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Hypocaloric liquid formula diets were given for one month to 20 moderately obese patients with non-insulin-dependent diabetes mellitus divided into two equal groups; group 1 was treated with weight loss alone; group 2 received glipizide in addition to the hypocaloric diet. Mean weight loss was similar in the two groups (6.5 +/- 0.6 v 6.4 +/- 0.5 kg) and was associated with a statistically significant fall in mean fasting plasma glucose values from 293 +/- 15 to 232 +/- 24 mg/dL (group 1) and from 281 +/- 15 to 152 +/- 7 mg/dL (group 2). This was associated with 13% (group 1) and 36% (group 2) decrements in total postprandial glucose response. Neither fasting nor postprandial insulin levels changed significantly with weight loss, but estimates of insulin-stimulated glucose disposal demonstrated a 15% (group 1) and 42% (group 2) improvement. Finally, fasting plasma cholesterol and triglyceride concentrations fell significantly in both groups.
Using this method, repeat analysis of samples can be avoided. This is useful for the bioanalysis of toxicokinetic studies with wide dose ranges and studies where the sample volume is limited.
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Long-term studies on the comparative efficacy and relative potency of glipizide and glyburide are sparse and controversial.
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Articles pertaining to the pharmacology of sitagliptin, its pharmacokinetics, safety and efficacy were reviewed.
The oral antidiabetics glibenclamide and glipizide, and the diuretics bendroflumethiazide and furosemide, all sulphonamide derived drugs, were investigated in vitro for phototoxic properties. Irradiation with broad-band UV induced phototoxic inhibition of colony forming ability in cell cultures. During irradiation, the substances lost one absorption maximum in the UVA region, demonstrated by UV spectroscopy. These findings correlate well with the UV applied, the action spectrum being in the UVA region. Photoproducts detected during and after irradiation showed a decomposition of the substances due to ionization and fragmentation. Incubation of these preirradiated drugs with the cell cultures revealed no phototoxic effects.
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To assess and compare healthcare utilization and costs over a 2-year period in older patients (> or = 60 years) with type 2 diabetes receiving combination therapy with rosiglitazone plus a sulfonylurea (glipizide) or progressive up-titration of glipizide monotherapy.
Glipizide-GITS was significantly more effective than immediate-release glipizide in reducing FPG levels. Both formulations reduced postprandial plasma glucose levels equally; however, glipizide-GITS exerted its control in the presence of lower plasma glipizide concentrations in addition to significantly lower insulin and C-peptide levels. This suggests that glipizide-GITS improves insulin sensitivity.
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Two cases of factitious hypoglycaemia due to intentional or inadvertent intake of glipizide by non-diabetic subjects were identified through the measurement of this sulphonylurea in plasma by a modified assay procedure.
Sulfonylureas are antidiabetic agents widely prescribed for the treatment of type-II diabetes. Detection of the presence of sulfonylureas in cases of unexplained hypoglycemia rules out other underlying pathophysiological conditions. The goal of this study was to develop and validate a qualitative liquid chromatography tandem mass spectrometry (LC-MS/MS) assay for the rapid identification of sulfonylureas in serum.
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An LC-MS/MS assay was developed using an Agilent HPLC with an AB Sciex 3200 LC-MS/MS operating in ESI positive mode. Linearity, LOD, precision, matrix effect, recovery, carry-over and stability of the final method were evaluated for method validation. Concordance with another clinically validated LC-MS/MS method was evaluated using remnant samples from patients prescribed a sulfonylurea.
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Ninety-five patients with type II diabetics were randomly divided into two groups. Fifty-three cases of SHJT group were given orally decoction and tablets of SHJT for 4-6 months. The efficacy was compared with that of 42 cases treated with Glipizide as the control. Before and after treatment standard steamed bread meal test was performed to measure the insulin peripheral sensitivity, insulin release to glucose and insulin sensitivity index.
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This study evaluated the relation of leptin with glycaemic control and the effect of 14 days of diet, or diet combined with gliclazide, glipizide-GITS or metformin treatment, on leptin concentration in 51 female patients with type 2 diabetes mellitus. Leptin levels were similar both at baseline and after treatment in diabetic and control groups. Diabetic patients with basal fasting plasma glucose (FPG) < 10 mmol/l or with basal postprandial plasma glucose (PPPG) < 13.9 mmol/l had significantly higher leptin levels than diabetic patients with basal FPG > or = 10 mmol/l or with basal PPPG > or = 13.9 mmol/l (19.6+/-8.7 vs. 13.65+/-5.4 microg/l, p < 0.05; and 20.2+/-7.9 vs. 12.9+/-5.2 microg/l, p < 0.05, respectively). Mode of treatment did not influence leptin levels. Delta leptin showed a weak correlation with basal FPG (r = 0.346; p < 0.05), basal and post-treatment PPPG (r = 0.335, p < 0.05 and r = 0.325, p < 0.05, respectively) and a moderate correlation with post-treatment FPG (r = 0.391, p < 0.01). In conclusion, leptin level is not affected by the presence of type 2 diabetes mellitus and by short-term treatment with diet or oral antidiabetic drugs but is directly related to glycaemic control in female patients with type 2 diabetes mellitus.
Glibenclamide and other sulphonylureas are extensively used as specific blockers for ATP-dependent potassium channels in vascular smooth muscle. However, glibenclamide has recently been shown to inhibit actions of some prostanoids in vascular smooth muscle. We extend our previous study by examining the relaxant actions of five different sulphonylureas in rat aorta. The inhibitory effects of sulphonylureas on the contractions induced by prostaglandins F2 alpha, E2 and D2, norepinephrine, 5-hydroxytryptamine (5-HT) or potassium chloride (KCl) were examined. Glibenclamide significantly inhibited the contractions produced by prostaglandins F2 alpha, E2 and D2 but was without effect on responses to norepinephrine, 5-HT or KCl. Glimepiride produced significant attenuation of the responses to all agents tested (5-HT, norepinephrine, KCl), although the inhibition of the responses to prostaglandin F2 alpha was most pronounced. Glipizide and tolbutamide had activities similar to that of glibenclamide, while chlorpropamide was devoid of any antagonist action in rat aorta. In rat aorta precontracted with norepinephrine, glibenclamide inhibited the relaxant responses to lemakalim and pinacidil. Thus, in addition to the effect on ATP-dependent potassium channels, glibenclamide inhibits responses to prostaglandins F2 alpha, E2 and D2 but not to other agents. This effect is shared by glimepiride, tolbutamide and glipizide.
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Diabetes was induced in albino rats by giving a single subcutaneous injection of alloxan in a dose of 150 mg/kg body weight. After 72 hours of giving alloxan injection, depending upon their blood glucose levels (350mg/dl and above), the rats were included into the study and they were divided into four groups, each comprising of 6 rats (n=24): Group 1 which was taken as control was given distilled water. Group 2 was treated with glipizide, a standard drug. Group 3 was treated with the test drug, bromocriptine and Group 4 was treated with sub therapeutic doses of test and standard drugs. The drugs were given to the diabetic rats once daily by oral route for 30 consecutive days, in order to assess their effects in terms of reduction in blood glucose levels. Blood glucose was estimated on 0(th), 10(th), 20(th), and 30(th) days of the study at fixed time intervals.
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Three muscle biopsies were performed in 53 overt type II diabetics over a period of approximately 2 years. At baseline, 21 (40%) had an abnormally increased capillary basement membrane width in muscle. Thirty-five subjects received glipizide and 18, placebo. At baseline, no statistically significant difference was found in the muscle capillary basement membrane width between the two groups (P = NS). In the subjects receiving placebo, the mean width of the muscle capillary basement membrane increased (P = NS), but in those receiving glipizide, the mean decreased from 193 +/- 13 nm (SEM) to 161 +/- 10 nm (P = .02). Fasting plasma glucose and glycosylated hemoglobin A1 significantly decreased (P less than .001) after two years in those receiving glipizide. In 15 subjects, mean glycosylated hemoglobin A1 reached the normal range, and mean muscle capillary basement membrane width decreased to a level close to that found in subjects without diabetes (P = NS). Determinations of enzyme activities involved in the synthesis and degradation of glycoproteins revealed a 2-year significant decrease of muscle glucosyltransferase (synthesis) activity (P less than .01) in the glipizide-treated subjects as opposed to a significant increase (P less than .001) in those receiving placebo. Muscle N-acetyl-beta-glucosaminidase activity (degradation) was statistically increased (P less than .001) in those subjects taking glipizide, but decreased in those taking placebo (P less than .001).
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The clinically effective duration of blood glucose lowering action of a new hypoglycaemic sulphonylurea, glipizide, given in single before breakfast dosage (up to 20 mg) has been studied in 20 apparently insulin-independent diabetics. All, on diet only, had persistent overnight 1-2% glycosuria, fasting glycaemia in excess of 150 mg/100ml, random mid-morning glycaemia of at least 250 mg/100ml and associated clinical symptoms. Eighteen were satisfactorily controlled over the observation period of six months by single daily dosage (mean 10 mg daily); in addition considerable improvement in glucose tolerance occurred. Complementary in-patients indicated that, within the range of dosage studied, there was no therapeutic advantage in taking glipizide twice daily.
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Separation of six drugs (including the internal standard) was accomplished in 5 min plus 5 min rinsing. The between-day CV of the ratio of the areas of the sulfonylurea drugs to internal standard was <1% (n = 10). Linearity (r(2) > or =0.998) and recovery (> or =80%) were good for all sulfonylurea drugs tested. Pharmacokinetic curves for gliclazide by CE and HPLC were superimposable. CE analysis confirmed the HPLC diagnosis of surreptitious abuse of gliclazide and tolbutamide.
In this study, the in vivo and in vitro anti-hyperglycemic activity of chalcone derivatives of 3,4-methylenedioxy, with a substituent electron-acceptor nitro group in the A or B ring, was investigated. As expected, the second generation sulfonylurea glipizide stimulated insulin secretion and reduced glycemia over the study period. Also, it was demonstrated for the first time that chalcones are able to increase insulin secretion and this event was coincident with serum glucose-lowering in the oral glucose tolerance test. Additionally, the chalcones studied had a similar effect on insulin secretion and serum glucose-lowering as glipizide. The effect of chalcones in terms of inducing insulin secretion was greater than that of glipizide after 30 min. Moreover, chalcones were not able to stimulate glucose uptake in soleus muscle, either in the presence of insulin or in the absence of this hormone. In addition, the oral treatment with chalcones did not alter glycemia in diabetic rats. These reports indicate that the effect of chalcones on serum glucose-lowering in hyperglycemic-normal rats is mainly a consequence of insulin secretion, highlighting these chalcones as novel compounds with strong anti-hyperglycemic properties.
A total of 900 patients with T2DM were enrolled in the study from four community health service centers in Beijing and followed up for one year. The following data were collected and analyzed, including patients characteristics, the proportion of patients with glycosylated hemoglobin A1c (HbA1c) less than 7% and the coverage rate of the hypoglycemic agents.
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CsA pharmacokinetics is not significantly altered by glipizide coadministration.