ライフサイエンスコーパス: hyperinsulinemia

1 atic model assessment-IR, hyperglycemia, and hyperinsulinemia).

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

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

4 ond effects accounted for by concurrent mild hyperinsulinemia.

5 ncer (TNBC) specifically under conditions of hyperinsulinemia.

6 ed improved insulin sensitivity and reversed hyperinsulinemia.

7 adipose tissue insulin resistance and worse hyperinsulinemia.

8 ice treated with LPS develop glucose-induced hyperinsulinemia.

9 decrease in liver triglyceride export during hyperinsulinemia.

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

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

12 offspring with normal glucose tolerance but hyperinsulinemia.

13 iver, insulin resistance, hyperlipidemia and hyperinsulinemia.

14 This appears to explain a phenotype of hyperinsulinemia.

15 P mice showed glucose intolerance and severe hyperinsulinemia.

16 type 2 diabetes: combined hyperglycemia and hyperinsulinemia.

17 re observed, which also were correlated with hyperinsulinemia.

18 rtantly, enhanced insulin secretion, causing hyperinsulinemia.

19 ently associated with insulin resistance and hyperinsulinemia.

20 ulin signaling, leading to hyperglycemia and hyperinsulinemia.

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

22 n have normal insulin sensitivity, with mild hyperinsulinemia.

23 portal glucose delivery, hyperglycemia, and hyperinsulinemia.

24 ommon origin that involves insulin-resistant hyperinsulinemia.

25 EPA's preventative role on hyperglycemia and hyperinsulinemia.

26 iates obesity-induced insulin resistance and hyperinsulinemia.

27 T1 in inflammation and insulin resistance in hyperinsulinemia.

28 increases in leptin, glucose intolerance and hyperinsulinemia.

29 ing associated with chronic inflammation and hyperinsulinemia.

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

31 stream of the HIF signaling pathway precedes hyperinsulinemia.

32 y improve glucose metabolism during systemic hyperinsulinemia.

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

34 ation of oxidative stress, inflammation, and hyperinsulinemia.

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

36 xes of oxidative stress and inflammation and hyperinsulinemia.

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

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

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

40 Hyperinsulinemia, a hallmark of these pathologies, is su

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

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

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

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

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

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

47 2KO/IRS1KO, exhibited insulin resistance and hyperinsulinemia and an absence of compensatory beta-cel

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

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

50 Hyperinsulinemia and decreased glucose utilization were

51 Diet-induced obesity causes hyperinsulinemia and diminishes visceral AT (VAT) T reg

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

53 g a propensity for obesity and fatty livers, hyperinsulinemia and glucose response defects.

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

55 Hyperinsulinemia and higher insulin-like growth factors

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

57 mia and hyperglycemia), and type 1 diabetes (hyperinsulinemia and hyperglycemia matching GCK-MODY).

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

59 of 18-HEPE, but not 18-HEPE itself, reversed hyperinsulinemia and hyperglycemia through the G-protein

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

61 RvE1's effects on hyperinsulinemia and hyperglycemia were divergent in div

62 Collectively, the data suggest EPA prevents hyperinsulinemia and hyperglycemia, in part, through RvE

63 We next investigated how EPA improved murine hyperinsulinemia and hyperglycemia.

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

65 impact physiological functions resulting in hyperinsulinemia and hyperglycemia.

66 Hyperinsulinemia and hyperleptinemia may therefore parti

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

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

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

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

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

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

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

74 ed central insulin signaling associated with hyperinsulinemia and insulin resistance due to unrestrai

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

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

79 Thus, hyperinsulinemia and its resultant increased signaling m

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

81 Factors of metabolic syndrome including hyperinsulinemia and obesity are well known to increase

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

83 loited as an alternative way to halt fasting hyperinsulinemia and the progression of type 2 diabetes.

84 in, adipose pathology, or insulin resistance/hyperinsulinemia and with inadequate documentation of li

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

86 g) to WT mice results in insulin resistance, hyperinsulinemia, and glucose intolerance and that Pg tr

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

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

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

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

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

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

93 evented obesity-induced glucose intolerance, hyperinsulinemia, and hyperglycemia in C57BL/6J mice.

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

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

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

97 Insulin resistance, hyperinsulinemia, and hyperproinsulinemia occur early in

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

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

100 iated with lower risk of insulin resistance, hyperinsulinemia, and inflammation, which are known pred

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

102 s Mellitus (T2DM), exhibiting hyperglycemia, hyperinsulinemia, and insulin resistance associated with

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

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

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

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

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

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

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

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

111 ingestion induced marked hyperaminoacidemia, hyperinsulinemia (approximately sixfold basal), and unpr

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

113 Insulin resistance and hyperinsulinemia are consistent characteristics of MetS,

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

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

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

117 offer a direct connection between peripheral hyperinsulinemia, as found in prediabetes, age-related n

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

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

120 provide a novel therapeutic approach against hyperinsulinemia-associated insulin resistance.

121 ooperativity and the mechanism of activated, hyperinsulinemia-associated, noncooperative variants.

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

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

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

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

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

127 control and GCK-MODY and the contribution of hyperinsulinemia by comparing GCK-MODY and type 1 diabet

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

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

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

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

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

133 garding the pathogenesis of diabetes because hyperinsulinemia causes insulin resistance and insulin h

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

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

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

137 Hyperinsulinemia contributes to cardiac hypertrophy and

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

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

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

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

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

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

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

145 act with the HFD to worsen hyperglycemia and hyperinsulinemia during an OGTT, HFD-fed rats that co-us

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

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

148 Thus, in both diet- and aging-associated hyperinsulinemia, excessive Insr signaling in T regs lea

149 Hyperinsulinemia generally increased both NOx FSR and ab

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

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

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

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

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

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

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

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

158 Hyperinsulinemia (HI) is elevated plasma insulin at basa

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

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

161 05; Vit D + CLA: 0.038 +/- 0.005 %.h-1), and hyperinsulinemia-hyperaminoacidemia increased myofibrill

162 %/h; Vit D + CLA: 0.040 +/- 0.007%/h) or the hyperinsulinemia-hyperaminoacidemia-induced increase in

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

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

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

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

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

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

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

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

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

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

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

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

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

176 ce in D734A INSR-expressing mice and reduced hyperinsulinemia in both S350L and D734A INSR-expressing

177 ells, leading to enlarged beta cell area and hyperinsulinemia in diet-induced obesity.

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

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

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

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

182 Hyperinsulinemia in NAFLD correlated strongly with impai

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

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

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

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

187 in peripheral glucose uptake and concomitant hyperinsulinemia in the alms1-/- animals.

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

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

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

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

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

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

194 2R knockout mice exhibit marked postprandial hyperinsulinemia in vivo.

195 A similar attenuation of hyperglycemia and hyperinsulinemia in wild-type mice with obesity but not

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

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

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

199 Hyperinsulinemia increased the synthesis of nearly half

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

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

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

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

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

205 lated and fasted rats, suggesting that acute hyperinsulinemia increases ENaC activity independent of

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

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

208 Maternal hyperinsulinemia (independent of maternal body weight an

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

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

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

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

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

214 = 0.80) but augmented the hyperaminoacidemia-hyperinsulinemia-induced increase in the rate of muscle

215 LDN improves hyperinsulinemia-induced insulin resistance by reorienti

216 Hyperglycemia- and hyperinsulinemia-induced insulin resistance causes alter

217 This, in turn, attenuates the hyperinsulinemia-induced release of pro-inflammatory cyt

218 Our observations suggest that hyperinsulinemia induces sirtuin1 (SIRT1) repression and

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

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

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

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

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

224 in the development of these conditions, and hyperinsulinemia is a central hallmark of peripheral ins

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

226 Hyperinsulinemia is a risk factor for late-onset Alzheim

227 Hyperinsulinemia is an adaptive mechanism that enables t

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

229 Hyperinsulinemia is induced by inflammatory stimuli as a

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

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

232 We show that prediabetic serum hyperinsulinemia is reflected in the cerebrospinal fluid

233 We propose a model in which hyperinsulinemia is the primary and causative defect und

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

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

236 However, how hyperinsulinemia leads to systemic insulin resistance is

237 that in various models of obesity/diabetes, hyperinsulinemia maintains heightened hepatic expression

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

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

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

241 wed that low-dose naltrexone (LDN) abrogates hyperinsulinemia-mediated SIRT1 repression and prevents

242 Peripheral hyperinsulinemia modestly increases ISF and plasma Abeta

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

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

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

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

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

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

249 largely prevented the suppressive effect of hyperinsulinemia on EGP.

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

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

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

253 roach to mitigate the detrimental effects of hyperinsulinemia on immunoregulation of metabolic syndro

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

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

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

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

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

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

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

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

262 0.05 mug/mL per mug protein; P < 0.05), and hyperinsulinemia (P < 0.05).

263 Previous studies show that in obese mice, hyperinsulinemia plays a crucial role in beta-AR desensi

264 Fasting hyperinsulinemia precedes the development of type 2 diab

265 These data suggest that iatrogenic hyperinsulinemia predominates in driving insulin resista

266 ts a second metabolic abnormality-iatrogenic hyperinsulinemia-principally drives insulin resistance a

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

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

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

270 We now provide evidence that hyperinsulinemia promotes the release of soluble pro-inf

271 demonstrate that organismal hyperinsulinemia promotes tumorigenesis by abrogating lo

272 Hyperinsulinemia reduced HGP due to a rapid transition f

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

274 Upon aging, chronic hyperinsulinemia resulted in insulin resistance and hepa

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

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

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

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

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

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

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

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

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

284 insulin clearance will result in peripheral hyperinsulinemia: this exacerbates insulin resistance, w

285 Meanwhile, miR-26a prevents hyperinsulinemia through targeting several critical regu

286 ontributions of hyperglycemia and iatrogenic hyperinsulinemia to insulin resistance using hyperinsuli

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

288 Insulin resistance and hyperinsulinemia underlie the pathogenesis of T2DM.

289 Hyperinsulinemia was caused by increased insulin secreti

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

291 Among nondiabetics, hyperinsulinemia was positively associated with Barrett'

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

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

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

295 Hyperinsulinemia, which is associated with aging and met

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

297 [-4.0 +/- 0.9 pmol/l]) and during sustained hyperinsulinemia with hypoglycemia (-14 +/- 2 pg/ml [-4.

298 They also developed hyperinsulinemia with transient insulin resistance durin

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

300 rather than severe hyperglycemia, sustained hyperinsulinemia without late failure of insulin product