ライフサイエンスコーパス: tolbutamide

1 t S(I(insulin)) was 29 +/- 4% lower than S(I(tolbutamide)).

2 TP have a Po of > 0.8 and are not blocked by tolbutamide).

3 nduce an outward current that was blocked by tolbutamide.

4 in gKATP because it persisted in 100 microM tolbutamide.

5 f glucose or by the K(ATP) channel inhibitor tolbutamide.

6 ons evoked by either agent were inhibited by tolbutamide.

7 e resultant hyperpolarization was blocked by tolbutamide.

8 y in extracts of MIN6 beta-cells affected by tolbutamide.

9 athway was to close the K(ATP) channels with tolbutamide.

10 nduce an outward current that was blocked by tolbutamide.

11 t is reversed by applying the sulphonylurea, tolbutamide.

12 unmasked a marked glucagonotropic effect of tolbutamide.

13 TP but were insensitive to glibenclamide and tolbutamide.

14 dual effect on electrical activity evoked by tolbutamide.

15 drugs, including midazolam, metoprolol, and tolbutamide.

16 50 on insulin release but not the effects of tolbutamide.

17 lfonylurea receptor 1 (SUR1) channel blocker tolbutamide.

18 rises in [Ca(2+)](i) but not the actions of tolbutamide.

19 ll membrane, an effect that was abolished by tolbutamide.

20 r the mitochondrial KATP channel antagonist, tolbutamide.

21 ion was reversed by the KATP channel blocker tolbutamide.

22 min, as did the depolarizing agents KCl and tolbutamide.

23 ime than that observed with stimulation with tolbutamide.

24 m permeabilized beta-cells was stimulated by tolbutamide (0.1-1 mmol/l) at 10(-8) but not at 10(-5) m

25 the postabsorptive basal state and during a tolbutamide (0.2 mg/min) infusion when their plasma gluc

26 Tolbutamide (1 mM) inhibited growth (p<0.001) and abolis

27 8 +/- 0.5 vs 2.1 +/- 2.2 hours, P < 0.0001), tolbutamide (1.4 +/- 1.8 vs 2.1 +/- 2.2 hours, P = 0.000

28 rtal-vein insulin pulse frequency (basal vs. tolbutamide, 10.1 +/- 0.6 vs. 11.1 +/- 0.8 pulses/h; P =

29 ted by the application of the sulphonylureas tolbutamide (100 microM) and glibenclamide (0.5 microM).

30 Tolbutamide (100 microM) was found to induce no effect o

31 ation of the secretory pulse mass (basal vs. tolbutamide, 167 +/- 37 vs. 362 +/- 50 pmol/pulse; P < 0

32 Perfusion of tolbutamide (200 microm) or wortmannin (100-200 nm) prev

33 the insulin secretory burst mass (basal vs. tolbutamide, 266 +/- 64 vs. 817 +/- 144 pmol/pulse; P <

34 Each subject underwent two FSIGTTs, one with tolbutamide (300 mg) and the other with insulin (0.03 U/

35 pmol/l; P < 0.01) and portal vein (basal vs. tolbutamide, 345 +/- 55 vs. 1,288 +/- 230 pmol/l; P < 0.

36 ted by apamin or by the KATP channel blocker tolbutamide (400 microM-1 mM).

37 ponse to local application of KCl (60 mM) or tolbutamide (50-200 microM), we recorded barrages of amp

38 urrents): the currents were > 90% blocked by tolbutamide (500 microM), meglitinide (10 microM) or gli

39 centrations in the carotid artery (basal vs. tolbutamide, 85 +/- 12 vs. 325 +/- 66 pmol/l; P < 0.01)

40 -cells because treatment of these cells with tolbutamide, a blocker of ATP-sensitive K+ channels, pro

41 s 7-hydroxylated metabolite was inhibited by tolbutamide, a Cyp2c isoform-specific substrate, and tha

42 Minoxidil and tolbutamide, a K(ATP) channel blocker, opposed each othe

43 Superfusion of tolbutamide, a K(ATP) channel sulfonylurea receptor bloc

44 When either tolbutamide, a KATP channel blocker, or ZIP were adminis

45 In contrast, the sulfonylurea tolbutamide, a specific blocker of KATP channels, closed

46 se effects were reversed by the sulfonylurea tolbutamide, a specific inhibitor of K(ATP).

47 were markedly inhibited by the sulfonylurea tolbutamide, accounting for the efficacy of sulfonylurea

48 that 8-pCPT-2'-O-Me-cAMP-AM potentiation of tolbutamide action may involve activation of a 2-APB-sen

49 Tolbutamide activated glucose-responsive neurons; howeve

50 subnormal positive glucose AIR, and impaired tolbutamide AIR.

51 cute insulin responses to glucose (AIRg) and tolbutamide (AIRt) during FSIGTs and as the 30-min incre

52 Oral (250 mg) tolbutamide also magnified the endogenous insulin secret

53 Furthermore, we show that tolbutamide, an antagonist of the ATP-sensitive K+ chann

54 Insulin secretion stimulated by both 200 muM tolbutamide and 20 muM gliclazide, concentrations that h

55 t there is a bimolecular interaction between tolbutamide and CFTR, causing open channel blockade.

56 sulin secretion with pharmacological agents (tolbutamide and diazoxide) suggested a possible role for

57 tive to K+(ATP)-sensitive channel modulators tolbutamide and diazoxide.

58 nifedipine (VDCC blocker), the sulfonylureas tolbutamide and glibenclamide (KATP channel blockers), a

59 arization were blocked by the sulphonylureas tolbutamide and glibenclamide and by the photorelease of

60 e to sulfonylureas, we studied the effect of tolbutamide and glibenclamide on PKC activity.

61 ed potassium channel openers and inhibitors (tolbutamide and glibenclamide), plus a novel, selective

62 the tissue specificity of the sulfonylureas tolbutamide and glibenclamide, and the benzamido-derivat

63 Tolbutamide and glibenclamide, KATP+-channel blockers, m

64 K(ATP) channel is involved in the binding of tolbutamide and glibenclamide.

65 annel that was blocked by the sulphonylureas tolbutamide and glibenclamide.

66 arization were blocked by the sulphonylureas tolbutamide and glibenclamide.

67 ur data demonstrate that the actions of both tolbutamide and gliclazide are strongly potentiated by 8

68 Thus tolbutamide and gliclazide block channels containing SUR

69 Tolbutamide and gliclazide block the K(ATP) channel K(ir

70 Both tolbutamide and gliclazide stimulated phospholipase C ac

71 interaction was reduced by the sulfonylureas tolbutamide and gliclazide, but not by the pore blocker

72 lar results were seen with the sulfonylureas tolbutamide and glipizide.

73 lies the inhibition of glucagon secretion by tolbutamide and glucose.

74 Thus the tolbutamide and insulin protocols must not be used inter

75 ) concentration ([Ca(2+)](i)) in response to tolbutamide and KCl, and these depolarizing stimuli prod

76 s glucose tolerance tests (FSIGTT), one with tolbutamide and three with the same insulin dosage (0.03

77 SG(tolbutamide) and SG(insulin) were not different among th

78 S(G(tolbutamide)) and S(G(insulin)) were not different (1.88

79 glucose concentrations, by the sulfonylurea tolbutamide, and by a depolarizing concentration of pota

80 al responses to glucose, leucine, diazoxide, tolbutamide, and extracellular CaCl2 omission or excess.

81 exceeded its initial intracellular pool and tolbutamide, and high K(+) increased IGF2 secretion only

82 hibited insulin secretion evoked by glucose, tolbutamide, and imidazolines.

83 sing MIN6 pseudoislets responded to glucose, tolbutamide, and KCl with insulin secretory profiles sim

84 were inhibited by glucose, the sulfonylurea tolbutamide, and the imidazoline compounds efaroxan and

85 of PKA inhibitors, the KATP channel blocker tolbutamide, and the L-type Ca(2+) channel blocker israd

86 y, insulin secretory response to glucose and tolbutamide, and tolbutamide clearance.

87 Diazoxide suppressed IS and tolbutamide antagonized the inhibition.

88 KATP currents, the blocking effect of 0.5 mM tolbutamide appeared greater in the presence of 100 micr

89 We chose tolbutamide because weak (i.e., fast-type) open channel

90 It did not affect the Ki for tolbutamide block at either the high- or low-affinity si

91 id not affect the gating, ATP sensitivity or tolbutamide block of a truncated isoform of Kir6.2, Kir6

92 The dose-response relation for tolbutamide block of Kir6.2 delta C36 (a truncated form

93 mechanism by which nucleotides modulate the tolbutamide block of the beta-cell ATP-sensitive K+ chan

94 The dose-response relation for tolbutamide block of wild-type KATP currents in the abse

95 High-affinity tolbutamide block was also abolished.

96 ensitivity and the fraction of high-affinity tolbutamide block, although to a lesser extent than for

97 ion of the protein involved in high-affinity tolbutamide block.

98 concomitantly with the loss of high-affinity tolbutamide block.

99 ted by sulfonylurea-sensitive K(+) channels: tolbutamide blocked DA modulation by glutamate and by GA

100 The sulfonylurea tolbutamide blocked heterozygous R50Q (89%) and R50P (84

101 Both 100 nM glibenclamide and 200 M tolbutamide, blockers of the -cell ATP-sensitive K+ chan

102 el (MINMOD) protocol was evaluated using the tolbutamide-boosted protocol as a reference.

103 were inhibited by diazoxide and restored by tolbutamide but were not further augmented by other agen

104 medium and was blocked by glibenclamide and tolbutamide, but not by charybdotoxin.

105 Loss of acute insulin response to tolbutamide can identify children with diffuse SUR1 defe

106 Tolbutamide caused a high-frequency Lorentzian (corner f

107 The concentration of tolbutamide causing a 50% reduction of Po Burst (540 +/-

108 Neither the infusion nor the ingestion of tolbutamide changed the calculated clearance rates of en

109 ory response to glucose and tolbutamide, and tolbutamide clearance.

110 component increased as a linear function of tolbutamide concentration, as expected for a pseudo-firs

111 Both S(I(insulin)) and S(I(tolbutamide)) correlated significantly with S(I(clamp))

112 cued to the cell surface by the sulfonylurea tolbutamide could be subsequently activated by metabolic

113 Tolbutamide decreased glucagon secretion at 1 mmol/L glu

114 s treatment with the KATP channel antagonist tolbutamide decreases survival and increases viral repli

115 Inhibition of K(ATP)-channels with tolbutamide depolarized alpha-cells by 10 mV and reduced

116 glutamate and GABA(A) receptor antagonists, tolbutamide depolarized and significantly increased the

117 ng insulin secretory response to intravenous tolbutamide despite a small response to intravenous gluc

118 While the bss mutants fed tolbutamide did not display a reduction in SLA, they did

119 KATP channels do not drive this, as tolbutamide did not trigger release.

120 echanical shock, the eas and tko mutants fed tolbutamide displayed less SLA and recovered quicker tha

121 ulin release studies documented that whereas tolbutamide failed to cause insulin secretion as a conse

122 pinephrine, and the K(ATP) channel inhibitor tolbutamide, failed to synchronize islets.

123 amperometric events evoked by application of tolbutamide followed the closure of ATP-sensitive K+ cha

124 of the insulinotropic antidiabetes compounds tolbutamide, glibenclamide, glimepiride, and nateglinide

125 I(KATP) was inhibited reversibly by tolbutamide (IC(50) of 34.1 microM) and irreversibly by

126 a 48-h infusion of 200 mg x kg(-1) x day(-1) tolbutamide in 20% glucose.

127 mmol/l lactate or the K(ATP) channel blocker tolbutamide increased their action potential frequency.

128 The greater response to glucose than to tolbutamide indicates that ATP-sensitive potassium (KATP

129 We conclude that sulfonylurea (tolbutamide) induced insulin secretion in vivo is achiev

130 treatment protocol also abolished 200 microm tolbutamide-induced insulin secretion from perifused isl

131 isobutyl-1-methylxanthine (IBMX-), KCl-, and tolbutamide-induced insulin secretion.

132 livery, saturation of insulin action, and/or tolbutamide-induced proinsulin release.

133 daily blood glucose values were equal in the tolbutamide-infused and control rats.

134 Pancreas amylin content was unchanged in the tolbutamide-infused rats as was amylin secretion, result

135 esponse to hypoglycemia was prevented during tolbutamide infusion (P < 0.0001).

136 in secretion in vivo directly in response to tolbutamide infusion or ingestion.

137 8 +/- 230 pmol/l; P < 0.01) increased during tolbutamide infusion, but the portal vein plasma flow di

138 Hypoglycemia with tolbutamide infusion, compared with similar hypoglycemia

139 nses to hypoglycemia were not reduced during tolbutamide infusion.

140 tively, during hypoglycemia with and without tolbutamide infusion.

141 The sulfonylurea drug tolbutamide inhibited 130 pS channel openings elicited b

142 Tolbutamide inhibited Kir6.2/SUR1 (Ki approximately 5 mi

143 er: (1) the sulfonylureas, glibenclamide and tolbutamide, inhibited NCCa-ATP channels with EC50 value

144 High-affinity tolbutamide inhibition could be conferred on SUR2A by re

145 M), there was no difference in the extent of tolbutamide inhibition in the presence or absence of MgA

146 Conversely, high-affinity tolbutamide inhibition of SUR1 was abolished by replacin

147 I uncovered an attenuated tolbutamide inhibition of the hyperstimulated mutant, wh

148 constitute the principal mechanism by which tolbutamide inhibits the KATP channel.

149 nsulin concentrations induced by glucose and tolbutamide injection did not cause any change in plasma

150 The Ki for tolbutamide interaction with either the high- or low-aff

151 imarily because of the lower partitioning of tolbutamide into phospholipid bilayers.

152 ree BS strains were fed a sulfonylurea drug (tolbutamide) known to both increase heamolymph glucose c

153 nnels that can respond to minoxidil and that tolbutamide may suppress hair growth clinically; novel d

154 response of the mutant channel complexes to tolbutamide, MgADP and diazoxide is disturbed.

155 isposition index (DI) were determined by the tolbutamide-modified intravenous glucose tolerance test

156 d tomography, and insulin sensitivity by the tolbutamide-modified, frequently sampled intravenous glu

157 Neither tolbutamide nor glibenclamide elicited translocation of

158 r major drug-metabolizing enzymes (caffeine, tolbutamide, omeprazole, dextromethorphan, and oral and

159 of this study was to quantify the effects of tolbutamide on CFTR gating in excised membrane patches c

160 secretion produced by high concentrations of tolbutamide or diazoxide, or disruption of K(ATP) channe

161 Purified brain PKC was not activated by tolbutamide or glibenclamide, whether tested in the abse

162 Ca(2+) transients stimulated by either tolbutamide or gliclazide were inhibited by thapsigargin

163 in the presence of nifedipine, diazoxide, or tolbutamide or if K(ATP) channel knockout mouse islets w

164 No sensitivity to tolbutamide or metabolic inhibition was observed when SU

165 the secretory responses of cells to glucose, tolbutamide, or a depolarizing concentration of KCl.

166 t that depolarization with high external K+, tolbutamide, or glucose caused a rapid increase in cAMP

167 4 +/- 1.9 pmol x kg(-1) x min(-1); basal vs. tolbutamide, P < 0.01).

168 19 metabolize many important drugs including tolbutamide, phenytoin, and (S)-warfarin.

169 cine, depolarizing concentrations of KCl and tolbutamide, pointing to a general phenomenon and common

170 annel inhibition with a low concentration of tolbutamide prevents electromechanical decline when oxyg

171 odel analysis (MINMOD) was compared with the tolbutamide protocol and the glucose clamp in 35 nondiab

172 ted that the sulfonylureas glibenclamide and tolbutamide reduced CFTR whole cell currents.

173 urrent records revealed that the addition of tolbutamide reduced the apparent single-channel current

174 quently activated by metabolic inhibition on tolbutamide removal.

175 +/- 5, 29 +/- 5, and 23 +/- 4% lower than SI(tolbutamide), respectively.

176 The properties of the tolbutamide response indicate that the drug disrupts the

177 on with 1 mM NaN3 revealed the presence of a tolbutamide-sensitive channel exhibiting a unitary condu

178 10 microM) in the pipette solution activated tolbutamide-sensitive KATP channels in CRI-G1 cells.

179 el recordings indicate that leptin activates tolbutamide-sensitive KATP channels in CRI-G1 insulin-se

180 ings, insulin prevented leptin activation of tolbutamide-sensitive KATP channels.

181 tion of 1-50 microM troglitazone depolarised tolbutamide-sensitive neurones in a poorly reversible ma

182 ubunits, which correlated with the diazoxide/tolbutamide sensitivity.

183 Finally, tolbutamide significantly increased GnRH secretion from

184 , since the ATP-sensitive K+ channel blocker tolbutamide substituted for glucose in inducing [Ca2+]i

185 (120 ng/min glibenclamide or 2.7 microg/min tolbutamide) suppressed counterregulatory (epinephrine a

186 With the same amount of tolbutamide, the decrease in pHin was much smaller, prim

187 t HI islets were challenged with glucose and tolbutamide, there was no rise in intracellular free cal

188 ion was also potentiated by the sulfonylurea tolbutamide (threefold at 3 mmol/l glucose and 50% at 15

189 A subset of hearts was perfused with 1 mum tolbutamide (TOLB) to identify the level of AP duration

190 m, the acute insulin response to intravenous tolbutamide was absent and did not overlap with the resp

191 effect was not specific for meglitinide, as tolbutamide was also unable to prevent MgADP activation

192 The effect of tolbutamide was blocked either by inhibition of PKC or w

193 latter occasions, the beta-cell secretagogue tolbutamide was infused in a dose of 1.0 g/h from 60 thr

194 entiation of insulin secretion stimulated by tolbutamide was markedly inhibited by 2-APB (25 muM) and

195 However, when the Po was decreased (by ATP), tolbutamide was unable to block Kir6.2DeltaN14/SUR1-K719

196 ed in the same units (dl/min per pU/ml), S(I(tolbutamide)) was on average 13 +/- 6% lower than S(I(cl

197 ic resonance spectroscopy, glibenclamide and tolbutamide, were found to incorporate into phospholipid

198 Tolbutamide, which activates glucose-stimulated neurons,

199 Stimulation of insulin release by tolbutamide, which inhibits the K(ATP) channel and depol

200 but not Kir6.2-SUR2A channels are blocked by tolbutamide with high affinity.

201 Our results indicate that interaction of tolbutamide with the high-affinity site (on SUR1) abolis