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Precose

Generic Precose is used for treating type 2 diabetes in adults whose diabetes cannot be managed with diet alone. Generic Precose may be used alone, in combination with other oral diabetes medicines, or with insulin.

Other names for this medication:
Acarbosa, Acarbosum, Asucrose, Byetta, Carbose, Decarbay, Deglu, Diabose, Dorobay, Glicobase, Glucar, Glucobay, Gluconase, Glucor, Glumida, Glynose, Incardel, Prandase, Sincrosa

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Also known as: Acarbose.

Description

Generic Precose is used for treating type 2 diabetes in adults whose diabetes cannot be managed with diet alone. Generic Precose may be used alone, in combination with other oral diabetes medicines, or with insulin.

Generic Precose is a glucosidase inhibitor. It works by slowing down the enzyme that turns carbohydrates into glucose; it decreases blood sugar levels following a meal.

Precose is also known as Acarbose, Glucobay, Glucor, Rebose.

Generic name of Generic Precose is Acarbose.

Brand name of Generic Precose is Precose.

Dosage

Take Generic Precose by mouth with food.

If you also take charcoal or digestive enzyme preparations, do not take them within 2 to 4 hours before after taking Generic Precose.

Temporary insulin therapy may be necessary during stressful periods (such as fever, trauma, infection, or surgery).

If you want to achieve most effective results do not stop taking Generic Precose suddenly.

Overdose

If you overdose Generic Precose and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store at room temperature below 25 degrees C (77 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Precose are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Generic Precose if you are allergic to Generic Precose components.

Be careful with Generic Precose if you're pregnant or you plan to have a baby, or you are a nursing mother.

Do not take Generic Precose if you have blockage of the stomach or intestine or are at risk for these problems.

Do not take Generic Precose if you have long-term (chronic) bowel inflammation, colon ulcers, or stomach or intestine problems that interfere with digestion or nutrient absorption.

Do not take Generic Precose if you have cirrhosis of the liver or unexplained abnormal liver function tests.

Do not take Generic Precose if you have diabetic ketoacidosis (high ketone levels) or severe kidney problems.

Try to be careful with Generic Precose if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Try to be careful with Generic Precose if you have allergies to medicines, foods, or other substances

if you have stomach or intestinal problems, liver problems, or kidney problems.

Try to be careful with Generic Precose if you are taking anticoagulants (eg, warfarin) because the risk of their side effects, including bleeding, may be increased by Generic Precose; calcium channel blockers (eg, verapamil), corticosteroids (eg, prednisone), diuretics (eg, hydrochlorothiazide), estrogen, isoniazid, nicotinic acid, oral contraceptives (birth control pills), phenothiazines (eg, chlorpromazine), phenytoin, sympathomimetics (eg, pseudoephedrine), or thyroid hormone because they may increase or decrease Precose 's effectiveness; insulin or sulfonylureas (eg, glyburide) because the risk of their side effects may be increased by Generic Precose; digoxin because its effectiveness may be decreased by Generic Precose.

Avoid alcohol.

Do not stop taking Generic Precose suddenly.

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Poorly controlled Type 2 diabetic patients treated with oral hypoglycaemic agents (OHA) were randomized into either acarbose (100 mg t.d.s.) or placebo treatment. The double-blind treatment lasted for 24 weeks. Four-day food diaries and blood samples for efficacy analysis were collected at 0, 4, 12, and 24 weeks. Thirty-six acarbose and 39 placebo-treated patients completed the trial and were included in the final analyses.

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In this study, we demonstrate the use of a PCR-based method for the detection of the specific genes involved in natural-product biosynthesis. This method was applied, using specifically designed PCR primers, to the amplification of a gene segment encoding for sedo-heptulose 7-phosphate cyclase, which appears to be involved in the biosynthetic pathways of C7N aminoacyclitol or its keto analogue-containing metabolites, in a variety of actinomycetes species. The sequences of DNA fragments (about 540 bp) obtained from three out of 39 actinomycete strains exhibited a high degree of homology with the sedo-heptulose 7-phosphate cyclase gene, which has been implicated in acarbose biosynthesis. The selective cultivation conditions of this experiment induced the expression of these loci, indicating that the range of C7 aminoacyclitol or its keto analogue-group natural products might be far greater than was previously imagined. Considering that a total of approximately 20 C7 aminoacyclitol metabolites, or its keto analogue-containing metabolites, have been described to date, it appears likely that some of the unknown loci described herein might constitute new classes of C7 aminoacyclitol, or of its keto analogue-containing metabolites. As these metabolites, some of which contain valienamine, are among the most potent antidiabetic agents thus far discovered, the molecular detection of specific metabolite-producing actinomycetes may prove a crucial step in current attempts to expand the scope and diversity of natural-product discovery.

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Acarbose, which is clinically widely used to treat Type 2 Diabetes, is thought to act at the small intestine by competitively inhibiting enzymes that delay the release of glucose from complex carbohydrates, thereby specifically reducing post prandial glucose excursion. The major side-effect of treatment with acarbose, flatulence, occurs when undigested carbohydrates are fermented by colonic bacteria, resulting in considerable amount of hydrogen. We propose that enteric benefits of acarbose is partly attributable to be their ability to neutralise oxidative stress via increased production of H2 in the gastrointestinal tract. Therefore, symptoms of ulcerative colitis in human beings can be ameliorated by acarbose.

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Databases and reference lists of clinical trials on acarbose were searched. Eligible studies were randomised controlled trials of acarbose monotherapy in populations with hyperglycaemia of more than 12-week duration that provided data on body weight (BW) or body mass index (BMI).

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Acarbose can prevent obesity and fat infiltration in islets and muscles, improve glucose and lipid metabolism, and insulin secretion in OLETF rats with IGT.

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The ability of an inhibitor of intestinal alpha-glucosiadase activity to prevent sucrose-induced hypertriglyceridemia was studied in nonobese rats. The results indicated that plasma triglyceride levels were approximately twice as high in untreated rats, and the reduction in plasma triglyceride levels of drug-treated rats was associated with lowered very low density lipoprotein-triglyceride secretion rates and plasma insulin levels. Since these changes could be produced with an amount of glucosidase inhibitor which did not prevent normal rate of weight gain, the possibility arises that this approach may be useful in the treatment of various hypertriglyceridemic states in man. Finally, the observation that the fall in plasma TG concentration was associated with a fall in plasma insulin concentration provides further evidence for the existence of a causal relationship between the two variables.

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A double-blinded, parallel group study was performed on 56 male subjects with hypertension, body mass index (BMI) 27-35 kg/m2, fasting blood glucose < or =6 mmol/l and a normal oral glucose tolerance test. Blood pressure, HbA1c, lipid profile and insulin resistance [homeostasis model assessment (HOMA) index] were determined initially and following 24 weeks of acarbose, 150 mg/day or placebo. The primary end point was the change in insulin resistance. Anti-hypertensive treatment and diet were kept constant during the study.

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The effects of the disaccharidase inhibitor acarbose on serum lipoprotein lipid concentrations were investigated in healthy subjects during prolonged feeding of a fiber-free formula diet. Acarbose was shown to decrease cholesterol and fasting triglyceride concentrations, whereas the postprandial increment of triglycerides was not diminished. The response of fasting triglycerides to acarbose treatment appeared to be related to dietary fat intake, but not to the drug-induced reduction of postprandial glucose and insulin concentrations. Both the triglyceride and the cholesterol lowering efficacy were less pronounced with a higher amount of saturated fat than with a lower intake of fat mainly composed of polyunsaturated fatty acids. The decrease in total cholesterol was shown to be a consequence of a significant reduction in low density lipoprotein (LDL) cholesterol. Since high density lipoprotein (HDL) cholesterol concentrations remained unaltered, the ratio of HDL/LDL cholesterol changed in a beneficial way.

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Both nateglinide and acarbose increase post-prandial ghrelin suppression. Improved ghrelin regulation is most likely to play a role in glucose stability in T2DM patients with nateglinide or acarbose therapy.

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The long-term benefit of acarbose treatment was studied prospectively 20 NIDDM patients on diet, and 20 IDDM patients were treated with acarbose and followed for six years. 5 NIDDM patients and 7 IDDM patients were dropped-out due to side-effects or planned pregnancy or price of the drug. In the NIDDM group, acarbose treatment had to be supplemented with sulfonylureas in six patients, and a conversion to insulin had to be carried out in two patients. At the end of the study, all of NIDDM patients had a significantly lowered fasting blood-glucose level as compared to the baseline value. In the IDDM group, the postprandial blood-glucose level (at 90 minutes after meal) was significantly decreased, whereas the fasting glucose level remained unchanged versus the baseline level. In both groups, the values of HbA1c and serum lipids were significantly better than before acarbose treatment. The frequency of hypoglycaemic episodes was decreased, the body weight was without significant change. In addition, five NIDDM patients with late sulfonylurea-resistance were also treated with acarbose and followed for two years. After six months of treatment, however, four out of the five patients had to be converted to insulin.

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It has been previously demonstrated that hyperglycaemia activates haemostasis; diabetes mellitus is considered a thrombosis-prone state. Acarbose, by inhibiting dietary carbohydrate absorption, reduces post-meal hyperglycaemia. In this study we evaluated the effect of post-meal hyperglycaemia on two markers of coagulation activation: prothrombin fragments 1 + 2 and D-dimer. Seventeen non-insulin-dependent diabetic patients maintained on diet therapy alone were randomly assigned to receive- with a cross-over study design-acarbose (100 mg orally) or placebo before a standard meal. Blood samples for measurement of plasma glucose, insulin, prothrombin fragments 1 + 2 and D-dimer were drawn at 0, 60, 120 and 240 min. After both placebo and acarbose, hyperglycaemia and hyperinsulinaemia which followed a standard meal were accompanied by a significant increase of plasma concentration of prothrombin fragments 1 + 2 and D-dimer in comparison to their baseline values. Acarbose administration significantly reduced the rise of glucose, insulin, prothrombin fragments 1 + 2 and D-dimer from 0 to 240 min in comparison to placebo. We conclude that post-meal hyperglycaemia, at the level reached by many diabetic patients on diet therapy alone, induces a coagulation activation. Acarbose, by decreasing post-meal hyperglycaemia, may be useful in reducing meal-induced activation of haemostasis in diabetic patients.

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Fifty-gram carbohydrate tolerance tests were performed on healthy volunteers to test the activity and specificity of an alpha-glucoside hydrolase inhibitor, acarbose (BAY g 5421). Two hundred milligrams acarbose reduced the area under the blood glucose response curve by 89% (P less than 0.001) after sucrose by 80% (P less than 0.002) after starch, by 19% (N.S.) after maltose, with no effect on glucose. Breath hydrogen measurements indicated an almost complete malabsorption of the sucrose. At 50 mg acarbose, some reduction in blood glucose and insulin response to sucrose was still seen, but no significant hydrogen production. It is suggested that at lower doses, acarbose may prolong the time course over which carbohydrate is absorbed as does dietary fiber; as with fiber, it may be a useful adjunct to diabetic therapy.

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buy precose online 2016-06-28

Insulin resistance is one of the determinants of post-prandial hyperglycaemia. Recently, acarbose, an alpha-glucosidase inhibitor that delays the absorption of carbohydrates from the small intestine, has been found to reduce the incidence of cardiovascular disease in patients with impaired glucose tolerance or diabetes. However, the molecular mechanism by which acarbose inhibits cardiovascular events remains unknown. In this study, we examined whether oral administration of acarbose could suppress expression of monocyte chemoattractant protein-1 (MCP-1) in fructose-fed rats, a widely used animal model of insulin resistance. Serum MCP-1 levels were elevated in fructose-fed rats after 4 weeks. Acarbose treatment for 4 weeks reduced the fructose-induced elevation of serum MCP-1 levels. Acarbose treatment for 8 Ponstel Generic Price weeks decreased MCP-1 mRNA levels in the aortae of fructose-fed rats. These results suggest that the cardioprotective effects of acarbose could be due, at least in part, to the suppression of MCP-1 expression.

precose generic 2017-08-05

A total of 20 trials evaluating 13 antihyperglycaemic agents were included. Compared with placebo/control, all antihyperglycaemic agents reduced HbA1c levels, albeit by differing magnitudes [range 7 mmol/mol (0. Cialis Online Kaufen 6%) for acarbose to 13 mmol/mol (1.20%) for liraglutide]. Sodium glucose cotransporter-2 inhibitors reduced weight (1.43-2.07 kg) whereas thiazolidinediones, glargine and sitagliptin caused weight gain (1.48-3.62 kg) compared with placebo/control. Sodium glucose cotransporter-2 inhibitors, rosiglitazone and liraglutide decreased systolic blood pressure compared with placebo/control, pioglitazone, glargine and sitagliptin (2.41-8.88 mm Hg). Glargine, thiazolidinediones, liraglutide, sitagliptin and canagliflozin increased hypoglycaemia risk compared with placebo/control (relative risk 1.92-7.47), while glargine and rosiglitazone increased hypoglycaemia compared with most antihyperglycaemic agents (relative risk 2.81-7.47). No antihyperglycaemic agent increased the risk of urinary tract infection, but canagliflozin increased the risk of genital tract infection by 3.9-fold compared with placebo/control.

precose generic name 2016-05-26

Acarbose inhibits intestinal alpha-glucosidases resulting in diminished and delayed postprandial hyperglycaemia (PPH). Studies on effects of acarbose on postprandial lipaemia (PPL) have been inconclusive. Little is known about the effects of acarbose on PPH and PPL following intake of a polysaccharide diet. We studied 30 type 2 diabetic patients on dietary and/or oral hypoglycaemic agent(s). Thirty patients were recruited for food A (nasi lemak), 28 for food B (mee goreng) and 28 for food C (roti telur), which represent the typical diets of the three main races in Malaysia. Serial blood samples were taken at 15 min before and up to 240 min after each food intake, without acarbose. Subsequently, three doses of 50 mg acarbose were given orally and the same procedure was repeated the following day. There were significantly lower mean increments in plasma glucose levels after compared to before acarbose treatment 30, 45 and 60 min for food A and at 30, 45, 60, 120, 180 and Buy Cheap Cialis 240 min for food C, but no significant difference was noted for food B. There was a significantly lower mean fasting glucose level after compared with before acarbose treatment following intake of food A and C but not food B. Short-term treatment with acarbose caused significant diminished and delayed PPH response with food A and C but not with food B. Acarbose was more effective in reducing PPH response in polysaccharide foods with a higher and earlier postprandial glucose peak than in those with a lower and lagged peak. There were no significant differences in the mean fasting or postprandial triglyceride levels before and after acarbose treatment, following intake of all three foods for up to 4 hours. Depending on the food absorption pattern, overnight low dose treatment with acarbose leads to diminished fasting and peak plasma glucose levels, and delayed PPH but insignificant reduction in postprandial lipaemia in poorly controlled type 2 diabetics following intake of racially different Malaysian food.

precose cost 2015-03-15

Two new flavonoids, bismilachinone (11) and smilachinin (14), were isolated from the leaves of Smilax china L. together with 14 known compounds. Their structures were elucidated using spectroscopic methods. The PTP1B, α-glucosidase, and DPP-IV inhibitory activities of compounds 1-16 were evaluated at the molecular level. Among them, compounds 4, 7, and 10 showed moderate DPP-IV inhibitory activities with IC50 values of 20.81, 33.12, and 32.93 μM, respectively. Compounds 3, 4, 6, 11, 12, and 16 showed strong PTP1B inhibitory activities, with respective IC50 values of 7.62, 10.80, 0.92, 2.68, 9.77, and 24.17 μM compared with the IC50 value for the positive control (ursolic acid: IC50 = 1.21 μM). Compounds 2-7, 11, 12, 15, and 16 showed potent α-glucosidase inhibitory activities, with respective IC50 values of 8.70, 81.66, 35.11, 35.92, 7.99, 26.28, 11.28, 62.68, 44.32, and 70.12 μM. The positive control, acarbose, displayed an IC50 value of 175.84 μM. In the kinetic study for the PTP1B enzyme, compounds 6, 11, and 12 displayed competitive inhibition with Ki values of 3.20, 8.56, and 5.86 μM, respectively. Compounds 3, 4, and 16 showed noncompetitive inhibition with Ki values of 18.75, 5.95, and 22.86 μM, respectively. Molecular docking study for the competitive inhibitors (6, 11, and 12) radically corroborates the binding affinities and inhibition of PTP1B enzymes. These results indicated that the leaves of Smilax china L. may Diamox Generic Name contain compounds with anti-diabetic activity.

precose online 2017-05-08

For the last 30 years, sulfonylureas have been the mainstay of treatment for patients with non-insulin-dependent diabetes mellitus (NIDDM). They offered patients an alternative to using insulin to lower their blood glucose. One of the advantages of these agents was that they could be taken orally as opposed to insulin, which required multiple daily injections. In addition, they are tolerable, with few side effects, and they cause less hypoglycemia than does insulin. In the past year, new agents (metformin and acarbose) have been introduced into the market and have offered practitioners an alternative to the traditional sulfonylureas Buy Brand Viagra . The sulfonylureas are still valuable agents in the treatment of NIDDM. Their efficacy is unsurpassed by any other oral medications. They possess the best tolerability profile of all oral agents on the market, and they possess very few contraindications or drug interactions. The sulfonylureas should still be considered first-line agents for NIDDM. Metformin and acarbose are agents that may benefit a specific patient population, but sulfonylureas are agents that can benefit most patients.

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Post-prandial hyperglycemia still remains a problem in the management of type 2 diabetes mellitus. Of all available anti-diabetic drugs, α-glucosidase inhibitors seem to be the most effective in reducing post-prandial hyperglycemia. We conducted a review analyzing the clinical efficacy and safety of α-glucosidase inhibitors, both alone and in combination with other anti-diabetic drugs, with respect to glycemic control, inflammation and atherosclerosis. α-Glucosidase inhibitors proved to be effective and safe both in monotherapy and as an add-on to other anti-diabetic drugs. Compared to miglitol and voglibose, acarbose seems to have some additive effects Clomid Pct Buy such as stabling carotid plaques, and reducing inflammation. Acarbose also proved to reverse impaired glucose tolerance to normal glucose tolerance.

precose generic 2015-10-23

Glucose tolerance declines with age, resulting in a high prevalence of diabetes and impaired glucose tolerance (IGT) in the older population. Hyperglycemia per se can lead to impaired beta-cell function (glucose toxicity). We tested the role of glucose toxicity in age-related beta-cell dysfunction in older people (65 +/- 8 yr) with IGT treated with the alpha-glucosidase inhibitor acarbose (n = 14) or placebo (n = 13) for 6 wk in a randomized, double-blind study. Baseline and posttreatment studies included 1) an oral glucose tolerance test (OGTT), 2) 1-h postprandial glucose monitoring, 3) a frequently sampled intravenous glucose tolerance test (insulin sensitivity, or S(I)), and 4) glucose ramp clamp (insulin secretion rates, or ISR), Astelin Generic in which a variable glucose infusion increases plasma glucose from 5 to 10 mM. The treatment groups had similar baseline body mass index; fasting, 2-h OGTT, and 1-h postprandial glucose levels; and S(I). In these carefully matched older people with IGT, both fasting (5.7 +/- 0.2 vs. 6.3 +/- 0.2 mM, P = 0.002) and 1-h postprandial glucose levels (6.9 +/- 0.3 vs. 8.2 +/- 0.4 mM, P = 0.02) were significantly lower in the acarbose than in the placebo group. Despite this reduction of chronic hyperglycemia in the acarbose vs. placebo group, measures of insulin secretion (ISR area under the curve: 728 +/- 55 vs. 835 +/- 81 pmol/kg, P = 0.9) and acute insulin response to intravenous glucose (329 +/- 67 vs. 301 +/- 54 pM, P = 0.4) remained unchanged and impaired. Thus short-term improvement of chronic hyperglycemia does not reverse beta-cell dysfunction in older people with IGT.

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ClinicalTrials.gov NCT01175486 Avelox Cost .

precose cost 2015-05-04

Digestion of starch requires activities provided by 6 interactive small intestinal enzymes. Two of these are luminal endo-glucosidases named alpha-amylases. Four are exo-glucosidases bound to the luminal surface of enterocytes. These mucosal activities were identified as 4 different maltases. Two maltase activities were associated with sucrase-isomaltase. Two remaining maltases, lacking other identifying activities, were named maltase-glucoamylase. These 4 activities are better described as alpha-glucosidases because they digest all linear starch oligosaccharides to glucose. Because confusion persists about the relative roles of these 6 enzymes, we ablated maltase-glucoamylase gene expression by homologous recombination in Sv/129 mice. We assayed the alpha-glucogenic activities of the jejunal mucosa with and without added recombinant pancreatic alpha-amylase, using a range of food starch substrates. Compared with wild-type mucosa, null mucosa or alpha-amylase alone had little alpha-glucogenic activity. alpha-Amylase amplified wild-type and null mucosal alpha-glucogenesis. alpha-Amylase amplification was most potent against amylose and model resistant starches but was inactive against its final product limit-dextrin and its constituent glucosides. Both sucrase-isomaltase and maltase-glucoamylase were active with limit-dextrin substrate. These mucosal assays were corroborated by a 13C-limit-dextrin breath test. In conclusion, the global effect of maltase-glucoamylase ablation was a slowing of rates of mucosal alpha-glucogenesis. Maltase-glucoamylase determined rates of digestion of starch in normal mice and alpha-amylase served as an amplifier for mucosal starch Celebrex Generic Cost digestion. Acarbose inhibition was most potent against maltase-glucoamylase activities of the wild-type mouse. The consortium of 6 interactive enzymes appears to be a mechanism for adaptation of alpha-glucogenesis to a wide range of food starches.

precose online 2016-08-30

Type I diabetes mellitus is a metabolic disease caused by chronic immune attack against the insulin-producing cells of the pancreas. It has recently been shown that the clinical course of this disease can be interrupted by immune ablation and PBSCT. In this report, we describe our experience with this treatment modality in a series of eight cases. Patients with newly diagnosed type I diabetes were received treatment consisting of two to three plasmaphereses, hematopoietic stem cell mobilization with CY and G-CSF, collection of at least 3 × 10(6) per kg of CD34+ cells, and conditioning with CY and anti-thymocyte globulin followed by stem cell infusion. All patients became independent of exogenous insulin after the transplantation. One patient resumed low-dose insulin 7 months after transplantation. Six out of eight Suprax Generic Available patients were given acarbose for better glycemic control after transplantation. All patients exhibited good glycemic control: the average HbA1c concentrations were 12.3% at diagnosis, and 5.6 and 6.2% at 3 and 6 months after transplantation, respectively. We conclude that at least temporary independence of exogenous insulin can be achieved in type I diabetes patients following immunoablation and reconstitution of the immune system with autologous PBSCs.

buy precose online 2015-02-16

The severity of the type 2 diabetes epidemic is widely acknowledged. Demographic, social, and cultural changes around the world are driving a dramatic increase in the prevalence of type 2 diabetes. Consequently, there is increasing interest in defining the target population and developing strategies for preventing or delaying the disease. Impaired glucose tolerance (IGT), an asymptomatic condition early in the disease continuum of dysglycemia, is the best target for intervention, as it is a strong predictor for the development of both type 2 diabetes and cardiovascular disease (CVD). Identifying individuals likely Precose Cost to have IGT using risk-prediction tools is simple and cost-effective; diagnosis can be confirmed with an oral glucose tolerance test. Numerous trials have examined the benefits of intervention in IGT populations. Lifestyle modification and some pharmacologic therapies, such as acarbose, have been shown to significantly reduce disease progression. Acarbose therapy has also been associated with significant reductions in cardiovascular events and new cases of hypertension. Trials assessing the potential preventive effects of various therapies are ongoing, but current evidence confirms that early intervention in individuals with IGT can reduce the risks of type 2 diabetes and CVD. Identification of high-risk individuals should therefore be standard in general practice and, if IGT is diagnosed, therapeutic intervention should be initiated promptly.

precose generic 2016-10-10

The efficacy and tolerability of acarbose was studied in type 2 diabetic patients eating a typical Jamaican diet. The study was an open label parallel group study without placebo control. Of the 51 subjects recruited, five (9.8%) did not complete the study and were excluded from further analysis. Six (13%) of the remaining 46 had adverse side effects and did not complete the protocol. Of the remaining 40 (Gp A), acarbose was added to their previous regime of diet alone (n = 15), [Gp B], oral hypoglycaemic agents, OHAs (n = 17), [Gp C], or insulin (n = 8), Gp D]. In addition, during the run-in period all subjects had one session each with a dietitian and a diabetes educator. Over a 3-month period, significant reductions in Buspar Generic Name average glucose (mmol) were observed in Gp B 10.5 +/- 1.1 to 8.4 +/- 0.9 (p < 0.027) and, from 11.0 +/- 1.0 to 8.7 +/- 0.7 (p < 0.01) in Gp C. Similarly, total glycosylated haemoglobin fell from 14.8 +/- 1.1% to 12.2 +/- 1.0% (p < 0.016) in Gp B, from 14.9 +/- 1.1 to 11.9 +/- 1.1% (p < 0.002) in Gp C, and from 14.1 +/- 1.4 to 11.8 +/- 1.4 (p < 0.02) in Gp D. Twenty-three per cent (23%) of the patients experienced flatulence; 7.5%, changes in bowel habits and 5%, abdominal cramps and discomfort. Acarbose is effective as monotherapy and as combination therapy with oral hypoglycaemic agents or insulin. Side effects were common, but tolerable.