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Starlix (Nateglinide)
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Starlix

Starlix is used for lowering blood sugar levels in patients with type 2 diabetes. It is used along with diet and exercise. It may also be used for other conditions.

Other names for this medication:

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Also known as:  Nateglinide.

Description

Starlix is used for lowering blood sugar levels in patients with type 2 diabetes. It is used along with diet and exercise. It may also be used for other conditions.

Starlix is an antidiabetic agent. It works by lowering blood glucose levels, causing insulin to be released from beta cells of the pancreas.

Starlix is also known as Nateglinide, Fastic, Glinate, Glunat, Starsis, Trazec.

Dosage

Take Starlix by mouth 1 to 30 minutes before meals. If you skip a meal, you must also skip your scheduled dose to avoid the risk of low blood sugar levels (hypoglycemia).

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

Overdose

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

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture 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 Starlix 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 Starlix if you are allergic to its components.

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

Do not take Starlix if you have type 1 diabetes.

Do not take Starlix if you have diabetic ketoacidosis.

Be careful with Starlix if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Starlix if you have allergies to medicines, foods, or other substances.

Be careful with Starlix if you have adrenocortical, pituitary, liver, or kidney problems

Be careful with Starlix if you have a high fever or are malnourished.

Be careful with Starlix if you are taking beta-adrenergic blockers (eg, metoprolol), gemfibrozil, imidazoles (eg, ketoconazole), monoamine oxidase inhibitors (MAOIs) (eg, phenelzine), nonsteroidal anti-inflammatory drugs (NSAIDs) (eg, ibuprofen), or salicylates (eg, aspirin) because the risk of low blood sugar may be increased; corticosteroids (eg, prednisone), rifampin, sympathomimetics (eg, pseudoephedrine), thiazides (eg, hydrochlorothiazide), or thyroid hormones (eg, levothyroxine) because they may decrease Starlix 's effectiveness

Avoid alcohol.

Do not stop taking Starlix suddenly.

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The aim of this work was to assess the efficacy and tolerability of nateglinide alone or in combination with metformin in elderly patients with type 2 diabetes (T2DM).

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Predictors of incident AF were analyzed in 8,943 patients without AF at baseline by Cox proportional hazards regression. Study treatments (valsartan vs no valsartan and nateglinide vs no nateglinide) and the time-dependent covariate for progression to type 2 diabetes mellitus were added separately to the model.

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A micellar chromatographic method has been developed and validated for simultaneous separation and determination of metformin(MF), nateglinide (NT) and gliclazide (GL). The separation was carried out using a Nucleosil C18 column, 150 mm × 4.6 mm i.d., 5 μm particle size, using micellar mobile phase consisting of sodium dodecyl sulphate (SDS), n-propanol with UV detection. The optimum conditions for the simultaneous separation of the three drugs were 0.12 M SDS, 10% (v/v) n-popanol, 0.3% triethylamine adjusted to pH5.6 with a flow rate of 1 ml.min(-1) and detection at 254 nm. The limit of detection (LOD) of MF, NT, GL were 0.047, 0.00115, 0.036 μg.mL(-1) respectively. The method showed good linearity in the ranges of 0.4-16 μg.mL(-1), (r(2)=0.999), 0.8-16 μg.ml(-1) (r(2)=0.999) and 1-40 μg.ml(-1) (r(2)=0.999) for MF, NT, GL respectively. The suggested method was successfully applied for the analysis of the three antidiabetic drugs in pharmaceutical preparations with average recoveries of 99.66%, 100.08% and 100.31% for MT, NT and GL respectively. The results obtained were in good agreement with those obtained from comparison methods. The method was validated regarding accuracy and precision.

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To investigate this, a meal was given to 15 T2D (age 52 +/- 2 years, BMI 25 +/- 0.8 kg m(-2)) on three different occasions: (1) without treatment, (2) after 120 mg of nateglinide before the meal (acute treatment), and (3) after 3 months of nateglinide (120 mg t.i.d., chronic treatment). Fifteen healthy subjects (CON, age 48 +/- 2 years, BMI 24 +/- 0.5 kg m(-2)) were also studied. Blood was withdrawn for 360 min from veins draining the anterior abdominal subcutaneous adipose tissue (AD) and from an arterialized hand vein. Blood flow (BF) in AD was measured with (133)Xe. Lipoprotein lipase activity (LPL) was calculated as the triacylglycerol (TAG) flux across AD, and hormone-sensitive lipase (HSL) as the glycerol flux minus LPL.

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The administration of A-4166 results in increased serum insulin and decreased serum glucose level in all rats irrespective of the diet. A significant diminution of serum NEFA levels was observed in A-4166 administered Wistar and HTG rats fed high fat diet. In both groups of rats fed basal diet the lipolysis was not affected by A-4166. However, a decrease of lipolysis was found after A-4166 in Wistar rats fed high fat diet. The stimulation of lipolysis by norepinephrine was not influenced by A-4166. A lowered basal lipolysis was found in HTG rats fed high fat diet. The stimulation of lipolysis by norepinephrine was diminished in HTG rats as compared to Wistar animals. Administration of A-4166 did not affect the stimulation of lipolysis by norepinephrine in HTG rats. A decrease of stimulatory action of insulin on lipogenesis was found in Wistar rats fed high fat diet and in all groups of HTG rats. The administration of A-4166 did not change the basal lipogenesis and also the effect of insulin on lipogenesis.

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The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, interactions, and dosage of nateglinide are reviewed. Nateglinide is an oral hypoglycemic agent approved for use alone or in combination with metformin as an adjunct to diet and exercise for the treatment of type 2 diabetes mellitus. Nateglinide, an amino acid derivative of D-phenylalanine, stimulates the secretion of insulin by binding to the ATP potassium channels in pancreatic beta cells. The result is an increase in beta-cell calcium influx, which leads to rapid, short-lived insulin release. The drug is rapidly and completely absorbed in the small intestine. The estimated bioavailability is 72%. Nateglinide is highly bound to plasma proteins, is metabolized extensively by the liver, and has an elimination half-life of 1.4 hours. Several clinical trials of nateglinide, alone and in combination with other oral hypoglycemic agents, have found the drug to be safe, effective, and well tolerated. The most common adverse effects are nausea, diarrhea, dizziness, and lightheadedness. There is a potential for interactions between nateglinide and medications affected by the cytochrome P-450 isoenzyme system. Dosage regimens ranging from 60 to 240 mg have been evaluated. The maximum effective dosage is 120 mg taken 10 minutes before meals three times a day. Nateglinide is an alternative to second-generation sulfonylureas for the treatment of type 2 diabetes mellitus. Additional comparative trials are needed to fully elucidate nateglinide's role.

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As newer oral diabetes agents continue to emerge on the market, comparative evidence is urgently required to guide appropriate therapy.

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Anti-diabetics such as sulfonylurea and thiazolidinedione derivatives are hypoglycemic drugs used for the treatment of diabetes. However, they can also be used as a stopper in horseracing. This paper describes a convenient method for the separation and simultaneous detection of 10 anti-diabetic drugs (namely glipizide, glibenclamide, glimepiride, gliclazide, tolazamide, tolbutamide, nateglinide, repaglinide, rosiglitazone and pioglitazone) in equine plasma and urine by LC-MS-MS.

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The prevalence of diabetes is increasing in epidemic proportion worldwide. Because of the morbidity and mortality associated with the disease, it is becoming a major burden for the health care system. With a better understanding of the pathogenesis of type 2 diabetes, the concept of primary prevention has emerged. A number of studies demonstrated that both lifestyle modification program and pharmacological interventions in subjects with impaired glucose tolerance (IGT) can prevent or delay the progression to diabetes. The Diabetes Prevention Study (DPS) and the Diabetes Prevention Program (DPP) convincingly showed that an intensive lifestyle modification program is highly effective in decreasing the risk of diabetes in a high risk population (risk reduction of 58%). Four other smaller studies have made similar observations. The DPP study showed that metformin can reduced the risk of diabetes by 31% in subjects with IGT. The STOP-NIDDM trial confirmed the efficacy of acarbose in decreasing the risk of diabetes by 36% in similar high risk population. The TRIPOD study showed that troglitazone can reduce the incidence of diabetes by 55% in Hispanic women with a history of gestational diabetes. And more recently, the XENDOS study showed that in very obese population on intensive lifestyle modification program, xenical treatment was associated with a 37% reduced incidence of diabetes compared to placebo. Three studies suggested that bariatric surgery in morbidly obese subjects with or without IGT can reduce the incidence of diabetes to near zero. Eight of 10 studies showed that treatment with inhibitors of the renin-angiotensin aldosterone system in high risk population for cardiovascular disease (CVD) were associated with a significant reduction in the subsequent development of diabetes as a secondary outcome. The WOSCOPS study and the HERS study examined the effect of pravastatin and estrogen/progestin respectively on cardiovascular events and observed that these pharmacological interventions were associated with a 30% and 35% reduction in the incidence of diabetes as secondary outcome. There are 3 major trials currently in progress examining the effect of rosiglitazone/ramipril (the DREAM study), nateglinide/valsartan (the NAVIGATOR study) and pioglitazone (the ACT NOW study) on the development of diabetes in IGT subjects as a primary outcome. We also have 3 studies studying the prevention of diabetes as secondary outcomes: the ONTARGET-TRANSCEND study examining telmisartan with or without ramipril, and the ORIGIN study testing glargine insulin/omega 3. The evidence is overwelming-diabetes can be prevented or delayed in high risk population through lifestyle modification or pharmacological interventions. This new information now has to be translated in the real world into well defined strategies for screening and treating high risk population. Prevention of the disease is our only chance to alleviate the ever growing burden of diabetes mellitus in the world.

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Postprandial hyperglycemia (PPHG) frequently occurs among renal transplant recipients (RTR). Reduced early insulin response (EIR) after a meal leads to impaired suppression of endogenous glucose production and subsequently PPHG, which is a risk factor for cardiovascular disease. Nateglinide is a rapid acting insulin secretagogue inducing an EIR after a meal. Our main objective was to investigate the safety and effect of nateglinide treatment on postprandial plasma glucose excursions and insulin secretion in RTR with PPHG.

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This study illustrates the use of an efficiency model that focuses directly on the relevant short-term end point: glycemic control. Starting patients with nateglinide is shown to be an efficient way of obtaining dual glycemic control during the first 3 years of treatment.

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The aim of this study was to clarify the role of an early insulin secretion in postprandial hyperglycaemia and hyperlipidaemia; a study using spontaneously type 2 diabetic Otsuka Long-Evans Tokushima Fatty rats with visceral obesity was performed to investigate the acute effect of nateglinide (NAT) vs. glibenclamide (GB) on increases in glucose after glucose loading and on increases in triglyceride (TG) after fat loading.

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PROSPERO CRD42014010567.

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Meglitinides are limited by their cost, frequency of administration, and minimal available data assessing clinical impact; however, mitiglinide shows selective action on the pancreatic β-cells, has greater affinity for β-cells, and limited metabolism when compared to other meglitinides. These properties may allow more utility in patients with chronic kidney disease or at high risk of hypoglycemia. The primary role in therapy for mitiglinide is the treatment of elevated postprandial glucose in patients with T2DM.

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MBF at rest and during adenosine did not change during the study. The percentage of flow increase from rest during cold pressor test did not improve significantly in the nateglinide group vs. placebo (from 26.1 +/- 37.2% to 29.1 +/- 27.8% between week 0 to week 16 for nateglinide vs. 14.9 +/- 37.1% to 18.1 +/- 28.4% for placebo; P = 0.07 for nateglinide when adjusted for higher baseline values). Nateglinide decreased HbA1c by 0.4% (from 7.6 +/- 0.9% to 7.2 +/- 1.3%) compared to an increase of 0.5% in the placebo group (from 7.9 +/- 0.8% to 8.4 +/- 1.7%; P = 0.02 for nateglinide). No differences between the two groups were observed in insulin levels and lipid status.

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In patients receiving initial CT, HbA(1c) decreased substantially (Delta = -1.6 +/- 0.1%, p < 0.0001 vs. baseline or placebo) from a mean baseline of 8.2 +/- 0.1%, an effect significantly greater than the 0.8% reduction observed with both monotherapies (p < 0.001); whereas, in placebo-treated patients, HbA(1c) increased modestly (Delta = +0.3 +/- 0.1%, p < 0.05) from an identical baseline value. Seventy percent of CT-treated patients achieved a target HbA(1c) of < 7.0%. Both fasting plasma glucose (FPG) and the 2-hour postprandial glucose excursion (PPGE) after a liquid meal challenge decreased by 2.3 mmol/L in patients receiving CT, while the changes from baseline values in FPG and PPGE were +0.2 +/- 0.3 mmol/L and -0.5 +/- 0.2 mmol/L, respectively, in placebo-treated patients. The incremental 30-minute post-load insulin levels increased by 88 +/- 32 pmol/L (p = 0.006) in patients receiving CT and did not change significantly in placebo-treated patients. patients receiving CT (vs. 27.9% in the metformin monotherapy, and 14.4% in the placebo groups). Confirmed hypoglycemia (glucose

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The anti-diabetics were isolated from equine plasma and urine by liquid-liquid extraction with 1,2-dichloroethane at acidic pH, and analysed by LC-MS-MS in the positive electrospray ionisation mode. Separation of 10 anti-diabetic drugs was achieved with a reversed phase C8 column using a mixture of aqueous ammonium formate (pH 3.0, 10 mM) and methanol as the mobile phase.

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Male GK rats and normal Wistar rats were used in this study, GK rats fed twice daily were given TLFA (300 mg/kg) or nateglinide (50mg/kg) orally before each meal for 12 weeks. Besides common evaluation indexes of hypoglycemic activity such as blood glucose level, oral glucose tolerance test (OGTT), glycated hemoglobin, as well as lipid metabolism parameters such as cholesterol (CHOL), triglycerides (TG), et al., in rat serum. The effects of TLFA on insulin secretion and pancreas tissue sections, the levels of serum glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), and the α-glucosidase inhibitory activity of TLFA in vitro were investigated.

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This multicenter, double-blind, randomized, parallel-group, fixed-dose study of 8 weeks' duration was performed in a total of 288 subjects with IGT using a 2:2:2:1 randomization. Subjects received nateglinide (30, 60, and 120 mg) or placebo before each main meal. Metabolic effectiveness was assessed during a standardized meal challenge performed before and after the 8-week treatment. All adverse events (AEs) were recorded, and confirmed hypoglycemia was defined as symptoms accompanied by a self-monitoring of blood glucose measurement < or =3.3 mmol/l (plasma glucose < or =3.7 mmol/l).

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Nateglinide and mitiglinide are immediate short-acting insulinotropic agents. Both are administered preprandially to control postprandial hyperglycemia. Glinide drugs are characterized by immediate onset as well as rapid disappearance of effect as compared with sulfonylurea drugs. We examined the rapidity of onset of the therapeutic effect between nateglinide and mitiglinide by pharmacokinetic/pharmacodynamic analysis using the receptor-binding-dissociation model in rats. Nateglinide or mitiglinide was administered orally or intravenously to rats and blood samples were collected at various time-points post administration. The plasma concentrations of the unbound drug forms and the blood glucose were measured. When the simultaneous fitting of oral administration and intravenous administration was performed using the receptor-binding-dissociation model, the measured values exhibited good correspondence with the fitting curve. Moreover, the time-courses of changes of the receptor-binding rate (sulfonylurea receptor) were examined using the parameters (k (on): second-order binding association constant to the receptor, Φ: receptor-binding occupancy ratio) obtained from the analysis. The results showed that the binding rate, which is important for glinide drugs in the early phase after administration, was obviously higher for nateglinide than that for mitiglinide from 10 min after oral administration and between 0 and 30 min after intravenous administration. These results suggest a more rapid onset of the therapeutic effect of nateglinide than that of mitiglinide after the drug is distributed into the blood.

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Nateglinide increased the early insulin secretion in healthy individuals submitted to a mild hyperglycemia, but not at high glucose concentrations.

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A simple reversed phase high performance liquid chromatographic (RP-HPLC) method was developed and validated for the simultaneous determination of Rosiglitazone (ROS) and Glimepiride (GLM) in combined dosage forms and human plasma. The separation was achieved using a 150 mm × 4.6 mm i.d., 5 μm particle size Symmetry® C18 column. Mobile phase containing a mixture of acetonitrile and 0.02 M phosphate buffer of pH 5 (60: 40, V/V) was pumped at a flow rate of 1 mL/min. UV detection was performed at 235 nm using nicardipine as an internal standard. The method was validated for accuracy, precision, specificity, linearity, and sensitivity. The developed and validated method was successfully used for quantitative analysis of Avandaryl™ tablets. The chromatographic analysis time was approximately 7 min per sample with complete resolution of ROS (tR = 3.7 min.), GLM (tR = 4.66 min.), and nicardipine (tR, 6.37 min). Validation studieswas performed according to ICH Guidelines revealed that the proposed method is specific, rapid, reliable and reproducible. The calibration plots were linear over the concentration ranges 0.10-25 μg/mL and 0.125-12.5 μg/mL with LOD of 0.04 μg/mL for both compounds and limits of quantification 0.13 and 0.11 μg/mL for ROS and GLM respectively.

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Plasma glucose reached 18.2+/-1.7 and 16.7+/-1.7 mmol/l at 90 min in control and placebo groups (P<0.001). These effects were accompanied by prompt 32% inhibition of DPP-IV activity after 10 min (19.9+/-1.6 nmol/ml per min, P<0.05), reaching a minimum of 1.9+/-0.1 nmol/ml per min at 120 min (P<0.001) after nateglinide. Insulin and C-peptide levels increased significantly compared with placebo, to peak after 90 min at 637.6+/-163.9 pmol/l (P<0.05) and 11.8+/-1.4 mg/l (P<0.01) respectively. DPP-IV-mediated degradation of GIP was significantly less in patients receiving nateglinide compared with placebo. Inhibition of DPP-IV activity corresponded with a time- and concentration-dependent inhibitory effect of nateglinide on DPP-IV-mediated truncation of GIP(1-42) to GIP(3-42) in vitro. Comparison of in vitro inhibition of DPP-IV by nateglinide and vildagliptin revealed IC(50) values of 17.1 and 2.1 microM respectively.

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Both in vitro and in vivo tests were conducted using NIT-1 and HEK293 cell lines, male normal and db/db mice and isolated perfused rat pancreas preparations.

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A monolithic molecularly imprinted polymer (monolithic MIP) was designed and prepared for chiral separation of nateglinide and its L-enantiomer. The enantiomers were rapidly separated on this novel monolithic MIP based chiral stationary phase (MIP-CSP), whereas the enantioseparation was not obtained on the non-imprinted polymer (NIP). Chiral recognition was found to be dependent on the stereo structures and the arrangement of functional groups of the imprinted molecule and the cavities on MIP. Thermodynamic data (deltadeltaH and deltadeltaS) obtained by Van't Hoff plots revealed an enthalpy-controlled enantioseparation. The binding capacity was evaluated by frontal analysis. Monolithic nateglinide-MIP had an effective number of binding sites Bt = 41.15 micromol g(-1) with a dissociation constant of Kd = 7.40 mM. The morphological characteristics of the monolithic MIP were investigated by pore analysis and scanning electron microscope (SEM). Results showed that both mesopores and macropores were formed in the monolith. Over all, this study presents a new and practical possibility for providing high rates of mass transfer, fast separations and high efficiencies without the pressure constraints of the traditional bulk molecularly imprinted polymers, through the monolithic MIPs.

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The fate of 3H- and 14C-labelled A-4166 was examined in rat pancreatic islets. The net uptake of the meglitinide analogue by islets incubated for 60 min in the presence of 0.1 mM A-4166 and then submitted to repeated washes was close to 0.1 pmol/islet. It was significantly increased when the concentration of D-glucose in the incubation medium was raised from 2.8 to 16.7 mM. No sizeable internalization of tritiated A-4166 into insulin-producing cells could be detected by autoradiography. These findings suggest that the interaction of A-4166 with the beta-cell may be restricted to its insertion on the plasma membrane and binding to sulphonylurea receptors.

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It is well known that the control of the crystallization of drugs to ensure that only the approved and desired polymorph is present in the formulation is a crucial point of a preformulation study. In this regard, the aim of the present work is to devise a method for the quantification of the polymorphic purity of nateglinide in mixtures formed by polymorphs H and B. In order to achieve this goal, binary systems of known composition have been prepared and the melting peaks of both polymorphs have been recorded by differential scanning calorimetry. Experiments have determined that the method of preparation of the mixtures has to be carefully evaluated. Indeed it has been shown that grinding the samples induces transition from B to H form. Furthermore, it could be observed that the enrichment of the binary mixture with H form is caused by heating. Therefore, after having prepared the mixture without grinding stage, we propose a method to evaluate the content of H polymorph in mixture with the B one from the melting peak of B.

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Nateglinide (Starlix, SDZ DJN 608 or A-4166), a new insulinotropic agent, is intended to be administered prior to a meal in order to improve early insulin release in non-insulin-dependent diabetes mellitus patients. The effects of a meal on the oral bioavailability and pharmacodynamic actions of nateglinide were investigated. Twelve healthy male subjects completed this randomized, single-dose, four-way crossover study in which each subject received a 60 mg dose of nateglinide 10 minutes before the start of and immediately after a high-fat breakfast meal. In addition, each subject received a single 30 and 60 mg dose of nateglinide underfasting conditions. Plasma and urine concentrations of nateglinide were determined by an HPLC method while plasma glucose and insulin concentrations were measured by standard immunoassay methods. Compared to the fasted state, administration of nateglinide 10 minutes before the meal was associated with an increase in the rate of absorption (12% increase in Cmax and 52% decrease in tmax), while there was no significant effect on the extent of absorption (AUC). Alternatively, when nateglinide was given after the meal, a food effect was observed that was characterized by a decrease in the rate of absorption: 34% decrease in Cmax and a 22% increase in tmax but no significant effect on AUC. Nateglinide was rapidly eliminated with plasma t 1/2 = 1.4 hours. Its plasma renal clearance, 20.7 ml/min, appears to be due mostly to active tubular secretion. However, only 13% to 14% of the dose is recovered as nateglinide in the urine. The 30 and 60 mg tablets were dose proportional in terms of both AUC and Cmax; both tmax and t 1/2 were dose independent. Regardless of timing, the combination of a meal and nateglinide produced a larger increase in insulin levels than did nateglinide alone. Meal-related glucose excursions were eliminated when nateglinide was taken prior to the meal. Thus, the rapid onset/short duration stimulation of insulin release by nateglinide should allow good control of prandial hyperglycemia while limiting exposure to hyperinsulinemia.

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Both drugs effectively reduced postprandial glucose levels compared with the insulin glargine monotherapy. No significant differences were found between nateglinide and acarbose in terms of mean glucose level, standard deviation of glucose levels, mean average glucose excursion and average daily risk range. Homeostasis model analysis (HOMA)% β, corrected insulin response and insulin-to-glucose ratio were significantly higher in the responder group compared with the non-responder. There was no episode of severe hypoglycemia.

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Nateglinide is a meglitinide analogue with antidiabetic action. A recent study showed that SLCO1B1 (which codes the OATP1B1 gene, also known as OATP-C, OATP2) is a major determinant which markedly affects the pharmacokinetics of repaglinide. Our objective was to assess the association between single nucleotide polymorphisms (SNPs) of SLCO1B1 and the pharmacokinetics of nateglinide.

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The expression meglitinide analogs was introduced in 1995 to cover new molecules proposed as non-sulfonylurea insulinotropic agents and displaying structural analogy with meglitinide, such as repaglinide, nateglinide, and mitiglinide. Meglitinide analogs display, as judged by conformation analysis, a U-shaped configuration similar to that of antihyperglycemic sulfonylureas such as glibenclamide (glyburide) and glimepiride. In rat pancreatic islets incubated in the presence of 7.0 mmol/L D-glucose, repaglinide and mitiglinide demonstrate comparable concentration-response relationships for stimulation of insulin release, with a threshold value < 10 nmol/L and a maximal secretory response at about 10 nmol/L. Several findings indicate that meglitinide analogs provoke the closing of adenosine triphosphate-sensitive potassium channels, with subsequent gating of voltage-sensitive calcium channels. The effects of meglitinide analogs upon the binding of [3H]glibenclamide to islet cells membranes reinforces this concept. At variance, however, with other meglitinide analogs, the ionic and secretory response to repaglinide (10 micromol/L) is not rapidly reversible in perifused rat islets. In experiments conducted in vivo in control and diabetic rats, repaglinide provokes a greater and more rapid increase in plasma insulin concentration and an earlier fall in glycemia than glibenclamide or glimepiride. Onset of effect is also more rapid and duration of effect shorter with nateglinide versus glibenclamide. In clinical studies, single or repeated daily administration of repaglinide increased plasma insulin concentration in a dose-dependent manner, with an incremental peak reached about 2 hours after repaglinide intake. Plasma concentrations of repaglinide are about 5.0 microg/L 2-2.5 hours after oral intake of the drug. Despite the slow reversibility of repaglinide action in vitro, this drug offers advantages over glibenclamide in terms of the possible occurrence of hypoglycemia if a meal is missed. In volunteers receiving a single oral dose of nateglinide (120mg) 10 minutes before a standardized 800 Kcal breakfast, the plasma insulin concentration was higher 5, 10, and 20 minutes after meal intake than when they received a single dose of repaglinide (0.5 or 2.0mg) or placebo 10 minutes before breakfast. Peak plasma concentrations of nateglinide were reached within 2 hours in most volunteers. Peak plasma concentrations of mitiglinide were reached 30 minutes after a single oral dose in a representative volunteer. Mitiglinide significantly suppressed meal-induced elevations in blood glucose concentrations in a study of patients with type 2 diabetes. In conclusion, two obvious differences among these meglitinide analogs should be underlined. First, on a molar basis, nateglinide is somewhat less potent than repaglinide or mitiglinide, as an insulinotropic agent. The maximal secretory responses evoked by these three meglitinide analogs are, however, identical to one another. Secondly, and as already mentioned, the functional effects of nateglinide and mitiglinide are more rapidly reversible than those of repaglinide, for instance in perifused rat islets. The meglitinide analogs offer the advantage over the long-acting antihyperglycemic sulfonylurea glibenclamide of minimizing the risk of undesirable hypoglycemia.

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Nateglinide is a D-phenylalanine derivative that stimulates fast insulin secretion with a short activity span. It has been suggested that the hypoglycemic effect of nateglinide is related to the glucose concentration, an aspect that still has not been completely evaluated in human beings.

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Longitudinal regression using weight as response value and physical activity as predictor value was conducted, adjusted for baseline covariates. Analysis was then repeated with physical activity as response value and weight as predictor value. Only participants with a response value preceded by at least three annual response values were included.

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Neutrophils transmigration across umbilical vein endothelial cells (in high insulin medium) with or without K(ATP) channel blockers was performed. Neutrophil migration was quantified by measuring myeloperoxidase, and surface expression of endothelial PECAM-1 was examined using cell-surface enzyme immunoassay.

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A randomized, parallel-group, open-label, multicenter 16-week clinical trial compared efficacy and safety of repaglinide monotherapy and nateglinide monotherapy in type 2 diabetic patients previously treated with diet and exercise.

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starlix reviews 2016-06-19

A 67-year-old Turkish woman with Alzheimer's disease was admitted to the hospital because of dizziness and syncope. Her medical history included diagnoses of hypertension (treated with amlodipine 5 mg daily) and diabetes mellitus (treated with nateglinide 120 mg daily). She had been taking both drugs for over five years. She had also been taking rivastigmine 6 mg p.o. daily for five months for the treatment of Alzheimer's disease. She had experienced dizziness since the onset of rivastigmine therapy but had not reported it to any health care provider. On admission, she had a blood pressure measurement of 90/60 mm Hg and a pulse rate of 34 beats/min. A 12-lead electrocardiogram revealed complete atrioventricular block. Echocardiography results, blood electrolyte levels, and cardiac biochemical markers were normal. After initial evaluation, a temporary transvenous pacemaker was implanted via the right femoral vein. Amlodipine and rivastigmine were discontinued. On the first day of hospitalization, a coronary angiogram revealed normal coronary anatomy. Two days later, the complete atrioventricular block resolved spontaneously to sinus rhythm. Rivastigmine 6 mg p.o. daily was reinitiated, and complete atrioventricular block recurred on the fourth day of therapy. A VVI permanent pacemaker was implanted on the fifth day of hospitalization. Amlodipine and rivastigmine were reinitiated. The patient continued rivastigmine 6 mg p.o. daily after permanent pacemaker implantation. A three-month follow-up appointment revealed that buy starlix online no further syncope episodes or dizziness had occurred.

starlix diabetes medication 2015-07-12

In patients buy starlix online stabilized on high-dose metformin, the addition of nateglinide improved glycaemic control. The combination of these agents was well tolerated and both doses of nateglinide proved effective. The efficacy of nateglinide 60 mg and the low rate of hypoglycaemia observed at this dose make it suitable for patients close to their therapeutic target on metformin monotherapy.

starlix medicine 2017-11-20

Cox proportional hazard regression models were constructed using variables (demographic data, medical history, clinical features, biochemical results and ECG findings) recorded buy starlix online at baseline to identify variables associated with and predictive of cardiovascular events.

starlix 120 mg 2017-12-15

Epidemiological studies demonstrated the importance of postprandial hyperglycemia on the progression of atherosclerosis. However, whether treatment of postprandial hyperglycemia by insulin or insulin secretagogues has a beneficial effect on atherosclerosis has not been elucidated. To elucidate the effects of reduction of postprandial rise of blood glucose by insulin and nateglinide on monocyte adhesion to endothelial cells, we used non-obese type 2 diabetic Goto-Kakizaki (GK) rats fed twice daily, as a model of repetitive postprandial hyperglycemia. We investigated the effects of insulin injection and nateglinide administration just before each meal for 12 weeks on monocyte adhesion to endothelial cells. By setting the doses of insulin and nateglinide, both treatment significantly reduced postprandial hyperglycemia without significant reduction of HbA1c buy starlix online . Nateglinide also reduced serum insulin level just after 1 h meal. Both nateglinide and insulin therapy reduced the number of monocytes adherent to the aortic endothelial layer. Nateglinide, but not insulin, reduced intimal thickness of the thoracic aorta. While increased serum insulin level might be regarded as a factor responsible for the progression of atherosclerosis, our data showed that treatment with pre-meal insulin or nateglinide, which reduces postprandial hyperglycemia, reduced monocyte adhesion to endothelial cells.

starlix maximum dose 2016-10-06

Addition of a short-acting insulin buy starlix online secretagogue at main meals improves postprandial hyperglycaemia during combination therapy with basal insulin and metformin, but increases the frequency of hypolycaemia.

starlix generic name 2015-01-11

Nateglinide and acarbose were comparably effective in reducing postprandial buy starlix online glycemic excursions in antihyperglycemic agent-naive Chinese patients with type 2 diabetes, possibly through different pathophysiological mechanisms.

starlix pill images 2016-08-12

A single dose of nateglinide (60, 120, or 180 mg) or placebo was given to eight diet-treated overnight-fasted type 2 diabetic patients and to seven patients 5 min before a standard breakfast. Plasma glucose, radioimmunoassay insulin, and nateglinide were measured at baseline and for a further 180 min buy starlix online .

starlix brand name 2016-01-12

The change in area under the curve (AUC) of glucose from 0 to 180 min (AUC0-180 min) during the meal test by nateglinide was similar to that by sitagliptin. As expected, the change in active glucagon like peptide-1 was significantly higher after a single-dose of sitagliptin than nateglinide. Then, insulin secretion relative to glucose elevation (ISG) (ΔISG0-180 min: ΔAUC0-180 min buy starlix online insulin/AUC0-180 min glucose) was significantly enhanced by nateglinide compared with sitagliptin. Conversely, glucagon level (ΔAUC0-180 min glucagon) was increased by administration of nateglinide, whereas the glucagon level was reduced by administration of sitagliptin.

starlix dosing 2015-03-23

We aimed to determine whether differences in this hypoglycemic effect existed between individuals consuming Eastern and Western diets with significantly different starch contents, a systematic meta-analysis of studies comparing acarbose with placebo or other hypoglycemic agents buy starlix online in patients with type 2 diabetes mellitus (T2DM) was performed.

starlix medication cost 2017-07-24

The model-derived parameters are sensitive measures of beta-cell function, buy starlix online showing improvements after nateglinide treatment and predicting changes in glucose tolerance.

starlix drug class 2016-10-27

Data were extracted from 27 studies meeting all inclusion criteria. IC(50) values for SUR1 were below those for SUR2A/SUR2B for all insulin secretagogues and addition of C(SS) values identified three distinct patterns. The C(SS) for gliclazide, glipizide, mitiglinide and nateglinide lie between IC(50) values for SUR1 and SUR2A/SUR2B, suggesting that these drugs bind selectively to pancreatic receptors. The C(SS) for glimepiride and buy starlix online glyburide (glibenclamide) was above IC(50) values for all three isoforms, suggesting these drugs are non-selective. Tolbutamide and repaglinide may have partial pancreatic receptor selectivity because IC(50) values for SUR1 and SUR2A/SUR2B overlapped somewhat, with the C(SS) in the midst of these values.

starlix 30 mg 2017-01-06

Diabetes was induced by a single intraperitoneal injection of STZ at a dose 55 mg kg(-1). buy starlix online The plasma glucose, total lipid, cholesterol, triglyceride and protein components were measured before and 15 and 30 days after the administration of the antidiabetic agents.

starlix cost 2015-12-30

We compared the acute effect of nateglinide, glibenclamide, and placebo on prandial plasma glucose and serum insulin, C-peptide, and glucagon excursions in 15 patients with MODY3. After an overnight fast, they received on three randomized occasions placebo, 1.25 mg glibenclamide, or buy starlix online 30 mg nateglinide before a standard 450-kcal test meal and light bicycle exercise for 30 min starting 140 min after the ingestion of the first test drug.

starlix and alcohol 2017-12-15

After the treatment, a significant reduction was observed in fasting blood glucose levels in all groups. Rosiglitazone or metformin were found to exhibit a hypolipidaemic effect in diabetic rats when administered alone or in combination. In comparison, nateglinide, when used alone, resulted in a significant increase in cholesterol and buy starlix online total lipid levels. This effect was masked when nateglinide was administered concurrently with metformin and hypolipidaemic effect was noticed.

starlix medication 2016-09-01

Type 2 diabetes mellitus, is a disease with a rising prevalence worldwide. It is currently estimated that 190 million people around the world suffer Eldepryl 5 Mg from diabetes mellitus, with over 330 million predicted to have the condition by 2025 and 366 million by the year 2030. It is predicted that the developing countries will contribute 77.6% of the total number of diabetic patients in the world by the year 2030. This rapidly growing prevalence among developing countries is attributed to the effects of urbanization, industrialization and globalization on these countries. There has been substantial progress over the last decade in the development of new agents for the treatment of type 2 diabetes especially focusing on the underlying pathophysiology. Despite this and the numerous guidelines from diabetes organisations only less than 40% of patients achieve recommended glycaemic targets. We therefore decided to do a review of the pharmacological treatment of type 2 diabetes mellitus to highlight the pharmacology and effectiveness of these agents and their roles in the management of type 2 diabetes.

starlix drug classification 2017-01-21

We performed an open labeled randomized prospective trial on 78 drug-naive type 2 diabetic patients whose HbA1c was less than 6.5%. Thirty-eight patients were randomly assigned to receive nateglinide (270 mg/dL) and 40 to control group (no treatment). After 12 months, a significant reduction in HbA1c was observed in the nateglinide group, whereas a significant increase of HbA1c was observed in the untreated group. The carotid intima-media thickness at the end of 1-year follow-up was significantly reduced in the nateglinide group compared with the untreated group (-0.017+/-0.054 mm/year versus 0.024+/-0.066 mm/year, P=0.0064). Whereas Buspar Generic nateglinide treatment also reduced triglyceride, highly-sensitive C-reactive protein, and E-selectin, multiple regression analysis identified HbA1c as the only significant independent determinant of the change in carotid intima-media thickness.

starlix generic cost 2016-01-04

Male Sprague Lopid 600 Dose Dawley fitted with indwelling jugular cannulas were used to compare the pharmacodynamic profiles of nateglinide (Nateg), glipizide (Glip) and repaglinide (Repag) through frequent blood samples following the administration of these compounds via oral gavage. In similar animals which were pretrained to consume their daily food intake in two discrete 45-min meals, the effects of compound induced changes in pre-meal, meal and post-meal insulin profiles on glycaemic control were assessed through frequent blood sampling following the administration of these compounds 10 min prior to a 30-min meal.

starlix 60 mg 2015-06-02

In T2D, restoration of early phase insulin secretion improved postprandial hyperglycaemia and suppressed endogenous lipolysis, resulting in suppression of NEFA levels. These results suggest that in nonobese Luvox 25 Mg T2D, metabolic defects may result, to a large extent, from the delay in prandial insulin secretion.

starlix tablet 2016-01-11

Nonalcoholic fatty liver disease (NAFLD) has a high prevalence in patients with type 2 diabetes mellitus (T2DM). In this study, we sought to provide a comprehensive assessment regarding the effects of Micardis Hct Reviews anti-diabetic agents on NAFLD in patients with T2DM.

starlix dosage 2016-05-02

The cardiometabolic risk cluster metabolic syndrome (MS) includes ≥3 of elevated fasting glucose, hypertension, elevated triglycerides, reduced high-density lipoprotein cholesterol (HDL-c), and increased waist circumference. Each can be affected by physical activity and diet. Our objective was to determine whether determine whether baseline physical activity and/ Strattera Daily Dosage or diet behavior impact MS in the course of a large pharmaceutical trial.

starlix tabs 2017-08-26

In this Diovan Generic Availability systematic review we present information relating to the effectiveness and safety of the following interventions: combined oral drug treatment, diet, education, insulin (continuous subcutaneous infusion), insulin, intensive treatment programmes, meglitinides (nateglinide, repaglinide), metformin, monotherapy, blood glucose self-monitoring (different frequencies), and sulphonylureas (newer or older).

starlix generic 2017-12-01

To investigate the safety, tolerability, pharmacokinetics and pharmacodynamics of Lopressor Iv Dose LY2189265 (LY), a novel, long-acting glucagen-like peptide-1 analogue, administered once weekly to subjects with type 2 diabetes.

starlix nateglinide generic 2016-02-10

An LC-MS-MS method has been developed for the simultaneous detection of 10 anti-diabetics Accutane Acne Medication in equine plasma and urine. This method can be used to detect the abuse of anti-diabetic drugs in racehorses.

starlix drug 2015-07-06

The aim of this study was to quantify the incidence of hypoglycaemic events and to describe the pattern of these incident events during the first 9 months of treatment with four oral antidiabetic drugs, rosiglitazone, pioglitazone, nateglinide and repaglinide, prescribed in general practice in England.

starlix drug information 2015-04-21

Clinical trial participants in 40 countries.

starlix reviews 2016-08-14

The projected rise in the incidence of type 2 diabetes mellitus (T2DM) could develop into a substantial health problem worldwide. Whether insulin secretagogues (sulphonylureas and meglitinide analogues) are able to prevent or delay T2DM and its associated complications in people at risk for the development of T2DM is unknown.