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Glucophage is efficacious medical preparation in fight against type 2 diabetes. Glucophage is created with extremely active ingredients with aim to make Glucophage ideal remedy against type 2 diabetes. Target of Glucophage is to control sugar level in blood.

Other names for this medication:
Glucophage, Glucophage XR, Glumetza, Fortamet, Riomet

Similar Products:
Metformin, Glycomet, Avandia, Actos

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Also known as:  Metformin.


Glucophage is a famous medication which provides treatment type 2 diabetes. Glucophage acts controlling and decreasing glucose (sugar in blood).

Glucophage is oral antihyperglycemic drug from the biguanide class.

Glucophage is also known as Metformin, Phage, Riomet, Fortamet, Glumetza, Obimet, Dianben, Diabex, Diaformin.

Glucophage is not taken to treat type 1 diabetes.

You can normally take insulin while using Glucophage.

Generic name of Glucophage is Metformin.

Brand names of Glucophage are Glucophage XR, Fortamet, Riomet, Glucophage, Glumetza, Diaformin, Diabex.


Glucophage can be taken in form of pills and extended-release pills which should be taken by mouth.

It is better to take Glucophage every day at the same time with meal or without it.

Usual Glucophage dosage is taken 2-3 times a day with meals.

Glucophage XR (extended-release tablets) is taken once a day with evening meal.

Take Glucophage and remember that its dosage depends on patient's health state.

Glucophage can't be used by patients under 10 years. Glucophage XR (extended-release tablets) can't be used by patients under 17 years.

It can be dangerous to stop Glucophage taking suddenly.


Do not take Glucophage tablets in large quantities. In case of Glucophage overdosage, you need to visit doctor or health care provider immediately.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. 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 Glucophage 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.


Do not use Glucophage if you are allergic to Glucophage components.

Try to be careful with Glucophage while you are pregnant or have nurseling.

Glucophage can't be used by patients under 10 years. Glucophage XR (extended-release tablets) can't be used by patients under 17 years.

Glucophage is not taken to treat type 1 diabetes.

You can normally take insulin while using Glucophage.

Do not use Glucophage in case of taking probenecid (Benemid); aspirin and other salicylates; sulfa drugs (Bactrim); beta-blockers; monoamine oxidase inhibitor (MAOI); allergies, colds, asthma medicines; thyroid medicine (Synthroid); seizure medicines (Dilantin); phenothiazines (Compazine); diet pills; isoniazid; steroids; hormones including birth control pills.

Try to be careful with Glucophage in case of using such medication as morphine (MS Contin, Kadian, Oramorph); quinidine (Cardioquin, Quinidex, Quinaglute); vancomycin (Vancocin, Lyphocin); cimetidine (Tagamet) or ranitidine (Zantac); nifedipine (Adalat, Procardia); procainamide (Procan, Pronestyl, Procanbid); trimethoprim (Proloprim, Primsol, Bactrim, Cotrim, Septra); amiloride (Midamor) or triamterene (Dyrenium); digoxin (Lanoxin); furosemide (Lasix).

Try to avoid Glucophage in case of having lung, kidney, heart or liver disease, high blood pressure, stroke, diabetic ketoacidosis, or kidney failure.

Try to avoid Glucophage in case you want to undergo an operation (dental or any other), x-ray or CT scan.

Try to avoid unhealthy food.

Glucophage can't be used by patients under 10 years. Glucophage XR (extended-release tablets) can't be used by patients under 17 years.

If you want to achieve most effective results without any side effects you need to avoid alcohol.

It can be dangerous to stop Glucophage taking suddenly.

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To assess the efficacy and safety of saxagliptin vs. glipizide as add-on therapy to metformin in patients with type 2 diabetes mellitus and inadequate glycaemic control on metformin alone.

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Efforts must be made to ease the burden of research participation on both pediatric T2D patients as well as pediatric endocrinologists.

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To assess the design and the Mainland China subgroup baseline characteristics of the study to evaluate the efficacy and safety of alogliptin versus placebo in subjects with type 2 diabetes (T2DM) as monotherapy, add-on to metformin or add-on to pioglitazone.

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This article describes a patient with type 2 diabetes mellitus achieving glycemic control after transitioning from premixed to basal-prandial insulin.

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An observational retrospective study was performed. Patients ≥30 years of age who were receiving treatment with metformin who started a second oral antidiabetes therapy in 2008 and 2009 were included. Patients were divided into two groups: (a) metformin plus DPP-4 inhibitors and (b) metformin plus other oral antidiabetes drugs. The main measures were compliance, persistence, metabolic control (glycosylated hemoglobin level of <7%), and complications (hypoglycemia and cardiovascular events). Healthcare and non-healthcare costs were calculated. Patients were followed up for 2 years. An analysis of covariance was carried out (P<0.05 was considered significant).

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Chronic EtOH consumption led to liver injury both histologically and biochemically accompanied by insulin resistance, reduced AMPK activity, and dysregulation of downstream enzymes. Decreased levels of circulating adiponectin and decreased expression of proliferator-activated receptor gamma coactivator-1α (PGC-1α) and peroxisome proliferator-activated receptors-α (PPAR-α) in the hepatic tissue were observed. Treatment with metformin attenuated the severity of liver injury, restored AMPK activity and normalized the expression of acetyl-CoA carboxylase and fatty acid synthase. In addition, metformin also increased the circulating adiponectin and liver adiponectin receptor 2 expression. Furthermore, PGC-1α and PPAR-α activities were also restored.

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To assess the clinical value and of metformin as mono-therapy versus other treatments for type 2 diabetes mellitus in children and adolescents. Major electronic databases, the reference lists of relevant articles and databases of ongoing trials were searched. Authors of reviews and metformin manufacturers were contacted in order to obtain more references and reports of unpublished trials. The methodological quality of these reports, included randomised controlled trials (RCTs) was assessed using the National Health System Centre for Reviews and Dissemination (NHS CRD) checklist. The search identified 1,825 studies. Three RCTs met the inclusion criteria. Two RCTs had been completed and one was still ongoing. In the metformin group there were significant reductions of mean change of HBA1c from baseline. It reduced by -0.71% (P = 0.0002) and in the other trial the result was reduced by -1.10 (95% CI: -1.19 to -1.01). In addition, more patients (48.1%) in the metformin group achieved good glycaemic control (<7%) at week 24. The mean changes in FPG from baseline were significantly (P < 0.05) different in the metformin group (-16.6%, for week 18 and week 24 20.6%. In the second trial there was a significant (P < 0.001) reduction in the adjusted mean of FPG from baseline in the metformin group, while there was an increase in the placebo group ( -42.9 mg/dl vs. +21.4mg/dl) with mean difference of -64.80 in favour of the metformin group. For BMI, significant (P < 0.001) differences were seen at week 12 and week 24 (0.07 and 0.55 kg(2)) for metformin and glimepiride respectively. There was no significant difference between the placebo and metformin in the other trials. For lipid value there was a significant decrease in LDL levels in the metformin group. No significant changes were found in the other lipid parameters after adjusting. There were more adverse events in the metformin group but they were not statistically significant. There was a limited but not convincing evidence to suggest that metformin can improve the glycaemic control in children and adolescent with type 2 diabetes compared with other interventions. This is may be the result of the limited number, poor quality and short duration of the included trials.

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Women aged 15-45 years.

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Lixisenatide (Lyxumia(®)) is a glucagon-like peptide-1 receptor agonist that acts in a glucose-dependent manner to improve glycemic control in adult patients with type 2 diabetes mellitus. Subcutaneous once-daily prandial lixisenatide is indicated for the treatment of adult patients with type 2 diabetes to achieve glycemic control in combination with oral antihyperglycemic drugs (OADs) and/or basal insulin when these antihyperglycemic drugs do not provide adequate glycemic control. In an extensive phase III clinical trial program, lixisenatide once daily in combination with OADs and/or basal insulin for 24 weeks improved glycemic control, had beneficial effects on bodyweight, and was generally well tolerated in adult patients with inadequately controlled type 2 diabetes despite treatment with OADs and/or basal insulin. At 24 weeks, in terms of the primary efficacy endpoint of each trial, combination therapy with lixisenatide was associated with better efficacy than placebo in patients inadequately controlled on OADs and/or basal insulin, was shown to be noninferior to exenatide in patients inadequately controlled on background metformin therapy, and showed similar efficacy to sitagliptin in patients inadequately controlled on background metformin therapy. Further clinical experience/post-marketing surveillance studies and long-term safety data, along with pharmacoeconomic analyses, are required to fully define the position of lixisenatide in relation to other antihyperglycemics. In the meantime, once-daily prandial lixisenatide in combination with OADs and/or basal insulin (plus diet and exercise) is an effective option for improving glycemic control in adult patients with type 2 diabetes, including in patients where bodyweight loss is an essential component in their management.

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We examined the effects of metformin, a commonly used antidiabetic drug, on gene expression in multiple arteries. Specifically, transcriptional profiles of feed arteries and second branch order arterioles in the soleus, gastrocnemius, and diaphragm muscles as well as aortic endothelial scrapes were examined from obese insulin-resistant Otsuka Long-Evans Tokushima Fatty rats treated with ( n = 9) or without ( n = 10) metformin from 20 to 32 weeks of age. Metformin-treated rats exhibited a reduction in body weight, adiposity, and HbA1c ( P < 0.05). The greatest number of differentially expressed genes (FDR < 15%) between those treated with and without metformin was found in the red gastrocnemius 2a arterioles (93 genes), followed by the diaphragm 2a arterioles (62 genes), and soleus 2a arterioles (15 genes). We also found that two genes were differentially expressed in aortic endothelial cells (LETMD1 and HMGCS2, both downregulated), one gene in the gastrocnemius feed artery (BLNK, downregulated), and no genes in the soleus and diaphragm feed arteries and white gastrocnemius 2a arterioles. No single gene was altered by metformin across all vessels examined. This study provides evidence that metformin treatment produces distinct gene expression effects throughout the arterial tree in a rat model of obesity and insulin resistance. Genes whose expression was modulated with metformin do not appear to have a clear connection with its known mechanisms of action. These findings support the notion that vascular gene regulation in response to oral pharmacological therapy, such as metformin, is vessel specific. Impact statement This study provides evidence that metformin treatment produces artery-specific gene expression effects. The genes whose expression was modulated with metformin do not appear to have a clear connection with its known mechanisms of action.

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An ever-increasing number of studies highlight the role of uncoupling protein 2 (UCP2) in a broad range of physiological and pathological processes. The knowledge of the molecular mechanisms of UCP2 regulation is becoming fundamental in both the comprehension of UCP2-related physiological events and the identification of novel therapeutic strategies based on UCP2 modulation. The study of UCP2 regulation is a fast-moving field. Recently, several research groups have made a great effort to thoroughly understand the various molecular mechanisms at the basis of UCP2 regulation. In this review, we describe novel findings concerning events that can occur in a concerted manner at various levels: Ucp2 gene mutation (single nucleotide polymorphisms), UCP2 mRNA and protein expression (transcriptional, translational, and protein turn-over regulation), UCP2 proton conductance (ligands and post-transcriptional modifications), and nutritional and pharmacological regulation of UCP2.

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Epithelial-mesenchymal transition (EMT) is a critical process for cancer metastasis and recurrence. Metformin, an effective oral antidiabetic drug, has been associated with decreased cancer risk and mortality. In this pilot study, we started to evaluate the effect of metformin on EMT in vivo and in vitro in endometrial cancer (EC).

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FOXO3a is a member of the forkhead O transcription factors. FOXO3a induces the factors that contribute to cell cycle arrest and is considered a tumor suppressor in several malignant tumors. Y-box binding protein-1 (YB-1) is a multifunctional protein whose high expression is correlated with poor prognoses in various malignant tumors. In the current study, we investigated the relationship between FOXO3a and YB-1 to validate their functional roles in prostate cancer.

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A total of 1,442 participants who successfully lost at least 3% of their baseline body weight after 12 months of participation in the randomized controlled Diabetes Prevention Program (DPP) continued in their assigned treatment group (metformin, intensive lifestyle, or placebo) and were followed into the Diabetes Prevention Program Outcome Study (DPPOS). Weight regain was defined as a return to baseline DPP body weight. Participant weight and antidepressant medication use were assessed every 6 months. Depression symptoms (Beck Depression Inventory [BDI] score ≥11) were assessed every 12 months.

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The effect of Fructus Mume formula and its separated prescription extract on insulin resistance in type 2 diabetic rats was investigated. The rat model of type 2 diabetes was established by feeding on a high-fat diet for 8 weeks and by subsequently intravenous injection of small doses of streptozotocin. Rats in treatment groups, including the Fructus Mume formula treatment group (FM), the cold property herbs of Fructus Mume formula treatment group (CFM), the warm property herbs of Fructus Mume formula treatment group (WFM), were administrated with Fructus Mume formula and its separated prescription extract by gavage, while the rats in diabetic model group (DM) and metformin group (MET) were given by gavage with normal saline and metformin correspondingly. The body weight before and after treatment was measured, and the oral glucose tolerance test (OGTT) and the insulin release test (IRT) were performed. The homeostasis model assessment-insulin resistance index (HOMA-IR) was calculated. The protein and mRNA expression levels of Insr, β-arrestin-2, Irs-1 and Glut-4 in the liver, skeletal muscle and fat tissues were detected by using Western blotting and RT-PCR respectively. The results demonstrated that, as compared with DM group, OGTT, IRT (0 h, 1 h) levels and HOMR-IR in treatment groups were all reduced, meanwhile their protein and mRNA expression levels of Insr, Irs-1 and Glut-4 in the liver, skeletal muscle and fat tissues were obviously increased, and their protein and mRNA expression levels of β-arrestin-2 in the liver and skeletal muscle tissues were also markedly increased. It was suggested that the Fructus Mume formula and its separated prescription extracts could effectively improve insulin resistance in type 2 diabetic rats, which might be related to the up-regulated expression of Insr, Irs-1 and Glut-4 in the liver, skeletal muscle and fat tissues, and β-arrestin-2 in the liver and skeletal muscle tissues.

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glucophage 750 mg 2015-05-26

Hepatocytes isolated from rat, mouse and human livers were treated with various concentrations of metformin. Isoform Mysoline Reviews -specific AMPKα abundance and activity, as well as intracellular adenine nucleotide levels and mitochondrial oxygen consumption rates were determined at different time points.

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In a population-based retrospective cohort study in Ontario Paxil 4 Mg from 2010 until 2012 involving adults aged 66 years and older, we studied those who were newly prescribed sitagliptin or an alternative hypoglycemic agent. Our primary outcome of interest was a hospital encounter (emergency department visit or hospital admission) with acute pancreatitis within 90 days. We used inverse probability of treatment weighting to balance the 2 groups and logistic regression with a robust variance estimate to calculate odds ratios (ORs) and 95% confidence intervals (CIs).

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A total of 13,702 patients were included in the study; median age 76 years, 42.5% males, 77.1% white. The most common anatomic site and stage at diagnosis were head of the pancreas (49.9%) and stage 4 (49.6%), respectively. Ninety-four percent of patients died in the follow-up period (median overall survival 5.3 mo). Multivariable Cox regression analysis showed that use of β-blockers, heparin, insulin, and warfarin were significantly associated with improved survival (P<0.05 for each one), whereas metformin, thiazolidinedione, statin, and combination Celexa Usual Dosage therapies were not.

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Co-presenting non-antibiotic drugs and pyrimidinethiol on gold nanoparticles (NPs) can generate broad-spectrum antibacterial and bactericidal activities against superbugs. Dimethylbiguanide (metformin), an anti-hyperglycemic drug, shows the best enhanced activity via increasing the ability to compromise bacterial cell walls. Synergistic effects are also reflected in the eradicating biofilm cells. Our findings suggest a large chemical space to develop new antibacterial materials Casodex Dosage to treat superbugs.

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Gestational diabetes mellitus (GDM) is associated with adverse pregnancy outcomes such as preeclampsia and macrosomia. Women with polycystic ovary syndrome (PCOS) are at increased risk of developing GDM. Today, GDM is diagnosed by oral glucose tolerance test (OGTT), a rather Best Luvox Dosage cumbersome test for the women and health care system. The objectives of this study were to investigate whether HbA1c in first trimester of pregnancy could be used as a screening test for GDM in first trimester and throughout pregnancy in order to reduce the number of OGTTs, and whether it could predict preeclampsia and macrosomia in women with PCOS.

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The ovulation rate did not differ between the groups (84.8% vs 87.7% between groups A and B, P=NS). Most of the women developed one follicle (91% in group A and 88.2% in group B, P=NS). The pregnancy rate in group A (46.4% per woman and 12.4% per ovulatory cycle) did not differ from that in group B (51.9% per woman and 13.2% per ovulatory cycle, P=NS). With regard to dosages, the ovulation rate in PCOS women without insulin resistance (IR) was significantly higher than those with IR. FI, Risperdal And Alcohol T and ADD were significantly decreased after 4 weeks of metformin in both groups.

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To determine whether metformin and/or pioglitazone are associated with a reduction in disease activity as measured by brain magnetic resonance imaging in patients with MS Hytrin Tablet 5mg and MetS and to evaluate the potential mechanisms underlying this anti-inflammatory effect.

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Sulfonylureas have been the preferred add-on therapy to metformin for T2DM, Abilify Generic Name but a study finds that DPP-4s have lower risks of death, CV events, and hypoglycemia.

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glucagon antagonism - potential side effects - type 2 diabetes mellitus.

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Phenformin, a metformin analogue, selectively induces apoptosis in LKB1-mutant NSCLC models.

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Aim of the Study was to investigate herb-drug interaction (HDI) of Ridayarishta formulation through human hepatic cytochrome P450 (CYP450) enzyme inhibition assay.