenylenediamine were prepared with oxalic acid. Most of the reactions were conducted using both the microwave and conventional methods to compare yields and reaction times. The operational simplicity, environmental friendly conditions and high yield in a significantly short reaction time were the major benefits. All substances' inhibitory activities against α-glucosidase were evaluated. The results may suggest a significant role for the nature of bisbenzimidazole compounds in their inhibitory action against α-glucosidase. They showed different range of α-glucosidase inhibitory potential with IC50 value ranging between 0.44±0.04 and 6.69±0.01μM when compared to the standard acarbose (IC50, 13.34±1.26μM). This has described a new class of α-glucosidase inhibitors. Molecular docking studies were done for all compounds to identify important binding modes responsible for inhibition activity of α-glucosidase.
We studied the efficacy and safety of acarbose in comparison with voglibose in type 2 diabetes patients whose blood glucose levels were inadequately controlled with basal insulin alone or in combination with metformin (or a sulfonylurea). This study was a 24-week prospective, open-label, randomized, active-controlled multi-center study. Participants were randomized to receive either acarbose (n=59, 300 mg/day) or voglibose (n=62, 0.9 mg/day). The mean HbA1c at week 24 was significantly decreased approximately 0.7% from baseline in both acarbose (from 8.43% ± 0.71% to 7.71% ± 0.93%) and voglibose groups (from 8.38% ± 0.73% to 7.68% ± 0.94%). The mean fasting plasma glucose level and self-monitoring of blood glucose data from 1 hr before and after each meal were significantly decreased at week 24 in comparison to baseline in both groups. The levels 1 hr after dinner at week 24 were significantly decreased in the acarbose group (from 233.54 ± 69.38 to 176.80 ± 46.63 mg/dL) compared with the voglibose group (from 224.18 ± 70.07 to 193.01 ± 55.39 mg/dL). In conclusion, both acarbose and voglibose are efficacious and safe in patients with type 2 diabetes who are inadequately controlled with basal insulin. (ClinicalTrials.gov number, NCT00970528).
At the highest concentration employed (100 μg/ml), NBF showed highest inhibition against α-glucosidase (75%) and α-amylase (87%) in vitro (IC50 = 2.40 ± 0.23 μg/ml and 58.50 ± 0.13 μg/ml, respectively) in a dose-dependent fashion; an effect found to be about 20% higher than acarbose (55%), a standard α-glucosidase inhibitor (IC50 = 3.45 ± 0.19 μg/ml). The ME and SFI also inhibited α-glucosidase (IC50 = 7.50 ± 0.15 μg/ml and 11.45 ± 0.28 μg/ml) and α-amylase (IC50 = 43.90 ± 0.19 μg/ml and 69.80 ± 0.25 μg/ml), but to a lesser extent. In in vivo studies with diabetic rats, NBF and SFI effectively reduced peak blood glucose (PBG) by 15.08% and 6.46%, and the area under the tolerance curve (AUC) by 14.23% and 12.46%, respectively, after an oral sucrose challenge (P < 0.05); thereby validating the observed in vitro action. These reduction effects on PBG and AUC were also demonstrated in glucose and starch tolerance tests, but to a lesser degree.
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To search alpha-glucosidase inhibitors from Rubia cordifolia.
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This article focuses on those patients where particular agents should not be used: i.e. 'when not to use what'.
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Combating Type-2 diabetes mellitus is a pivotal challenge in front of the present world. Several lines of therapy are in practice for resisting this deadly disease which often culminates with cardiovascular complexities, neuropathy and retinopathy. Among various therapies, administration of alpha glucosidase inhibitors is common and widely practiced. Sulfonylurea category of anti diabetic drug often suffers from cross reactivity with sulfamethoxazole (SMX), a common drug in use to treat a handful of microbial infections. However the specific cellular target generating postprandial hypoglycemia on SMX administration is till date unraveled. The present work has been initiated to elucidate the effects of a group of sulfonamide drugs inclusive of SMX for their amylase inhibitory role. SMX inhibits porcine pancreatic amylase (PPA) in a noncompetitive mode with an average IC50 value 0.94 mM respectively. Interaction of SMX with PPA is manifested with gradual quenching of tryptophan fluorescence with concomitant shift in lambda max value (λmax). Binding is governed by entropy driven factor (24.8 cal mol(-1) K(-1)) with unfavorable contribution from enthalpy change. SMX interferes with the activity of acarbose in a synergistic mode to reduce the effective dose of acarbose as evident from the in vitro PPA inhibition study. In summary, loss of PPA activity in presence of SMX is indicative of structural changes of PPA which is further augmented in the presence of acarbose as explained in the schematic model and docking study.
In general however, it must be remembered that problems with oral hypoglycaemics are rare. The great majority of patients have no problems with their prescribed hypoglycaemic medication.
There were significantly more responders in the acarbose-treated group compared with the placebo group (20/24 patients vs. 10/19 patients; p < 0.05). The mean daily insulin dose after 24 weeks of treatment was 16.4 +/- 10.1 IU in the acarbose group and 22.4 +/- 12.2 IU in the placebo group (mean +/- s.d.; p < 0.07). Postprandial increases in blood glucose, insulin and C-peptide were consistently lower in the acarbose-treated group than in the placebo group. For example, the mean increase in 2-h postprandial serum insulin remained almost unchanged in the acarbose group at the end of 24 weeks of treatment compared to an increase to 43 +/- 29 microU/ml (mean +/- s.d.) at the end of the study period for the placebo group.
Diabetes is an increasingly prevalent disease state with a global impact. It is important that effective and cost-efficient methods be developed to treat this disease state. Zucker diabetic fatty rats, an animal model of type 2 diabetes, were treated with montbretin A (MbA), a selective human pancreatic α-amylase inhibitor, isolated from the corms of the Crocosmia crocosmiiflora plant that may have potential as a glucose-lowering agent. The study purpose was to determine if MbA was an orally effective treatment for diabetes. The effect of MbA was compared to a current clinical treatment modality, acarbose that is associated with gastrointestinal side effects known to affect patient compliance. MbA and acarbose were administered daily in the drinking water. Body weight and fluid intake were measured daily to calculate dose consumption. Plasma glucose levels were determined twice weekly in both the fed and fasted state. At termination samples were collected to assess increased risk of secondary complications related to diabetes and oxidative stress. There was no effect of either MbA or acarbose treatment on insulin levels. Plasma glucose levels were significantly lower following MbA treatment in the ZT group which persisted throughout the study period (day 49: 12.1 ± 1.2 mM). However, while there was an initial decrease in plasma glucose levels in the acarbose-treated fatty group, this effect was not sustained (day 49: 20.6 ± 1.3 mM) through to termination. MbA improved the oxidative status of the fatty diabetic animals as well as attenuated markers for increased risk of cardiovascular complications associated with diabetes. This study demonstrated that, at a lower dose as compared to acarbose (10 mg/kg/day), chronic oral administration of MbA (7.5 mg/kg/day) was an effective glucose-lowering agent in the treatment of type 2 diabetes.
Almost three out of ten patients with a total attachment to the pharmacological treatment have chances of being controlled.
Five subjects completed the pilot study. The AUC(gluc) from dosing until 1 h post-dose (AUC(gluc,1 h)) was significantly different between the placebo and acarbose. A total of 33 subjects completed the main study. The mean differences in G(max) (ΔG(max)) and AUC(gluc,1 h) (ΔAUC(gluc,1 h)) for the reference formulation compared with placebo were 22·0 ± 18·3 mg/dL and 928·2 ± 756·0 mg min/dL, respectively. The corresponding values for the test formulation were 23·3 ± 21·2 mg/dL and 923·0 ± 991·4 0 mg min/dL, respectively. The geometric mean ratios (GMRs) of the test formulation to the reference formulation for ΔG(max) and ΔAUC(gluc, 1 h) were 1·06 and 1·00, respectively, and the 90% confidence intervals (CIs) corresponding values were 0·79-1·39 and 0·64-1·36, respectively.
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The effect of the alpha-glucosidase inhibitor acarbose on pancreatic exocrine and endocrine function was studied using the isolated perfused pancreata prepared from rats fed a normal (control diet) or an acarbose-containing sucrose- (ACS diet) or glucose-supplemented diet (ACG diet) for 10 days. Pancreatic amylase and insulin contents in rats fed the ACS diet were significantly decreased compared with those in rats with the control diet. Rats fed the ACG diet, however, had normal enzyme and hormone contents. Basal and cerulein-stimulated flow rates of pancreatic juice in rats with the ACS or ACG diet were similar to those in rats fed the control diet, suggesting that the pancreata from rats treated with acarbose have normal sensitivity and responsiveness to cerulein. On the other hand, cerulein-stimulated amylase output was significantly decreased in rats with the ACS diet, but was normal in rats with the ACG diet. Insulin secretion to both glucose and cerulein stimulation in rats fed the ACS diet was reduced by approximately 55% compared with the control rats. On the other hand, rats fed the ACG diet showed normal insulin secretion to glucose stimulation, although the insulin response to cerulein stimulation was reduced by 30%. These results suggest that the addition of acarbose to the sucrose-rich diet decreases the secretory responsiveness of amylase to cerulein stimulation and that of insulin to both glucose and cerulein stimulation. All these alterations, except the sensitivity of B cells to cerulein, can be normalized by replacing sucrose with glucose.
Randomized trials at least 24 weeks in duration. Studies evaluated the effects of adding a third antihyperglycemic drug to treatment of adults aged 18 years or older with type 2 diabetes and a hemoglobin A(1c) (HbA(1c)) level greater than 7.0% who were already receiving a combination of metformin and a sulfonylurea.