ライフサイエンスコーパス: sulfonylurea

1 he same chemical class of active ingredient (sulfonylurea).

2 y controlled with metformin (with or without sulfonylureas).

3 and cardiovascular mortality (compared with sulfonylureas).

4 ients, 2948 added insulin and 39,990 added a sulfonylurea.

5 rticipant who added insulin to 5 who added a sulfonylurea.

6 008 who subsequently added either insulin or sulfonylurea.

7 iovascular benefit compared with addition of sulfonylurea.

8 formin either alone or in combination with a sulfonylurea.

9 Hypoglycemia was more frequent with sulfonylureas.

10 f exercise will reduce the patients need for sulfonylureas.

11 ce a greater acute and sustained response to sulfonylureas.

12 well as C-peptide in response to glucose and sulfonylureas.

13 nted events occurred only in patients taking sulfonylureas.

14 the patient responded to treatment with oral sulfonylureas.

15 s biphasic diabetes that can be treated with sulfonylureas.

16 and the patient is successfully treated with sulfonylureas.

17 n "A" site that confers SUR1 selectivity for sulfonylureas.

18 ant beta cells to stimulation by glucose and sulfonylureas.

19 ecretion and are the targets of antidiabetic sulfonylureas.

20 rthermore, immunofluorescent localization of sulfonylurea 1 and 2 failed to show expression of a sulf

21 escription for an AHM, with insulin (39.5%), sulfonylureas (32.4%), and metformin (17%) being the mos

22 enzyme inhibitor, 171 (12.9%) were taking a sulfonylurea), 45 (3.4%) were taking metformin despite a

23 s 28.8%), with metformin (6.1% versus 4.9%), sulfonylurea (8.7% versus 6.9%), dipeptidyl peptidase-4

24 e if glycemic control is accomplished with a sulfonylurea, a glinide, or insulin, particularly in the

25 nds that clinicians consider adding either a sulfonylurea, a thiazolidinedione, an SGLT-2 inhibitor,

26 roved glycemic control to the same degree as sulfonylureas (absolute decrease in hemoglobin A1c level

27 idiabetic drugs (GLP-1 receptor agonists and sulfonylureas) activate this pathway and thereby paradox

28 n=2220) or to a combination of metformin and sulfonylurea (active control group, n=2227).

29 Therapeutic channel inhibition using sulfonylurea agents has proved disappointing, although a

30 +BCAA but not in CDM-BCAA in the presence of sulfonylurea AHAS inhibitors.

31 statins adjusted for lipids, and biguanides, sulfonylureas, alpha-glycosidase inhibitors [AGIs], and

32 Observations that sulfonylureas also reverse trafficking defects caused by

33 xenatide became nominally significant in the sulfonylurea and any glucose-lowering medication groups,

34 Sulfonylurea and glinide drugs, which bind to SUR1, clos

35 9.58) mg/dL vs. 8.36 (7.96-8.77) mg/dL), and sulfonylurea and insulin use were not associated with la

36 e provides novel mechanistic insights of how sulfonylureas and ATP interact with the KATP channel com

37 Channel inhibitors, including sulfonylureas and carbamazepine, have been shown to corr

38 subunits have a high sensitivity toward many sulfonylureas and certain K(ATP) channel-opening drugs.

39 Cox models with exposure to sulfonylureas and DPP-4 inhibitors included as time-vary

40 ere propensity score matched to new users of sulfonylureas and followed to determine whether they wer

41 Sulfonylureas and glinides were associated with higher r

42 k for congestive heart failure compared with sulfonylureas and increased risk for bone fractures comp

43 The effects of sulfonylureas and metformin on outcomes of cardiovascula

44 glitinides), older agents (second-generation sulfonylureas and metformin) have similar or superior ef

45 Sulfonylureas and repaglinide were associated with great

46 se overactive channels remained sensitive to sulfonylurea, and treatment with sulfonylureas resulted

47 69 (CI, 0.54 to 0.87) for saxagliptin versus sulfonylureas, and 0.61 (CI, 0.50 to 0.73) for saxaglipt

48 86 (CI, 0.77 to 0.95) for sitagliptin versus sulfonylureas, and 0.71 (CI, 0.64 to 0.78) for sitaglipt

49 olesterol levels compared with pioglitazone, sulfonylureas, and DPP-4 inhibitors.

50 Although use of thiazolidinediones, sulfonylureas, and glinides were associated with weight

51 ted with an NHA2 inhibitor exhibited reduced sulfonylurea- and secretagogue-induced insulin secretion

52 Strikingly, the mutations rescued by sulfonylureas are all located in the first transmembrane

53 Sulfonylureas are anti-diabetic medications that act by

54 Sulfonylureas are commonly used to treat type 2 diabetes

55 fied C. albicans AHAS and shown that several sulfonylureas are inhibitors of this enzyme and possess

56 Sulfonylureas are widely prescribed for the treatment of

57 (HR, 0.43 [CI, 0.33 to 0.56]) compared with sulfonylureas as add-on therapy to metformin but had no

58 Our results show that sulfonylureas, as chemical chaperones, can dictate manif

59 ics, nitrates, statins, insulin, biguanides, sulfonylureas, aspirin, and other nonsteroidal anti-infl

60 Prior studies reported sulfonylurea-associated cardiovascular death but not ser

61 tations in a way that is dependent on intact sulfonylurea binding sites in SUR1 further support this

62 on ATP-sensitive potassium (KATP) channels, sulfonylureas boost insulin release from the pancreatic

63 iation in TCF7L2 would influence response to sulfonylureas but not metformin.

64 2 variants influence therapeutic response to sulfonylureas but not metformin.

65 tion of rosiglitazone to either metformin or sulfonylurea compared with the combination of the two ov

66 Use of sulfonylureas compared with metformin for initial treatm

67 7 to receive a combination of metformin plus sulfonylurea (control group).

68 r-maximal doses of OAD, mostly metformin and sulfonylureas; control subjects (n = 1,216) were patient

69 Sulfonylurea derivatives exert their insulinotropic effe

70 ions included metformin, thiazolidinediones, sulfonylureas, dipeptidyl peptidase-4 (DPP-4) inhibitors

71 Compared with sulfonylureas, DPP-4 inhibitors were associated with low

72 ceptibility, the three BS strains were fed a sulfonylurea drug (tolbutamide) known to both increase h

73 /rat Kir6.2 channel bound to a high-affinity sulfonylurea drug glibenclamide and ATP at 3.63 A resolu

74 these channel variants to inhibition by the sulfonylurea drug glibenclamide, a potential pharmacothe

75 site-specific binding that occurred between sulfonylurea drugs or as the level of HSA glycation was

76 This pathway is engaged by the anti-diabetic sulfonylurea drugs to exert their full glucose-lowering

77 columns to examine the changes in binding by sulfonylurea drugs to in vivo glycated HSA that had been

78 L225P did not alter channel inhibition by sulfonylurea drugs, and, consistent with this, the patie

79 is placed on a combination of Metformin and sulfonylurea drugs.

80 itiated treatment with thiazolidinediones or sulfonylureas during the years 1997 through 2005 and had

81 Compared with sulfonylurea exposure, metformin reduced the mean log-tr

82 tolerated doses of metformin alone or with a sulfonylurea for at least 3 months, a stable bodyweight

83 e, determined in the presence of ATP and the sulfonylurea glibenclamide, at 6 A resolution reveals a

84 y glycemia regulation, a comparison with the sulfonylurea glimepiride was done.

85 yl peptidase 4 inhibitor linagliptin and the sulfonylurea glimepiride.

86 a mixed meal and after administration of the sulfonylurea glimepiride.

87 of carotid wall thickness compared with the sulfonylurea glimepiride.

88 k of SCA/VA among users of second-generation sulfonylureas: glimepiride, glyburide, and glipizide.

89 th nine classes of approved drugs (insulins, sulfonylureas, glinides, biguanides, alpha-glucosidase i

90 Although biguanides, sulfonylurea, glitazones, and dipeptidyl peptidase 4 inh

91 When added to metformin and sulfonylurea, GLP-1 receptor agonists were associated wi

92 Sulfonylureas had a 4-fold higher risk for mild or moder

93 Sulfonylureas have a 100- to 1000-fold greater affinity

94 Active ingredients from the sulfonylurea herbicide and carbamate insecticide classes

95 been developed for the determination of four sulfonylurea herbicides (SUHs): flazasulfuron (FS), pros

96 The sulfonylurea herbicides exert their activity by inhibiti

97 There was no association with treatment with sulfonylureas (HR=0.99, 95% CI 0.91 to 1.08) or insulin

98 ary electrophoresis method to determine four sulfonylureas in grain samples was developed using 10mM

99 e insulin-resistant diabetes cluster and for sulfonylureas in patients in the mild age-related diabet

100 greater 1-year hemoglobin A(1c) reduction to sulfonylureas in the Genetics of Diabetes Audit and Rese

101 ular outcomes of linagliptin vs glimepiride (sulfonylurea) in patients with relatively early type 2 d

102 lycemic control while receiving metformin or sulfonylurea, in which 2220 patients were assigned to re

103 PC1 or TPC2 channels attenuates glucose- and sulfonylurea-induced membrane currents, depolarization,

104 ent, the G334D mutation has no effect on the sulfonylurea inhibition of reconstituted channels in exc

105 Sulfonylurea inhibitors, such as glibenclamide, are pote

106 oral hypoglycemic agents (generally stopping sulfonylureas) initially, and later, prandial insulin ca

107 idence rate, 13.0 [95% CI, 10.9-15.3]) among sulfonylurea initiators, corresponding to an adjusted po

108 idence rate, 20.8 [95% CI, 18.1-23.8]) among sulfonylurea initiators, corresponding to an adjusted po

109 mediated K(+) currents and Ca(2+)-activated, sulfonylurea-insensitive Na(+) currents in the same patc

110 cause DEND and suggest the possibility that sulfonylurea insensitivity of such patients may be a sec

111 In disagreement with the sulfonylurea insensitivity of the affected patient, the

112 In the sulfonylurea-insulin group, relative reductions in risk

113 utcome of patients treated with antidiabetic sulfonylureas is being considered.

114 on the Kir pore is elevated and blockade by sulfonylureas is preserved.

115 jected the fourth generation photoswitchable sulfonylurea JB253 to comprehensive toxicology assessmen

116 design and development of a photoswitchable sulfonylurea, JB253, which reversibly and repeatedly blo

117 For patients taking sulfonylureas, K(ATP) channel inhibition may exacerbate

118 -like properties and apparently sensitive to sulfonylureas, leading to the postulation that post-trau

119 globin A1c (HbA1c) control despite metformin-sulfonylurea (Met-SU) dual therapy, a third-line glucose

120 or currently treated with diet and exercise, sulfonylurea, metformin, insulin, or a combination there

121 Insulin use was higher and sulfonylurea/metformin use was lower among patients with

122 New users of metformin or sulfonylurea monotherapy who continued treatment with th

123 atients with type 2 diabetes on metformin or sulfonylurea monotherapy with mean haemoglobin A(1c) (Hb

124 incident treatment with either metformin or sulfonylurea monotherapy.

125 tment was available in a subset of patients (sulfonylurea n = 579; metformin n = 755).

126 Sulfonylurea (odds ratio [OR], 3.13 [95% CI, 2.39 to 4.1

127 ating glucagonlike peptide-1 agonists versus sulfonylureas on cardiovascular events and all-cause mor

128 ry restriction) or intensive therapy (either sulfonylurea or insulin or, in overweight patients, metf

129 f blood pressure or statin treatment than of sulfonylurea or insulin treatment.

130 Adding a sulfonylurea or metformin to insulin was associated with

131 d type 2 diabetes and were on treatment with sulfonylurea or sulfonylurea plus metformin, 260 (63% ma

132 nction upon trafficking rescue by reversible sulfonylureas or carbamazepine was facilitated by the KA

133 ts could be corrected by treating cells with sulfonylureas or diazoxide.

134 reated with oral antidiabetic agents such as sulfonylureas or dipeptidyl peptidase-4 antagonists, whi

135 bolishing the ability of mutant SUR1 to bind sulfonylureas or glinides by the following mutations: Y2

136 Use of sulfonylureas or insulin was associated with 1.49- (95%

137 itiser used in combination with metformin, a sulfonylurea, or both, for lowering blood glucose in peo

138 been receiving a stable dose of metformin or sulfonylurea, or both, or basal insulin with or without

139 HbA1c) of 7.0% or more, receiving metformin, sulfonylureas, or basal insulin, or combinations of thes

140 Previously, we reported that sulfonylureas, oral hypoglycemic drugs widely used to tr

141 6 metformin + insulin and 12,180 metformin + sulfonylurea patients.

142 .2 [95% CI, 1.4 to 3.0] more CVD events with sulfonylureas per 1000 person-years; adjusted hazard rat

143 There were 67 749 metformin and 28 976 sulfonylurea persistent monotherapy users; the weighted

144 s and were on treatment with sulfonylurea or sulfonylurea plus metformin, 260 (63% male, 37% female)

145 Their differential affinity for hypoglycemic sulfonylureas provides a basis for the selectivity of th

146 iant in the gene encoding a component of the sulfonylurea receptor (ABCC8 p.A1369S) promotes closure

147 he ATP-gated K(+) (K(ATP)) metabolic sensor [sulfonylurea receptor (SUR) 1 and potassium inwardly rec

148 rd rectifier potassium channel (Kir) 6.2 and sulfonylurea receptor (SUR) 1 critically regulate pancre

149 Mutations in either the Kir6.2 or sulfonylurea receptor (SUR) 1 subunit of the channel hav

150 eter regulation of wild-type [SUR2(+/+)] and sulfonylurea receptor (SUR) 2-deficient [SUR2(-/-)] mous

151 Using putative sulfonylurea receptor (SUR) coiled-coil domains as baits

152 The sulfonylurea receptor (SUR) is another atypical ABC prot

153 el subunit (Kir6.1, Kir6.2) and a regulatory sulfonylurea receptor (SUR) subunit, an ATP-binding cass

154 -forming Kir6.2 subunits and four modulatory sulfonylurea receptor (SUR) subunits.

155 ATP/ADP-sensing (sulfonylurea receptor (SUR)/K(IR)6)(4) K(ATP) channels r

156 novo L225P mutation in the L0 region of the sulfonylurea receptor (SUR)1, the regulatory subunit of

157 sized that the mitoK(ATP) channel contains a sulfonylurea receptor (SUR)2 regulatory subunit and aime

158 channel, composed of the beta-cell proteins sulfonylurea receptor (SUR1) and inward-rectifying potas

159 Recent studies demonstrated that sulfonylurea receptor 1 (SUR 1) regulated nonselective c

160 eric complexes, (SUR1/Kir6.2)(4), comprising sulfonylurea receptor 1 (SUR1 or ABCC8) and a K(+)-selec

161 tive potassium (K(ATP)) channels composed of sulfonylurea receptor 1 (SUR1) and Kir6.2 regulate insul

162 h defects in ABCC8 and KCNJ11 genes encoding sulfonylurea receptor 1 (SUR1) and Kir6.2 subunits, whic

163 ATP-sensitive K(+) (K(ATP)) channel proteins sulfonylurea receptor 1 (SUR1) and Kir6.2, encoded by AB

164 caused by mutations in the channel proteins: sulfonylurea receptor 1 (SUR1) and Kir6.2, results in lo

165 sitive potassium (KATP) channels composed of sulfonylurea receptor 1 (SUR1) and Kir6.2.

166 tive potassium (KATP) channels consisting of sulfonylurea receptor 1 (SUR1) and the potassium channel

167 ed glucose sensitivity after deletion of the sulfonylurea receptor 1 (SUR1) both in man and mouse.

168 outward current that was antagonized by the sulfonylurea receptor 1 (SUR1) channel blocker tolbutami

169 Sulfonylurea receptor 1 (SUR1) is a molecule with more d

170 tions in ABCC8 or KCNJ11, genes encoding the sulfonylurea receptor 1 (SUR1) or the inwardly rectifyin

171 tudies using transfected COSm6 cells, mutant sulfonylurea receptor 1 (SUR1) protein was expressed on

172 ium channel and a regulatory ABC transporter sulfonylurea receptor 1 (SUR1) regulate insulin secretio

173 s to nucleotide binding fold-1 (NBF1) of the sulfonylurea receptor 1 (SUR1) subunit of the KATP chann

174 ctifying potassium channel (Kir6.2) and four sulfonylurea receptor 1 (SUR1) subunits.

175 in ischemic astrocytes that is regulated by sulfonylurea receptor 1 (SUR1), is opened by depletion o

176 The sulfonylurea receptor 1 (Sur1)-NC(Ca-ATP) channel plays

177 scovery of a disease-causing mutation in the sulfonylurea receptor 1 (SUR1)/ABCC8 from a patient with

178 ATP-sensitive K(+) channel (K(ATP) channel) sulfonylurea receptor 1 subunit, and decreased inhibitor

179 ying potassium channel Kir6.2 assembles with sulfonylurea receptor 1 to form the ATP-sensitive potass

180 Kir6.2 or its associated regulatory subunit, sulfonylurea receptor 1, causes congenital hyperinsulini

181 cervical SCI, we tested the hypothesis that sulfonylurea receptor 1-regulated (SUR1-regulated) Ca(2+

182 nes were generated and independently bred to sulfonylurea receptor 2 (SUR2) null mice to generate mic

183 ABCC9 (c.1320 + 1 G > A), which encodes the sulfonylurea receptor 2 (SUR2) subunit of K(ATP) channel

184 tations in the genes encoding the regulatory sulfonylurea receptor 2 (SUR2) subunits of the ATP-sensi

185 The sulfonylurea receptor 2B (SUR2B) forms the regulatory su

186 Sulfhydration of sulfonylurea receptor 2B (SUR2B) was induced by NaHS and

187 Superfusion of tolbutamide, a K(ATP) channel sulfonylurea receptor blocker, elicited identical glucos

188 a transgenic strategy where the full-length sulfonylurea receptor containing exon 40 was expressed u

189 lurea 1 and 2 failed to show expression of a sulfonylurea receptor in the parietal cell, thus further

190 Transgenic expression of the sulfonylurea receptor in vascular smooth muscle cells wa

191 aining a pore-forming subunit (Kir6.1) and a sulfonylurea receptor subunit (SUR2B).

192 ed from pore-forming (Kir6.x) and regulatory sulfonylurea receptor subunits, are critical electrical

193 itive potassium (K(ATP)) channel composed of sulfonylurea receptor SUR1 and potassium channel Kir6.2

194 The sulfonylurea receptor SUR1 associates with Kir6.2 or Kir

195 ; however, the evidence is strong that SUR1 (sulfonylurea receptor type 1) subunits are also expresse

196 K(ATP) channels, (SUR1/Kir6.2)(4) (sulfonylurea receptor type 1/potassium inward rectifier

197 -rectifier potassium channel 6.2) and SUR2A (sulfonylurea receptor type 2A) subunits; however, the ev

198 s tissues contain subtypes of the regulatory sulfonylurea receptor, SUR, and pore-forming, K(+) inwar

199 Sulfonylurea receptor- 1 was quantified by enzyme-linked

200 There was no association between mean/peak sulfonylurea receptor-1 and mean/peak intracranial press

201 There was a temporal delay between peak sulfonylurea receptor-1 and peak intracranial pressure i

202 is available, assessing cerebrospinal fluid sulfonylurea receptor-1 in larger studies is warranted t

203 Because a therapy inhibiting sulfonylurea receptor-1 is available, assessing cerebros

204 We hypothesized that sulfonylurea receptor-1 is measurable in human cerebrosp

205 However, decreasing sulfonylurea receptor-1 trajectories between 48 and 72 h

206 Sulfonylurea receptor-1 trajectories between 48 and 72 h

207 Sulfonylurea receptor-1 was detected in severe traumatic

208 Mean and peak sulfonylurea receptor-1 was higher in patients with CT e

209 MAIN Sulfonylurea receptor-1 was present in all severe trauma

210 Sulfonylurea receptor-1-transient receptor potential cat

211 report quantifying human cerebrospinal fluid sulfonylurea receptor-1.

212 They comprise four sulfonylurea receptors (SUR) and four potassium channel

213 mponent gene expression including regulatory sulfonylurea receptors (SUR) SUR1 and SUR2B but not SUR2

214 mily (Kir6.1, KCNJ8, and Kir6.2 KCNJ11) with sulfonylurea receptors (SUR1, ABCC8, and SUR2, ABCC9) of

215 Sulfonylurea receptors SUR1 and SUR2 are the regulatory

216 osynthesis and were thought to interact with sulfonylurea receptors that mediate chitin vesicle trans

217 ic ATP-binding cassette regulatory subunits (sulfonylurea receptors), which counterbalance the nearly

218 inwardly rectifying Kir channel (Kir6.x) and sulfonylurea receptors.

219 rvations and the unexpected partnership with sulfonylurea-receptors (SURs) makes the TRPM4 channel a

220 he mechanistic and structural basis on which sulfonylureas rescue K(ATP) channel surface expression d

221 tudy, we investigated the mechanism by which sulfonylureas rescue these mutants.

222 Sulfonylureas rescued a subset of the trafficking mutant

223 outcome among patients who added insulin vs sulfonylureas, respectively (42.7 vs 32.8 events per 100

224 is considerable interindividual variation in sulfonylurea response in type 2 diabetes.

225 s do exhibit a decreased, but still present, sulfonylurea response.

226 e-insulin formulation added to metformin and sulfonylurea resulted in a glycated hemoglobin level of

227 ensitive to sulfonylurea, and treatment with sulfonylureas resulted in euglycemia.

228 The mutation does not affect sulfonylurea sensitivity, and the patient is successfull

229 Compared with metformin, sulfonylurea (standardized mean difference [SMD], 0.18 [

230 In rat models of stroke, sulfonylurea (SU) drugs such as glibenclamide (adopted U

231 e, two widely used antidiabetic drugs of the sulfonylurea (SU) family, showed greatly reduced efficac

232 l the smooth muscle channel is composed of a sulfonylurea subunit (SUR2B) and a pore-forming subunit

233 he inward rectifier subunit, Kir6.2, and the sulfonylurea subunit, SUR2B.

234 Block of SUR 1 with sulfonylurea such as glibenclamide has been shown to be

235 the potential importance of block of SUR1 by sulfonylureas such as glibenclamide (glyburide) in condi

236 Sulfonylureas (SUs) provide an efficacious first-line tr

237 For the sulfonylureas tested there was a strong correlation betw

238 ors, and compared with thiazolidinediones or sulfonylureas, the mean differences in body weight were

239 lar mortality was lower for metformin versus sulfonylureas; the evidence on all-cause mortality, card

240 The patient was wholly unresponsive to sulfonylurea therapy (up to 1.14 mg . kg(-1) . day(-1))

241 0 patients initiating treatment (98 665 with sulfonylurea therapy and 155 025 with metformin therapy)

242 S) promotes closure of the target channel of sulfonylurea therapy and is associated with increased in

243 lso provide an update on known mutations and sulfonylurea therapy in neonatal diabetes mellitus.

244 tolbutamide, accounting for the efficacy of sulfonylurea therapy in the patient.

245 an wild-type channels (98%), suggesting that sulfonylurea therapy may be of benefit for patients with

246 bility that, at least for some CS mutations, sulfonylurea therapy may not prove to be successful and

247 association with increased weight, long-term sulfonylurea therapy may reduce the risk of coronary hea

248 treatment of type 2 diabetes, the impact of sulfonylurea therapy on cardiovascular outcomes remains

249 with important implications when considering sulfonylurea therapy or dissecting the role of cardiac K

250 This realization has led to sulfonylurea therapy replacing insulin injections in man

251 Sulfonylurea therapy was replaced by a second type of in

252 ced mortality compared with controls (mostly sulfonylurea therapy): 23% versus 37% (pooled adjusted r

253 hemoglobin levels while taking metformin and sulfonylurea therapy.

254 be successfully transferred from insulin to sulfonylurea therapy.

255 lin secretion, thus mimicking the effects of sulfonylurea therapy.

256 ian, 1.0 year for metformin vs 1.2 years for sulfonylurea), there were 1048 MACE outcomes (23.0 per 1

257 no HF harm was seen in CVOTs for insulin or sulfonylureas, they should be used only with caution in

258 ts, and SGLT-2 inhibitors and increased with sulfonylureas, thiazolidinediones, and insulin (between-

259 h all noninsulin treatments after metformin (sulfonylureas, thiazolidinediones, dipeptidyl peptidase

260 Bottom Line: Adding a sulfonylurea to insulin was associated with more hypogly

261 g maximally tolerated doses of metformin and sulfonylurea to receive biphasic insulin aspart twice da

262 Patients adding either SGLT2i or sulfonylureas to baseline GLP-1RA were identified within

263 r outcomes of adding DPP-4 inhibitors versus sulfonylureas to metformin therapy remain scarce.

264 The sulfonylurea tolbutamide blocked heterozygous R50Q (89%)

265 0 mutants rescued to the cell surface by the sulfonylurea tolbutamide could be subsequently activated

266 In contrast, the sulfonylurea tolbutamide, a specific blocker of KATP cha

267 F35V channels were markedly inhibited by the sulfonylurea tolbutamide, accounting for the efficacy of

268 sing glucose, nifedipine (VDCC blocker), the sulfonylureas tolbutamide and glibenclamide (KATP channe

269 P = 0.0004), and fewer patients responded to sulfonylurea treatment (48% vs. 73%, P = 0.038).

270 reatment, with improved glycaemic control on sulfonylurea treatment for most patients with potassium

271 At least in a subset of animals, early sulfonylurea treatment leads to permanent remission of N

272 nt groups, previous background metformin and sulfonylurea treatment was continued throughout the tria

273 h reduced penetrance, reduced sensitivity to sulfonylurea treatment, and no effect on birth weight.

274 ss of beta-cells are both avoided by chronic sulfonylurea treatment.

275 ol (mean HbA(1c) 7.58 before and 6.18% after sulfonylurea treatment; P < 0.007).

276 98 patients) of drugs added to metformin and sulfonylurea (triple therapy).

277 R, 0.174; 95% CI, 0.131-0.230), preoperative sulfonylurea use (RYGB: OR, 0.616; 95% CI, 0.505-0.752 a

278 ower IOP and systemic ACEI, ARB, statin, and sulfonylurea use was associated with higher IOP in this

279 e to diagnosis of Parkinson disease than was sulfonylurea use, regardless of duration of exposure.

280 person-years of metformin use compared with sulfonylurea use.

281 cohort included 24 679 metformin and 24 799 sulfonylurea users (median age, 70 years [interquartile

282 e outcome were 18.2 per 1000 person-years in sulfonylurea users and 10.4 per 1000 person-years in met

283 A total of 901 incident sulfonylurea users and 945 metformin users were identifi

284 e-matched pairs of DPP-4 inhibitor users and sulfonylurea users were examined.

285 We identified 624,406 and 491,940 sulfonylurea users, and 714 and 385 SCA/VA events, in Me

286 nce interval: 0.71, 1.66) when compared with sulfonylurea users.

287 94 events (29.2 per 1000 person-years) among sulfonylurea users.

288 lied to an analysis comparing the effects of sulfonylureas versus metformin on body mass index, where

289 ving metformin, the addition of insulin vs a sulfonylurea was associated with an increased risk of a

290 y, treatment with metformin, compared with a sulfonylurea, was associated with a lower risk of MACE.

291 Glibenclamide (GBC), a sulfonylurea, was used as a conformational probe to comp

292 were found for RCTs where second-generation sulfonylureas were used as a proxy for placebo regarding

293 bolization, closing KATP channels similar to sulfonylureas, which also stimulated secretion.

294 ly used oral glucose-lowering agents include sulfonylureas, which are insulin secretagogues, and thia

295 ating cells with the oral hypoglycemic drugs sulfonylureas, which we have shown previously to act as

296 74 882 persistent new users of metformin and sulfonylureas who reached a reduced kidney function thre

297 e risk allele were less likely to respond to sulfonylureas with an odds ratio (OR) for failure of 1.9

298 Our result supports the association of sulfonylureas with weight gain.

299 ycemic agents (metformin, thiazolidinedione, sulfonylurea) with stable body weight, and glycated hemo

300 n was 0.80 (95% CI, 0.75-0.86) compared with sulfonylureas, yielding an adjusted rate difference of 5