ライフサイエンスコーパス: euglycemia

1 l/l (hypoglycemia) and to 102 +/- 10 pmol/l (euglycemia).

2 01) by day 1 hypoglycemia (relative to day 1 euglycemia).

3 nosis >=50% (OR, 3.01 [1.79-5.08]; reference=euglycemia).

4 G(i) signaling is essential for maintaining euglycemia.

5 high-dose cortisol, compared with antecedent euglycemia.

6 levels were not linked to the restoration of euglycemia.

7 eased MVo(2) and is insulin resistant during euglycemia.

8 and treatment with sulfonylureas resulted in euglycemia.

9 gical and behavioral responses that maintain euglycemia.

10 with type I diabetes is required to restore euglycemia.

11 lamp was decreased appropriately to maintain euglycemia.

12 ay hypoglycemia (2.9 mmol/l) or previous-day euglycemia.

13 eeks after engraftment or until remission of euglycemia.

14 al state and that they are saturated even at euglycemia.

15 lamp was decreased appropriately to maintain euglycemia.

16 r-cultured, islets were necessary to produce euglycemia.

17 normal after 3 days of insulin treatment and euglycemia.

18 ed the islet mass required to achieve stable euglycemia.

19 d undergoes compensatory changes to maintain euglycemia.

20 lycemia compared with insulin with (clamped) euglycemia.

21 GO) both at baseline and during steady-state euglycemia.

22 smaller increase in EGP compared with day 1 euglycemia.

23 ation day 1 hypoglycemia compared with day 1 euglycemia.

24 change is sustained upon re-establishment of euglycemia.

25 nsive to therapy aimed at restoring relative euglycemia.

26 in therapy when diet alone fails to maintain euglycemia.

27 lasma glucose concentrations were clamped at euglycemia.

28 y 1 cortisol infusion compared to antecedent euglycemia.

29 es, 28% remained preDM, and 38% regressed to euglycemia.

30 pathway plays a decisive role in maintaining euglycemia.

31 -a is critical for maintaining interprandial euglycemia.

32 ne that drives catabolic actions to maintain euglycemia.

33 ingle or repeated hypoglycemia compared with euglycemia.

34 sion of 20% dextrose as required to maintain euglycemia.

35 cemia, 65 h at hyperglycemia, and 1,258 h at euglycemia.

36 during nocturnal hypoglycemia compared with euglycemia.

37 counterregulatory hormone release to restore euglycemia.

38 (EGP) increased by ~25%, thereby maintaining euglycemia.

39 -cell glucose sensing and the maintenance of euglycemia.

40 ctivity to levels otherwise only observed at euglycemia.

41 ginal mass islet transplants did not restore euglycemia.

42 rk (DMN) also was seen in both groups during euglycemia.

43 fter anti-CD3 mAb treatment despite baseline euglycemia.

44 key facet of leptin-mediated restoration of euglycemia.

45 Brain glucose values during euglycemia (1.1 +/- 0.4 mumol/g vs. 1.1 +/- 0.3 mumol/g;

46 as blood glucose levels were increased from euglycemia (100 mg/dl) to 200 mg/dl and to 300 mg/dl, re

47 8 +/- 2 mg/dl) on one occasion and nocturnal euglycemia (109 +/- 1 mg/dl) on the other.

48 llowing a decrease in zinc-free insulin with euglycemia (-14 +/- 3 pg/ml [-4.0 +/- 0.9 pmol/l]) and d

49 red with insulin administration with clamped euglycemia (165 +/- 12 vs. 118 +/- 21 spikes/s [P < 0.05

50 ound that MT islets extended the duration of euglycemia 2-fold longer than nontransgenic islets.

51 and dissociated mouse islet cells to restore euglycemia, 3) the generation of a human immune system f

52 llowing outcomes were measured under clamped euglycemia (4 to 6 mmol/L): inulin (GFR) and para-aminoh

53 uring hypoglycemia but did not change during euglycemia (4.3 +/- 0.2 mmol/l).

54 ce with otherwise identical hyperinsulinemic euglycemia (4.8 +/- 0.1 mmol/l, 86 +/- 5 mg/dl) between

55 ose infusion rate (GIR) required to maintain euglycemia (40.1 +/- 5.7 and 38.1 +/- 4.8 micromol / kg

56 resent across worsening glycemic categories (euglycemia, 43%; prediabetes, 58%; diabetes, 69%), and s

57 luxes ([3-(3)H]glucose) were measured during euglycemia (5 mmol/l) and after abrupt onset of hypergly

58 ness and 7 with hypoglycemia unawareness--at euglycemia (5 mmol/l) and hypoglycemia (2.6 mmol/l), in

59 1 (n = 6), plasma glucose was maintained at euglycemia (5 mmol/l) throughout.

60 ycemia (interstitial glucose 3.5 mmol/L) and euglycemia (5-10 mmol/L) matched for time of day.

61 erinsulinemic (12.0 pmol x kg(-1) x min(-1)) euglycemia (5.0 mmol/l) and hypoglycemia (2.8 mmol/l).

62 perinsulinemic (3 mU x kg-1 x min-1 for 3 h) euglycemia (5.0 mmol/l) and hypoglycemia (2.8 mmol/l).

63 two separate occasions, on one occasion with euglycemia (5.0 mmol/l) and on the other occasion with h

64 with type 2 diabetes were studied twice, at euglycemia (5.2 +/- 0.2 mmol/L) or hyperglycemia (12.3 +

65 bral blood flow (CBF) four times each during euglycemia (5.2 +/- 0.2 mmol/liter) and hypoglycemia (3.

66 g hypoglycemia, but it did not change during euglycemia (5.20 +/- 0.19 vs. 5.05 +/- 0.15 micromol/ml)

67 Despite similar euglycemia (5.3 +/- 0.1 mmol/L) and insulinemia (46 +/-

68 0.6 micromol x kg(-1) x min(-1)) than during euglycemia (5.73 +/-0.6 micromol x kg(-1) x min(-1), P <

69 minal glucose infusion in both groups during euglycemia (+5.8 x 10(4) and +5.8 x 10(4) copies, respec

70 ol/l; n = 12; ANTE EUG), 2) hyperinsulinemic euglycemia (6.0 +/- 0.1 mmol/l; n = 8) plus simultaneous

71 Glucose was maintained at euglycemia (6.0 mmol/L) or hypoglycemia (2.5 mmol/L) for

72 a (6.2 +/- 0.1 mmol/l; n = 12; ANTE EUG), or euglycemia (6.2 +/- 0.1 mmol/l) plus simultaneous intrac

73 mia (2.8 +/- 0.1 mmol/l; n = 12; ANTE HYPO), euglycemia (6.2 +/- 0.1 mmol/l; n = 12; ANTE EUG), or eu

74 hyperinsulinemic (30 pmol. kg(-1). min(-1)) euglycemia (6.2 +/- 0.2 mmol/l; n = 12; ANTE EUG), 2) hy

75 ion glucose was used to stratify patients in euglycemia (71-140 mg/dL), mild hyperglycemia (141-199 m

76 after day 1 hypoglycemia compared with day 1 euglycemia (8.8+/-2.2 vs. 0.6+/-0.6 micromol x kg(-1) x

77 2 h clamped hypoglycemia (53 +/- 2 mg/dl) or euglycemia (93 +/- 3 mg/dl) was obtained during morning

78 ement in subsequent cognitive performance at euglycemia, accompanied by alterations in cognitive meta

79 als vs. 63 +/- 3% in controls; P < 0.001) at euglycemia, accompanied by reversal of the task-associat

80 During fasting euglycemia, administration of glucagon caused blood gluc

81 ta) mice also showed a much faster return to euglycemia after beta-cell ablation, suggesting that the

82 Euglycemia after CKPT may have a protective role in nati

83 l-l-arginine (l-NMMA) slowed the recovery to euglycemia after hypoglycemia.

84 Achieving euglycemia after ICT may not reverse CAN once establishe

85 arkedly decreases the time needed to restore euglycemia after intraportal transplantation of syngenei

86 oline chloride (0.3 to 10 microg/min) during euglycemia, after 6 hours of hyperglycemia (300 mg/dL) c

87 stimulation after hypoglycemia compared with euglycemia, although it was less pronounced in patients

88 es were studied twice: 1) insulin-controlled euglycemia and 2) insulin deprivation and endotoxin admi

89 oline chloride (0.3 to 10 microg/min) during euglycemia and after 6 hours of hyperglycemic clamp.

90 After euglycemia and after hypoglycemia, rates of blood-to-bra

91 in diabetes, AGE accumulation also occurs in euglycemia and aging, albeit to lower degrees, driven by

92 autologous non-beta cell leading to fasting euglycemia and an improved glucose tolerance, thereby su

93 Identical euglycemia and basal insulin levels were successfully ma

94 ation were compared between hypoglycemia and euglycemia and between hyperglycemia and euglycemia matc

95 lycemia, glucose utilization is increased at euglycemia and decreased after acute hypoglycemia, which

96 ning PVPON/TA-encapsulated islets maintained euglycemia and delayed graft rejection significantly lon

97 planted with precultured BM/islets exhibited euglycemia and detectable human insulin levels (157 muU/

98 Hypoglycemia, euglycemia and hyperglycemia are continuously monitored

99 arginine infusions for the 3 groups both at euglycemia and hyperglycemia as well as their C-peptide-

100 A consecutive 2-day assessment of clamped euglycemia and hyperglycemia was evaluated at baseline a

101 : euinsulinemic euglycemia, hyperinsulinemic euglycemia and hyperinsulinemic hyperglycemia.

102 uent changes in MBFR during hyperinsulinemic euglycemia and hyperinsulinemic hypoglycemia in DM patie

103 ress at baseline and during hyperinsulinemic euglycemia and hyperinsulinemic hypoglycemia.

104 Blood was drawn during euglycemia and hypoglycemia and 1, 3, and 7 days later t

105 tween plasma and brain glucose levels during euglycemia and hypoglycemia in healthy subjects and pati

106 ysiological responses to hyperinsulinemia at euglycemia and hypoglycemia were intermediate relative t

107 succeeded in restoring long-term, drug-free euglycemia and immune tolerance to beta cells in overtly

108 sulin-producing beta cells and restores both euglycemia and immune tolerance to beta cells.

109 The beta2 mutant animals failed to maintain euglycemia and muscle ATP levels during fasting.

110 ting and improved glucose tolerance, despite euglycemia and normal insulin levels.

111 gical functions including the maintenance of euglycemia and peripheral insulin sensitivity.

112 Maintenance of euglycemia and physiologic control of insulin responses

113 tic alpha-cells, is critical for maintaining euglycemia and plays a key role in the pathophysiology o

114 (i.e. treatment with rosiglitazone) restored euglycemia and reversed high fat diet-induced insulin re

115 nt a prototype for therapies able to restore euglycemia and self-tolerance in T1DM.

116 d glucose infusion rate required to maintain euglycemia and showed a significant increase in muscle-s

117 d into a SC, neovascularized device restored euglycemia and sustained function long-term.

118 f zinc, suppresses glucagon secretion during euglycemia and that a decrease in insulin per se stimula

119 nnel activity is critical for maintenance of euglycemia and that overactivity can cause diabetes by i

120 ose infusion rate (GIR) required to maintain euglycemia and the rate of glucose utilization (R(d)) we

121 with severity and duration of deviation from euglycemia and with increased variability.

122 ctively, during the initial hyperinsulinemic euglycemia, and 15 +/- 1 vs. 22 +/- 2 pmol/l, respective

123 es of exogenous glucose required to maintain euglycemia, and hypoglycemia was a potential problem.

124 Eight subjects were studied after euglycemia, and nine were studied after approximately 24

125 At euglycemia, antecedent recurrent hypoglycemia increased

126 The mechanisms of benefit of euglycemia appear to be multifactorial.

127 ne function, body weight, energy metabolism, euglycemia, appetite function, and gut function can also

128 Plasma glucose levels were clamped at euglycemia ( approximately 5.0 mmol/l, approximately 90

129 Glulisine was infused with clamped euglycemia ( approximately 95 mg/dl [5.3 mmol/l]) from 0

130 easure regional cerebral blood flow (CBF) at euglycemia ( approximately 95 mg/dl) on one occasion and

131 erinsulinemia (approximately 600 pmol/l) and euglycemia (approximately 4.9 mmol/l), women with GDM ha

132 FFA group (Liposyn-infused) were clamped at euglycemia (approximately 6 mM)-hyperinsulinemia (10 mil

133 nous insulin in a dose that maintains stable euglycemia are receiving biologically optimal insulin re

134 flow (rCBF) during hypoglycemia relative to euglycemia are similar for two imaging modalities-pulsed

135 h epinephrine responses following antecedent euglycemia (area under the curve/time 312 +/- 38 pg/ml),

136 lycemia (bolus insulin), 2) hyperinsulinemic euglycemia (bolus insulin and glucose infusion), and 3)

137 FD mice maintain euglycemia but develop insulin resistance, with an inter

138 -aminobutyric acid (GABA)ergic inhibition at euglycemia but much greater loss of this tone at low bat

139 sed (9.30 +/- 0.70 vs. 5.65 +/- 0.50) during euglycemia but not during hypoglycemia (9.80 +/- 0.50 vs

140 2) increases insulin sensitivity only during euglycemia but not during the more physiological conditi

141 ical leptin levels were necessary to restore euglycemia but simultaneously increased risk of hypoglyc

142 ose load in whom islet function is normal at euglycemia, but who have marked defects in both alpha- a

143 ects, MBFR increased during hyperinsulinemic euglycemia by 0.57 U (22%) above baseline (B coefficient

144 e glucose infusion rate required to maintain euglycemia by 18 and 49% at indinavir concentrations of

145 antly, CDN1163-treated ob/ob mice maintained euglycemia comparable with that of lean mice for >6 week

146 cose infusion rate was necessary to maintain euglycemia compared with placebo.

147 r agonist, exendin-4 (Ex-4), to test whether euglycemia could be achieved, whether pancreatic dysfunc

148 Compared with euglycemia, DbCM was significantly associated with highe

149 At comparable euglycemia, diabetic patients had similar ISR but higher

150 uscle insulin resistance, KO mice maintained euglycemia due to increased liver insulin sensitivity.

151 f glucose infusion were required to maintain euglycemia during exercise after day 1 hypoglycemia comp

152 Glucose was infused as needed to maintain euglycemia during exercise.

153 ount of exogenous glucose needed to maintain euglycemia during exercise.

154 Glucagon is important for maintaining euglycemia during fasting/starvation, and abnormal gluca

155 the glucose infusion rate needed to maintain euglycemia during hyperinsulinemia, indicating enhanceme

156 e glucose infusion rate required to maintain euglycemia during hyperinsulinemic clamp, primarily due

157 he glucose infusion rates needed to maintain euglycemia during hyperinsulinemic clamping) changed in

158 glucose infusion rates required to maintain euglycemia during steady state were significantly lower

159 e glucose infusion rate required to maintain euglycemia during the hyperinsulinemic-euglycemic clamp

160 Reducing systemic hyperglycemia to euglycemia, exenatide still increased total glucose turn

161 scaffolds adsorbed with collagen IV achieved euglycemia fastest and their response to glucose challen

162 (FGU) during insulin infusion with 60 min of euglycemia followed by 60 min of hypoglycemia.

163 +/- 0.2% [37 +/- 3 mmol/mol]) during fasting euglycemia followed by a 60-min +5.5 mmol/L hyperglycemi

164 single kidney capsule, stable restoration of euglycemia for >/=120 days was achieved.

165 Restoration of euglycemia for 2 weeks with insulin implants normalized

166 Glucose was infused to maintain euglycemia for 3 h and then to allow limited peripheral

167 ansplanted with RIP.B7-H4 islets established euglycemia for 42.3+/-18.4 days (mean+/-SD; n=9) compare

168 r diabetic mice also restored and maintained euglycemia for at least 45 days.

169 ntal cortex, and globus pallidum compared to euglycemia for both PASL-MRI and PET methodologies.

170 healthy control subjects (euinsulinemia and euglycemia), glucokinase-maturity-onset diabetes of the

171 esis, and glucose cycling (GC) during 2 h of euglycemia (glucose approximately 8 mmol/l) followed by

172 and vertebral arteries to maintain cerebral euglycemia (H-EU group) concurrently with peripheral hyp

173 at 10- to 15-min intervals for 90 min after euglycemia had been restored.

174 s transplantation (CKPT) with its associated euglycemia has been shown to prevent or reduce recurrent

175 main goal of treatment is the achievement of euglycemia; however, in patients at risk of, or with kno

176 During clamped euglycemia, hyperfiltration was attenuated by -33 mL/min

177 els at 5.6 mmol/l (approximately 100 mg/dl) (euglycemia-hyperinsulinemia group).

178 three physiologic conditions: euinsulinemic euglycemia, hyperinsulinemic euglycemia and hyperinsulin

179 pe 1 diabetic subjects (those studied during euglycemia, hyperlipidemia, and a hyperinsulinemic-eugly

180 Compared with euglycemia, hypoglycemia produced a greater increase in

181 on, ablates invasive insulitis, and restores euglycemia, immune tolerance to beta cells, normal insul

182 Prolonged exposure to diet-induced euglycemia improves retinal function but does not reesta

183 y rapidly advances and our ability to ensure euglycemia improves, iatrogenic insulin resistance will

184 whereas islet-alone transplantation achieved euglycemia in 3 of 10 recipients.

185 diabetes; however, PDGF + IGF-1 resulted in euglycemia in 6 of 6, with a mean of 36+/-14 days (P<0.0

186 the kidney capsule of diabetic mice restored euglycemia in 77.8% of recipients compared with 18.2% an

187 on of blood glucose, the role of maintaining euglycemia in a broader group of patients (including the

188 issociated mouse islets, required to restore euglycemia in chemically diabetic NOD-scid IL2rgamma(nul

189 SA-FasL-engineered islet grafts established euglycemia in chemically diabetic syngeneic mice indefin

190 I greatly improves the rate of conversion to euglycemia in diabetic rats.

191 This resulted in restoration of euglycemia in diabetic rats.

192 isolated venous sac with ability to restore euglycemia in diabetic rats.

193 cemia, corneal swelling was less than during euglycemia in diabetic subjects, which suggests that hyp

194 t and neonatal pigs are capable of restoring euglycemia in experimental animal models of diabetes.

195 ntral leptin action is sufficient to restore euglycemia in insulinopenic type 1 diabetes (T1D); howev

196 nasal insulin than after placebo to maintain euglycemia in lean but not in overweight people.

197 f Ad-IGF-II-transduced rat islets to restore euglycemia in nonobese diabetic/severe combined immunode

198 elegant and effective method for preserving euglycemia in patients undergoing near-total or total pa

199 most effective treatment strategy to restore euglycemia in patients with type 1 diabetes mellitus.

200 Restoration of euglycemia in Pdx1-treated diabetic mice was evident by

201 during pregnancy are crucial for maintaining euglycemia in response to increased metabolic demands pl

202 Leptin has been shown to effectively restore euglycemia in rodent models of T1D; however, the mechani

203 Leptin administration restores euglycemia in rodents with severe insulin-deficient diab

204 endoplasmic reticulum stress and establishes euglycemia in severely obese and diabetic mice.

205 ith a trend toward higher insulin levels and euglycemia in the fructose diet (FD)--fed mice.

206 cin-induced diabetes resulted in a return to euglycemia in the recipients within 24 hr.

207 nstrates that infusion of insulin to restore euglycemia in these patients results in a marked reducti

208 apability or ability to achieve and maintain euglycemia in vivo.

209 e show that physiological levels of glucose (euglycemia) increase RUNX2 DNA binding and transcription

210 related conditions influence cell fate, with euglycemia inducing several Ppy+ cell markers and hyperg

211 In contrast, during euglycemia, insulin potently inhibits glucagon's effect

212 Euglycemia is defined here as glucose < 200 mg/dl for 3

213 It remains enigmatic how euglycemia is preserved under these conditions.

214 y to withstand food deprivation and maintain euglycemia, is not known.

215 ich an increase in insulin was induced, with euglycemia maintained by peripheral glucose infusion.

216 and euglycemia and between hyperglycemia and euglycemia matched for time of day.

217 agent in this setting, although maintaining euglycemia may reduce the prevalence of critical illness

218 After the establishment of stable euglycemia, mice were reconstituted with allogeneic huma

219 the insulin-deficient diabetic rats restored euglycemia, minimized body weight loss due to food restr

220 gases were monitored during either constant euglycemia (n = 5) or initial hyperglycemia with gradual

221 BAT transplants result in euglycemia, normalized glucose tolerance, reduced tissue

222 of glucose-stimulated insulin secretion and euglycemia occurs only when tolerance is also induced by

223 All recipients were restored to stable euglycemia, off exogenous insulin, within 1-2 weeks afte

224 tain blood glucose at 4.5 mmol/l (81 mg/dl) (euglycemia) on separate occasions.

225 r morning and afternoon 2-h hyperinsulinemic euglycemia or 2-h hyperinsulinemic hypoglycemia (2.9 mmo

226 with peripheral glucose infusion to maintain euglycemia or create mild hyperglycemia.

227 ects who at different times displayed either euglycemia or hyperglycemia.

228 80-min hyperinsulinemic period during either euglycemia or hypoglycemia.

229 y dependent spatial memory, tested either at euglycemia or under acute hypoglycemia.

230 hen, glulisine was discontinued with clamped euglycemia or with clamped hypoglycemia ( approximately

231 P < 0.01) during zinc-free hyperinsulinemic euglycemia over the first 60 min.

232 kg(-1) x min(-1)) during hypoglycemia versus euglycemia (P < 0.05) could account for nearly 60% of al

233 h were higher after hypoglycemia than after euglycemia (P <or= 0.01 for each subject), indicating in

234 odilation during hyperglycemia compared with euglycemia (P=.07 by ANOVA; maximal response, 13.3+/-2.8

235 +/- 0.3 mg x kg(-1) x min(-1) compared with euglycemia, P = NS), and hepatic glycogen concentration

236 - SE] 2.592 +/- 0.188 vs. 2.018 +/- 0.174 at euglycemia; P = 0.027).

237 After resting euglycemia, patients displayed normal counterregulatory

238 No responses were observed during euglycemia (peak change within 5-10 min = 48 +/- 35 pg/m

239 of 9 pmol x kg(-1) x min(-1) and 2-h clamped euglycemia (plasma glucose 5.2 +/- 0.2 mmol/l) or differ

240 scopy, during 2 h of either hyperinsulinemic euglycemia (plasma glucose 92 +/- 4 mg/dl) or hypoglycem

241 with maintained sequential hyperinsulinemic euglycemia (plasma glucose, 90 mg/dL [5.0 mmol/L]) follo

242 Compared with values during euglycemia, plasma epinephrine and NE and rates of SNESO

243 130 +/- 25 (hypoglycemia) and to 102 +/- 10 (euglycemia) pmol/l.

244 In adjusted analyses, compared with euglycemia, prediabetes and diabetes were each associate

245 articipants (49.5% women), the prevalence of euglycemia, prediabetes, and diabetes was 63%, 30%, and

246 In contrast, euglycemia preferentially activated the medial prefronta

247 ate of glucose infusion required to maintain euglycemia (reflecting glucose uptake) was reduced by >5

248 During euglycemia, renal glucose balance switched from a net ou

249 er release, is required for leptin action on euglycemia restoration and that hyperglucagonemia is not

250 Further, leptin action on euglycemia restoration was abrogated in these mice, whic

251 l mice responded normally to leptin-mediated euglycemia restoration, which was associated with expect

252 ling to test the effect of central leptin on euglycemia restoration.

253 A(A) activation with alprazolam during day 1 euglycemia resulted in significant blunting (P < 0.05) o

254 BA A activation with alprazolam during day 1 euglycemia resulted in significant blunting of plasma ep

255 Plasma catecholamines (unchanged during euglycemia) rose during hypoglycemia with epinephrine, i

256 g insulin-induced hypoglycemia (2.0 U/kg) or euglycemia (saline control).

257 ents suggests that the benefits of sustained euglycemia, shorter cold ischemia times, lower rates of

258 n, the LSF-treated recipient mice maintained euglycemia significantly longer than the saline-treated

259 Thus, euglycemia supports RUNX2 activity and promotes normal m

260 hesis that plasma cortisol elevations during euglycemia that are comparable to those that occur durin

261 During euglycemia, the mean +/- SE PRPH was less in diabetic su

262 gh this process is essential for maintaining euglycemia, the underlying intracellular mechanisms that

263 During euglycemia, the WMT activated the bilateral frontal and

264 ht be an indicator to begin hyperinsulinemia-euglycemia therapy.

265 urnal hypoglycemia, in contrast to nocturnal euglycemia, there was less deterioration of cognitive fu

266 on day 1 compared with 30 +/- 6 pg/ml during euglycemia.) These data are consistent with the hypothes

267 on by the absence of Sur1, thereby allowing euglycemia to be maintained.

268 periods as long as 1-2 decades in returning euglycemia to type 1 diabetic patients by restoring endo

269 a after placebo treatment (P=0.009 by ANOVA, euglycemia versus hyperglycemia) but not after treatment

270 g fasting to maintain energy homeostasis and euglycemia via metabolic processes mainly orchestrated b

271 0.6 to 7.7 +/- 1.4 mg.kg-1.min-1, P < 0.001, euglycemia vs. hyperglycemia), this increase was blunted

272 Euglycemia was achieved in 6 of 12 animals that received

273 e amount of glucose required for maintaining euglycemia was highest with 2 mg inhaled insulin.

274 Instead, the restoration of euglycemia was linked to relief from an inflammatory sta

275 l, i.e., threefold over basal), while strict euglycemia was maintained (approximately 130 mg/dl, coef

276 Euglycemia was maintained and glucose metabolism was ass

277 n (3.6 pmol. kg(-1). min(-1)) was given, and euglycemia was maintained by glucose infusion.

278 Euglycemia was maintained by glucose infusion.

279 levels were fixed in all studies, and basal euglycemia was maintained by peripheral glucose infusion

280 Euglycemia was maintained for 24 hours by insulin infusi

281 ne (n = 10) or CSII plus metformin (n = 10); euglycemia was maintained for another 6-7 weeks.

282 Thereafter, euglycemia was maintained for more than 100 days in 32/4

283 Euglycemia was maintained throughout the clamp with no d

284 Euglycemia was maintained, and glucagon was clamped at b

285 In group 3, when euglycemia was maintained, the insulin and glucagon leve

286 In group 3, saline was infused, and euglycemia was maintained.

287 By contrast, euglycemia was not restored in rats treated by intraport

288 g B task was impaired for up to 10 min after euglycemia was restored (P = 0.024, eta(2) = 0.158).

289 After parturition, euglycemia was restored in FoxM1(Deltapanc) females, but

290 numbers of donors held constant, the time to euglycemia was significantly shorter in syngenic recipie

291 ecretory response to intravenous arginine at euglycemia was similar in the control and diabetic group

292 sal, including mean time required to achieve euglycemia, weight gain, and glucose levels during an in

293 ulin, but glucose infusion rates to maintain euglycemia were higher in mutation carriers, indicating

294 Mice in which the transplant restored euglycemia were humanized with allogeneic peripheral blo

295 nfusion rates were increased following prior euglycemia with alprazolam.

296 g and afternoon 2-h clamped hyperinsulinemic euglycemia with cortisol infused to stimulate levels of

297 ustification for the benefits of maintaining euglycemia with insulin infusions in hospitalized patien

298 ecipients established fasting and nonfasting euglycemia within 1-2 weeks, and none required exogenous

299 P 0.83 +/- 0.14 mg x kg(-1) x min(-1) during euglycemia yet approximately 50% higher with hypoglycemi

300 Fibronectin and laminin similarly promoted euglycemia, yet required more time than collagen IV and