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1 ography) and insulin sensitivity (euglycemic insulin infusion).
2 glycemia ( approximately 100 mg/dl; variable insulin infusions).
3 ucose was clamped at basal levels during the insulin infusion.
4 psies basally and after 30, 45, or 60 min of insulin infusion.
5 ence of severe hyperglycemia unresponsive to insulin infusion.
6 ha had no effect on the SNP response without insulin infusion.
7 nfusion, but not during basal conditions and insulin infusion.
8 Euglycemia was maintained for 24 hours by insulin infusion.
9 c endogenous glucose production (EGP) during insulin infusion.
10 volume was measured at 0, 30, and 90 min of insulin infusion.
11 AAs and EAs after the 20-25 min intravenous insulin infusion.
12 scle were obtained before and after each 3-h insulin infusion.
13 5.5 mmo/l during the night using a variable insulin infusion.
14 (2)H(4)]tyrosine, with and without exogenous insulin infusion.
15 tic subjects during the low but not the high insulin infusion.
16 : the CSF-to-plasma insulin ratio during the insulin infusion.
17 and 50-60% lower (P < 0.05) during the high insulin infusion.
18 ic subjects (P < 0.05) and were unchanged by insulin infusion.
19 muscle and was decreased similarly after 3-h insulin infusion.
20 tion of a high dose continuous peripheral IV insulin infusion.
21 mal levels in the NIDDM group after 4-5 h of insulin infusion.
22 se (100 min, 40 mU x m-2 x min-1) euglycemic insulin infusion.
23 Plasma amino acid concentrations fall during insulin infusion.
24 was evident in response to glucose gavage or insulin infusion.
25 Subcutaneous insulin aspart vs IV regular insulin infusion.
26 use catheters for continuous intraperitoneal insulin infusion.
27 tients do not respond to increasing rates of insulin infusion.
28 n of continuous glucose monitoring (CGM) and insulin infusion.
29 r hour) vs standard-dose (0.1 U/kg per hour) insulin infusion.
30 , and participants with T2D before and after insulin infusion.
31 n was observed in patients given a high-dose insulin infusion.
32 Hypoglycemia was induced and maintained by insulin infusion.
33 cle excitability in vivo from a glucose plus insulin infusion.
34 ral glucose tolerance test and by a low-dose insulin infusion.
35 uppression of HGP by intracerebroventricular insulin infusion.
36 .75 +/- 0.07) and during (0.67 +/- 0.05) the insulin infusion.
37 ose flux was minimal and constant during all insulin infusions.
38 els were lower than in control (portal vein) insulin infusions.
39 dial (-3.1 +/- 0.4 vs. -3.0 +/- 0.6 pmol/kg) insulin infusions.
40 56 +/- 0.14 vs. 0.56 +/- 0.10 mol/l per 6 h) insulin infusions.
41 , and subjects received a 180-min peripheral insulin infusion (0.250 mU kg(-1) x min(-1)) with a vari
45 min), a basal period (-40 to 0 min), and an insulin infusion (1 mU x kg(-1) x min(-1)) period (0-150
46 we compared the effect of a very low dosage insulin infusion (10 mU x m[-2] x min[-1]) with that of
47 after the basal period, a hyperinsulinemic (insulin infusion = 120 mU x m(-2) min(-1)), hyperglycemi
48 lower mean glucose at the end of 18 hours of insulin infusion (135 +/- 12 mg/dL moderate vs 103 +/- 1
49 n impaired increase in glucose uptake during insulin infusion (169 +/- 28.1% compared with 67 +/- 9.6
50 ncentrations were significantly decreased by insulin infusion (28,450 +/- 9270 vs. 20,830 +/- 8110 mi
52 ects: NEFA levels (muM) during 8 mU/m(2)/min insulin infusion = 370 +/- 27 vs. 185 +/- 25, P < 0.0001
53 d (P < 0.05 vs. basal) during both AICAR and insulin infusion; [3H]2-deoxy-D-glucose transport activi
54 etes had a higher likelihood of requiring an insulin infusion (44.3% vs 29.3%; p < 0.0001), a higher
58 ved an insulin bolus (10 units/kg i.v.) plus insulin infusion (50 mU/kg/min i.v.) until hypoglycemia
61 asted state, 0.99 +/- 0.07 (r = 0.74) during insulin infusion and 1.00 +/- 0.05 (r = 0.92) when both
62 n in the nondiabetic subjects during the low insulin infusion and 50-60% lower (P < 0.05) during the
64 We compared standard continuous subcutaneous insulin infusion and closed-loop delivery (n=13; APCam01
65 extent of safety and usability by combining insulin infusion and continuous glucose measurement in a
66 crease in Akt phosphorylation observed after insulin infusion and could theoretically play a role in
67 rd transport of glucose was not increased by insulin infusion and did not differ from values in NIDDM
68 This was accomplished by stopping the portal insulin infusion and giving insulin peripherally at half
69 ng of the test period by stopping the portal insulin infusion and infusing insulin peripherally at tw
70 lamped at approximately 165 mg dl(-1) during insulin infusion and insulin levels reached approximatel
72 investigated the intraportal versus systemic insulin infusion and transendothelial transport of insul
73 relative increase in glucose disposal during insulin infusion) and a 4-fold increase in hepatic insul
74 into a control algorithm calculating rate of insulin infusion, and a nurse adjusted the insulin pump.
75 he first hour, plasma glucose was lowered by insulin infusion, and the second hour constituted a "rec
76 , the use of peritransplantation heparin and insulin infusions, and islet transplant mass remained si
77 GU in NIDDM, but only after several hours of insulin infusion; and 3) The kinetic defect in NIDDM and
78 t a 120-min clamp (2.5-mU . kg(-1) . min(-1) insulin infusion; approximately 120-130 mg/dl glucose) w
84 oxy-2[18F]fluoro-D-glucose ([18F]FDG) during insulin infusions at three rates (0, 40, and 120 mU/m2 p
85 onditions and during combined amino acid and insulin infusion before and after the supplementation pe
88 Plasma leptin remained stable during that insulin infusion, but fell by 37+/-2% in the control exp
90 monitoring (CGM) and continuous subcutaneous insulin infusion can be used to improve the treatment of
92 breakdown was significantly decreased during insulin infusion compared with controls (7.98 +/- 1.82 v
93 caused a greater vasodilator response during insulin infusion compared with during sham insulin infus
94 sulin concentration increased 20-fold during insulin infusion compared with saline infusion control (
95 blood glucose measurements and titration of insulin infusion, continuous glucose monitors, and stand
96 ly injections (MDI), continuous subcutaneous insulin infusion (CSII) and islet transplantation to red
97 emic with 4 weeks of continuous subcutaneous insulin infusion (CSII) before randomization to CSII plu
99 ) with insulin pump (continuous subcutaneous insulin infusion [CSII]), known as artificial pancreas,
100 nsulin pump therapy (continuous subcutaneous insulin infusion; CSII) in patients with type 1 diabetes
103 ls between 120 and 180 mg/dL with continuous insulin infusions decreases morbidity in diabetic patien
104 of a chemical sensing unit combined with an insulin infusion device controlled by an algorithm capab
105 he interval before automated glucose-sensing insulin infusion devices become available for the intens
108 Preventing the fall in plasma FFAs during insulin infusion either by administering intralipids or
112 kept euglycemic overnight by a variable rate insulin infusion, followed by a 4-h, two-step (insulin 0
114 2 weeks, whereas a daily repeated acute DVC insulin infusion for 12 days conversely decreased food i
115 s and children regarding a preference for an insulin infusion for the acute management of hyperglycem
116 n update of the guidelines for the use of an insulin infusion for the management of hyperglycemia in
117 ollected immediately after glucose gavage or insulin infusion) from controls showed significant incre
126 od glucose standardization (to 6-7 mmol/L by insulin infusion, if needed) and at 90 min after the mea
128 synthesis was not significantly affected by insulin infusion in either normal control subjects or CF
131 d NO was assessed without insulin and during insulin infusion in the forearm circulation of healthy s
133 se, were suppressed by >50% during AICAR and insulin infusions in both lean and obese rats (P < 0.05
135 ose production higher (P < 0.01) during both insulin infusions in the diabetic compared with the nond
136 als of strict glycemic control achieved with insulin infusions in this patient population are warrant
137 ed that switching off intrapancreatic artery insulin infusions in vivo during hypoglycemia greatly im
138 roprusside infusions, and control continuous insulin infusions-in effect, an artificial pancreas.
143 sal (5.9 +/- 1.1 mmol/l) throughout, whereas insulin infusion increased the arterial insulin level to
144 investigated whether intracerebroventricular insulin infusion increases SNA more in obese male than f
145 ressed in IFG and NFG groups during prandial insulin infusion, indicating that hepatic insulin resist
147 se monitoring (CGM), continuous subcutaneous insulin infusion (insulin pumps [CSII]), and glucometers
158 ial infusions, each group received saline or insulin infusion (n = 6 or 7 each) for an additional 5 h
160 and hepatic glucose output during low-dosage insulin infusion of a hyperinsulinemic clamp (HGO; a mea
161 tic glucose output [HGO] during the low-dose insulin infusion of a hyperinsulinemic clamp) and acute
163 (GRADE) methodology to assess the impact of insulin infusions on outcome for general intensive care
164 o blood glucose control to 80-110 mg/dL with insulin infusion or conventional glucose management, whe
165 onventional therapy (continuous subcutaneous insulin infusion or multiple daily insulin injections wi
166 rovascular volume increased within 20 min of insulin infusion (P < 0.01), whereas an effect to increa
169 .001), and this inhibition was larger during insulin infusion (P=0.01) but not further increased by N
171 evels during a 90-min euglycemic intravenous insulin infusion (plasma insulin approximately 700 pmol/
173 or insulin therapy include use of a reliable insulin infusion protocol, frequent blood glucose monito
176 lunting of the renal vasodilator response to insulin infusion (R(2) = 0.36, P = 0.02) and sensitizing
180 echnique combined with indirect calorimetry (insulin infusion rate (1.5 mU x kg-1 x min-1)) in 12 mal
181 (24 micromol x kg[-1] x min[-1]) and maximal insulin infusion rate (240 micromol x kg[-1] x min[-1]).
184 ved a 7-h euglycemic-hyperinsulinemic clamp (insulin infusion rate = 100 mU x m(-2) x min(-1)), and a
187 reas even with the 1.0 mU x kg(-1) x min(-1) insulin infusion rate, splanchnic FFA release decreased
189 mal (4 mU/kg/min) and maximal (25 mU/kg/min) insulin infusion rates and demonstrated the presence of
190 rotocols were used: 1) euglycemic clamp with insulin infusion rates at 40, 120, 300, and 1,200 mU / m
191 s were randomly assigned and were studied at insulin infusion rates of 0, 20, 40 and 120 mU/min/m2 bo
194 identical glucose levels during the similar insulin infusion rates were substantially lower in diabe
195 The effects of these identical AICAR and insulin infusion rates were then examined in the obese Z
196 (calculated by C-peptide deconvolution) and insulin infusion rates were used as inputs to a new two-
200 ogy and device-related challenges, including insulin infusion set failure and sensor signal attenuati
209 ptying of hypoglycemia induced by a 5 mU/min insulin infusion (t = 5-90 min) was assessed in consciou
210 yl-L-arginine was significantly higher after insulin infusion than in the absence of hyperinsulinemia
211 insulin by somatostatin, with and without an insulin infusion that elevated insulin to 24.6 +/- 5.2 a
212 ns should be avoided and instead replaced by insulin infusions that normalize and maintain blood gluc
213 howed a dosage-dependent increase during the insulin infusions that was evident within 30-60 min.
214 During fasting conditions (i.e., absence of insulin infusion), the LC for skeletal muscle was slight
216 rity of the literature supporting the use of insulin infusion therapy for critically ill patients lac
218 ements that contribute to safe and effective insulin infusion therapy were determined through literat
219 initive, there are patients who will receive insulin infusion therapy, and the suggestions in this ar
220 were randomly assigned to receive continuous insulin infusion to maintain intraoperative glucose leve
225 the activation of Akt/PKB, and 3) prolonged insulin infusion under clamp conditions results in a blu
226 n uptake and clearance during an intravenous insulin infusion using compartmental modeling in 10 dogs
229 ctional phosphorylation of [(18)F]FDG during insulin infusion was also significantly lower in T2D (P
230 6-P concentration in response to the glucose-insulin infusion was approximately 50% less in the IDDM
233 Leg glucose uptake in response to the 40-mU insulin infusion was higher in the lean control subjects
237 rom 60 to 150 min of exercise, the simulated insulin infusion was sustained (C; n = 7), modified to s
241 y (percent increase in glucose uptake during insulin infusion) was greatest in the Lean group (576% +
242 ed insulin pumps for continuous subcutaneous insulin infusion were randomly assigned to 2 months of A
243 ion rates during both low-dose and high-dose insulin infusions were lower in pancreas-transplant pati
246 ximately 700 pmol/l by means of an exogenous insulin infusion, while EGP, SGU, and leg glucose uptake
247 s were maintained constant with an exogenous insulin infusion, while endogenous hormone secretion was
250 s/kg/min) and maximal (20 milliunits/kg/min) insulin infusions, whole-body glucose disposal was 77% (
251 ff), and forearm glucose uptake (FGU) during insulin infusion with 60 min of euglycemia followed by 6
252 e MiniMed 640G pump (continuous subcutaneous insulin infusion) with self-monitoring of blood glucose