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Prandin (Repaglinide)
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Prandin

Prandin is an efficacious medical preparation in fight against type 2 diabetes. Prandin acts by controlling and decreasing glucose (sugar in blood).

Other names for this medication:

Similar Products:
Glucophage, Actos, Glucotrol, Avandia, Starlix, Metformin, Insulin aspart, Glipizide, Glimepiride, Januvia, Victoza, Pioglitazone, Glyburide, Tradjenta, Amaryl, Welchol, Lantus, Levemir, Onglyza, Sitagliptin, Farxiga, Humalog, Novolog, Bydureon, Glucotrol, Toujeo

 

Also known as:  Repaglinide.

Description

Prandin is created with extremely active ingredients with aim to make Prandin ideal remedy against type 2 diabetes. Target of Prandin is to control sugar level in blood.

Prandin acts by controlling and decreasing glucose (sugar in blood). You can use it in case exercise and diet does not help.

Prandin is also known as Repaglinide, Eurepa, GlucoNorm, NovoNorm, Rapilin.

Prandin is an oral anti-diabetic drug. It can be taken together with anti-diabetic medication as Glucophage.

Prandin is not taken to treat type 1 diabetes.

You can normally take insulin while using Prandin.

Dosage

It is better to take Prandin orally every day at the same time.

Usual Prandin dosage is 0.5mg - 4mg, which is taken 2-4 times a day before meal.

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

Overdose

If you overdose Prandin and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Prandin overdosage: troublesome, retching, flushing, migraine, short breath, weakness, sweating, coma, fainting, muscle pain, hunger, pain of stomach, tremors, extreme fatigue, dizziness, seizure, slow heartbeat, dyspepsia, feeling cold, lack of appetite, fast heartbeat.

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 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 Prandin 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 Prandin if you are allergic to Prandin components.

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

Prandin is not taken to treat type 1 diabetes.

You can normally take insulin while using Prandin.

Do not use Prandin in case of having type 1 diabetes, diabetic ketoacidosis, liver disease, poor adrenal, pituitary function.

Try to be careful with Prandin in case of using such medication as sulfa drugs (Gantanol); isoniazid; niacin (Nicobid); water pills (thiazide diuretics HydroDIURIL, Dyazide); beta blockers (blood pressure medications as Tenormin, Inderal); barbiturates (sedatives as Nembutal, Seconal); calcium channel blockers (blood pressure medications as Procardia, Cardizem); Rifampin (Rimactane, Rifadin); oral contraceptives; ketoconazole (Nizoral); chloramphenicol (Chloromycetin); nonsteroidal anti-inflammatory drugs (Voltaren, Motrin, Advil, Naprosyn); blood thinners (Miradon, Dicumarol); steroids as prednisone; furosemide as Lasix; clarithromycin as Biaxin; thyroid medications as Synthroid; phenytoin as Dilantin; Probenecid (ColBENEMID, Benemid); estrogens (Premarin); aspirin; erythromycin (PCE, Eryc, Ery-Tab); MAO inhibitors (antidepressants Parnate, Marplan, Nardil); glucose lowering agents (Micronase, Glucotrol); carbamazepine (Tegretol); major tranquilizers (Stelazine, Mellaril).

You can use Prandin in case exercise and diet does not help.

Prandin can be taken together with anti-diabetic medication as Glucophage.

Try to avoid unhealthy food.

Avoid consuming alcohol.

Do not stop taking Prandin suddenly.

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Repaglinide is a short-acting insulin secretagogue, which often results in considerable interindividual variability in therapeutic efficacy when widely used in a clinical setting. Among various reasons under discussion is genetic polymorphism, especially the genes related to insulin secretion and resistance. Recent studies have described the importance of PPARD in regulating the secretion and resistance of insulin. However, little is known about the impacts of PPARD genetic polymorphism on the efficacy of repaglinide. Therefore, the current study was designed to investigate the associations of PPARD rs2016520 polymorphism with type 2 diabetes mellitus (T2DM) susceptibility and repaglinide therapeutic efficacy in Chinese Han T2DM patients. A total of 338 T2DM patients and 200 healthy subjects were genotyped for PPARD rs2016520 polymorphism by polymerase chain reaction-restriction fragment length polymorphism assay. A total of 84 patients with the same genotypes of CYP2C8*3 139Arg and OATP1B1 521TT were randomized to orally take repaglinide for 8 weeks. Then the pharmacodynamic parameters of repaglinide and biochemical indicators were determined before and after repaglinide treatment. No significant difference was found in either allelic frequency (P = 0.298) or genotype distribution (P = 0.151) of PPARD rs2016520 between T2DM patients and healthy subjects. However, T2DM patients carrying genotype TC showed a significantly lower increase in postprandial serum insulin (mU/L) than those with wild-type TT (P < 0.05). These findings suggest that PPARD rs2016520 polymorphism might influence the therapeutic effect of repaglinide rather than T2DM susceptibility in Chinese Han T2DM patients.

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18F-labeled non-sulfonylurea hypoglycemic agent (S)-2-(2-[(18)F]fluoroethoxy)-4-((3-methyl-1-(2-piperidin-1-yl-phenyl)-butylcarbamoyl)-methyl)-benzoic acid ([(18)F]repaglinide), a derivative of the sulfonylurea-receptor (SUR) ligand repaglinide, was synthesized as a potential tracer for the non-invasive investigation of the sulfonylurea 1 receptor status of pancreatic beta-cells by positron emission tomography (PET) in the context of type 1 and type 2 diabetes. [(18)F]Repaglinide could be obtained in an overall radiochemical yield (RCY) of 20% after 135 min with a radiochemical purity higher than 98% applying the secondary labeling precursor 2-[(18)F]fluoroethyltosylate. Specific activity was in the range of 50-60 GBq/micromol. Labeling was conducted by exchanging the ethoxy-moiety into a 2-[(18)F]fluoroethoxy group. To characterize the properties of fluorinated repaglinide, the affinity of the analogous non-radioactive (19)F-compound for binding to the human SUR1 isoform was assessed. [(19)F]Repaglinide induced a complete monophasic inhibition curve with a Hill coefficient close to 1 (1.03) yielding a dissociation constant (K(D)) of 134 nM. Biological activity was proven via insulin secretion experiments on isolated rat islets and was comparable to that of repaglinide. Finally, biodistribution of [(18)F]repaglinide was investigated in rats by measuring the concentration of the compound in different organs after i.v. injection. Pancreatic tissue displayed a stable accumulation of approximately 0.12% of the injected dose from 10 min to 30 min p.i. 50% of the radioactive tracer could be displaced by additional injection of unlabeled repaglinide, indicating that [(18)F]repaglinide might be suitable for in vivo investigation with PET.

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Two authors independently extracted data and assessed trial quality.

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To compare the effects of treatment with repaglinide and glibenclamide on platelet function and endothelial markers in patients with Type 2 diabetes mellitus, before and after a standardized meal.

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Exaggerated postprandial glucose (PPG) excursions are associated with a derangement of both global, executive, and attention functioning. A tighter control of PPG may prevent cognitive decline in older diabetic individuals.

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Persons with Type 2 diabetes who were poorly controlled on oral therapy were randomly assigned to monotherapy with repaglinide or combination therapy with repaglinide plus metformin. Brachial artery flow-mediated vasodilation was assessed by ultrasonography at randomization and following 16 weeks of therapy. The primary outcome was change in brachial artery endothelial function from baseline. Comparison of randomized groups was a secondary aim.

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Insulin therapy safely reversed chronic weight loss in patients with CFRD FH-.

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Post-prandial hyperglycaemia, which occurs early in the development of impaired glucose tolerance and Type 2 diabetes mellitus (T2DM), has been receiving increased attention recently. Post-prandial hyperglycaemia is likely to promote or aggravate fasting hyperglycaemia and contributes entirely to HbA1c elevation, which is associated with microvascular and macrovascular complications in people with T2DM. Moreover, post-prandial hyperglycaemia is coupled with coagulation activation and may be associated with an increased risk of cardiovascular disease in people with or without diabetes. For these reasons, reduction of post-prandial hyperglycaemia is an important target in patients with impaired glucose tolerance or T2DM. Several treatments have therefore been developed to reduce post-prandial hyperglycaemia; of these, repaglinide, a prandial glucose regulator taken orally before each meal, is now available. Drugs that reduce post-prandial hyperglycaemia significantly also decrease HbA1c (up to 2% with repaglinide) and fasting glucose concentrations (up to 3.9 mmol/l with repaglinide), with consequent decreases in coagulation activation and, in some studies, post-prandial lipidaemia. In clinical trials in patients with T2DM, repaglinide significantly reduced 2-hr post-prandial glucose concentrations and significantly reduced the risk of hypoglycaemia, compared with sulphonylureas, especially when participants missed or postponed a meal. Treatment with the prandial glucose regulator repaglinide allows patients with T2DM to have a more flexible lifestyle, which is likely to improve their quality of life and compliance.

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Repaglinide is a prandial glucose regulator indicated for management of type 2 diabetes. This post-marketing study used the observational cohort technique of prescription-event monitoring (PEM) to monitor safety of repaglinide prescribed in primary care in England. Patients were identified from dispensed prescriptions issued by general practitioners (GPs) between December 1998 and January 2001. Demographic and clinical event data were collected from questionnaires posted to GPs at least six months after the date of first prescription for each patient. The cohort consisted of 5731 patients [median age 60 (IQR 51-68), 49.9% male]. Event incidence densities (IDs) [no. 1st reports/1000 patient-months of exposure] were calculated for all events reported. The most frequently recorded clinical events in the first month were diarrhoea (ID(1) 10.3), malaise/lassitude (ID(1) 8.1) and nausea/vomiting (ID(1) 7.9). The most frequently reported reason for stopping was 'not effective' (647), with the most common clinical reasons being diarrhoea (60), malaise/lassitude (55) and intolerance (54). One hundred and thirteen adverse drug reactions (ADRs) were reported, with the most frequently specified being diarrhoea (10), abdominal pain (10) and nausea/vomiting (9). We concluded that repaglinide is generally well tolerated when used in general practice in England and did not identify any serious unrecognised adverse events.

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This review has not found any significant conclusive evidence that long-acting insulins, short-acting insulins or oral hypoglycemic agents have a distinct advantage over one another in controlling hyperglycemia or clinical outcomes associated with cystic fibrosis-related diabetes. While some cystic fibrosis centers use oral medications to help control diabetes, the Cystic Fibrosis Foundation (USA) clinical practice guidelines support the use of insulin therapy and this remains the most widely-used treatment method. Randomized controlled trials specifically related to controlling diabetes with this impact on the course of pulmonary disease process in cystic fibrosis continue to be a high priority.There is no demonstrated advantage yet established for using oral hypoglycemic agents over insulin, and further studies need to be evaluated to establish whether there is clear benefit for using hypoglycemic agents. Agents that potentiate insulin action, especially agents with additional anti-inflammatory potential should be further investigated to see if there may be a clinical advantage to adding these medications to insulin as adjuvant therapy.

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In older patients with type 2 diabetes hospitalized for IHD, prior use of gliclazide, glyburide, or repaglinide appears to be associated with a similar risk of adverse cardiovascular sequelae.

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To compare the effect on glycemic control and weight gain of repaglinide versus metformin combined with bedtime NPH insulin in patients with type 2 diabetes.

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Coprescribing of clopidogrel and other drugs is common. Available reviews have addressed the drug-drug interactions (DDIs) when clopidogrel is as an object drug, or focused on combination use of clopidogrel and a special class of drugs. Clinicians may still be ignorant of those DDIs when clopidogrel is a precipitant drug, the factors determining the degree of DDIs, and corresponding risk management.

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Repaglinide and glibenclamide, respectively, were >or=30 and >or=1,000 times more potent in closing the pancreatic than the cardiovascular channels and they did not lead to complete inhibition of the myocardial channel. Binding assays showed that the selectivity of glibenclamide was essentially based on high affinity for the pancreatic SUR, whereas binding of repaglinide to the SUR subtypes was rather non-selective. After coexpression with Kir6.x to form the assembled channels, however, the affinity of the pancreatic channel for repaglinide was increased 130-fold, an effect much larger than with the cardiovascular channels. This selective effect of coexpression depended on the piperidino substituent in repaglinide.

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Patients were aged 68±10 years, 57.1% were males, Body Mass Index was 30±5 kg/m2, glycated hemoglobin 8±1%, systolic and diastolic blood pressure values were 138±15/80±9 mmHg. Serum creatinine was 1.03±0.35 mg/dL and GFR 71±21 mL/min/1.73 m2. In 504 patients (30%) GFR was lower than 60 mL/min/1.73 m2. The different treatment groups had different GFR and hypoglycaemic drugs were prescribed differently in the different K/DIGO stages. The majority of subjects in stage 3A and 3B were treated with repaglinide, however a significant percentage of them were treated with metformin and sulfonylureas. Nearly half of subjects with CKD stage 4 were treated with metformin and sulfonylureas.

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Hyperglycemia is a modifiable risk factor that has a deleterious effect on the development and progression of microvascular and macrovascular complications in patients with type 2 diabetes. The UK Prospective Diabetes Study revealed how reductions in hemoglobin A1c (HbA1c) correlate with a significant reduction in all-cause mortality and the incidence of myocardial infarction. The Diabetes Intervention Study showed that poor control of fasting glycemia does not increase the risk of myocardial infarction or mortality, whereas poor control of post-prandial glucose is associated with a high all-cause mortality rate. HbA1c is the standard measure for metabolic control and therapeutic efficacy, but does not reflect fluctuations in glycemic control. Plasma glucose concentrations in healthy subjects remain within a narrow range, which suggests that the fluctuations in glucose levels caused by inappropriate treatment may have negative consequences. These fluctuations have been associated with acute adverse effects (particularly excessive post-prandial hyperglycemia, pre-meal hypoglycemia and weight gain) that counteract the positive effect of lowering fasting plasma glucose and HbA1c. Post-prandial hyperglycemia and spikes also have deleterious effects on insulin secretion and sensitivity. Prandial oral antidiabetic agents such as alpha-glucosidase inhibitors (acarbose, miglitol) and rapidly acting insulin secretagogues (nateglinide, repaglinide) have recently been introduced to improve the control of post-prandial hyperglycemia.

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This study was designed to compare diurnal blood glucose excursions and the effects of accidental dietary noncompliance in type 2 diabetic patients who are well-controlled on either repaglinide or glyburide treatment.

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A total of 22 healthy young male participants were recruited from a pool of pharmacogenetically characterized participants genotyped for SLCO1B1, CYP3A4, and CYP2C8 SNPs by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Volunteers with CYP2C8*3 and CYP3A4*4 alleles were excluded from the clinical study. Then selected volunteers took part in the clinical pharmacokinetic study, receiving 2 mg repaglinide.

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CYP2C8 is an important member of the cytochrome P450 family of enzymes; it affects the activity of various drugs used in routine clinical practice, including amiodarone, chloroquine, amodiaquine, and repaglinide, as well as endogenous compounds, such as arachidonic acid and retonic acid. It is also the main enzyme involved in the metabolism of the widely used anticancer drug Paclitaxel, which has a very narrow therapeutic index. There is evidence that single nucleotide polymorphisms in the CYP2C8 gene influence the adverse reactions and/or the efficacy of drugs metabolized by this enzyme. We examined the allele and genotype frequencies of widely studied functional polymorphisms of the CYP2C8 gene in a North Indian population. We assayed the genomic DNA of at least 251 healthy unrelated North Indians for CYP2C8*2, CYP2C8*3 (G416A, A1196G), and CYP2C8*4 genetic polymorphisms by RFLP technique. These results were compared to information on other populations. The allelic frequencies of CYP2C8*2, CYP2C8*3, and CYP2C8*4 were found to be 3, 4, and 4% respectively. The two CYP2C8*3 polymorphisms (G416A and A1196G) were found to be completely linked to each other. Allele frequencies of CYP2C8 genetic variants in northern Indians were found to have a distinct pattern that differs from that of southern Indian and other global populations. This is the first report from North India on CYP2C8 polymorphisms. Ethnic differences with respect to polymorphisms are the molecular basis of interethnic variability in pharmacokinetics. Our study may help in rational use of drugs that are substrates for CYP2C8 in this population.

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The current study involves the development of oral bioadhesive hydrophilic matrices of repaglinide and the optimization of their in vitro drug release and ex vivo bioadhesion. A simplex lattice design was employed to systematically optimize the drug delivery containing two polymers and a filler. The proportions of polyethylene oxide (PEO), microcrystalline cellulose (MCC) and lactose were varied to be fitted in simplex lattice design. Mucoadhesion (M), drug release at 2 h (Q2) and drug release at 8 h (Q8) were taken as responses. Response surface plots were drawn and the optimum formulation was selected by desirability function. The criteria for optimized formulation were set for mucoadhesion as maximum, Q2 as 20% and Q8 as 80%. The formulations were also checked for their swelling index and showed good swelling characteristic. In vitro drug release study was carried out using simulated gastric fluid (SGF) pH 1.2. The experimental values of M, Q2 and Q8 for check point batch were found to be 0.211N, 21.87% and 80.86% respectively. The release profile indicated anomalous (non-Fickian) transport mechanism. The optimized formulation was further checked for its compatibility with other excipients by studying FTIR and DSC studies and they indicated the absence of any significant chemical interaction within drug and excipients.

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In the past few years, oral antihyperglycaemic agents have been considered as an alternative to insulin therapy in the treatment of gestational diabetes. There is still little information available on the safety of these drugs during pregnancy, but there have been several studies published regarding their use. Here we report on the case of a woman who took repaglinide up to the seventh week of pregnancy. Delivery occured with no complications and the newborn showed no malformations. Further studies are required to confirm the safety of repaglinide during pregnancy.

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A change in the function or expression of hepatic drug transporters may have significant effect on the efficacy or safety of orally administered drugs. Although a number of clinical drug-drug interactions associated with hepatic transport proteins have been reported, in practice it is not always straightforward to discriminate other pathways (e.g. drug metabolism) from being involved in these interactions. The present study was designed to assess the interactions between organic anion transporting polypeptide (Oatp) substrates (pravastatin or repaglinide) and inhibitors (spironolactone or diphenhydramine) in vivo in rats. The mechanisms behind the interactions were then investigated using in vitro tools (isolated hepatocytes and rat liver microsomes). The results showed a significant increase in the systemic exposures of pravastatin (2.5-fold increase in AUC) and repaglinide (1.8-fold increase in AUC) after co-administration of spironolactone to rats. Diphenhydramine increased the AUC of repaglinide by 1.4-fold. The in vivo interactions observed in rats between Oatp substrates and inhibitors may a priori be classified as transport-mediated drug-drug interactions. However, mechanistic studies performed in vitro using both isolated rat hepatocytes and rat liver microsomes showed that the interaction between pravastatin and spironolactone may be solely linked to the inhibition of pravastatin uptake in liver. On the contrary, the inhibition of cytochrome P450 seemed to be the reason for the interactions observed between repaglinide and spironolactone. Although the function and structure of transport proteins may vary between rats and humans, the approach used in the present study can be applied to humans and help to understand the role of drug transport and drug metabolism in a given drug-drug interaction. This is important to predict and mitigate the risk of drug-drug interactions for a candidate drug in pre-clinical development, it is also important for the optimal design of drug-drug interactions studies in the clinic.

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Pharmacokinetic profiles of single- and multiple-dose regimens of repaglinide were evaluated in 12 elderly subjects with type 2 diabetes. On day 1, following a 10-hour fast, subjects received a single 2-mg dose of repaglinide. Starting on day 2 and continuing for 7 days, each subject received a 2-mg dose of repaglinide 15 minutes before each of the three main meals. On day 9, subjects received a single 2-mg dose of repaglinide. Pharmacokinetic profiles, including area under the curve (AUC), log(AUC), maximal concentration (Cmax), log(Cmax), time to maximal concentration (Tmax), and half-life (T(1/2)), were determined at completion of the single- and multiple-dose regimens (days 1 and 9, respectively). Trough repaglinide values were collected on days 2 through 7. The mean log(AUC) values after multiple dosing were significantly higher than the values obtained after a single dose. The mean values for log(Cmax), and Tmax were comparable after each dosing regimen. The T(1/2) of repaglinide after multiple dosing was 1.7 hours. The trough values for repaglinide were low. No hypoglycemic events were reported. The pharmacokinetic profiles of repaglinide after single- and multiple-dose regimens were similar, and repaglinide was well tolerated by elderly subjects with type 2 diabetes.

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Genome-wide association studies (GWASs) identified that SLC30A8 genetic polymorphism was a risk of type 2 diabetes mellitus (T2DM) in several populations. This study aimed to investigate whether the SLC30A8 rs13266634 and rs16889462 polymorphisms were associated with T2DM susceptibility and repaglinide therapeutic efficacy in Chinese T2DM patients.

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In vitro data have recently suggested that sulfonylureas (SUs) enhance GH secretion by modulating the effects of GHRH and somatostatin in pituitary cells. The present study was undertaken to explore in more detail a possible influence of a single dose of SU (glibenclamide) and a non-SU (repaglinide) insulin secretagogue on circulating GH dynamics. Ten C-peptide-negative type 1 diabetic individuals were examined on three occasions in random order. Either glibenclamide (10.5 mg), repaglinide (8 mg), or placebo was administered after overnight normalization of plasma glucose by iv insulin infusion. Subsequently, GH concentrations were measured regularly after stimulation with GHRH (bolus 0.1 micro g/kg) alone and during concomitant infusion with somatostatin (7 ng.kg(-1).min(-1)). Insulin was replaced at baseline levels (0.25 mU.kg(-1).min(-1)) and plasma glucose clamped at 5-6 mmol/liter. Overall, there were no significant statistical differences in GH responses determined as either GH peak concentrations, integrated levels of GH, or secretory burst mass of GH during the experimental protocol. In contrast, plasma glucagon concentrations were significantly increased during glibenclamide and repaglinide exposure. The present experimental design does not support the hypothesis that acute administration of pharmacological doses of the oral antihyperglycemic agents glibenclamide and repaglinide per se enhance GH release in humans. Additionally, this study shows that these potassium channel inhibitors seem to stimulate glucagon secretion in people who have severe intraislet insulin deficiency (e.g. type 1 diabetes). However, extrapolation of our findings to type 2 diabetic individuals should be done with some caution.

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Of 20 drugs for which the DDD value has changed in the 5 year period, 5 were used in Rijeka hospital: erythropoietin parenteral, budesonide nasal spray, repaglinide oral, amoxicillin with clavulanic acid parenteral, and fentanyl transdermal. Graphs for individual drugs with the year by year method showed artificial jerks in the years proceeding the year of DDD change. Representation of total hospital consumption did not differ notably with the two methods.

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prandin renal dose 2017-12-22

Repaglinide reduced HbA(1c) by 1.25 and 1.07% in the post-prandial and pre-prandial groups, respectively (P for difference = 0.6), and achieved target buy prandin glucose levels in 80.7 and 66.7%, respectively (P = 0.16). The effect of titration strategy differed by baseline drug therapy, and was more effective in the metformin-treated individuals who experienced a HbA(1c) fall of 0.6 vs. 1.10% with pre-prandial vs. post-prandial titration (P for metformin-allocated group interaction = 0.043). The rate of hypoglycaemia did not differ by group.

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Cross- buy prandin sectional analysis.

prandin reviews 2017-06-06

A rapid, simple, and precise RPLC method was developed for the simultaneous determination of the widely used oral antidiabetic, metformin hydrochloride (MTF), with some commonly coadministered oral antidiabetics from different pharmacological classes-glipizide (GPZ), pioglitazone hydrochloride (PGZ), glimepiride (GLM), and repaglinide (RPG)-in bulk, laboratory-prepared mixtures and pharmaceutical formulations in the presence of metformin-reported impurity [1-cyanoguanidine (CNG)]. Chromatographic separation was achieved using isocratic buy prandin elution mode with a mobile phase of acetonitrile: 0.02 M potassium dihydrogen phosphate (pH 3.17; 50-50, v/v) flowing through a CN Phenomenex column (Phenosphere Next, 250 × 4.6 mm, 5 μm) at a rate of 1.5 mL/min at ambient temperature. UV detection was carried out at 220 nm. The method was validated according to International Conference on Harmonization guidelines. Linearity, accuracy, and precision were satisfactory for concentration ranges: 0.175-350 μg/mL for MTF, 0.0525-105 μg/mL for GPZ, 0.125-250 μg/mL for PGZ, and 0.05-100 μg/mL for GLM and RPG. Correlation coefficients were >0.99 for all analytes. LOQs were 0.009 μg/mL for MTF, 0.009 μg/mL for GPZ, 0.04 μg/mL for GLM, 0.124 μg/mL for PGZ, and 0.044 μg/mL for RPG. The developed method is specific, accurate, and suitable for the QC and routine analysis of the cited drugs in their pharmaceutical products.

prandin 5 mg 2016-03-20

Potentiometric and spectrophotometric titrations were used for the determination of ionization behaviour, lipophilicity and solubility profile of repaglinide. Acid-base equilibria were characterized by means of protonation macro- and microconstants using Target Factor Analysis of spectrophotometric data. Lipophilicity profiles were evaluated by determination of partition coefficients of neutral and ionized forms of repaglinide in biphasic octanol/water system. The intrinsic solubilities of repaglinide were determined from the solubility data and temperature dependence of intrinsic solubilities were evaluated using van't Hoff equation. Repaglinide possesses two protonation sites and in aqueous solutions exhibits ampholitic properties. At isoelectric pH the zwitterionic form of the molecule predominates over the uncharged form with the tautomeric ratio, logKz=1.9. The difference between calculated and measured logP values, as well as the difference between logP values of uncharged form of repaglinide, HR0, and either one of mono-charged forms indicated the significant partition of zwitterion into octanol. Temperature dependence of solubility data revealed buy prandin exothermic dissolution process with DeltasolH=-36 kJmol-1 and negative entropy of solution of DeltasolS=-0.19 kJK-1mol-1.

prandin dosing 2017-07-07

Dyslipidemia is common in patients with type 2 diabetes. Statins are used as the first choice in treatment of diabetic dyslipidemia. Atorvastatin represents a first-line treatment option, alongside other hydroxyl methylglutaryl coenzyme A reductase inhibitors. Repaglinide is a short-acting, oral, insulin secretagogue that is used in the buy prandin treatment of type 2 diabetes mellitus. Both the category of drugs undergo extensive metabolism with cytochrome enzyme system. This may lead to drug-drug interaction problems with altered repaglinide activity which is cautious. Repaglinide/atorvastatin/atorvastatin + repaglinide were administered orally to normal, diabetic rats, and to normal rabbits. Blood samples were collected at different time intervals and were analyzed for blood glucose by GOD-POD method using commercial glucose kits and repaglinide estimation in plasma by HPLC method. Diabetes was induced by alloxan 100 mg/kg body weight administered by I.P route. In the presence of atorvastatin, repaglinide activity was increased and maintained for longer period in diabetic rats compared with repaglinide matching control. The present study concludes co-administration of atorvastatin was found to improve repaglinide responses significantly in diabetic rats and improved glucose metabolism of atorvastatin played an important role and increased repaglinide levels by competitive CYP 3A4 enzyme inhibition by atorvastatin could be added advantage for anti hyperglycemic activity.

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ADA = antidiabetes agent BG = blood glucose CKD = chronic kidney disease DPP-4 = buy prandin dipeptidyl peptidase 4 eGFR = estimated glomerular filtration rate ESRD = end-stage renal disease GFR = glomerular filtration rate HD = hemodialysis NPH = neutral protamine Hagedorn PD = peritoneal dialysis SA = short acting SU = sulfonylurea.

prandin 3 mg 2016-03-16

End-of-treatment levels of haemoglobin A(1c) (HbA(1c)), fasting plasma glucose, mean of seven-point home-monitored plasma glucose and fasting levels of high-sensitivity C-reactive protein and adiponectin were not significantly different between treatments. However, body weight, waist circumference, fasting serum levels of insulin and C-peptide were lower and less number of patients experienced hypoglycaemia during treatment with metformin vs. repaglinide. Both drugs were well tolerated buy prandin .

prandin user reviews 2016-04-27

The objective of the present investigation was to evaluate gastro-retentive performance and pharmacokinetic parameters of optimized floating microspheres (RgFMCS4) consisting of (i) calcium silicate (CS) as porous carrier; (ii) repaglinide (Rg), an oral hypoglycemic agent; and (iii) Eudragit S (ES) as polymer. The optimized formulation demonstrated favorable in-vitro-floating and drug release characteristics. The gastro-retentive behavior of this optimized formulation was compared with non-floating microspheres (RgNFM) prepared from the identical polymer. Stability test of (99m)Tc-labeled formulations were carried out using appropriate standard buffer solutions of pH 2.0, 6.8 and 7.4. The organ distribution study was performed in albino rats in order to measure labeling efficiency of the formulation with (99m)Tc. The gamma scintigraphy of the formulations was carried out in albino rabbits to monitor the transit of RgFMCS4 and RgNFM buy prandin in the gastrointestinal (GI) tract. Prolonged gastric residence time (GRT) of over 6 h was achieved in all animals for calcium silicate based floating microspheres of Rg. Rg loaded optimized formulation was orally administered to albino rabbits and blood samples were used to determine pharmacokinetic parameters of Rg from floating microspheres, which were compared with pharmacokinetic parameters of the marketed tablet formulation. The relative bioavailability of Rg loaded floating microspheres was found to be increased about 3.17 times in comparison to that of the marketed tablet. The enhanced bioavailability and eliminated half-lives of Rg formulation observed in the present study are attributed to the floating nature of the designed formulations.

prandin tablet 2017-08-18

1. Liver distribution and systemic exposure of pravastatin were the determinant factors of efficacy and toxicity of pravastatin. Aim of the present study was to investigate the effect of paroxetine on the liver distribution and systemic exposure of pravastatin in diabetic rats induced by combining high fat diet (HFD) and low-dose streptozotocin (STZ). 2. Plasma concentrations and liver distribution of pravastatin were measured in the presence of paroxetine. Effect of paroxetine on pravastatin excretion via bile, intestine, feces and urine, as well as pravastatin absorption via intestine was documented. Freshly isolated hepatocytes and Caco-2 cells were used to investigate the effect of paroxetine on pravastatin transport. 3. Paroxetine increased the systemic exposure of pravastatin and decreased hepatic distribution of pravastatin in diabetic rats. In buy prandin vitro, paroxetine inhibited the hepatic uptake of pravastatin and promoted the efflux of pravastatin in freshly isolated hepatocytes, which may partly explain the decreased hepatic distribution of pravastatin by paroxetine. It was also observed that paroxetine promoted the absorption of pravastatin via jejunum and the uptake of pravastatin in Caco-2 cells. 4. We concluded that paroxetine increased the systemic exposure of pravastatin partly via promoting absorption via jejunum and inhibiting hepatic uptake of pravastatin.

prandin tablets generic 2015-11-02

Evidence obtained in the 1990's strongly supports the notion that glycaemic control is important not only in Type I (insulin-dependent), but also in Type II (non-insulin-dependent) diabetes mellitus. Although measurement of HbA(1c) is the standard for assessing the effect of glucose control in the occurrence and prevention of diabetic sequelae, more recent evidence indicates that other glucose parameters are also important. Postchallenge and postprandial hyperglycaemic peaks seem to be prospective determinants of vascular damage in early Type II diabetes. Currently, there is no overall accepted standard approach for the pharmacological management of Type II diabetes. The United Kingdom Prospective Diabetes Study has shown that reaching a near-normal glycaemic target is critically important and the pharmacotherapy of this progressive disease is difficult. Loss of endogenous insulin secretion has been substantiated to cause the progression of Type II diabetes in the United Kingdom Prospective Diabetes Study. Early insulinization, however, was not advantageous over other forms of therapy. The advent of polypharmacy in recent years has greatly strengthened the treatment of this disease. This synergy has been extended of late with the development of early-phase insulin secretion agents. buy prandin Two such agents, nateglinide and repaglinide, can be used to reduce mealtime glucose excursions and HbA(1c) as monotherapy, and in combination with metformin; their antidiabetic potential is similar to the combination treatment with glibenclamide and metformin. Additional substantiation of their long-term effect on improving life expectancy and reducing diabetic complications in Type II diabetic patients is now required.

prandin medication 2016-12-01

Thirty-two healthy volunteers with different SLCO1B1 genotypes ingested a 0.5-mg dose of repaglinide and 60-mg dose of nateglinide with a washout period of 1 week. Participants with SLCO1B1 c.521CC genotype (n = 4) had buy prandin a 59% (P = 0.001) or 72% (P < 0.001) greater mean area under the plasma repaglinide concentration-time curve (AUC(0-infinity)) than participants with c.521TC (n = 12) or c.521TT (n = 16) genotypes. The AUC(0-infinity) of repaglinide metabolites M2 and M4 were 112% (P = 0.004) and 81% (P = 0.002) larger in participants with c.521CC genotype than in those with c.521TT genotype, but no differences existed in the pharmacokinetics of M1. Maximum decrease in blood glucose concentration correlated with repaglinide AUC(0-infinity) (r = 0.412, P = 0.019). SLCO1B1 polymorphism had no significant effect on the pharmacokinetics or pharmacodynamics of nateglinide or its M7 metabolite. Thus, in contrast to repaglinide, the disposition of nateglinide is unaffected by the SLCO1B1 c.521T>C polymorphism.

prandin drugs 2017-08-09

Patient perceptions of prandial oral therapy with repaglinide were predominantly positive, due mostly to the perception that glucose buy prandin control was achieved, with minimal perception of any increase in hypoglycemic episodes.

prandin generic launch 2016-06-01

Type 2 diabetes is a progressive disease associated with high levels of morbidity and mortality and for which there is both a large and growing prevalence worldwide. Lifestyle advice plus metformin is commonly recommended initially Eldepryl Drug Classification to manage hyperglycemia and to minimize the risk of vascular complications. However, additional agents are required when glycemic targets cannot be achieved or maintained due to the progressive nature of the disease. Repaglinide/metformin fixed-dose combination (FDC) therapy (PrandiMet(®); Novo Nordisk, Bagsværd, Denmark) has been approved for use in the USA. This FDC is a rational second-line therapy given the complementary mechanisms of action of the components. Repaglinide is a rapidly absorbed, short-acting insulin secretagogue targeting postprandial glucose excursions; metformin is an insulin sensitizer with a longer duration of action that principally regulates basal glucose levels. A pivotal, 26-week, randomized study with repaglinide/metformin FDC therapy has been conducted in patients experiencing suboptimal control with previous oral antidiabetes therapy. Repaglinide/metformin FDC improved glycemic control and weight neutrality without adverse effects on lipid profiles. There were no major hypoglycemic episodes and patients expressed greater satisfaction with repaglinide/metformin FDC than previous treatments. Repaglinide/metformin FDC is expected to be more convenient than individual tablets for patients taking repaglinide and metformin in loose combination, and it is expected to improve glycemic control in patients for whom meglitinide or metformin monotherapies provide inadequate control.

prandin generic name 2016-04-23

Treating patients with diabetes is one of the most challenging and important activities a physician (primary care physician or specialist) can undertake. A key to successful therapy for type 2 diabetes is the insight that this condition is progressive and that the need for additional agents over time is normative. The ability to individualize therapy by patient and medication characteristics comes from experience and knowledge of pertinent clinical studies. However, guidelines from expert bodies such as the American Diabetes Association/European Association for the Study of Diabetes and American Oxytrol Dosage Association of Clinical Endocrinologists/American College of Endocrinology can help clinicians of all levels of expertise to approach therapy choices more rationally. There is unity across these guidelines about the role and benefits of metformin as first-line pharmacological treatment, probability of good efficacy, low risk of hypoglycemia, modest weight loss, and overall long-term data. Unfortunately, this unity does not extend to recommendations for subsequent pharmacological agents and their use in combination to intensify treatment when insulin is not (yet) appropriate. Across both statements, some drug classes seem more prominent, and looking at their benefit-risk profile, it is clear why this is the case. The most profound recent change in diabetes therapy has been the introduction of incretin therapies. Incretin therapies minimize 2 important adverse effects seen with many other therapies: hypoglycemia and weight gain. These agents have increased the range of options available for early intensification of treatment of type 2 diabetes. In combination with more established therapies, there are more opportunities than ever to accommodate patient preferences while improving glycemic control and harnessing extraglycemic benefits of a second (or third) agent.

prandin drug interactions 2016-03-17

In this study, the development and validation of a high-performance liquid chromatography (HPLC) assay for determination of repaglinide concentration in human plasma for pharmacokinetic studies is described. Singulair 5mg Tablet Plasma samples containing repaglinide and an internal standard, indomethacin were extracted with ethylacetate at pH 7.4. The recovery of repaglinide was 92%+/-55.31. Chromatographic separations were performed on Purospher STAR C-18 analytical column (4.8 mm x 150 mm; 5 microm particle size). The mobile phase composed of acetonitrile-ammonium formate (pH 2.7; 0.01 M) (60:40, v/v). The flow rate was 1 ml/min. The retention time for repaglinide and indomethacin were approximately 6.2 and 5.3 min, respectively. Calibration curves of repaglinide were linear in the concentration range of 20-200 ng/ml in plasma. The limits of detection and quantification were 10 ng/ml and 20 ng/ml, respectively. The inter-day precision was from 5.21 to 11.84% and the intra-day precision ranged from 3.90 to 6.67%. The inter-day accuracy ranged 89.95 to 105.75% and intra-day accuracy ranged from 92.37 to 104.66%. This method was applied to determine repaglinide concentration in human plasma samples for a pharmacokinetic study.

prandin dose range 2015-01-08

1. In order to evaluate the inhibition activity of 1-aminobenzotriazole (ABT) and (-)-borneol (borneol) against cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT), the substrates of these metabolic enzymes were incubated with ABT and borneol in human hepatocytes. We found that 3 mM ABT and 300 μM borneol Biaxin Medicine were the most suitable experimental levels to specifically inhibit CYP and UGT. 2. Montelukast, mefenamic acid, flufenamic acid, diclofenac, tienilic acid, gemfibrozil, ibufenac and repaglinide were markedly metabolized in human hepatocytes, and the metabolism of gemfibrozil, mefenamic acid and flufenamic acid was inhibited by borneol. With regard to repaglinide, montelukast, diclofenac and tienilic acid, metabolism was inhibited by ABT. Ibufenac was partly inhibited by both inhibitors. Zomepirac, tolmetin, ibuprofen, indomethacin and levofloxacin were moderately metabolized by human hepatocytes, and the metabolism of zomepirac, ibuprofen and indomethacin was equally inhibited by both ABT and borneol. The metabolism of tolmetin was strongly inhibited by ABT, and was also inhibited weakly by borneol. Residual drugs, telmisartan, valsartan, furosemide, naproxen and probenecid were scarcely metabolized. 3. Although we attempted to predict the toxicological risks of drugs containing carboxylic groups from the combination chemical stability and CLint via UGT, the results indicated that this combination was not sufficient and that clinical daily dose is important.

prandin generic cost 2015-10-30

When repaglinide was given, together with the last rifampicin dose, on day 7, an almost 50% reduction of the median repaglinide area under the plasma concentration-time curve (AUC) was observed. Neither the peak plasma concentration (C(max)), time to reach Feldene Gel Dosage C(max) (t(max)) nor terminal half-life (t(1/2)) was statistically significantly affected. When repaglinide was given on day 8, 24 h after the last rifampicin dose, an almost 80% reduction of the median repaglinide AUC was observed. The median C(max) was now statistically significantly reduced from 35 ng/ml to 7.5 ng/ml. Neither t(max) nor t(1/2) was significantly affected.

prandin diabetes medicine 2017-11-18

Anthropometric measurements and fasting plasma glucose (FPG), postprandial plasma glucose Strattera 80mg Tablet , hemoglobin A1c , fasting serum insulin (FINS), postprandial serum insulin, homeostasis model assessment for insulin resistance (HOMA-IR), triglyceride, total cholesterol, low-density lipoprotein-cholesterol, and high-density lipoprotein-cholesterol tests were obtained before and after repaglinide treatment. The risk C allelic frequency of NOS1AP rs12742393 was higher in patients with T2DM than in healthy volunteers (p<0.001). Patients with T2DM and genotypes AA and AC at NOS1AP rs12742393 had a significant reduction in FPG (mmol/l) compared with those with genotype CC (p<0.01). Patients with CC homozygotes and AC heterozygotes had a greater increase in FINS (mU/l) than those with wild-type AA (p<0.05). In addition, the carriers of genotype CC at NOS1AP rs12742393 had higher differential values of HOMA-IR compared with genotypes AC and AA carriers (p<0.001). The effects of repaglinide treatment on FPG (p<0.01), FINS (p<0.05) and HOMA-IR (p<0.001) were reduced in patients with T2DM carrying the NOS1AP rs12742393 risk C allele compared with the AA genotype carriers.

dose of prandin 2015-12-29

Treatment with repaglinide significantly improved glycemic control with respect to baseline and placebo, reducing HbA1c by 1.14% from Voltaren 400 Mg baseline and fasting plasma glucose by 1.8 mmol/l. Improvement in glycemic control was independent of the meal pattern adopted by patients, including those most commonly taking two or four meals daily, with no correlation between meal pattern and risk of hypoglycemia. The improvement in glycemic control was also independent of degree of obesity and age < or =65 or >65 years. There was no significant body weight increase in the repaglinide group.

prandin e gel 2016-06-24

Drug-drug interactions with insulin secretagogues are associated with increased risk of serious hypoglycemia in patients with type Risperdal Reviews Schizophrenia 2 diabetes. We aimed to systematically screen for drugs that interact with the five most commonly used secretagogues-glipizide, glyburide, glimepiride, repaglinide, and nateglinide-to cause serious hypoglycemia.

prandin tab 2015-07-05

Observational and multicentre study in 14 Cymbalta 300 Mg nursing homes in Cádiz (Spain).

prandin repaglinide tablets 2015-08-07

When rifampicin and repaglinide are administered concomitantly, rifampicin seems to act as both an inducer and an inhibitor of the metabolism of repaglinide. After discontinuing rifampicin administration, while the inductive effect on CYP3A4 and probably also CYP2C8 is still present, an even more marked reduction in the plasma concentration of repaglinide was observed. Our results suggest that concomitant administration of rifampicin and repaglinide may cause a Paxil High Dose clinically relevant decrease in the glucose-lowering effect of repaglinide, in particular when rifampicin treatment is discontinued or if the drugs are not administered simultaneously or within a few hours of each other.

prandin dosage diabetes 2015-09-12

Glycaemic normalisation improved skin microcirculation but not endothelial function in patients with type 2 Requip Maximum Dosage diabetes with mild cardiovascular engagement.

prandin diabetes medication 2016-09-24

The ability of Gelucire 50/13 to nanosize various solid lipids was evaluated. The ability of Gelucire 50/13 to yield NLC was evaluated by using Precirol ATO 5 as a model solid lipid and various liquid lipids (oils). Gelucire 50/13 based NLC (GeluPearl) were evaluated for their ability to improve the efficacy Tegretol Medicine of RPG on oral administration in comparison to RPG tablets. The short term stability of RPG-GeluPearl was evaluated at 25 °C/60% RH.

prandin gel 2015-01-11

Metformin did not inhibit the uptake of OATP and OCT1 substrates. However, OATP-mediated BSP and pravastatin uptake and OCT1-mediated MPP(+) and metformin uptake were significantly inhibited by repaglinide (half-maximal inhibitory concentration [IC(50)] 1.6-5.6 micromol/l) and rosiglitazone (IC(50) 5.2-30.4 micromol/l).

prandin max dose 2017-07-25

The NeuroD1/BETA2 and PAX4 polymorphisms were substantially associated with plasma glucose level after repaglinide monotherapy.

prandin cost 2017-03-07

OLETF (Otsuka Long-Evans Tokushima Fatty) rats are characterized by obesity-related insulin resistance, which is a phenotype of type 2 diabetes. Sulfonylurea drugs or benzoic acid derivatives as inhibitors of the ATP-sensitive potassium (K(ATP)) channel are commercially available to treat diabetes. The present study compared sulfonylurea drugs (glimepiride and gliclazide) with one of benzoic acid derivatives (repaglinide) in regard to their long-term effect on ameliorating insulin sensitivity in OLETF rats. Each drug was dissolved and fed with drinking water from 29 weeks of age. On high glucose loading at 45 weeks of age, response of blood glucose recovery was the greatest in the group treated with glimepiride. On immunohistochemistry analysis for the Kir6.2 subunit of K(ATP) channels, insulin receptor beta-subunits, and glucose transporters (GLUT) type 2 and 4 in liver, fat and skeletal muscle tissues, the sulfonylurea drugs (glimepiride and gliclazide) were more effective than repaglinide in recovery from their decreased expressions in OLETF rats. From these results, it seems to be plausible that K(ATP)-channel inhibitors containing sulfonylurea moiety may be much more effective in reducing insulin resistance than those with benzoic acid moiety. In contrast to gliclazide, non-tissue selectivity of glimepiride on K(ATP) channel inhibition may further strengthen an amelioration of insulin sensitivity unless considering other side effects.

prandin generic 2015-04-26

Cerebral insulin can regulate glucose homeostasis via activation of the parasympathetic nervous system, which results in the reduction of hepatic glucose output. However, the precise mechanism(s) through which cerebral insulin directly exerts an effect on insulin secretion remains unclear. In the present study, we found that cerebral administration of insulin caused an increase of plasma insulin concentration and a concomitant decrease in plasma glucose levels within one hour. These effects were blocked by vagotomy or intraperitoneal injection of 1,1-dimethyl-4-diphenylacetoxypiperidinium iodide, a specific M (3) antagonist. The mediating influence of parasympathetic activation can thus be considered. The adenosine triphosphate-sensitive potassium (K-ATP) channel is a key mediator of the cerebral action of insulin. The plasma glucose-lowering action of insulin was abolished by cerebral administration of glibenclamide or repaglinide at concentrations sufficient to block K-ATP channels. In conclusion, our findings suggest that cerebral insulin may induce insulin release by stimulating the opening of K-ATP channels, which in turn activate parasympathetic tone in pancreatic tissue.

prandin drug 2017-04-27

Nowadays, diabetes mellitus (DM) and hypertension are considered as the most common causes of end-stage renal disease (ESRD). In this paper, other than presenting the role of DM in ESRD, glucose metabolism and the management of hyperglycemia in these patients are reviewed. Although in several large studies there was no significant relationship found between tight glycemic control and the survival of ESRD patients, it is recommended that glycemic control be considered as the main therapeutic goal in the treatment of these patients to prevent damage to other organs. Glycemic control is perfect when fasting blood sugar is less than 140 mg/dL, 1-h postprandial blood glucose is less than 200 mg/dL, and glycosylated hemoglobin (HbA1c) is 6-7 in patients with type 1 diabetes and 7-8 in patients with type 2 diabetes. Administration of metformin should be avoided in chronic renal failure (CRF) because of lactic acidosis, the potentially fatal complication of metformin, but glipizide and repaglinide seem to be good choices.