ライフサイエンスコーパス: serum insulin

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.

8 mol/l vs. 5.5 +/- 0.3 micromol/g wet wt when serum insulin = 668 +/- 81 pmol/l, P = NS).

9 For a one SD higher level of serum insulin (7.14 micro U/ml), C-peptide (0.45 Deltamo

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

16 related with adult growth, liver weight, and serum insulin and cholesterol levels.

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

19 Serum insulin and estradiol values measured previously w

20 ood glucose levels and increased circulating serum insulin and FGF-21 concentrations.

21 reases of body weight, body fat content, and serum insulin and free fatty acid (FFA) levels compared

22 Serum insulin and glucose concentrations during the oral

23 To characterize 7-year changes in fasting serum insulin and glucose concentrations, the authors an

24 annelRhodopsin2 (ChR2) in cholinergic cells, serum insulin and glucose were measured in response to (

25 to less weight loss and smaller decreases in serum insulin and HOMA-IR (all P </= 0.02 in an additive

26 oss (P=0.008) but became null for changes in serum insulin and HOMA-IR resulting from weight regain.

27 challenge, and induction of higher levels of serum insulin and IGF1 were observed when diabetic mice

28 e of the normal inverse relationship between serum insulin and IGFBP-1 levels in glucoregulation and

29 rosin A significantly reversed the increased serum insulin and insulin resistance (IR) in dexamethaso

30 abetes, soy protein has been shown to reduce serum insulin and insulin resistance.

31 Serum insulin and plasma flow areas under the curve (AUC

32 Serum insulin and plasma flow areas under the curve (AUC

33 Protein co-ingestion resulted in elevated serum insulin and plasma glucagon compared with FRU and

34 Similarly, serum insulin and plasma glucagon concentrations were ma

35 Others reported inverse relations between serum insulin and sex hormone-binding globulin (SHBG).

36 nificant correlation between the decrease in serum insulin and the increase in urinary NO(X) (r2=0.68

37 Serum, insulin and insulin-like growth factor, but not e

38 t-1 cells blocked DNA synthesis initiated by serum, insulin and various purified growth factors, but

39 lucose, blood pressure, body mass index, and serum insulin) and incident diabetes differed by case de

40 um biomarkers of islet distress (e.g., acute serum insulin) and inflammation (e.g., leptin and alpha2

41 tokinin, peptide YY, ghrelin, blood glucose, serum insulin, and appetite were measured during 60-min,

42 men-by-time interactions for plasma glucose, serum insulin, and blood lactate concentrations.

43 erol intake and risk of T2D, plasma glucose, serum insulin, and C-reactive protein were mainly nonsig

44 Blood glucose, plasma total GLP-1 and GIP, serum insulin, and gastric emptying were determined.

45 es, and free fatty acids, but blood glucose, serum insulin, and glucose tolerance are normal.

46 All mice were evaluated for blood glucose, serum insulin, and glucose tolerance up to postoperative

47 (P < 0.05) positively with serum C-peptide, serum insulin, and glycated hemoglobin and inversely wit

48 y significantly decreased the blood glucose, serum insulin, and glycated hemoglobin levels.

49 is reduced 52% (p < 0.001) despite decreased serum insulin, and homeostasis model assessment insulin

50 insulin tolerance, higher levels of fasting serum insulin, and lower pancreatic insulin content.

51 mal protein S6 could be rapidly activated by serum, insulin, and phorbol ester in transiently transfe

52 None of the infants developed serum insulin antibodies.

53 apples significantly decreased postprandial serum insulin [area under the curve (AUC): 25.6 (17.4, 3

54 tion at the TR-->FO checkpoint, 2) abrogated serum insulin autoantibodies, 3) reduced the severity of

55 18 mmol l(-1), P = 1.1 x 10(-6)) and fasting serum insulin (beta = -8.3 pmol l(-1), P = 0.0014), and

56 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))

57 - 0.006; P = 8.04 x 10-5), increased fasting serum insulin (beta: 0.004 +/- 0.0013; P = 5.83 x 10-3),

58 The detection of picomolar levels of serum insulin binding to the surface antibody was achiev

59 iastolic indexes included sex, age, baseline serum insulin, blood pressure, and heart rate.

60 y after an overnight fast for measurement of serum insulin, C-peptide, and glucose.

61 d 2.65 (95% CI, 1.25 to 5.62; P = 0.008) for serum insulin, C-peptide, HbA1c levels, and HOMA-insulin

62 ogressively higher with increasing levels of serum insulin, C-peptide, HbA1c, and HOMA-insulin resist

63 nse to glucose, and determination of fasting serum insulin, C-peptide, triglyceride, and free fatty a

64 e, day 1, and week 4, respectively), fasting serum insulin (CDP571: 21.2 +/- 2.8, 21.0 +/- 2.8, 24.8

65 Deletion studies showed that serum, insulin, cholera toxin, and FGF7 were necessary f

66 Serum insulin, cholesterol, and triglyceride levels were

67 lin-dependent PKB/Akt phosphorylation, lower serum insulin, cholesterol, and triglyceride levels, as

68 +/- 10.1 vs. +1.8 +/- 8.1 mg/dL, P < 0.001), serum insulin concentration (-2.1 +/- 6.5 vs. +5.7 +/- 1

69 The serum insulin concentration also was slightly elevated a

70 Fasting serum insulin concentration and the insulin sensitivity

71 Serum insulin concentration at 30 minutes after a 75-g d

72 Serum insulin concentration increased 20-fold during ins

73 Serum insulin concentration increased more for C+P than

74 Serum insulin concentration increased to maximal on day

75 (OGTT), with 7 samples of plasma glucose and serum insulin concentration measurements.

76 An increase in serum insulin concentration of > 200 pM for > 24 h was n

77 Serum insulin concentration, net forearm carnitine balan

78 ard ketogenesis (+232%) due to reductions in serum insulin concentrations (-53%) and hepatic citrate

79 s with T2DM treated with DXM showed enhanced serum insulin concentrations and glucose tolerance.

80 d at 52 weeks of age had significantly lower serum insulin concentrations and percent body fat compar

81 Fasting serum insulin concentrations differed among groups (F(33

82 etect genes influencing variation in fasting serum insulin concentrations in 391 nondiabetic individu

83 later life, and with lower blood glucose and serum insulin concentrations in infancy.

84 However, serum insulin concentrations provide an imprecise index

85 Profiles for blood glucose and serum insulin concentrations revealed higher peaks and l

86 Peak plasma glucose and serum insulin concentrations were greater after the HGI

87 However, remarkably decreased serum insulin concentrations were observed in Adipoq(-/-

88 Serum insulin concentrations were significantly increase

89 The cord-serum insulin concentrations were similar in the two gro

90 th the polycystic ovary syndrome, decreasing serum insulin concentrations with metformin reduces ovar

91 ycerides, 2-hour postload plasma glucose and serum insulin concentrations, and blood pressure.

92 ted in impaired glucose tolerance, increased serum insulin concentrations, and increased percent body

93 otein synthesis independently of a change in serum insulin concentrations.

94 ecrease in plasma glucose but did not affect serum insulin concentrations.

95 c diameter) and detecting the binding of MNP-serum insulin conjugate to the surface insulin-antibody

96 mit was further lowered to 5 pM by designing serum insulin conjugates with poly(acrylic acid)-functio

97 n 12-mo changes in weight, body composition, serum insulin, CRP, and 25(OH)D were compared between gr

98 clomiphene, the mean (+/-SE) area under the serum insulin curve after oral glucose administration de

99 metformin, the mean (+/- SE) area under the serum insulin curve after oral glucose administration de

100 Serum insulin decreased significantly in the SFD group,

101 Serum insulin decreased subsequent to the second meal at

102 uced but expression of Pepck increased while serum insulin decreased, glucose tolerance improved and

103 days in medium containing charcoal-stripped serum, insulin, epidermal growth factor, hepatocyte grow

104 t, waist-hip ratio, body mass index, fasting serum insulin, fasting plasma glucose, and type 2 diabet

105 Fasting blood sugar, serum insulin, fasting serum lipids and serum alanine am

106 Serum insulin, fatty acid, and triglyceride levels were

107 ic ATGL completely abrogated the increase in serum insulin following either 1 or 12 wk of feeding a h

108 disproportionately high level of circulating serum insulin for a given glucose concentration ( approx

109 Measured were serum insulin, free fatty acid (FFA), cortisol, and grow

110 in-sensitivity ChecK Index (QUICKI), fasting serum insulin (FSI), homeostasis model assessment of ins

111 into this phenotype, we show that, although serum insulin, glucose, and cholesterol levels are entir

112 are hyperphagic, and have elevated levels of serum insulin, glucose, and leptin.

113 During the fasting and postprandial periods, serum insulin, glucose, triacylglycerol, and nonesterifi

114 auterine growth restriction (IUGR) decreases serum insulin growth factor-1 (IGF-1) levels.

115 the development of hyperinsulinemia (fasting serum insulin > or = 90th percentile, 19.1 micro U/ml).

116 ancreatic cancer cells, and elevated fasting serum insulin has been linked to pancreatic cancer risk.

117 body composition (lean or fat mass); fasting serum insulin; HbA1c; glucose dynamics during glucose to

118 (omental and retroperitoneal), food intake, serum insulin, hepatic triglycerides or in the exercise-

119 essed the prognostic value of adding fasting serum insulin, HOMA-IR (homeostasis model assessment-ins

120 ge in HbA1c, fasting plasma glucose, fasting serum insulin, HOMA-IR or 2-h oral glucose tolerance at

121 ssfully for calibration-free measurements of serum insulin in 30 samples from individuals with type 1

122 educing weight gain, insulin resistance, and serum insulin in DIO mice.

123 ersus placebo (84 +/- 5 mg/dL); mean fasting serum insulin increased nearly fivefold (23 +/- 12 vs. 5

124 Fasting serum insulin, insulin-like growth factor I, fatty acids

125 rin is activated by pertussis toxin, whereas serum, insulin, insulin-like growth factor-1, and ligati

126 This is associated with increased serum insulin, islet insulin content, and insulin mRNA i

127 Body weight, serum insulin, leptin, glucose, cholesterol, and triglyc

128 Serum insulin level was associated with Barrett's esopha

129 y mass index but not with waist:hip ratio or serum insulin level.

130 blood glucose level and a marked rise in the serum insulin level.

131 tingly, LID mice show a fourfold increase in serum insulin levels (2.2 vs. 0.6 ng/ml in control mice)

132 veloped a time-dependent increase in fasting serum insulin levels (from 3.6 +/- 1.1 ng ml-1 at baseli

133 ent in glucose tolerance without a change in serum insulin levels and an increase in serum leptin lev

134 he formation of adenomas results in elevated serum insulin levels and decreased blood glucose levels.

135 body weight, as well as the normalization of serum insulin levels and glucose tolerance.

136 We observed reduced serum insulin levels and insulin-to-glucose ratios in hi

137 severe hyperglycemia with markedly decreased serum insulin levels and nearly normal insulin tolerance

138 Insulin infusion significantly increased serum insulin levels and the insulin/glucagon ratio.

139 Serum insulin levels are altered in insulin resistance a

140 tardation, mild hyperglycemia, and decreased serum insulin levels at 6 months of age when compared wi

141 n noted as a potential breast cancer marker (serum insulin levels being found to be raised in compari

142 We measured serum insulin levels by a validated radioimmunoassay, an

143 seven most strongly linked families had high serum insulin levels during fasting and 2-h post-glucose

144 Stable serum insulin levels during hyperglycemic clamping in pa

145 Intranasal insulin transiently increased serum insulin levels followed by a gradual lowering of b

146 Consistently, HGF concomitantly increased serum insulin levels in diabetic mice.

147 distinguishing the type of diabetes based on serum insulin levels in diabetic patients.

148 s associated with a significant reduction in serum insulin levels in fed and fasting mice.

149 Several studies have implicated serum insulin levels in the upregulation of leptin gene

150 In these subjects, the systemic serum insulin levels increased significantly during the

151 Among women higher fasting serum insulin levels increased the risk of gallbladder d

152 nt compared with control mice and had higher serum insulin levels on day 28.

153 red insulin indicated a sustained profile as serum insulin levels plateaued after 3 h for the duratio

154 dy weight, fasting blood glucose levels, and serum insulin levels than wild-type (WT) mice.

155 th retardation and Turner syndrome; however, serum insulin levels were elevated.

156 Serum insulin levels were reduced in vivo in ritonavir-t

157 Serum insulin levels were significantly decreased in ani

158 Serum insulin levels were significantly different betwee

159 red first-phase insulin secretion, increased serum insulin levels, and greatly decreased levels of gl

160 induced hyperglycemia, a decrease in fasting serum insulin levels, and mild elevation of fasting seru

161 eficiency improves glucose tolerance, lowers serum insulin levels, and reduces TNFalpha gene expressi

162 , such as a reduced increase in body fat and serum insulin levels, compared to steroids.

163 tv3 or THADA tv5 correlated positively with serum insulin levels, of CDK5 tv1 positively with % HbA1

164 um lipid, fasting serum glucose, and fasting serum insulin levels, or blood pressure.

165 tly improved glucose tolerance with enhanced serum insulin levels, reduced beta cell death, and incre

166 ition, Munc18c transgenic mice had depressed serum insulin levels, reflecting a threefold reduction i

167 ed by a 607 +/- 136 % (P < 0.01) increase in serum insulin levels.

168 to insulin and high fasting and postprandial serum insulin levels.

169 glycemia were associated with a decrease in serum insulin levels.

170 ice had impaired glucose tolerance and lower serum insulin levels.

171 sponse to a glucose load in vivo, with lower serum insulin levels.

172 Serum insulin-like growth factor (IGF) -1 is secreted ma

173 ogenesis (4 months), the LF group had higher serum insulin-like growth factor (IGF) binding protein-1

174 Furthermore, MIA-690 decreased serum insulin-like growth factor (IGF)-1 levels in mice

175 Serum insulin-like growth factor (IGF)-I levels were dim

176 Clinical studies have established elevated serum insulin-like growth factor (IGF-I) content and IGF

177 ent epidemiologic studies unequivocally link serum insulin-like growth factor 1 (IGF-1) levels with r

178 te proliferation by modulating a decrease in serum insulin-like growth factor 1 (IGF-1) that allows G

179 Serum insulin-like growth factor 1 (IGF-1) was further r

180 smaller and had severely depressed levels of serum insulin-like growth factor 1 (IGF-1).

181 No difference in serum insulin-like growth factor 1 (IGF1) levels was obs

182 of in utero growth retardation, and had low serum insulin-like growth factor 1 (IGF1) levels.

183 Serum insulin-like growth factor 1 (IGF1) was low in SCD

184 Serum insulin-like growth factor 1 (IGF1) was not reduce

185 Serum insulin-like growth factor 1 (sIGF-1) is an import

186 Serum insulin-like growth factor 1 levels and body weigh

187 ance and restored GH activation of STAT5 and serum insulin-like growth factor 1 levels in colitic mic

188 poor survival and postnatal growth with low serum insulin-like growth factor 1 levels.

189 rior cingulate, treatment-related changes in serum insulin-like growth factor 1 were positively corre

190 We also determined serum insulin-like growth factor binding protein-1 in fo

191 Serum insulin-like growth factor binding protein-1 level

192 Serum insulin-like growth factor binding protein-1 level

193 Serum insulin-like growth factor binding protein-1 level

194 receiver-operating-characteristic curve for serum insulin-like growth factor binding protein-1 was 0

195 ents with available measurements of baseline serum insulin-like growth factor binding protein-1.

196 Serum insulin-like growth factor I (IGF-I) levels consis

197 ory bowel disease (IBD) present with reduced serum insulin-like growth factor I (IGF-I).

198 addition, there was about a 30% decrease in serum insulin-like growth factor I (IGF1), and while the

199 p also experienced a 10% greater increase in serum insulin-like growth factor I (P < 0.05) and a 16%

200 HR and GH binding protein, greatly decreased serum insulin-like growth factor I and elevated serum GH

201 higher serum alkaline phosphatase activity, serum insulin-like growth factor I and insulin-like grow

202 y corticosterone output, but only CR reduced serum insulin-like growth factor I and leptin.

203 ED decreased serum insulin-like growth factor I concentrations and in

204 for 18 months at a dose adjusted for normal serum insulin-like growth factor I level.

205 olic rate, nutrient and electrolyte balance, serum insulin-like growth factor I levels, D-xylose abso

206 ased urinary deoxypyridinoline and increased serum insulin-like growth factor I without affecting par

207 rease in marrow adiposity and a reduction in serum insulin-like growth factor-1 (IGF-1) and the bindi

208 fference (95% CI) was computed for levels of serum insulin-like growth factor-1 (IGF-1), leptin, and

209 zed panel of serologic testing that included serum insulin-like growth factor-1, insulin-like growth

210 axonal and neuropsychological recovery, and serum insulin-like growth factor-I (IGF-I) may mediate t

211 as drawn 0, 10, 20, and 40 days postburn and serum insulin-like growth factor-I (IGF-I), insulin-like

212 72%) weight, (iii) significant inhibition in serum insulin-like growth factor-I and restoration of in

213 nced growth hormone secretion, and increased serum insulin-like growth factor-I by threefold to sixfo

214 tochemical concentrate and green tea reduced serum insulin-like growth factor-I concentrations in bot

215 tudies individualising GH doses to normalize serum insulin-like growth factor-I level have shown a si

216 ROS, which was stimulated by growth factors (serum, insulin-like growth factor I, or fibroblast growt

217 free medium increased after 8 to 16 hours in serum, insulin-like growth factor-I (IGF-I), epidermal g

218 in the presence of nicotinamide, but with no serum, insulin-like growth factor-I or butyrate.

219 A combination of fetal calf serum, insulin-like growth factor-I, nicotinamide and so

220 achieved in vitro by addition of fetal calf serum, insulin-like growth factor-I, nicotinamide, and s

221 hemical indicators including plasma glucose, serum insulin, lipid profile, liver markers (ALT, AST an

222 5 h of intravenous L-carnitine infusion with serum insulin maintained at fasting (7.4+/-0.4 mIU*l(-1)

223 nitoring, 10 patients had plasma glucose and serum insulin measurements, and 5 patients had repeated

224 nist CL 316,243 (CL) increased lipolysis and serum insulin more in KO mice, but blood glucose reducti

225 here were no abnormalities in serum glucose, serum insulin or the ability of insulin to stimulate glu

226 with winter season, waist circumference, and serum insulin (P < 0.005 for all).

227 0001), lower serum glucose (P = 0.04), lower serum insulin (P = 0.03), lower serum IL-(P = 0.0022), l

228 p < 0.001) and was inversely correlated with serum insulin (r = -0.163, p = 0.025), HOMA-IR (r = -0.1

229 d (r = 0.197), fat tissue index (r = 0.150), serum insulin (r = 0.280), and homeostatic model assessm

230 ne increased (P = 0.036) and correlated with serum insulin (r = 0.91, P = 0.002).

231 ely to be responsible, including much higher serum insulin responses to total parenteral nutrition th

232 Blood glucose and serum insulin returned to physiological levels during th

233 ants, LQT2 patients had 56% to 78% increased serum insulin, serum C-peptide, plasma GLP-1, and plasma

234 plant to assess fasting blood glucose (FBG), serum insulin (SI) levels, and i.v. glucose tolerance (I

235 plasma total fatty acid concentration, BMI, serum insulin, statin use, season, and longitudinal time

236 Serum insulin, thyroxine (T4), corticosterone, and adipo

237 tiVIP) gene therapy was required to increase serum insulin to a level sufficient to suppress non-fast

238 tion in A-ZIP/F1 mice reduced blood glucose, serum insulin, triglyceride levels, and the rate of trig

239 knockout mice were not obese and had normal serum insulin, triglyceride, and leptin levels, with a t

240 Herein we report the first serum insulin voltammetric immunosensor for diagnosis of

241 Among nonusers of hormone therapy, fasting serum insulin was associated with a statistically signif

242 Serum insulin was decreased, and plasma glucagon was inc

243 vs 8.7 mmol/L [157 mg/dL] for placebo), and serum insulin was increased in the sulfonylurea studies

244 At Post, postprandial serum insulin was reduced in the Sedentary group (-49%;

245 RESULTS.: Blood glucose was the lowest and serum insulin was the highest in the islet+bone marrow g

246 Among the components of serum, insulin was identified as the key factor that mai

247 tration of uric acid, mean concentrations of serum insulin were 66.2, 66.7, 79.9, and 90.9 pmol/L for

248 and fed conditions, fat-free mass (FFM), and serum insulin were determined on the final day of each t

249 significant differences in plasma glucose or serum insulin were observed during exercise.

250 However, both basal and 2-h OGTT serum insulin were significantly correlated with SAT as

251 a activation in mature adipocytes normalizes serum insulin without increased adipogenesis.