ライフサイエンスコーパス: hyperinsulinemia

1 ing associated with chronic inflammation and hyperinsulinemia.

2 ed improved insulin sensitivity and reversed hyperinsulinemia.

3 adipose tissue insulin resistance and worse hyperinsulinemia.

4 ice treated with LPS develop glucose-induced hyperinsulinemia.

5 y improve glucose metabolism during systemic hyperinsulinemia.

6 decrease in liver triglyceride export during hyperinsulinemia.

7 Jun NH(2)-terminal kinase activation during hyperinsulinemia.

8 ere independent of age, body mass index, and hyperinsulinemia.

9 offspring with normal glucose tolerance but hyperinsulinemia.

10 iver, insulin resistance, hyperlipidemia and hyperinsulinemia.

11 This appears to explain a phenotype of hyperinsulinemia.

12 [(18)F]-fluorodeoxyglucose during euglycemic hyperinsulinemia.

13 type 2 diabetes: combined hyperglycemia and hyperinsulinemia.

14 re observed, which also were correlated with hyperinsulinemia.

15 rtantly, enhanced insulin secretion, causing hyperinsulinemia.

16 ently associated with insulin resistance and hyperinsulinemia.

17 ulin signaling, leading to hyperglycemia and hyperinsulinemia.

18 to a sustained state of hyperglycemia and/or hyperinsulinemia.

19 n have normal insulin sensitivity, with mild hyperinsulinemia.

20 portal glucose delivery, hyperglycemia, and hyperinsulinemia.

21 ommon origin that involves insulin-resistant hyperinsulinemia.

22 e livers of mice with insulin resistance and hyperinsulinemia.

23 ation of oxidative stress, inflammation, and hyperinsulinemia.

24 ed in the presence of insulin resistance and hyperinsulinemia.

25 aged at the baseline and under conditions of hyperinsulinemia.

26 ed in the presence of insulin resistance and hyperinsulinemia.

27 lucose-induced insulin secretion, leading to hyperinsulinemia.

28 s, likely reflecting the lipogenic effect of hyperinsulinemia.

29 ty in the presence of insulin resistance and hyperinsulinemia.

30 etic signaling results in a leptin-dependent hyperinsulinemia.

31 was higher in OB+DM than OB and Lean during hyperinsulinemia.

32 ls are inversely correlated with obesity and hyperinsulinemia.

33 hereas Osteocalcin inactivation halves their hyperinsulinemia.

34 istance of liver and skeletal muscle, and 3) hyperinsulinemia.

35 xes of oxidative stress and inflammation and hyperinsulinemia.

36 n the setting of pre-diabetes and endogenous hyperinsulinemia.

37 bolism and, when challenged with HFD, marked hyperinsulinemia.

38 stream of the HIF signaling pathway precedes hyperinsulinemia.

39 y also promoting insulin resistance (IR) and hyperinsulinemia.

40 ond effects accounted for by concurrent mild hyperinsulinemia.

41 In response to acute physiologic hyperinsulinemia, 1) HGP is suppressed primarily through

42 ned hyperglycemia (202.0 +/- 10.6 mg/dL) and hyperinsulinemia (110.6 +/- 59.0 muU/mL) were, despite i

43 r disease risk factor prevalence was fasting hyperinsulinemia (74%), elevated high-sensitivity C-reac

44 Hyperinsulinemia, a hallmark of these pathologies, is su

45 Hyperinsulinemia, a key factor in obesity, pre-diabetes

46 (-1) x min(-1), P < 0.05) in the presence of hyperinsulinemia, accompanied by smaller increments in R

47 Sirolimus alone resulted in hyperinsulinemia after oral glucose challenge compared t

48 Hyperglycemia and hyperinsulinemia also impaired the PI3K/Akt while enhanc

49 ) were resistant to diet-induced obesity and hyperinsulinemia, although systemic glucose intolerance

50 tor for type 2 diabetes, is characterized by hyperinsulinemia and accelerated body fat recovery.

51 s relevant to understanding the link between hyperinsulinemia and AD.

52 2KO/IRS1KO, exhibited insulin resistance and hyperinsulinemia and an absence of compensatory beta-cel

53 ctive to understand the relationship between hyperinsulinemia and cancer evolution.

54 reatment of type 1 diabetes, or when chronic hyperinsulinemia and central insulin resistance develops

55 erest in relation to the association between hyperinsulinemia and colorectal cancer.

56 Hyperinsulinemia and decreased glucose utilization were

57 Accordingly, Esp inactivation doubles hyperinsulinemia and delays glucose intolerance in ob/ob

58 This may be attributed to hyperinsulinemia and dysregulation of adipokine levels a

59 lpha-reductase inhibitor finasteride induced hyperinsulinemia and hepatic steatosis (10.6 +/- 1.2 vs.

60 ssant-like effects, LAC corrected a systemic hyperinsulinemia and hyperglicemia in rFSL and failed to

61 o GcgR(-/-),LepR(-/-) mice caused the severe hyperinsulinemia and hyperglycemia of LepR(-/-) mice to

62 strated that PoG infusion in the presence of hyperinsulinemia and hyperglycemia triggered an increase

63 as performed in the presence of postprandial hyperinsulinemia and hyperglycemia with exenatide (20 mi

64 With hyperinsulinemia and hyperglycemia, exenatide produced a

65 impact physiological functions resulting in hyperinsulinemia and hyperglycemia.

66 pearance of the GcgR transgene abolished the hyperinsulinemia and hyperglycemia.

67 Hyperinsulinemia and hyperleptinemia may therefore parti

68 sed food intake and obesity accompanied with hyperinsulinemia and hyperleptinemia.

69 ic steatohepatitis (NASH) is associated with hyperinsulinemia and increased FFA-blood levels, the int

70 A role for hyperinsulinemia and increased insulin-like growth facto

71 overt insulin resistance, which is masked by hyperinsulinemia and increased pancreatic islet mass, to

72 n oxidant-mediated protein modifications and hyperinsulinemia and increased plasma adiponectin.

73 Endogenous hyperinsulinemia and insulin receptor (IR)/IGF-I recepto

74 ce were protected against the development of hyperinsulinemia and insulin resistance because of enhan

75 Although hyperinsulinemia and insulin resistance have been hypoth

76 protein kinase Map4k4 drives obesity-induced hyperinsulinemia and insulin resistance in part by promo

77 igen-related cell adhesion molecule 1 causes hyperinsulinemia and insulin resistance, which result fr

78 in obese mice and resulted in a reduction of hyperinsulinemia and insulin resistance.

79 elative contribution of insulin clearance to hyperinsulinemia and its relationship to liver histology

80 Thus, hyperinsulinemia and its resultant increased signaling m

81 cific inducible CEACAM1 expression prevented hyperinsulinemia and markedly limited insulin resistance

82 this, Smad3-deficient mice exhibit moderate hyperinsulinemia and mild hypoglycemia.

83 ine protease inhibitor) levels increase with hyperinsulinemia and obesity.

84 uesters fat within adipose tissue because of hyperinsulinemia and results in adaptive suppression of

85 ty in the presence of insulin resistance and hyperinsulinemia and the associated mechanism.

86 emic load (GL) may influence cancer risk via hyperinsulinemia and the insulin-like growth factor axis

87 gment the MBV increase seen with physiologic hyperinsulinemia and whether free fatty acid (FFA)-induc

88 ring and the earlier onset of hyperglycemia, hyperinsulinemia and/or hyperlipidemia.

89 including hyperbilirubinemia, hypoglycemia, hyperinsulinemia, and birth trauma.

90 nce suggests an association between obesity, hyperinsulinemia, and colorectal cancer risk.

91 emic CLGI, compromised glycemic homeostasis, hyperinsulinemia, and early symptoms of liver steatosis.

92 ond pathway broadly associated with obesity, hyperinsulinemia, and free IGF-I.

93 kedly exacerbated HFD-induced hyperglycemia, hyperinsulinemia, and glucose intolerance in TgKO mice.

94 sterolemia, with aggravated hyperleptinemia, hyperinsulinemia, and glucose intolerance.

95 f PKD1 in beta-cells worsened hyperglycemia, hyperinsulinemia, and glucose intolerance.

96 ulation, hepatic steatosis, hyperleptinemia, hyperinsulinemia, and glucose intolerance.

97 enuated comorbidities such as hyperglycemia, hyperinsulinemia, and hepatic steatosis and normalized l

98 her GlyRa, lower ATIS at baseline and during hyperinsulinemia, and higher lipid oxidation.

99 reases in lipid uptake, de novo lipogenesis, hyperinsulinemia, and hyperglycemia accompanied with sev

100 Physiological responses to hypoglycemia, hyperinsulinemia, and hyperglycemia include a critical a

101 trol-fed PXR-KO mice exhibited hepatomegaly, hyperinsulinemia, and hyperleptinemia but hypoadiponecti

102 c disorders, including obesity, hyperphagia, hyperinsulinemia, and hyperleptinemia, similar to those

103 s-induced diabetes, including hyperglycemia, hyperinsulinemia, and hyperlipidemia.

104 Insulin resistance, hyperinsulinemia, and hyperproinsulinemia occur early in

105 gous mice exhibit progressive hyperglycemia, hyperinsulinemia, and impaired glucose tolerance from 12

106 unction with low grade chronic inflammation, hyperinsulinemia, and increased body fat, which are sign

107 knockout mice develop obesity, fatty liver, hyperinsulinemia, and insulin insensitivity on chow diet

108 it has been hypothesized that hyperglycemia, hyperinsulinemia, and insulin resistance are involved in

109 -induced weight gain, adipocyte hypertrophy, hyperinsulinemia, and insulin resistance, which occur in

110 abolic dysfunction, including hyperglycemia, hyperinsulinemia, and insulin resistance.

111 end on experimental models of hyperglycemia, hyperinsulinemia, and insulin resistance.

112 in sensitivity, normalized hyperglycemia and hyperinsulinemia, and lowered postprandial insulin resis

113 iet caused excess weight gain, dyslipidemia, hyperinsulinemia, and mild glucose intolerance, however,

114 Rs in the early phase of the disease develop hyperinsulinemia, and show a strong inverse correlation

115 diet-induced body weight gain but exhibited hyperinsulinemia, and their adipose tissues were similar

116 (GB) surgery is associated with postprandial hyperinsulinemia, and this effect is accentuated in post

117 ted levels of biomarkers of inflammation and hyperinsulinemia are associated with a higher risk of HC

118 Insulin resistance (IR) and hyperinsulinemia are hallmarks of the metabolic syndrome

119 lin triggers CB, highlighting a new role for hyperinsulinemia as a stimulus for CB overactivation.

120 inciding with the onset of hyperglycemia and hyperinsulinemia as well as the induction of P2X(7) in a

121 nderlies the development of glucose-mediated hyperinsulinemia associated with endotoxemia.

122 all-molecule diabetes therapeutic agents and hyperinsulinemia-associated GCK mutations share a striki

123 L/6 mice, in vivo physiological responses to hyperinsulinemia at euglycemia and hypoglycemia were int

124 onstrated that in canines, physiologic brain hyperinsulinemia brought about by infusion of insulin in

125 ng insulin resistance may depend not only on hyperinsulinemia but also on the ability to suppress glu

126 oincides with the onset of hyperglycemia and hyperinsulinemia but, unexpectedly, is not mediated by t

127 Insulin clearance was not saturated at hyperinsulinemia, but metabolic clearance of C-peptide,

128 low circulating SHBG has been attributed to hyperinsulinemia, but no mechanistic evidence has been d

129 asculature beyond that seen with physiologic hyperinsulinemia by a distinct mechanism that is not blo

130 Importantly, with correction of hyperinsulinemia by inhibition of hepatic aPKC and impro

131 sulin resistance but also be responsible for hyperinsulinemia by stimulating secretion and reducing c

132 erol during physiologic and supraphysiologic hyperinsulinemia, by combining microdialysis with oral g

133 She presented the Banting Lecture, "Hyperinsulinemia: Cause or Consequence?" on Sunday, 26 J

134 ression reversed the glucose intolerance and hyperinsulinemia caused by the HFD and protected against

135 ent of HFF GcgR(-/-) to simulate HFF-induced hyperinsulinemia caused obesity and mild T2D.

136 S1 and IRS2 in the heart and examine whether hyperinsulinemia causes myocardial insulin resistance an

137 , sex, race, ethnicity, body mass index, and hyperinsulinemia, children with metabolic syndrome had 5

138 tations in KCNQ1, includes, besides long QT, hyperinsulinemia, clinically relevant symptomatic reacti

139 els of triglycerides and were protected from hyperinsulinemia compared with HFD PBS-treated mice.

140 Hyperinsulinemia contributes to cardiac hypertrophy and

141 In summary, our data suggest that hyperinsulinemia could induce breast cancer progression

142 , respectively; P < 0.05), while FFAs during hyperinsulinemia decreased and GDR increased significant

143 in tolerance, protection against LPS-induced hyperinsulinemia, decreased macrophage infiltration into

144 insulin signaling in response to peripheral hyperinsulinemia, despite detecting increased signaling

145 erglycemia, hypertriglyceridemia and greater hyperinsulinemia developed in the MKR mice treated with

146 Less marked hyperglycemia and hyperinsulinemia developed with NVP-BEZ235 than NVP-BKM1

147 adipose tissue, or lipodystrophy, results in hyperinsulinemia, diabetes mellitus, and severe hepatic

148 -resistant patients with T2DM, hyperglycemic-hyperinsulinemia did not increase ER stress response mar

149 Furthermore, acute hyperinsulinemia downregulates H19, a phenomenon that oc

150 vide evidence that higher BMI levels precede hyperinsulinemia during childhood, and this one-directio

151 Physiologic hyperinsulinemia during FFA elevation paradoxically decr

152 prevalence of CVD risk factors (ie, fasting hyperinsulinemia, elevated high-sensitivity C-reactive p

153 Hyperinsulinemia failed to suppress adipose tissue inter

154 Hyperinsulinemia generally increased both NOx FSR and ab

155 ion of p31(comet) causes insulin resistance, hyperinsulinemia, glucose intolerance, and hyperglycemia

156 e correlated with measures of hyperglycemia, hyperinsulinemia, glucose intolerance, and insulin resis

157 normal weight loss; however, they developed hyperinsulinemia, glucose intolerance, increased express

158 Increasing levels of ALT and fasting hyperinsulinemia (>12 muU/mL) synergized with increasing

159 itine infusion in the presence or absence of hyperinsulinemia had no effect on muscle TC content in v

160 reases breast cancer risk and mortality, and hyperinsulinemia has been identified as a major factor l

161 g hyperglycemia, impaired glucose tolerance, hyperinsulinemia, hepatic steatosis and diminished insul

162 are protected from the glucose intolerance, hyperinsulinemia, hepatic steatosis, adiposity, hyperten

163 s of Lep-null mutant rats including obesity, hyperinsulinemia, hepatic steatosis, nephropathy, and in

164 rose-enriched diet was sufficient to provoke hyperinsulinemia, hepatosteatosis, hepatic insulin resis

165 Hyperinsulinemia (HI) is elevated plasma insulin at basa

166 The progressive hyperinsulinemia, however, caused a dose-dependent incre

167 ain in response to excess caloric intake and hyperinsulinemia; however, the mechanism by which GH is

168 sting and amino acid-induced hypoglycemia in hyperinsulinemia hyperammonemia (HI/HA).

169 uent studies demonstrated that wild-type and hyperinsulinemia/hyperammonemia forms of GDH are inhibit

170 developed glucoregulatory defects including hyperinsulinemia, hyperglucagonemia, hyperglycemia, and

171 uding increased circulating estrogen levels, hyperinsulinemia, hyperglycemia, and chronic inflammatio

172 identify hepatocellular changes elicited by hyperinsulinemia, hyperglycemia, and PoG signaling in no

173 paired fasting glucose, glucose intolerance, hyperinsulinemia, hyperleptinemia and dyslipidemia marke

174 ly and raised on an Se-adequate diet exhibit hyperinsulinemia, hyperleptinemia, glucose intolerance,

175 ountered in humans, including hyperglycemia, hyperinsulinemia, hyperleptinemia, insulin and leptin re

176 mon metabolic dysregulation such as obesity, hyperinsulinemia, hypertension, and type 2 diabetes.

177 eveloped along with aspects of MS, including hyperinsulinemia, hypertension, hypertriglyceridemia, an

178 ated ChREBP, and caused glucose intolerance, hyperinsulinemia, hypertriglyceridemia, and hepatic stea

179 ith obesity and metabolic risk, specifically hyperinsulinemia, hypertriglyceridemia, hyperleptinemia,

180 ion (anti-incretin effect) to defend against hyperinsulinemia-hypoglycemia.

181 suppressed development of hyperglycemia and hyperinsulinemia, improved systemic glucose tolerance, r

182 perfusion and amino acid availability during hyperinsulinemia improves the muscle protein anabolic ef

183 We found that physiological hyperinsulinemia in awake, behaving mice does not increa

184 igh fat (HF) diet-induced diabetic mice with hyperinsulinemia in ECIRS1 TG versus wild type (WT), but

185 is unknown but may involve the influence of hyperinsulinemia in enhancing free or bioavailable conce

186 urthermore, the role of hyperglycemia versus hyperinsulinemia in exenatide-mediated glucose disposal

187 ricular dAG failed to regulate FM and induce hyperinsulinemia in GHSR-deficient (Ghsr(-/-)) mice.

188 emonstrate that pharmacological induction of hyperinsulinemia in mice down-regulates myocardial UCP3.

189 iled to cause glucose intolerance or promote hyperinsulinemia in mixed background A/A or S/S mice.

190 Hyperinsulinemia in NAFLD correlated strongly with impai

191 limus and sirolimus induce hyperglycemia and hyperinsulinemia in normal rats.

192 eased birth weight as a consequence of fetal hyperinsulinemia in Pima Indians, missense and common no

193 s were few but consistent with prevention of hyperinsulinemia in some but not all overweight persons.

194 data provide evidence for a direct role for hyperinsulinemia in stimulating hepatic Cd36 expression

195 y be a useful tool for reducing postprandial hyperinsulinemia in T2DM, thereby potentially improving

196 a mechanism that involves hyperglycemia and hyperinsulinemia in the development of malformations.

197 mice exhibited decreased glucose levels and hyperinsulinemia in the fasting and fed state.

198 parameters, baroreflex sensitivity (BRS) and hyperinsulinemia in the high fructose-drinking (HFD) rat

199 tential to revert the unfavorable effects of hyperinsulinemia in these patients.

200 cose metabolism caused by normal physiologic hyperinsulinemia in this large animal model.

201 ycemia was linked to glucose intolerance and hyperinsulinemia in TLR4(+/+) mice, but not in TLR4(-/-)

202 lating and tissue endocannabinoid levels and hyperinsulinemia in type 2 diabetes.

203 these molecular events during physiological hyperinsulinemia in vivo in a large animal model.

204 In the presence of hyperglycemic-hyperinsulinemia in ZDF, reduced glycogenic flux partial

205 olon cancer recurrence in states of relative hyperinsulinemia, including sedentary lifestyle, obesity

206 In normal subjects, hyperglycemia-hyperinsulinemia increased after/before mRNA ratios of s

207 Superimposing contraction on physiologic hyperinsulinemia increased MBV within 10 min by 37 and 6

208 Hyperinsulinemia increased the synthesis of nearly half

209 can influence breast cancer development via hyperinsulinemia, increased estrogen, and/or inflammatio

210 causes improved glucose tolerance, decreased hyperinsulinemia, increased insulin sensitivity and decr

211 and LepR(-/-),GcgR(+/+) mice both developed hyperinsulinemia, increased liver sterol response elemen

212 glucagon receptor-null mice did not develop hyperinsulinemia, increased liver sterol response elemen

213 In addition, hyperinsulinemia increases C-peptide clearance, which ma

214 We hypothesized that endogenous hyperinsulinemia increases mammary tumor growth by direc

215 ppear to rapidly alleviate hyperglycemia and hyperinsulinemia independent of weight loss.

216 Maternal hyperinsulinemia (independent of maternal body weight an

217 on rate needed to maintain euglycemia during hyperinsulinemia, indicating enhancement of peripheral i

218 we conclude that combined hyperglycemia and hyperinsulinemia induce short-term myocardial lipid accu

219 T2DM patients, was associated with decreased hyperinsulinemia-induced ER stress responses.

220 lin-signaling pathway and with a decrease of hyperinsulinemia-induced ER stress responses.

221 but appears to result partly from increased hyperinsulinemia-induced hypothalamic fatty acid synthas

222 = 0.80) but augmented the hyperaminoacidemia-hyperinsulinemia-induced increase in the rate of muscle

223 Hyperglycemia- and hyperinsulinemia-induced insulin resistance causes alter

224 eight gain (21.6 +/- 1.4 vs 16.2 +/- 2.4 g), hyperinsulinemia (insulin area under the curve during gl

225 mice, including glucose intolerance, marked hyperinsulinemia, insulin resistance in skeletal muscle

226 levels by >50% beginning at 21 days, causing hyperinsulinemia, insulin resistance, and elevation in h

227 L-iNOS-Tg mice exhibited mild hyperglycemia, hyperinsulinemia, insulin resistance, and impaired insul

228 D16 pregnant dams in association with basal hyperinsulinemia, insulin-resistant endogenous glucose p

229 We conclude that hyperinsulinemia is a key programming factor and therefo

230 Hyperinsulinemia is a risk factor for late-onset Alzheim

231 Hyperinsulinemia is an adaptive mechanism that enables t

232 Hyperinsulinemia is believed to play a key role in the p

233 Hyperinsulinemia is induced by inflammatory stimuli as a

234 ta-cell replication when acute hyperglycemia/hyperinsulinemia is induced.

235 nce in prediabetic individuals, postprandial hyperinsulinemia is reduced only when a low-GI diet is c

236 Because hyperinsulinemia is typically characterized by a 3-fold

237 Whether this hyperinsulinemia itself is part of a feedback loop that

238 n muscle TC during l-carnitine infusion with hyperinsulinemia, l-carnitine infusion in the presence o

239 rp78(+/-) mice are resistant to diet-induced hyperinsulinemia, liver steatosis, white adipose tissue

240 These data suggest that hyperinsulinemia may contribute to the development of ob

241 Sustained down-regulation of cardiac UCP3 by hyperinsulinemia may partly explain the poor prognosis o

242 rom long-standing systemic hyperglycemia and hyperinsulinemia, may be generalized to the brain, resul

243 Peripheral hyperinsulinemia modestly increases ISF and plasma Abeta

244 plasma free fatty acid concentration during hyperinsulinemia most strongly predicted infant birth we

245 temporal and mechanistic connections between hyperinsulinemia, obesity and insulin resistance.

246 ue inflammation corresponded with the robust hyperinsulinemia observed in APOE2 mice after being fed

247 l model systems consistently have shown that hyperinsulinemia occurs in animals with periodontitis co

248 ype II (MODY-II) and persistent hypoglycemic hyperinsulinemia of infancy (PHHI).

249 n was an important mediator in the effect of hyperinsulinemia on breast cancer metastasis.

250 largely prevented the suppressive effect of hyperinsulinemia on EGP.

251 e were evaluated to understand the impact of hyperinsulinemia on estimates of beta-cell function.

252 could mediate some of the adverse effects of hyperinsulinemia on HCC.

253 Here, we have explored the effect of hyperinsulinemia on hepatic Cd36 expression, development

254 -/-) mice had similar weight, adiposity, and hyperinsulinemia on high-fat diets, and Ffar1(-/-) mice

255 We investigated the effect of chronic hyperinsulinemia on proteostasis by generating a time-re

256 The in vivo effects of insulin (hyperinsulinemia) on omentin-1 levels were also assessed

257 d 11 adults, respectively, during euglycemic hyperinsulinemia or after oral niacin to suppress FFA co

258 risk for hypoglycemia, nor did it rely upon hyperinsulinemia or beta-cell hyperplasia, although PKA

259 ing on net hepatic glycogen synthesis during hyperinsulinemia or hepatic portal vein glucose infusion

260 LepR(-/-),GcgR(-/-) did not develop hyperinsulinemia or hyperglycemia.

261 ia, and low HDL cholesterol), and markers of hyperinsulinemia or insulin resistance (insulin and C-pe

262 of prediabetes, and the patients may develop hyperinsulinemia or type 2 diabetes in the future.

263 response of the liver to normal physiologic hyperinsulinemia over 4 h.

264 easures of oxidative stress (P < 0.001), and hyperinsulinemia (P < 0.01).

265 0.05 mug/mL per mug protein; P < 0.05), and hyperinsulinemia (P < 0.05).

266 de the first evidence that hyperglycemia and hyperinsulinemia promote insulin resistance and impair l

267 (NEFAs) in the liver, whereas IR-associated hyperinsulinemia promotes hepatic de novo lipogenesis.

268 gate the mechanisms through which endogenous hyperinsulinemia promotes mammary tumor metastases.

269 Hyperinsulinemia reduced HGP due to a rapid transition f

270 Thirty minutes of hyperinsulinemia resulted in an increase in phospho-FOXO

271 hepatic insulin extraction to cause chronic hyperinsulinemia, resulting in insulin resistance and vi

272 duced postprandial hyperglycemia and fasting hyperinsulinemia significantly correlated with tumor inc

273 ting FFAs; however, decreases in FFAs during hyperinsulinemia significantly determined GDR improvemen

274 Rather, brain hyperinsulinemia slowly caused a modest reduction in net

275 y liver disease, and thus it correlates with hyperinsulinemia, steatosis, and insulin resistance.

276 Hyperinsulinemia stimulates liver production of IGF-I, p

277 Pathologic conditions associated with hyperinsulinemia, such as obesity, metabolic syndrome, a

278 ciated with high levels of serum FFAs during hyperinsulinemia, suggesting impaired insulin action in

279 y pharmacological inhibition of DPP-4 caused hyperinsulinemia, suppression of glucagon release, and g

280 Here we show in a model of chronic hyperinsulinemia that adipocytes develop selective insul

281 of the human GLUT4 promoter, can prevent the hyperinsulinemia that results from obesity.

282 ity, thereby accelerating the development of hyperinsulinemia that will ultimately lead to advanced m

283 In contrast, reducing hyperinsulinemia to basal levels, exenatide-increased to

284 However, mechanisms linking hyperinsulinemia to NAFLD and HCC require clarification.

285 Insulin resistance and hyperinsulinemia underlie the pathogenesis of T2DM.

286 Hyperinsulinemia was caused by increased insulin secreti

287 A 2-fold increased hyperinsulinemia was maintained for the first 4 weeks of

288 t was elevated in the transgenics, and their hyperinsulinemia was more marked, suggesting greater ins

289 Among nondiabetics, hyperinsulinemia was positively associated with Barrett'

290 A higher fasting insulin concentration or hyperinsulinemia was significantly associated with an in

291 Glucose and lipid kinetics during hyperinsulinemia were also measured in a subset of parti

292 Insulin resistance and hyperinsulinemia were induced in mice by a high fat diet

293 Tumors from mice with endogenous hyperinsulinemia were larger and had greater IR phosphor

294 sal, and suppression of fat oxidation during hyperinsulinemia were significantly lower in Ab- compare

295 xhibited impairment of insulin clearance and hyperinsulinemia, which caused insulin resistance beginn

296 Hyperinsulinemia, which is associated with aging and met

297 pically from Irs1 single mutants and exhibit hyperinsulinemia, while maintaining normal beta cell mas

298 [-4.0 +/- 0.9 pmol/l]) and during sustained hyperinsulinemia with hypoglycemia (-14 +/- 2 pg/ml [-4.

299 They also developed hyperinsulinemia with transient insulin resistance durin

300 d to 3 days of high caloric intake exhibited hyperinsulinemia without hyperglycemia and a decrease in