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1 nia and/or systemic hypoglycemia (2.8 mmol/l glucose clamp).
2 cemic (5.0 mmol/L)-hypoglycemic (2.8 mmol/L) glucose clamp.
3 els were similar among all groups during the glucose clamp.
4 ng recovery (5-6 mmol/L) by hyperinsulinemic glucose clamp.
5 th a stepped hyperinsulinaemic hypoglycaemic glucose clamp.
6 liver and the peripheral tissues during the glucose clamp.
7 Insulin sensitivity was assessed by glucose clamps.
8 ovement in glucose disposal rates during the glucose clamps.
9 ormed on the day before the second and third glucose clamps.
10 ximately 3.6 mmol/l, approximately 65 mg/dl) glucose clamps.
12 during a 100-min hyperinsulinemic-euglycemic glucose clamp (40 mU x m(-2) x min(-1)) before and after
16 in sensitivity (hyperinsulinemic-isoglycemic glucose clamp) and insulin-stimulated changes in brachia
17 intravenous (ivGTT) glucose tolerance tests, glucose clamps, and body composition assessed between 15
18 er changes in HK-II expression seen during a glucose clamp are likely to be physiologically relevant,
19 tudies were conducted with maternal arterial glucose clamped at 5 micromol ml(-1) and fetal glucose a
20 emission tomography during hyperinsulinemic glucose clamps at nominal plasma glucose concentrations
21 . m(-2). min(-1) hyperinsulinemic-euglycemic glucose clamp before and after 3 months' treatment with
22 was assessed by hyperinsulinemic-euglycemic glucose clamp before and after intranasal application of
25 n contrast, insulin action (hyperinsulinemic glucose clamp) did not correlate with the age at onset o
26 l range (2.0-2.5-microm wavelength) during a glucose clamp experiment in order to identify the presen
31 lucose uptake by euglycemic-hyperinsulinemic glucose clamp in 15 normal-weight and 15 obese participa
32 mpared with the tolbutamide protocol and the glucose clamp in 35 nondiabetic subjects (age 38 +/- 2 y
34 is, we performed euglycemic-hyperinsulinemic glucose clamps in conscious dogs (n = 8) in which FFA we
35 and plasma FFA concentrations throughout the glucose clamps in control (r = 0.996) and GDM (r = 0.995
36 lin therapy displayed a significantly higher glucose clamp infusion rate posttreatment (9.1 +/- 1.3 i
37 e test (OGTT) and an isoglycemic intravenous glucose clamp (iso-IVGC) in: 1) 16 severely obese patien
38 blood glucose levels were manipulated using glucose clamp methodologies with continuous basal insuli
39 nsitivity during late pregnancy, but neither glucose clamp nor minimal model measures of insulin sens
41 those based on an intravenous test (e.g., a glucose clamp or an intravenous glucose tolerance test).
43 few data using direct measures of IR such as glucose clamps or frequently sampled intravenous glucose
44 t and exercise using a pancreatic clamp with glucose clamped (PC/GC; n = 5), a pancreatic clamp with
46 mmol/l) or hypoglycemic (2.9 +/- 0.1 mmol/l) glucose clamps (prolonged hypoglycemia) were carried out
47 old (by intralipid infusion during 11 mmol/l glucose clamp) resulted in a robust, approximate twofold
48 was assessed by hyperinsulinemic-isoglycemic glucose clamp (SI(Clamp)) and endothelial function evalu
49 rnoon 2-h hyperinsulinemic (528+/-30 pmol/l) glucose clamp studies of 5.3+/-0.1 mmol/l (euglycemic co
51 ests (ITTs), and hyperinsulinemic euglycemic glucose clamp studies, we demonstrated that mice lacking
52 essed during a hyperinsulinemic-hypoglycemic glucose clamp study in chronically catheterized awake ma
53 g field data (Raman spectra) acquired from a glucose clamping study on an animal model subject, we pe
54 Insulin sensitivity was measured using the glucose clamp technique (40 mU.m-2.min-1), in conjunctio
56 dy and individual skeletal muscles using the glucose clamp technique combined with D-[3-3H]glucose in
65 mmol/L) and hypoglycemic (3 mmol/L) [1-(13)C]glucose clamps were performed in eight healthy subjects
66 hyperinsulinemic euglycemic and hypoglycemic glucose clamps were performed on separate days, using [1
67 and type 2 diabetic volunteers (n = 8 each); glucose clamps were used to assess insulin sensitivity.
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