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 formin either alone or in combination with a sulfonylurea.

5 h PTDM may be safely treated with ROSI +/- a sulfonylurea.

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

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

8 008 who subsequently added either insulin or sulfonylurea.

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

10 nted events occurred only in patients taking sulfonylureas.

11 the patient responded to treatment with oral sulfonylureas.

12 s biphasic diabetes that can be treated with sulfonylureas.

13 and the patient is successfully treated with sulfonylureas.

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

15 ant beta cells to stimulation by glucose and sulfonylureas.

16 tions in KATP are amenable to treatment with sulfonylureas.

17 ecretion and are the targets of antidiabetic sulfonylureas.

18 Hypoglycemia was more frequent with sulfonylureas.

19 f exercise will reduce the patients need for sulfonylureas.

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

21 global intracerebroventricular perfusion of sulfonylurea (120 ng/min glibenclamide or 2.7 microg/min

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

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

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

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

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

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

31 We report here that sulfonylureas also function as chemical chaperones to re

32 Observations that sulfonylureas also reverse trafficking defects caused by

33 9.58) mg/dL vs. 8.36 (7.96-8.77) mg/dL), and sulfonylurea and insulin use were not associated with la

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

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

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

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

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

39 Sulfonylureas and glinides were associated with higher r

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

41 isk for hypoglycemia when treatment includes sulfonylureas and insulin.

42 The effects of sulfonylureas and metformin on outcomes of cardiovascula

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

44 Sulfonylureas and repaglinide were associated with great

45 between the study group (40 patients taking sulfonylureas) and control group (48 patients taking alt

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

55 Sulfonylureas are widely prescribed for the treatment of

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

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

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

59 a method for preparing sterically congested sulfonylureas based on N,N'-sulfuryldiimidazole that is

60 he possibility of defining the glibenclamide/sulfonylurea binding pocket.

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

62 elevation during AMI, and pretreatment with sulfonylureas blunts these ST-segment changes.

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

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

65 2 variants influence therapeutic response to sulfonylureas but not metformin.

66 decreased open probability due to rundown or sulfonylureas caused an increase in ATP sensitivity in t

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

68 Use of sulfonylureas compared with metformin for initial treatm

69 Two sulfonylurea compounds investigated by 1H nuclear magnet

70 7 to receive a combination of metformin plus sulfonylurea (control group).

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

72 Sulfonylurea derivatives exert their insulinotropic effe

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

74 We examined whether the delivery of sulfonylureas directly into the brain to close K(ATP) ch

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

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

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

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

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

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

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

82 nsulin secretion and serve as the target for sulfonylurea drugs used to treat type 2 diabetes.

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

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

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

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

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

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

89 ppression of DA release was prevented by the sulfonylurea glibenclamide, implicating ATP-sensitive K+

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

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

92 of carotid wall thickness compared with the sulfonylurea glimepiride.

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

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

95 Displacement by KATP channel blockers, the sulfonylurea glyburide, and the cyanoguanidine N-[1-(3-c

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

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

98 Active ingredients from the sulfonylurea herbicide and carbamate insecticide classes

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

100 The sulfonylurea herbicides exert their activity by inhibiti

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

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

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

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

105 Sulfonylureas inhibit K(ATP) channel activities by bindi

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

107 Sulfonylurea inhibitors, such as glibenclamide, are pote

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

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

118 Sulfonylureas markedly increased cell surface expression

119 Thus, sulfonylureas may be used to treat congenital hyperinsul

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 obic group in glibenclamide, adjacent to the sulfonylurea moiety, to provide selectivity for SUR1, wh

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 Adding a sulfonylurea or metformin to insulin was associated with

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

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

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

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

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

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

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

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

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

139 6 metformin + insulin and 12,180 metformin + sulfonylurea patients.

140 .2 [95% CI, 1.4 to 3.0] more CVD events with sulfonylureas per 1000 person-years; adjusted hazard rat

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

142 Sulfonylureas prepared from anilines were obtained in hi

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

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

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

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

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

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

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

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

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

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

153 It is comprised of sulfonylurea receptor (SUR)-1 and Kir6.2 proteins.

154 provides a template for the MDR-like core of sulfonylurea receptor (SUR)-1.

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 The genes for the sulfonylurea receptor (SUR1; encoded by ABCC8) and its a

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

161 otassium (K(ATP)) channel, a complex of four sulfonylurea receptor 1 (SUR1) and four potassium channe

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

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

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

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

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

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

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

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

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

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

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

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 Diazoxide, a sulfonylurea receptor 1 (SUR1)selective KATP-channel ope

179 racellular calcium in islets from normal and sulfonylurea receptor 1 knockout (SUR1-/-) mice.

180 ns in ABCC8 or KCNJ11, genes that encode the sulfonylurea receptor 1 or the inward rectifier Kir6.2 s

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

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

183 cases are associated with mutations in SUR1 (Sulfonylurea receptor 1) or KIR6.2 (Inward rectifier K(+

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

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

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

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

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

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

190 kidney 293 cell-attached patches expressing sulfonylurea receptor 2B and Kir6.2, we found K(ATP) sti

191 ed equivalent of this channel comprising the sulfonylurea receptor 2B and the inward rectifier 6.1 su

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

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

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

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

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

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

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

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

200 ective opener for K(ATP) channels containing sulfonylurea receptor SUR1 subunits, but not with cromak

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

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

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

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

205 rough association of the Kir6.2 pore and the sulfonylurea receptor, the stress-responsive ATP-sensiti

206 Sulfonylurea receptor- 1 was quantified by enzyme-linked

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

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

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

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

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

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

213 Sulfonylurea receptor-1 trajectories between 48 and 72 h

214 Sulfonylurea receptor-1 was detected in severe traumatic

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

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

217 Sulfonylurea receptor-1-transient receptor potential cat

218 report quantifying human cerebrospinal fluid sulfonylurea receptor-1.

219 enzymes, beta-cell-specific glucokinase and sulfonylurea receptor.

220 Administration of the sulfonylurea-receptor inhibitor glibenclamide promptly r

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

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

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

224 Sulfonylurea receptors SUR1 and SUR2 are the regulatory

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

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

227 nnels, with SUR 1 and SUR 2, probably SUR2B, sulfonylurea receptors.

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

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

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

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

232 Sulfonylureas rescued a subset of the trafficking mutant

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

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

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

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

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

238 ion of DA release by H(2)O(2) is mediated by sulfonylurea-sensitive K(+) channels: tolbutamide blocke

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

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

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

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

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

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

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

246 For the sulfonylureas tested there was a strong correlation betw

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

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

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

250 0 patients initiating treatment (98 665 with sulfonylurea therapy and 155 025 with metformin therapy)

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

252 Sulfonylurea therapy appears to attenuate the magnitude

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

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

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

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

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

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

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

260 Sulfonylurea therapy was replaced by a second type of in

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

262 hemoglobin levels while taking metformin and sulfonylurea therapy.

263 be successfully transferred from insulin to sulfonylurea therapy.

264 ese individuals with type 2 diabetes failing sulfonylurea therapy.

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

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

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

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

269 apy, whereas 25/40 (63%) required ROSI and a sulfonylurea to meet this goal.

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

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

272 The sulfonylurea tolbutamide blocked heterozygous R50Q (89%)

273 0 mutants rescued to the cell surface by the sulfonylurea tolbutamide could be subsequently activated

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

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

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

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

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

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

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

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

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

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

284 98 patients) of drugs added to metformin and sulfonylurea (triple therapy).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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