ライフサイエンスコーパス: L-glucose

1 cose (LG, 5.5 mmol/L D-glucose and 17 mmol/L L-glucose).

2 nhibition of S6K1 phosphorylation by 20 mmol/l glucose.

3 ed with levels in control islets at 5.5 mmol/l glucose.

4 ncreased insulin secretion by 46% at 11 mmol/l glucose.

5 4 h in media containing 0, 3, 6, or 25 mmol/l glucose.

6 hibition by the transition from 5 to 20 mmol/l glucose.

7 4% below that of islets cultured at 5.5 mmol/l glucose.

8 marked stimulation was observed at 8.3 mmol/;l glucose.

9 was added to the perfusate containing 5 mmol/l glucose.

10 ycling rate was further increased at 11 mmol/L glucose.

11 eversible manner in B6 MC exposed to 25 mmol/l glucose.

12 onectin synthesis, as compared with 5.5 mmol/l glucose.

13 e and significantly so only at < or = 2 mmol/l glucose.

14 lete within 15 min and occurred in 5-10 mmol/l glucose.

15 nd zeta) was detected in response to 25 mmol/l glucose.

16 l/l unlabeled palmitate, at 2.8 or 16.7 mmol/l glucose.

17 was increased in myocytes exposed to 25 mmol/l glucose.

18 ure) with half-maximal stimulation at 6 mmol/l glucose.

19 for 4 days with 0.25 mmol/l oleate/5.5 mmol/l glucose.

20 compared with muscles incubated with 0 mmol/l glucose.

21 iflozin-induced glucagon secretion at 6 mmol/L glucose.

22 e increasing AII by 25% compared with 5 mmol/l glucose.

23 e silent below 1 mmol/l and active at 5 mmol/l glucose.

24 exposed to 25 mmol/L compared with 5.6 mmol/L glucose.

25 red with culture in medium containing 5 mmol/l glucose.

26 neurons by the transition from 5 to 20 mmol/l glucose.

27 diabetic donors were exposed to 5 or 30 mmol/l glucose.

28 se, but not when they were exposed to 5 mmol/l glucose.

29 origin in the presence of both 5 and 30 mmol/l glucose.

30 lated islets of rats maintained at 1.67 mmol/l glucose.

31 reached a maximum rate between 8 and 10 mmol/l glucose.

32 f reperfusion with buffer containing 11 mmol/L glucose.

33 se or high-glucose medium containing 25 mmol/l glucose.

34 ore sensitive to substimulatory 4 and 6 mmol/L glucose.

35 ed the oscillatory pattern induced by 7 mmol/L glucose.

36 to a control culture condition with 5.1 mmol/L glucose.

37 maly was a large stimulation of IS by 1 mmol/L glucose.

38 mmol/L and was further increased by 15 mmol/L glucose.

39 aline (PBS) supplemented with 0 to 55.6 mmol/L glucose.

40 cells showing spontaneous activity at 1 mmol/l glucose.

41 s; maximal inhibition was observed at 6 mmol/l glucose.

42 lpha-cells are electrically active at 1 mmol/l glucose.

43 hibited insulin secretion elicited by 6 mmol/l glucose.

44 ) kappaB translocation in both 5 and 25 mmol/l glucose.

45 ompared with either continuous 10 or 15 mmol/l glucose.

46 GLP-1 secretion in the ileum at >/=200 mmol/L glucose.

47 (IC(50) = 0.025 micromol/l) held at 0.5 mmol/l glucose.

48 d PKCbetaII levels were increased in 25 mmol/L glucose.

49 potential frequency in both low and 2.5 mmol/l glucose.

50 ose concentration (25 mmol/l) than at 5 mmol/l glucose.

51 lated by insulin in the presence of 0.1 mmol/l glucose.

52 rved in 17 of 30 islets exposed to 11.1 mmol/l glucose.

53 l as increase the synthesis of glycogen from L-glucose.

54 ompetitive inhibition with D-glucose but not L-glucose.

55 t was observed with 2-deoxy-glucose, but not L-glucose.

56 brain was inhibited by d-glucose, but not by l-glucose.

57 ites were competitive with D-glucose but not L-glucose.

58 cells with the nonmetabolizable stereoisomer L-glucose.

59 ls are rapidly degraded by D-glucose but not L-glucose.

60 not produced by nontransported sugars, e.g., L-glucose.

61 5.4 g/L L-homoalanine was produced from 30 g/L glucose (0.18 g/g glucose yield, 26% of the theoretica

62 nificant increase in MDA in VSMCs in 25 mmol/l glucose (1.34 +/- 0.11 vs. 1.88 +/- 0.24 nmol/mg prote

63 deoxy-D-glucose (2-DG, 1 microM), but not to L-glucose (1 microM), significantly attenuated (P<0.05)

64 s were made under control conditions: 5 mmol/L glucose, 1 mmol/L lactate, 0.1 mmol/L pyruvate, 0.3 mm

65 Hindquarters were perfused with 7 mmol/l glucose, 1,000 micromol/l albumin-bound palmitate, and

66 After a 40-min exposure to 16.7 mmol/l glucose, 10.2% of the granules (approximately 1,060) w

67 l/l glucose/10 mmol/l arginine, and 5.5 mmol/l glucose/10 mmol/l arginine were reduced in parallel, e

68 responses to 16.7 mmol/l glucose, 16.7 mmol/l glucose/10 mmol/l arginine, and 5.5 mmol/l glucose/10

69 a doubling of insulin secretion to 16.7 mmol/l glucose/10 nmol/l GIP.

70 acking glucose, or with (b) nonmetabolizable L-glucose (100 mM).

71 Insulin responses to 16.7 mmol/l glucose, 16.7 mmol/l glucose/10 mmol/l arginine, and 5

72 timulation by 15 mmol/l compared with 3 mmol/l glucose), 17% of the clones were moderately responsive

73 inger bicarbonate buffer containing 2.8 mmol/l glucose, 20 micromol/l mastoparan stimulated insulin s

74 um withdrawal (rat VSMCs in normal [5.5 mmol/L] glucose 28+/-1%, high D-glucose 19+/-2%; P:<0.0001).

75 release to a similar extent (46%) as 10 mmol/l glucose (55%), and the selective GABA(A) receptor (GAB

76 er equilibration in RPMI containing 5.6 mmol/l glucose, 6.4% of the granules (approximately 700) were

77 ycogen synthesis and GS activity at 0.1 mmol/l glucose-6-phosphate, and reduced GS protein content by

78 F mice, P < 0.05) and in vitro (at 22.2 mmol/l glucose: 640 +/- 120.1 vs. 1,615 +/- 196.9 pg. microg

79 At 20 mmol/l glucose, a blocker of sarcoendoplasmic reticulum calci

80 th Krebs-Henseleit buffer containing 10 mmol/L glucose; a second group, with the buffer containing 5

81 Increasing plasma glucose levels to 18 mmol/l glucose, after clamp at 11 mmol/l, increased insulin s

82 -galacturonic acid, d-talose, l-altrose, and l-glucose, all of which failed as wild-type GalK substra

83 ucose, and 2-deoxyglucose but not galactose, l-glucose, alpha-methyl-d-glucoside, or fructose.

84 n to 30 micromol/l during fusion at 5.5 mmol/l glucose also did not alter basal GS FV (10.61 +/- 1.69

85 f fructose and mannose (but not galactose or L-glucose) also inhibit the release of IL-1 activity, su

86 d human islets to overnutrition with 25 mmol/L glucose and 0.5 mmol/L palmitic acid (glucolipotoxicit

87 l/l glucose and the combination of 16.7 mmol/l glucose and 10 mmol/l arginine, 0.1 mmol/l 3-isobutyl-

88 mol/l glucose for 5 weeks followed by 6 mmol/l glucose and 19 mmol/l mannitol for an additional 5 wee

89 in media containing either normal (5.5 mmol/l glucose and 22 pmol/l insulin) or increased concentrat

90 ulfonylurea tolbutamide (threefold at 3 mmol/l glucose and 50% at 15 mmol/l glucose) and was abolishe

91 e PKC isozymes occurs in response to 25 mmol/l glucose and ANG II; and 3) AT-1R-dependent PKC isozyme

92 Compared with 5 mmol/l glucose and no insulin (control), high glucose alone,

93 l preparation/min in the presence of 10 mmol/l glucose and pulsatile (3.7 +/- 0.4 min/pulse).

94 cacy at EC(50) = 0.06 micro mol/l) at 8 mmol/l glucose and shifted the glucose dose response curve to

95 TGF-beta in MCs cultured in 5.6 or 30.0 mmol/l glucose and suppressed or abolished increases in TGF-b

96 I, and IRI secretion compared with 1.67 mmol/l glucose and the combination of 16.7 mmol/l glucose and

97 uced insulin secretion stimulated by 11 mmol/l glucose and the subsequent response to stimulation wit

98 Glucose oxidation was doubled at 2.8 mmol/l glucose and unchanged at 27.7 mmol/l glucose in the FA

99 on did not alter the time profiles of plasma L-glucose and 3-O-methylglucose after an intravenous inj

100 e uptake of five different sugars, including L-glucose and D-xylose, is described in this issue (Mein

101 efold at 3 mmol/l glucose and 50% at 15 mmol/l glucose) and was abolished by diazoxide, which demonst

102 6 M for d-glucose, and 0.032 +/- 0.007 M for l-glucose) and similar sweetness intensities at suprathr

103 0.006 M for d-glucose, and 0.032 0.007 M for l-glucose) and similar sweetness intensities at suprathr

104 fter 210 min (range 1.4-3.6 vs. 4.1-5.3 mmol/L glucose), and 24-h glucose profiles showed that the pa

105 albumin, washed bovine erythrocytes, 8 mmol/l glucose, and +/-2 mmol/AICA-riboside or +/-60 nmol/l i

106 (P)H autofluorescence in response to 25 mmol/l glucose, and this was reduced by approximately 95% in

107 e carried out for three small solutes-water, L-glucose, and hydrocortisone-covering a wide range of m

108 At 6 mmol/L glucose, ANP readily elicited Ca(2+) influx in control

109 ol/L [2-13C]acetate plus supplemental 5 mmol/L glucose, any potential differences in endogenous carbo

110 ctive (alphaMDG > D-glucose > D-galactose >> L-glucose approximately D-mannose), 2) inhibited by phlo

111 pt for the first phase response to 16.7 mmol/l glucose/arginine.

112 -triol has been developed using either d- or l-glucose as the starting material.

113 atly stimulated insulin release at 0-30 mmol/l glucose but affected the concentration of free ADP onl

114 d no effect on insulin secretion at 2.8 mmol/l glucose but increased insulin secretion by 46% at 11 m

115 levels increased in B6 MC exposed to 25 mmol/l glucose but returned to baseline levels when the gluco

116 axis occurred in a serum gradient in 25 mmol/L glucose (but not in 5 mmol/L glucose) in association w

117 sequent response to stimulation with 30 mmol/l glucose, but it was without significant effect when th

118 at 90 kDa when cells were exposed to 30 mmol/l glucose, but not when they were exposed to 5 mmol/l gl

119 aseline and increased in response to 25 mmol/l glucose, but remained elevated when glucose concentrat

120 ells maintained in medium containing 25 mmol/l glucose can respond.

121 Exposure of GMC to 25 mmol/l glucose caused the activation of JAK2, STAT1, STAT3, a

122 ofold (by intralipid infusion during 11 mmol/l glucose clamp) resulted in a robust, approximate twofo

123 penia and/or systemic hypoglycemia (2.8 mmol/l glucose clamp).

124 to a hyperinsulinemic-hypoglycemic (2.5 mmol/l) glucose clamp for 90 min.

125 fternoon 2-h hyperinsulinemic (528+/-30 pmol/l) glucose clamp studies of 5.3+/-0.1 mmol/l (euglycemic

126 glycemic (5.0 mmol/L)-hypoglycemic (2.8 mmol/L) glucose clamp.

127 .32 mmol/L) hypoglycemic (2.80 +/- 0.12 mmol/L) glucose clamp.

128 .1 mmol/l) or hypoglycemic (2.9 +/- 0.1 mmol/l) glucose clamps (prolonged hypoglycemia) were carried

129 ion was increased by both 11.1 and 33.3 mmol/l glucose compared with 5.5 mmol/l.

130 Dd-Glucose, but not L-glucose, competed for D-chiro-[3-3H]inositol uptake ov

131 values up to 18.5% (3.78 vs 3.19) at 8-mmol/L glucose concentration after 7 days in culture (P < .00

132 amount of insulin secreted over the 5-9 mmol/l glucose concentration range in the control subjects an

133 prathreshold (6.8 mmol/l) or high (16.8 mmol/l) glucose concentration in the presence of the phosphod

134 prandial (14.1 +/- 0.6 vs. 15.9 +/- 0.9 mmol/l) glucose concentrations were lower (P < 0.01) after vi

135 at optimal (10 mmol/l) or elevated (30 mmol/l) glucose concentrations.

136 fold higher than the prestimulated 1.67 mmol/l glucose condition.

137 ly two- to sixfold higher than the 16.7 mmol/l glucose condition.

138 to 2.8 mmol/L glucose (P<0.05), and 20 mmol/L glucose conditions.

139 murine cardiac biopsies under high (25 mmol/L) glucose conditions reduced CSC yield (P=0.003), impai

140 ured under low (5.5 mmol/l) or high (25 mmol/l) glucose conditions.

141 human monocytic cell line) under HG (15 mmol/l glucose) conditions, whereas AT supplementation inhibi

142 crophages, even under hyperglycemic (50 mmol/l glucose) conditions.

143 lizers tested (glycerol, sucrose, trehalose, L-glucose, D-glucose, and D-galactose), and in each case

144 As a result of this analysis, l-glucose, d-glucose, l-allose, d-allose, d-gulose, d-ga

145 ts interactions with nonspecific substrates (L-glucose, D-mannose, and 2-deoxy-D-glucose).

146 Exposure of beta-HC9 cells to 5 mmol/l glucose decreased intracellular Na(+) levels monitored

147 cultured in 5 mmol/l glucosamine or 20 mmol/l glucose demonstrated only 3.79 +/- 0.60 or 1.6 +/- 0.7

148 Interestingly, both l-glucose-derived ligands are partial agonists: they are

149 l-Glucose-derived ligands, methyl alpha-l-glucopyranosid

150 re media from myocytes maintained in 25 mmol/l glucose detected a twofold increase in ANG II.

151 Exposure of HRECs to 25 mmol/l glucose did not stimulate endogenous ROS production, a

152 2-deficient islets stimulated with 22.8 mmol/L glucose exhibited potentiation of insulin release comp

153 ontrast, adding 15 mmol/l pyruvate to 5 mmol/l glucose failed to activate glucose-responsive neurons,

154 ebs-Henseleit buffer with or without 11 mmol/L glucose, followed by 32 minutes of reperfusion with bu

155 ed with both exogenous insulin and 16.7 mmol/l glucose, followed by switching off both the insulin an

156 ricytes were cultured in either 5 or 25 mmol/l glucose for 10 days.

157 Incubation of INS-1 cells at 25 mmol/l glucose for 24 h led to an 18-fold increase in TXNIP p

158 .05) and by 75% in cells switched to 20 mmol/l glucose for 3 days (P < 0.005).

159 f mesangial cells (MCs) in 5.6 vs. 30.0 mmol/l glucose for 3 weeks induced a sustained increase in pr

160 Exposure of ROP mesangial cells to 25 mmol/l glucose for 35 days induces both clonal selection and

161 SFs were cultured in medium with 25 mmol/l glucose for 36 h.

162 enic mouse embryos cultured in 30 or 50 mmol/l glucose for 48 h exhibited a higher incidence of morph

163 Thus exposure of GK+/- islets to 30 mmol/l glucose for 48-96 h enhanced their ability to sense an

164 ained in islets incubated in 11.6 or 30 mmol/l glucose for 48-96 h were compared.

165 MC were exposed to 25 mmol/l glucose for 5 weeks followed by 6 mmol/l glucose and 1

166 ndothelial cells (HUVECs) with 30 vs. 5 mmol/l glucose for 72 h causes a significant increase in apop

167 half-maximal values at approximately 1 mmol/l glucose for both respiration and secretion.

168 xposed to normal (5 mmol/l) or high (25 mmol/l) glucose for 12-24 h.

169 n (<2.8 mmol/L glucose) vs. 0 min (<3.9 mmol/L glucose) for the control participants.

170 the third group, the buffer contained 5 mmol/L glucose; for the fourth, 5 mmol/L glucose plus 0.4 mmo

171 definitive and cheap synthesis of 99.4% pure L-glucose from D-glucose which requires purification of

172 At 2.5 mmol/l glucose, fura-2 Ca(2+) imaging of dissociated ventrome

173 amide decreased glucagon secretion at 1 mmol/L glucose (G1) but stimulated it at 7 mmol/L glucose (G7

174 l/L glucose (G1) but stimulated it at 7 mmol/L glucose (G7).

175 ted mouse islets in the presence of 0.5 mmol/l glucose, gamma-aminobutyric acid (GABA) inhibited gluc

176 HAECs cultured for 7 days in 25 mmol/L glucose had a 2-fold elevation in interleukin-8 (IL-8)

177 der the same Ca2+-free conditions, 11.1 mmol/l glucose had no effect on insulin release alone, but au

178 rmal adult rats for up to 1 day with 50 mmol/l glucose had no effect; however, 1.0 nmol/l insulin inc

179 l-glucose had no effect.

180 mentation with the nonmetabolized enantiomer L-glucose had no effect.

181 Treatment of MES cells with 25 mmol/l glucose (HG) for 48 h increases cellular fibronectin l

182 Exposure of mesangial cells to 30 mmol/l glucose (high glucose) vs. 5 mmol/glucose (normal gluc

183 proximal tubular epithelial cells by 30 mmol/l glucose (high glucose), 1 nmol/l insulin (high insulin

184 phosphate (P(i)) was decreased with 30 mmol/l glucose in contrast to the decreased level of PCr and

185 activities was altered between 5 and 25 mmol/l glucose in either cell type.

186 Preincubation for 4 h with 25 mmol/l glucose in the absence of insulin produced a similar a

187 Islets were also exposed to 16.7 mmol/l glucose in the absence or presence of 10 micromol/l ni

188 .8 mmol/l glucose and unchanged at 27.7 mmol/l glucose in the FA-cultured islets despite a 35% decrea

189 at contained 400 mg/dl mannitol or 400 mg/dl L-glucose in addition to 100 mg/dl D-glucose did not inc

190 ient in 25 mmol/L glucose (but not in 5 mmol/L glucose) in association with increased phosphorylation

191 lucose (5.5 mmol/l glucose) or HG (25.5 mmol/l glucose) in the presence or absence of metformin or th

192 to 5 +/- 2% of events by culture at 30 mmol/l glucose, in line with decreases in Glut2 and glucokina

193 solated beta-cells in the presence of 3 mmol/l glucose increased [Ca(2+)](i) to 178 +/- 10% of basal

194 ontrast, exposure of GK+/+ islets to 30 mmol/l glucose increased their basal insulin secretion but re

195 Incubation of cells with 30 mmol/l glucose increased total TGF-beta1 secretion, which was

196 However, 5 mm l-glucose increased the P(f) of T310I, consistent with a

197 potoxicity (0.5 mmol/L palmitate and 25 mmol/L glucose) increases LC3 II, a marker of autophagy.

198 dependent manner, with incubation in 30 mmol/l glucose increasing AII by 25% compared with 5 mmol/l g

199 variate analysis (odds ratio = 1.08 per mmol/L glucose increment; p < 0.001) but not after adjustment

200 Thus, 25 mmol/l glucose induced reversible changes in MMP-2, TGF-beta(

201 -kappaB inhibited the hyperglycemia (25 mmol/l glucose)-induced cell death in retinal endothelial cel

202 fold elevated rate of both basal and 10 mmol/l glucose-induced insulin secretion.

203 In NOD mice beta-cells, 8 mmol/L glucose-induced synchronized short [Ca2+]c events dimi

204 for the first time that 10 mm d-glucose and l-glucose inhibit P(f) by approximately 45% in the WT bu

205 Switching from 1 to 7 mmol/L glucose inhibited glucagon release.

206 f embryo tissue in medium containing 15 mmol/l glucose inhibited Pax-3 expression compared with cultu

207 Preincubation with 25 mmol/l glucose + insulin (10 mU/ml) led to a 70% decrease in

208 bserved in muscles preincubated with 25 mmol/l glucose + insulin for 5 min.

209 During the first 2 h of the clamp (11 mmol/l glucose), insulin secretion and insulin resistance (S(

210 Furthermore, in the presence of 15 mmol/l glucose, insulin secretion was potentiated significant

211 conclusion, chemotaxis to PDGF-BB in 25 mmol/L glucose is PKCbetaII-dependent and requires activation

212 In 5 mmol/L glucose, islets from C57BL/6J chow-fed mice cycled app

213 beta-D- and beta-L-glucose, L-mannose, and the 6-deoxy-6-N-analogue of be

214 , high glucose (HG, 23 mmol/L D-glucose), or L-glucose (LG, 5.5 mmol/L D-glucose and 17 mmol/L L-gluc

215 raised in 25 mmol/l compared with 5.56 mmol/l glucose media also demonstrated reduced morphine-induc

216 Cells exposed to 20 mmol/l glucose medium for 3 days demonstrated increases in GL

217 dothelial (RME) cells grown in high (30 mmol/l)-glucose medium for 9 days had reduced Cx43 expression

218 s) grown in normal (5 mmol/l) or HG (30 mmol/l glucose) medium for 7 days were assessed for expressio

219 After exposure to 5 or 30 mmol/l glucose, no changes were detected in mRNA levels in MM

220 also secretory responses induced by 20 mmol/l glucose or by 50 mumol/l arachidonic acid.

221 ecrete glucagon in response to either 1 mmol/L glucose or dapagliflozin, indicating a functional impa

222 ys in either normal medium containing 5 mmol/l glucose or high-glucose medium containing 25 mmol/l gl

223 f normal platelets in high concentrations of L-glucose or insulin.

224 beta cells with equimolar amounts (25 mM) of l-glucose or mannitol had no effect on TXNIP expression

225 imicked by the nonmetabolizable carbohydrate L-glucose or the glucokinase inhibitor glucosamine or wh

226 control animals perfused with either 100 mM L-glucose or the iso-osmotic solution lacking glucose.

227 ompared with those incubated with either the l-glucose or untreated controls.

228 medium with either normal glucose (5.5 mmol/l glucose) or HG (25.5 mmol/l glucose) in the presence o

229 ther 100 mmol/L mannitol (control), 100 mmol/L glucose, or no additional solute (hypotonic solution).

230 as exposed to D-mannose, D-fucose, D-ribose, L-glucose, or L-galactose, but it changed markedly in th

231 m arabic (GA) to a 90 mmol/L sodium-111 mmol/L glucose oral rehydration solution (ORS) enhances its e

232 pared with that at a basal level of 2.8 mmol/l glucose (P < or = 0.05).

233 tion over control cells cultured in 5.5 mmol/L glucose (P<0.001).

234 cultured without NGF in response to 2.8 mmol/L glucose (P<0.05), and 20 mmol/L glucose conditions.

235 e neurons, although pyruvate added to 0 mmol/l glucose permitted neurons to maintain activity.

236 Perifusion with 16.7 mmol/l glucose plus 0.1 mmol/l IBMX caused a biphasic secreti

237 ond group, with the buffer containing 5 mmol/L glucose plus 0.4 mmol/L oleate and 1 mU/mL insulin.

238 ned 5 mmol/L glucose; for the fourth, 5 mmol/L glucose plus 0.4 mmol/L oleate.

239 ive when islets were pretreated with 25 mmol/l glucose plus Q2.

240 ut not to high osmotic conditions (25 mmol/L L-glucose plus 5 mmol/L D-glucose) significantly lowered

241 denum and ileum, but not the colon, 300 mmol/L glucose potently stimulated GLP-1 release.

242 In wild-type mice, D-, but not L-glucose produced a phloridzin-sensitive, 4.1-mV hyperp

243 and then challenged with a 5-min, 11.1 mmol/l glucose pulse.

244 6h OGD, cells were reoxygenated with 11mmol/L glucose+/-pyruvate (8mmol/L) and/or rtPA (10microg/ml)

245 ing a subsequent 20-min incubation at 6 mmol/l glucose (r(2) = 0.93, P < 0.001).

246 al hyperinsulinemia a.m. and p.m. (~150 pmol/L), glucose Ra and glycerol Ra were both less suppressed

247 iosynthesis in the appropriate 2.8-16.7 mmol/l glucose range as defined in normal pancreatic islets.

248 pretreated for 40 min with 0, 5, or 15 mmol/l glucose, respectively.

249 a 45-min infusion of either 3.7 or 11.1 mmol/l glucose, rested for 20 min in the absence of glucose,

250 ed by (23)Na(+)-NMR spectroscopy and 30 mmol/l glucose resulted in a further decrease in cytosolic Na

251 tion of both these cell lines with 16.7 mmol/l glucose resulted in a two- to fourfold increase in hum

252 30 mM D-glucose, but not 30 mM L-glucose, resulted in the elevation of VEGF mRNA in RPT

253 terized by large insulin responses to 1 mmol/L glucose, resulting in very high basal secretion rates

254 high glucose (25 mmol/L) for 2 h, and 5 mmol/L glucose served as the control.

255 /- islets that had been incubated in 30 mmol/l glucose showed improved although not normal insulin se

256 ucose among other hexoses while fructose and L-glucose showed no inhibition.

257 bolizable (zero-calorie) sugar (sucralose or L-glucose), starved Gr5a; Gr64a double mutants preferred

258 pectively, P = 0.03) and during the 3.3-mmol/l glucose step (0.5 +/- 0.1 vs. 5.2 +/- 1.2 micromol.kg(

259 ructose infusion studies during the 3.9-mmol/l glucose step (4.6 +/- 0.9 vs. 7.4 +/- 1.1 micromol.kg(

260 eparations, the transition from 5 to 20 mmol/l glucose stimulated approximately 17% of the neurons (a

261 ceraldehyde, glycerol, and lactate to 5 mmol/l glucose stimulated glucose-responsive neurons.

262 In contrast, after 11 mmol/l glucose stimulation for 7 days, the relative levels of

263 ose mimicked the effects of d-glucose, while l-glucose, sucrose or mannitol were without effect.

264 rotein synthesis above a threshold of 4 mmol/l glucose that reached a maximum rate between 8 and 10 m

265 At 5 mmol/l glucose, the EC(50) for GKA50 in MIN6 cells was approx

266 At basal 2.8 mmol/l glucose, the muscarinic receptor agonist carbamylcholi

267 y, in islets stimulated for 2 h with 17 mmol/l glucose, the relative EDG-1 mRNA levels increased almo

268 ytotic events in cells maintained at 10 mmol/l glucose, this value was reduced reversibly to 5 +/- 2%

269 tory phenotype in the presence of up to 50 g/L glucose to a yeast strain, V5 hxt1-7Delta, in which on

270 t islets were first perifused with 16.7 mmol/l glucose to increase endogenous insulin secretion, foll

271 or impaired (IGT; 2-h glucose 7.8-11.1 mmol/l) glucose tolerance: NFG/NGT (n = 307), IFG/NGT (n = 11

272 We therefore tested the hypotheses that (l) glucose transport into myocytes is a critical limitin

273 Basal and acute insulin-stimulated (100 nmol/l) glucose transport was measured after re-equilibration

274 Maximal insulin-stimulated (100 nmol/l) glucose transport was reduced 70% in isolated adipocy

275 eased the uptake of 3H2-DOG by 28% in 8 mmol/l glucose-treated cells (P < 0.05) and by 75% in cells s

276 We concluded that 1) 25 mmol/l glucose triggers the release of ANG II by myocytes, re

277 mol/L glucose) with 36 +/- 10 min (<2.8 mmol/L glucose) vs. 0 min (<3.9 mmol/L glucose) for the contr

278 ic hyperglycemic clamp at 5, 10, and 15 mmol/l glucose was given in increasing steps as a single "spi

279 Glucagon secretion at 1 mmol/l glucose was inhibited by 40-70% by tetrodotoxin, heter

280 Glucagon secretion at 1 mmol/l glucose was inhibited by insulin but not by ZnCl(2).

281 GSIS at 20 mmol/l glucose was modestly impaired on incubation with exoge

282 f age, hypersecretion of insulin at 5.0 mmol/l glucose was observed in perifused islets from both obe

283 of total cell insulin releasable at 10 mmol/l glucose) was unchanged in beta-cells overexpressing th

284 is to PDGF-BB (360 pmol/L), absent in 5 mmol/L glucose, was present in raised glucose and could be bl

285 eonatal SCs with 20-30 mm d-glucose, but not l-glucose, was sufficient to inhibit transcription from

286 h KCl was not affected by culture at 30 mmol/l glucose, we conclude that hyperglycemia causes the abn

287 aortic endothelial cells exposed to 30 mmol/L glucose, we observed a similar loss of mitochondrial n

288 lar ATP levels after incubation with 10 mmol/l glucose were about 2.5 times lower in Foxa1-/- islets

289 TC1-9 cells such that mRNA levels at 16 mmol/l glucose were approximately 3.0-fold (alpha4), 2.0-fold

290 horylated analogues derived from both d- and l-glucose were synthesized.

291 ally cultured in medium containing 11.1 mmol/l glucose, were transfected with STF-1 alone or cotransf

292 islets, no effect was observed at 2.8 mmol/;l glucose, whereas a marked stimulation was observed at

293 activity in HIRc-B cells cultured in 1 mmol/l glucose, while cells cultured in 5 mmol/l glucosamine

294 in a subset of beta-cells resumed at 8 mmol/L glucose, while the long Ca2+ events were significantly

295 Preincubation of GMC cultured in 25 mmol/l glucose with a specific JAK2 or STAT1 antisense oligon

296 y, compared with embryos cultured in 10 mmol/l glucose with no abnormalities and a lower frequency of

297 cells (BREC) cultured in either 5 or 30 mmol/l glucose with or without 1 micro mol/l fidarestat.

298 abolically active (d-) rather than inactive (l-) glucose with a response profile that followed a bell

299 n per 24 h in hypoglycemic states (<3.9 mmol/L glucose) with 36 +/- 10 min (<2.8 mmol/L glucose) vs.

300 ase to a subsequent challenge with 16.7 mmol/l glucose, without changing the typical biphasic pattern