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 key facet of leptin-mediated restoration of euglycemia.

4 levels were not linked to the restoration of euglycemia.

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

6 and treatment with sulfonylureas resulted in euglycemia.

7 with type I diabetes is required to restore euglycemia.

8 lamp was decreased appropriately to maintain euglycemia.

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

10 eeks after engraftment or until remission of euglycemia.

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

12 lamp was decreased appropriately to maintain euglycemia.

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

14 normal after 3 days of insulin treatment and euglycemia.

15 ed the islet mass required to achieve stable euglycemia.

16 d undergoes compensatory changes to maintain euglycemia.

17 lycemia compared with insulin with (clamped) euglycemia.

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

19 pathway plays a decisive role in maintaining euglycemia.

20 smaller increase in EGP compared with day 1 euglycemia.

21 ation day 1 hypoglycemia compared with day 1 euglycemia.

22 change is sustained upon re-establishment of euglycemia.

23 nsive to therapy aimed at restoring relative euglycemia.

24 in therapy when diet alone fails to maintain euglycemia.

25 ingle or repeated hypoglycemia compared with euglycemia.

26 lasma glucose concentrations were clamped at euglycemia.

27 y 1 cortisol infusion compared to antecedent euglycemia.

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

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

30 during nocturnal hypoglycemia compared with euglycemia.

31 counterregulatory hormone release to restore euglycemia.

32 -cell glucose sensing and the maintenance of euglycemia.

33 ctivity to levels otherwise only observed at euglycemia.

34 gical and behavioral responses that maintain euglycemia.

35 ginal mass islet transplants did not restore euglycemia.

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

37 fter anti-CD3 mAb treatment despite baseline euglycemia.

38 high-dose cortisol, compared with antecedent euglycemia.

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

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

41 8 +/- 2 mg/dl) on one occasion and nocturnal euglycemia (109 +/- 1 mg/dl) on the other.

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

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

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

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

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

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

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

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

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

51 1 (n = 6), plasma glucose was maintained at euglycemia (5 mmol/l) throughout.

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

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

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

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

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

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

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

59 0.6 micromol x kg(-1) x min(-1)) than during euglycemia (5.73 +/-0.6 micromol x kg(-1) x min(-1), P <

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

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

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

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

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

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

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

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

68 2 h clamped hypoglycemia (53 +/- 2 mg/dl) or euglycemia (93 +/- 3 mg/dl) was obtained during morning

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

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

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

72 Euglycemia after CKPT may have a protective role in nati

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

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

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

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

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

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

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

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

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

82 Identical euglycemia and basal insulin levels were successfully ma

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

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

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

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

87 : euinsulinemic euglycemia, hyperinsulinemic euglycemia and hyperinsulinemic hyperglycemia.

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

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

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

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

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

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

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

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

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

97 Maintenance of euglycemia and physiologic control of insulin responses

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

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

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

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

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

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

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

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

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

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

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

109 At euglycemia, antecedent recurrent hypoglycemia increased

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 Restoration of euglycemia for 2 weeks with insulin implants normalized

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

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

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

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

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

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

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

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

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

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

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

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

160 Compared with euglycemia, hypoglycemia produced a greater increase in

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

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

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

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

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

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

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

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

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

170 This resulted in restoration of euglycemia in diabetic rats.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 80-min hyperinsulinemic period during either euglycemia or hypoglycemia.

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

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

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

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

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

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

212 +/- 0.3 mg x kg(-1) x min(-1) compared with euglycemia, P = NS), and hepatic glycogen concentration

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

214 After resting euglycemia, patients displayed normal counterregulatory

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

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

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

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

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

220 130 +/- 25 (hypoglycemia) and to 102 +/- 10 (euglycemia) pmol/l.

221 In contrast, euglycemia preferentially activated the medial prefronta

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

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

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

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

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

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

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

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

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

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

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

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

234 Thus, euglycemia supports RUNX2 activity and promotes normal m

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

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

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

238 During euglycemia, the WMT activated the bilateral frontal and

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

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

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

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

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

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

245 0.6 to 7.7 +/- 1.4 mg.kg-1.min-1, P < 0.001, euglycemia vs. hyperglycemia), this increase was blunted

246 Euglycemia was achieved in 6 of 12 animals that received

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

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

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

250 Euglycemia was maintained and glucose metabolism was ass

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

252 Euglycemia was maintained by glucose infusion.

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

254 Euglycemia was maintained for 24 hours by insulin infusi

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

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

257 Euglycemia was maintained throughout the clamp with no d

258 Euglycemia was maintained, and glucagon was clamped at b

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

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

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

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

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

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

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

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

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

268 nfusion rates were increased following prior euglycemia with alprazolam.

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

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

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

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

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