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1 se and serum C-reactive protein but not with serum insulin.
2 te or cocoa due to significant reductions in serum insulin.
3 ter glucose dosing and varies inversely with serum insulin.
4 /- 1.2 compared with 4.7 +/- 1.6 mmol/L) and serum insulin (138 +/- 76 compared with 136 +/- 116 pmol
5 roughout (5.3 +/- 0.3 micromol/g wet wt when serum insulin = 16 +/- 7 pmol/l vs. 5.5 +/- 0.3 micromol
6 /- 0.5 compared with 4.9 +/- 0.9 mmol/L) and serum insulin (244 +/- 93 compared with 151 +/- 57 pmol/
7 red with -0.9 +/- 16.6 mg/dL; P < 0.001) and serum insulin (-3.08 +/- 6.62 compared with +1.34 +/- 6.
10 euglycemic-hyperinsulinemic clamps (n = 10, serum insulin = 89 +/- 7 microU/dl), PAI-1 in blood incr
11 tically elevated levels of blood glucose and serum insulin accompanied by extreme insulin resistance.
12 arotenoids were inversely related to fasting serum insulin after adjustment for confounders (p < 0.05
13 activity, increased thermogenesis, and lower serum insulin, all of which correlate with a higher leve
14 , and this effect was associated with higher serum insulin, amylin, and glucagon-like peptide 1 level
15 intravenous insulin to mimic the changes in serum insulin and blood glucose levels observed after in
17 ectomy reduced the levels of plasma glucose, serum insulin and corticosterone, and food intake toward
18 glycemic control, corresponding to increased serum insulin and enhanced glucose-stimulated insulin re
20 reases of body weight, body fat content, and serum insulin and free fatty acid (FFA) levels compared
22 To characterize 7-year changes in fasting serum insulin and glucose concentrations, the authors an
23 to less weight loss and smaller decreases in serum insulin and HOMA-IR (all P </= 0.02 in an additive
24 oss (P=0.008) but became null for changes in serum insulin and HOMA-IR resulting from weight regain.
25 challenge, and induction of higher levels of serum insulin and IGF1 were observed when diabetic mice
26 e of the normal inverse relationship between serum insulin and IGFBP-1 levels in glucoregulation and
27 rosin A significantly reversed the increased serum insulin and insulin resistance (IR) in dexamethaso
32 nificant correlation between the decrease in serum insulin and the increase in urinary NO(X) (r2=0.68
34 t-1 cells blocked DNA synthesis initiated by serum, insulin and various purified growth factors, but
35 lucose, blood pressure, body mass index, and serum insulin) and incident diabetes differed by case de
36 um biomarkers of islet distress (e.g., acute serum insulin) and inflammation (e.g., leptin and alpha2
37 tokinin, peptide YY, ghrelin, blood glucose, serum insulin, and appetite were measured during 60-min,
39 erol intake and risk of T2D, plasma glucose, serum insulin, and C-reactive protein were mainly nonsig
42 All mice were evaluated for blood glucose, serum insulin, and glucose tolerance up to postoperative
43 (P < 0.05) positively with serum C-peptide, serum insulin, and glycated hemoglobin and inversely wit
45 is reduced 52% (p < 0.001) despite decreased serum insulin, and homeostasis model assessment insulin
47 mal protein S6 could be rapidly activated by serum, insulin, and phorbol ester in transiently transfe
48 tion at the TR-->FO checkpoint, 2) abrogated serum insulin autoantibodies, 3) reduced the severity of
49 18 mmol l(-1), P = 1.1 x 10(-6)) and fasting serum insulin (beta = -8.3 pmol l(-1), P = 0.0014), and
50 eta = 3.8 mmol l(-1), P = 2.5 x 10(-35)) and serum insulin (beta = 165 pmol l(-1), P = 1.5 x 10(-20))
54 d 2.65 (95% CI, 1.25 to 5.62; P = 0.008) for serum insulin, C-peptide, HbA1c levels, and HOMA-insulin
55 ogressively higher with increasing levels of serum insulin, C-peptide, HbA1c, and HOMA-insulin resist
56 nse to glucose, and determination of fasting serum insulin, C-peptide, triglyceride, and free fatty a
57 e, day 1, and week 4, respectively), fasting serum insulin (CDP571: 21.2 +/- 2.8, 21.0 +/- 2.8, 24.8
60 lin-dependent PKB/Akt phosphorylation, lower serum insulin, cholesterol, and triglyceride levels, as
61 +/- 10.1 vs. +1.8 +/- 8.1 mg/dL, P < 0.001), serum insulin concentration (-2.1 +/- 6.5 vs. +5.7 +/- 1
71 d at 52 weeks of age had significantly lower serum insulin concentrations and percent body fat compar
73 etect genes influencing variation in fasting serum insulin concentrations in 391 nondiabetic individu
81 th the polycystic ovary syndrome, decreasing serum insulin concentrations with metformin reduces ovar
83 ted in impaired glucose tolerance, increased serum insulin concentrations, and increased percent body
86 c diameter) and detecting the binding of MNP-serum insulin conjugate to the surface insulin-antibody
87 mit was further lowered to 5 pM by designing serum insulin conjugates with poly(acrylic acid)-functio
88 n 12-mo changes in weight, body composition, serum insulin, CRP, and 25(OH)D were compared between gr
89 clomiphene, the mean (+/-SE) area under the serum insulin curve after oral glucose administration de
90 metformin, the mean (+/- SE) area under the serum insulin curve after oral glucose administration de
93 uced but expression of Pepck increased while serum insulin decreased, glucose tolerance improved and
94 days in medium containing charcoal-stripped serum, insulin, epidermal growth factor, hepatocyte grow
97 ic ATGL completely abrogated the increase in serum insulin following either 1 or 12 wk of feeding a h
98 disproportionately high level of circulating serum insulin for a given glucose concentration ( approx
100 in-sensitivity ChecK Index (QUICKI), fasting serum insulin (FSI), homeostasis model assessment of ins
101 into this phenotype, we show that, although serum insulin, glucose, and cholesterol levels are entir
103 During the fasting and postprandial periods, serum insulin, glucose, triacylglycerol, and nonesterifi
105 the development of hyperinsulinemia (fasting serum insulin > or = 90th percentile, 19.1 micro U/ml).
106 ancreatic cancer cells, and elevated fasting serum insulin has been linked to pancreatic cancer risk.
107 (omental and retroperitoneal), food intake, serum insulin, hepatic triglycerides or in the exercise-
108 essed the prognostic value of adding fasting serum insulin, HOMA-IR (homeostasis model assessment-ins
110 rin is activated by pertussis toxin, whereas serum, insulin, insulin-like growth factor-1, and ligati
116 tingly, LID mice show a fourfold increase in serum insulin levels (2.2 vs. 0.6 ng/ml in control mice)
117 veloped a time-dependent increase in fasting serum insulin levels (from 3.6 +/- 1.1 ng ml-1 at baseli
118 ent in glucose tolerance without a change in serum insulin levels and an increase in serum leptin lev
119 he formation of adenomas results in elevated serum insulin levels and decreased blood glucose levels.
122 severe hyperglycemia with markedly decreased serum insulin levels and nearly normal insulin tolerance
125 tardation, mild hyperglycemia, and decreased serum insulin levels at 6 months of age when compared wi
126 n noted as a potential breast cancer marker (serum insulin levels being found to be raised in compari
128 seven most strongly linked families had high serum insulin levels during fasting and 2-h post-glucose
130 Intranasal insulin transiently increased serum insulin levels followed by a gradual lowering of b
142 red first-phase insulin secretion, increased serum insulin levels, and greatly decreased levels of gl
143 induced hyperglycemia, a decrease in fasting serum insulin levels, and mild elevation of fasting seru
144 eficiency improves glucose tolerance, lowers serum insulin levels, and reduces TNFalpha gene expressi
147 tly improved glucose tolerance with enhanced serum insulin levels, reduced beta cell death, and incre
148 ition, Munc18c transgenic mice had depressed serum insulin levels, reflecting a threefold reduction i
154 ogenesis (4 months), the LF group had higher serum insulin-like growth factor (IGF) binding protein-1
156 Clinical studies have established elevated serum insulin-like growth factor (IGF-I) content and IGF
157 ent epidemiologic studies unequivocally link serum insulin-like growth factor 1 (IGF-1) levels with r
158 te proliferation by modulating a decrease in serum insulin-like growth factor 1 (IGF-1) that allows G
165 ance and restored GH activation of STAT5 and serum insulin-like growth factor 1 levels in colitic mic
167 rior cingulate, treatment-related changes in serum insulin-like growth factor 1 were positively corre
172 receiver-operating-characteristic curve for serum insulin-like growth factor binding protein-1 was 0
173 ents with available measurements of baseline serum insulin-like growth factor binding protein-1.
175 addition, there was about a 30% decrease in serum insulin-like growth factor I (IGF1), and while the
176 p also experienced a 10% greater increase in serum insulin-like growth factor I (P < 0.05) and a 16%
177 HR and GH binding protein, greatly decreased serum insulin-like growth factor I and elevated serum GH
178 higher serum alkaline phosphatase activity, serum insulin-like growth factor I and insulin-like grow
182 olic rate, nutrient and electrolyte balance, serum insulin-like growth factor I levels, D-xylose abso
183 ased urinary deoxypyridinoline and increased serum insulin-like growth factor I without affecting par
184 rease in marrow adiposity and a reduction in serum insulin-like growth factor-1 (IGF-1) and the bindi
185 fference (95% CI) was computed for levels of serum insulin-like growth factor-1 (IGF-1), leptin, and
186 zed panel of serologic testing that included serum insulin-like growth factor-1, insulin-like growth
187 axonal and neuropsychological recovery, and serum insulin-like growth factor-I (IGF-I) may mediate t
188 as drawn 0, 10, 20, and 40 days postburn and serum insulin-like growth factor-I (IGF-I), insulin-like
189 72%) weight, (iii) significant inhibition in serum insulin-like growth factor-I and restoration of in
190 nced growth hormone secretion, and increased serum insulin-like growth factor-I by threefold to sixfo
191 tochemical concentrate and green tea reduced serum insulin-like growth factor-I concentrations in bot
192 tudies individualising GH doses to normalize serum insulin-like growth factor-I level have shown a si
193 ROS, which was stimulated by growth factors (serum, insulin-like growth factor I, or fibroblast growt
194 free medium increased after 8 to 16 hours in serum, insulin-like growth factor-I (IGF-I), epidermal g
197 achieved in vitro by addition of fetal calf serum, insulin-like growth factor-I, nicotinamide, and s
198 5 h of intravenous L-carnitine infusion with serum insulin maintained at fasting (7.4+/-0.4 mIU*l(-1)
199 nitoring, 10 patients had plasma glucose and serum insulin measurements, and 5 patients had repeated
200 nist CL 316,243 (CL) increased lipolysis and serum insulin more in KO mice, but blood glucose reducti
201 here were no abnormalities in serum glucose, serum insulin or the ability of insulin to stimulate glu
203 0001), lower serum glucose (P = 0.04), lower serum insulin (P = 0.03), lower serum IL-(P = 0.0022), l
205 ely to be responsible, including much higher serum insulin responses to total parenteral nutrition th
207 ants, LQT2 patients had 56% to 78% increased serum insulin, serum C-peptide, plasma GLP-1, and plasma
208 plant to assess fasting blood glucose (FBG), serum insulin (SI) levels, and i.v. glucose tolerance (I
209 plasma total fatty acid concentration, BMI, serum insulin, statin use, season, and longitudinal time
211 tion in A-ZIP/F1 mice reduced blood glucose, serum insulin, triglyceride levels, and the rate of trig
212 knockout mice were not obese and had normal serum insulin, triglyceride, and leptin levels, with a t
214 Among nonusers of hormone therapy, fasting serum insulin was associated with a statistically signif
216 vs 8.7 mmol/L [157 mg/dL] for placebo), and serum insulin was increased in the sulfonylurea studies
218 RESULTS.: Blood glucose was the lowest and serum insulin was the highest in the islet+bone marrow g
220 tration of uric acid, mean concentrations of serum insulin were 66.2, 66.7, 79.9, and 90.9 pmol/L for
221 and fed conditions, fat-free mass (FFM), and serum insulin were determined on the final day of each t
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