ライフサイエンスコーパス: insulin infusion

1 ography) and insulin sensitivity (euglycemic insulin infusion).

2 glycemia ( approximately 100 mg/dl; variable insulin infusions).

3 psies basally and after 30, 45, or 60 min of insulin infusion.

4 ence of severe hyperglycemia unresponsive to insulin infusion.

5 ha had no effect on the SNP response without insulin infusion.

6 nfusion, but not during basal conditions and insulin infusion.

7 Euglycemia was maintained for 24 hours by insulin infusion.

8 tion of a high dose continuous peripheral IV insulin infusion.

9 volume was measured at 0, 30, and 90 min of insulin infusion.

10 scle were obtained before and after each 3-h insulin infusion.

11 5.5 mmo/l during the night using a variable insulin infusion.

12 was evident in response to glucose gavage or insulin infusion.

13 (2)H(4)]tyrosine, with and without exogenous insulin infusion.

14 tic subjects during the low but not the high insulin infusion.

15 : the CSF-to-plasma insulin ratio during the insulin infusion.

16 and 50-60% lower (P < 0.05) during the high insulin infusion.

17 ic subjects (P < 0.05) and were unchanged by insulin infusion.

18 muscle and was decreased similarly after 3-h insulin infusion.

19 tients do not respond to increasing rates of insulin infusion.

20 mal levels in the NIDDM group after 4-5 h of insulin infusion.

21 se (100 min, 40 mU x m-2 x min-1) euglycemic insulin infusion.

22 Plasma amino acid concentrations fall during insulin infusion.

23 n of continuous glucose monitoring (CGM) and insulin infusion.

24 r hour) vs standard-dose (0.1 U/kg per hour) insulin infusion.

25 , and participants with T2D before and after insulin infusion.

26 n was observed in patients given a high-dose insulin infusion.

27 Hypoglycemia was induced and maintained by insulin infusion.

28 cle excitability in vivo from a glucose plus insulin infusion.

29 ral glucose tolerance test and by a low-dose insulin infusion.

30 c endogenous glucose production (EGP) during insulin infusion.

31 uppression of HGP by intracerebroventricular insulin infusion.

32 AAs and EAs after the 20-25 min intravenous insulin infusion.

33 .75 +/- 0.07) and during (0.67 +/- 0.05) the insulin infusion.

34 ucose was clamped at basal levels during the insulin infusion.

35 ose flux was minimal and constant during all insulin infusions.

36 els were lower than in control (portal vein) insulin infusions.

37 dial (-3.1 +/- 0.4 vs. -3.0 +/- 0.6 pmol/kg) insulin infusions.

38 56 +/- 0.14 vs. 0.56 +/- 0.10 mol/l per 6 h) insulin infusions.

39 , and subjects received a 180-min peripheral insulin infusion (0.250 mU kg(-1) x min(-1)) with a vari

40 In stage 1, a 2-h low-dose insulin infusion (0.4 mU.kg-1.min-1) was used to partial

41 The GIR and R(d) rose with increasing insulin infusions (0.8, 2.5, 4, and 20 mU . kg(-1) . min

42 After the control period, plasma insulin infusion 1) was discontinued, creating insulin d

43 min), a basal period (-40 to 0 min), and an insulin infusion (1 mU x kg(-1) x min(-1)) period (0-150

44 we compared the effect of a very low dosage insulin infusion (10 mU x m[-2] x min[-1]) with that of

45 after the basal period, a hyperinsulinemic (insulin infusion = 120 mU x m(-2) min(-1)), hyperglycemi

46 lower mean glucose at the end of 18 hours of insulin infusion (135 +/- 12 mg/dL moderate vs 103 +/- 1

47 n impaired increase in glucose uptake during insulin infusion (169 +/- 28.1% compared with 67 +/- 9.6

48 ncentrations were significantly decreased by insulin infusion (28,450 +/- 9270 vs. 20,830 +/- 8110 mi

49 Three-hour euglycemic-hyperinsulinemic (insulin infusion 30 mU / m / min) clamps were performed

50 ects: NEFA levels (muM) during 8 mU/m(2)/min insulin infusion = 370 +/- 27 vs. 185 +/- 25, P < 0.0001

51 d (P < 0.05 vs. basal) during both AICAR and insulin infusion; [3H]2-deoxy-D-glucose transport activi

52 etes had a higher likelihood of requiring an insulin infusion (44.3% vs 29.3%; p < 0.0001), a higher

53 Peripheral insulin infusion (5 mU/kg per min for 3 h) decreased pla

54 +/-0.09 mmol/l) was induced via jugular vein insulin infusion (50 mU x kg(-1) x min(-1)).

55 +/- 0.1 mmol/l) was induced via jugular vein insulin infusion (50 mU x kg(-1) x min[-1]).

56 ved an insulin bolus (10 units/kg i.v.) plus insulin infusion (50 mU/kg/min i.v.) until hypoglycemia

57 Neither the 40 mU nor the 240 mU insulin infusion affected HK activity.

58 In contrast, insulin infusion after exercise significantly decreased

59 asted state, 0.99 +/- 0.07 (r = 0.74) during insulin infusion and 1.00 +/- 0.05 (r = 0.92) when both

60 n in the nondiabetic subjects during the low insulin infusion and 50-60% lower (P < 0.05) during the

61 We compared standard continuous subcutaneous insulin infusion and closed-loop delivery (n=13; APCam01

62 extent of safety and usability by combining insulin infusion and continuous glucose measurement in a

63 crease in Akt phosphorylation observed after insulin infusion and could theoretically play a role in

64 rd transport of glucose was not increased by insulin infusion and did not differ from values in NIDDM

65 This was accomplished by stopping the portal insulin infusion and giving insulin peripherally at half

66 ng of the test period by stopping the portal insulin infusion and infusing insulin peripherally at tw

67 lamped at approximately 165 mg dl(-1) during insulin infusion and insulin levels reached approximatel

68 Continuous subcutaneous insulin infusion and MDI have similar effects on glycemi

69 investigated the intraportal versus systemic insulin infusion and transendothelial transport of insul

70 relative increase in glucose disposal during insulin infusion) and a 4-fold increase in hepatic insul

71 into a control algorithm calculating rate of insulin infusion, and a nurse adjusted the insulin pump.

72 he first hour, plasma glucose was lowered by insulin infusion, and the second hour constituted a "rec

73 , the use of peritransplantation heparin and insulin infusions, and islet transplant mass remained si

74 GU in NIDDM, but only after several hours of insulin infusion; and 3) The kinetic defect in NIDDM and

75 t a 120-min clamp (2.5-mU . kg(-1) . min(-1) insulin infusion; approximately 120-130 mg/dl glucose) w

76 In group 2, in response to insulin infusion, arterial insulin (pmol/l) was elevated

77 Insulin infusion at 0.4 U kg (-1)min(-1) decreased blood

78 cute fetal hypoglycaemia induced by maternal insulin infusion at 125 dGA.

79 tions and separately during a 6-h euglycemic insulin infusion at 40 mU . m(-2) . min(-1).

80 Insulin infusion at rest did not change the rate of prot

81 oxy-2[18F]fluoro-D-glucose ([18F]FDG) during insulin infusions at three rates (0, 40, and 120 mU/m2 p

82 Exogenous continuous low-dose insulin infusion, beta blockade with propranolol, and us

83 e I diabetes can be properly controlled with insulin infusion between 0.45 and 0.7muU/mlmin.

84 Plasma leptin remained stable during that insulin infusion, but fell by 37+/-2% in the control exp

85 ly suppressed in the nNOS and WT mice during insulin infusion, but not in the eNOS mice.

86 monitoring (CGM) and continuous subcutaneous insulin infusion can be used to improve the treatment of

87 optical oxygen sensor is integrated into the insulin infusion catheter of an insulin pump.

88 breakdown was significantly decreased during insulin infusion compared with controls (7.98 +/- 1.82 v

89 caused a greater vasodilator response during insulin infusion compared with during sham insulin infus

90 sulin concentration increased 20-fold during insulin infusion compared with saline infusion control (

91 ly injections (MDI), continuous subcutaneous insulin infusion (CSII) and islet transplantation to red

92 emic with 4 weeks of continuous subcutaneous insulin infusion (CSII) before randomization to CSII plu

93 ) with insulin pump (continuous subcutaneous insulin infusion [CSII]), known as artificial pancreas,

94 nsulin pump therapy (continuous subcutaneous insulin infusion; CSII) in patients with type 1 diabetes

95 During Flux 2 (low-dose insulin infusion), D were 89 +/- 3, 98 +/- 6, and 94 +/-

96 During Flux 3 (high-dose insulin infusion): D were 77 +/- 3, 82 +/- 7, and 84 +/-

97 ls between 120 and 180 mg/dL with continuous insulin infusions decreases morbidity in diabetic patien

98 he interval before automated glucose-sensing insulin infusion devices become available for the intens

99 Before RSG treatment, insulin infusion did not significantly increase insulin

100 Insulin infusion during low dose hyperinsulinemic-euglyc

101 Preventing the fall in plasma FFAs during insulin infusion either by administering intralipids or

102 With the 0.125 mU/min/kg insulin infusion, FFA fell 40% and HGO fell 33%; prevent

103 With 0.5 mU/min/kg insulin infusion, FFA levels fell 64% while HGO declined

104 kept euglycemic overnight by a variable rate insulin infusion, followed by a 4-h, two-step (insulin 0

105 Seventy patients receiving insulin infusion for >8 hrs were included in data analys

106 2 weeks, whereas a daily repeated acute DVC insulin infusion for 12 days conversely decreased food i

107 ollected immediately after glucose gavage or insulin infusion) from controls showed significant incre

108 Thirty minutes after cessation of insulin infusion, glucose uptake, glycogen synthase acti

109 During both the basal and prandial insulin infusions, glucose disappearance promptly increa

110 In euglycemic clamp studies, insulin infusion greatly increased tyrosine phosphorylat

111 Pharmacologic insulin infusion (group 2) established steady-state huma

112 Saturating insulin infusion (group 3) achieved steady-state human i

113 However, switching off zinc-free insulin infusions had no effect.

114 Hyperinsulinemia induced by insulin infusion, however, did not produce a similar eff

115 od glucose standardization (to 6-7 mmol/L by insulin infusion, if needed) and at 90 min after the mea

116 Conversely, insulin infusion improves coronary flow, even in the set

117 synthesis was not significantly affected by insulin infusion in either normal control subjects or CF

118 obtained by needle biopsy basally and after insulin infusion in four healthy volunteers.

119 d NO was assessed without insulin and during insulin infusion in the forearm circulation of healthy s

120 Acute insulin infusion in the third cerebral ventricle inhibit

121 se, were suppressed by >50% during AICAR and insulin infusions in both lean and obese rats (P < 0.05

122 the benefits of maintaining euglycemia with insulin infusions in hospitalized patients.

123 ose production higher (P < 0.01) during both insulin infusions in the diabetic compared with the nond

124 als of strict glycemic control achieved with insulin infusions in this patient population are warrant

125 ed that switching off intrapancreatic artery insulin infusions in vivo during hypoglycemia greatly im

126 roprusside infusions, and control continuous insulin infusions-in effect, an artificial pancreas.

127 Unlike leptin, i.c.v. insulin infusion increased basal and baroreflex control

128 Insulin infusion increased plasma renin activity (P < 0.

129 Insulin infusion increased protein synthesis at rest (51

130 sal (5.9 +/- 1.1 mmol/l) throughout, whereas insulin infusion increased the arterial insulin level to

131 ressed in IFG and NFG groups during prandial insulin infusion, indicating that hepatic insulin resist

132 Peripheral IV insulin infusion infiltration should be considered when

133 When patients were given a low-dose insulin infusion, insulin sensitivity increased by 28.0%

134 We discovered that the IV insulin infusion line infiltrated, resulting in a large

135 timulate (epinephrine infusion) and inhibit (insulin infusion) lipolysis of adipose tissue TGs.

136 Euglycemic insulin infusion lowered arterial concentrations of free

137 Lipid changes caused by insulin infusion may improve outcomes more than glycemic

138 Insulin infusions may improve outcomes in patients with

139 At baseline and after insulin infusion, MBV and MFV were measured by CEU durin

140 During the insulin infusion, muscle fatty acid oxidation was reduce

141 ere administered either a low or medium dose insulin infusion (n = 10 each group).

142 ial infusions, each group received saline or insulin infusion (n = 6 or 7 each) for an additional 5 h

143 c clamp studies after a 24-h fast, during an insulin infusion of 20 mU x kg(-1) x min(-1).

144 and hepatic glucose output during low-dosage insulin infusion of a hyperinsulinemic clamp (HGO; a mea

145 tic glucose output [HGO] during the low-dose insulin infusion of a hyperinsulinemic clamp) and acute

146 The effects of amino acid supply and insulin infusion on skin protein kinetics (fractional sy

147 (GRADE) methodology to assess the impact of insulin infusions on outcome for general intensive care

148 o blood glucose control to 80-110 mg/dL with insulin infusion or conventional glucose management, whe

149 rovascular volume increased within 20 min of insulin infusion (P < 0.01), whereas an effect to increa

150 -60 min (0.68 +/- 0.17 vs. 1.52 +/- 0.26) of insulin infusion (P < 0.05 for both).

151 g insulin infusion compared with during sham insulin infusion (P = 0.02).

152 .001), and this inhibition was larger during insulin infusion (P=0.01) but not further increased by N

153 During insulin infusion, pancreas-transplant patients showed a

154 evels during a 90-min euglycemic intravenous insulin infusion (plasma insulin approximately 700 pmol/

155 Intracoronary insulin infusion produced an approximately 3-fold increa

156 or insulin therapy include use of a reliable insulin infusion protocol, frequent blood glucose monito

157 Intraportal insulin infusions (pulsatile, constant, or reproducing t

158 Continuous insulin infusion pumps have been widely available for ov

159 lunting of the renal vasodilator response to insulin infusion (R(2) = 0.36, P = 0.02) and sensitizing

160 the renal vasodilator response to ARB during insulin infusion (R(2) = 0.59, P < 0.01).

161 Insulin infusion raised plasma insulin concentrations by

162 Intravenous insulin infusion rapidly increases plasma insulin, yet g

163 echnique combined with indirect calorimetry (insulin infusion rate (1.5 mU x kg-1 x min-1)) in 12 mal

164 (24 micromol x kg[-1] x min[-1]) and maximal insulin infusion rate (240 micromol x kg[-1] x min[-1]).

165 The insulin infusion rate (4 mU.kg(-1).min(-1)) was selected

166 ved a 7-h euglycemic-hyperinsulinemic clamp (insulin infusion rate = 100 mU x m(-2) x min(-1)), and a

167 At the insulin infusion rate used, the magnitude of this defect

168 At the 0.5 mU x kg(-1) x min(-1) insulin infusion rate, leg FFA release was almost comple

169 reas even with the 1.0 mU x kg(-1) x min(-1) insulin infusion rate, splanchnic FFA release decreased

170 1]) or maximal (240 pmol x kg(-1) x min[-1]) insulin infusion rate.

171 mal (4 mU/kg/min) and maximal (25 mU/kg/min) insulin infusion rates and demonstrated the presence of

172 rotocols were used: 1) euglycemic clamp with insulin infusion rates at 40, 120, 300, and 1,200 mU / m

173 s were randomly assigned and were studied at insulin infusion rates of 0, 20, 40 and 120 mU/min/m2 bo

174 nificantly suppressed glycerol appearance at insulin infusion rates of 10 mU. m(-2). min(-1).

175 The 72-hour average insulin infusion rates were 3.37 +/- 0.61 and 4.57 +/- 1

176 identical glucose levels during the similar insulin infusion rates were substantially lower in diabe

177 The effects of these identical AICAR and insulin infusion rates were then examined in the obese Z

178 (calculated by C-peptide deconvolution) and insulin infusion rates were used as inputs to a new two-

179 In fact, the rates of insulin infusion required to maintain basal hepatic gluc

180 The rates of insulin infusion required to maintain plasma glucose lev

181 2 at baseline to 8 +/- 2 and 10 +/- 3 during insulin infusion, respectively.

182 ogy and device-related challenges, including insulin infusion set failure and sensor signal attenuati

183 phorescence based CGM system into a standard insulin infusion set.

184 e the adhesion of the sensor elements on the insulin infusion set.

185 Whether an insulin infusion should be used for tight control of hyp

186 Insulin infusion significantly increased serum insulin l

187 The essential components of an insulin infusion system include use of a validated insul

188 ptying of hypoglycemia induced by a 5 mU/min insulin infusion (t = 5-90 min) was assessed in consciou

189 yl-L-arginine was significantly higher after insulin infusion than in the absence of hyperinsulinemia

190 insulin by somatostatin, with and without an insulin infusion that elevated insulin to 24.6 +/- 5.2 a

191 ns should be avoided and instead replaced by insulin infusions that normalize and maintain blood gluc

192 howed a dosage-dependent increase during the insulin infusions that was evident within 30-60 min.

193 During fasting conditions (i.e., absence of insulin infusion), the LC for skeletal muscle was slight

194 During the insulin infusion, the mean total peripheral glucose upta

195 rity of the literature supporting the use of insulin infusion therapy for critically ill patients lac

196 ements that contribute to safe and effective insulin infusion therapy were determined through literat

197 initive, there are patients who will receive insulin infusion therapy, and the suggestions in this ar

198 were randomly assigned to receive continuous insulin infusion to maintain intraoperative glucose leve

199 Both groups were treated with insulin infusion to maintain normoglycemia after surgery

200 We also showed that chronic insulin infusion to normal C57BL/6J mice resulted in inc

201 Subjects received an overnight insulin infusion to normalize glucose levels, then under

202 the activation of Akt/PKB, and 3) prolonged insulin infusion under clamp conditions results in a blu

203 n uptake and clearance during an intravenous insulin infusion using compartmental modeling in 10 dogs

204 Premeal insulin infusion was also associated with platelet activ

205 ctional phosphorylation of [(18)F]FDG during insulin infusion was also significantly lower in T2D (P

206 6-P concentration in response to the glucose-insulin infusion was approximately 50% less in the IDDM

207 The response to insulin or sham insulin infusion was defined as the change from time 0 t

208 Omental insulin infusion was extracted at approximately 27%, suc

209 Leg glucose uptake in response to the 40-mU insulin infusion was higher in the lean control subjects

210 In group 3 (n = 4), the human insulin infusion was increased to a saturating dose (120

211 In a control group (n=5), the portal insulin infusion was not changed and glucose was infused

212 No response was observed when the SPDa insulin infusion was not turned off (peak change within

213 rom 60 to 150 min of exercise, the simulated insulin infusion was sustained (C; n = 7), modified to s

214 After a basal sampling period, insulin infusion was switched from the portal vein to a

215 SPDa insulin infusion was switched off simultaneously when bl

216 Glucose infusion rate in response to insulin infusion was used to define insulin resistance (

217 y (percent increase in glucose uptake during insulin infusion) was greatest in the Lean group (576% +

218 ed insulin pumps for continuous subcutaneous insulin infusion were randomly assigned to 2 months of A

219 ion rates during both low-dose and high-dose insulin infusions were lower in pancreas-transplant pati

220 This was confirmed during preprandial insulin infusion when glucose disposal was lower (P < 0.

221 After the low-dose insulin infusion, which achieved postabsorptive insulin

222 ximately 700 pmol/l by means of an exogenous insulin infusion, while EGP, SGU, and leg glucose uptake

223 s were maintained constant with an exogenous insulin infusion, while endogenous hormone secretion was

224 During high-dose insulin infusion, whole-body glucose disposal was low an

225 After 2 h of insulin infusion, whole-body glucose infusion rate was s

226 s/kg/min) and maximal (20 milliunits/kg/min) insulin infusions, whole-body glucose disposal was 77% (

227 ff), and forearm glucose uptake (FGU) during insulin infusion with 60 min of euglycemia followed by 6