ライフサイエンスコーパス: insulin resistance

1 (Roux-en-Y gastric bypass [RYGB]) surgery on insulin resistance.

2 enotypes without markedly causing peripheral insulin resistance.

3 teins that play a role in the development of insulin resistance.

4 y changes of homeostasis model assessment of insulin resistance.

5 expenditure, impaired lipid metabolism, and insulin resistance.

6 hanistically link nutrient excess to adipose insulin resistance.

7 T) and may contribute to AT inflammation and insulin resistance.

8 approach against hyperinsulinemia-associated insulin resistance.

9 pocyte lipolysis in promoting stress-induced insulin resistance.

10 easing beta-cell mass during obesity-related insulin resistance.

11 lipogenesis, oxidative stress, fibrosis, and insulin resistance.

12 critical step in the progression of hepatic insulin resistance.

13 pendent glucose utilization does not promote insulin resistance.

14 development of hepatosteatosis resulting in insulin resistance.

15 egative feedback loop of "glucose-dependent" insulin resistance.

16 to reduce systemic inflammation and reverse insulin resistance.

17 on of diet-induced obesity, fatty liver, and insulin resistance.

18 inuria and with increased RPF, fat mass, and insulin resistance.

19 late insulin secretion and cause exacerbated insulin resistance.

20 ndent mitochondrial oxidants failed to cause insulin resistance.

21 ative stress, mitochondrial dysfunction, and insulin resistance.

22 d insulin secretion and increased peripheral insulin resistance.

23 ulinemia is a central hallmark of peripheral insulin resistance.

24 pants with features of central adiposity and insulin resistance.

25 thereby avoid the complications of life-long insulin resistance.

26 abolic health by lowering blood pressure and insulin resistance.

27 are paradoxically normal in the presence of insulin resistance.

28 uscle of IRMOE mice, indicating postreceptor insulin resistance.

29 olved in the pathogenesis of obesity-induced insulin resistance.

30 er-body fat, enlarged gluteal adipocytes and insulin resistance.

31 reversed diet-induced hepatic steatosis and insulin resistance.

32 intended metabolic consequence of whole-body insulin resistance.

33 ssary to explore the genetic architecture of insulin resistance.

34 nonalcoholic fatty liver disease (NAFLD) and insulin resistance.

35 nd protects against diet-induced obesity and insulin resistance.

36 disease and steatohepatitis (NAFLD/NASH) and insulin resistance.

37 c and proinflammatory cytokine that promotes insulin resistance.

38 creatic beta-cell dysfunction and peripheral insulin resistance.

39 in the adipose tissue during obesity-induced insulin resistance.

40 variants of SH2B1 display severe obesity and insulin resistance.

41 tion upon insulin stimulation, indicative of insulin resistance.

42 metabolism and growth in obesity-associated insulin resistance.

43 ng skeletal muscle and liver and to systemic insulin resistance.

44 ic lipid deposition-induced lipotoxicity and insulin resistance.

45 hus, can ameliorate diet-induced obesity and insulin resistance.

46 e-related and diet-induced fat mass gain and insulin resistance.

47 tribute to a state of local inflammation and insulin resistance.

48 including hyperglycemia, hyperlipidemia, and insulin resistance.

49 prevent hepatosteatosis, hyperlipidemia, and insulin resistance.

50 d offspring adiposity or markers of systemic insulin resistance.

51 ed impaired glucose tolerance and peripheral insulin resistance.

52 unction, giving rise to "lipodystrophy-like" insulin resistance.

53 reased in males indicating susceptibility to insulin resistance.

54 s not directly contribute to skeletal muscle insulin resistance.

55 lites known to contribute to skeletal muscle insulin resistance.

56 ue (AT) inflammation contributes to systemic insulin resistance.

57 nd protects mice from developing obesity and insulin resistance.

58 as an attractive target against obesity and insulin resistance.

59 and is not simply a compensatory response to insulin resistance.

60 sity-induced adipose tissue inflammation and insulin resistance.

61 mice were prone to diet-induced obesity and insulin resistance.

62 2 protects mice from HFD-induced obesity and insulin resistance.

63 -fat diet-induced obesity and development of insulin resistance.

64 ators from macrophages that lead to systemic insulin resistance.

65 meliorates liver inflammation, steatosis and insulin resistance.

66 and remarkably reverses already established insulin-resistance.

67 sociated with impaired glucose tolerance(2), insulin resistance(3) and mitochondrial disease(4), and

68 ecrease in body weight and decreased hepatic insulin resistance (-58%) despite an increase in NEFA co

69 Epidemiological studies suggest that insulin resistance accelerates progression of age-based

70 ons of betaine, were associated with greater insulin resistance (all P < 0.02).

71 Type 2 diabetes (T2D) is characterized by insulin resistance along with pancreatic beta cell failu

72 LincIRS2 loss causes elevated blood glucose, insulin resistance and aberrant glucose output in lean m

73 Insulin resistance and altered energy metabolism is comm

74 ts when investigating the pathophysiology of insulin resistance and associated risk factors such as b

75 m and adipose tissue (AT) in obesity-induced insulin resistance and correlates inversely with insulin

76 ntrations of very small TRLPs are related to insulin resistance and could be important mediators of c

77 CD36 deficiency led to hepatic insulin resistance and decreased insulin-stimulated tyro

78 The prevalence of obesity, insulin resistance and diabetes is increasing rapidly.

79 with HIV and alters the relationship between insulin resistance and DM.

80 nsitivity, but surgery alone did not resolve insulin resistance and ECM remodeling.

81 apo-RBP4 injection in wild-type mice causes insulin resistance and elevates PGWAT inflammatory marke

82 2 deficiency may be associated with obesity, insulin resistance and gestational diabetes; and with ob

83 letion of hepatic ApoJ or muscle LRP2 causes insulin resistance and glucose intolerance.

84 Insulin resistance and hepatic lipid accumulation consti

85 vestigated on therapeutic actions mitigating insulin resistance and hepatic steatosis in high-fat-suc

86 aging, chronic hyperinsulinemia resulted in insulin resistance and hepatic steatosis through activat

87 ence of JNK activation is the development of insulin resistance and hepatic steatosis through inhibit

88 reatment reduced miR-802 levels and improved insulin resistance and hepatosteatosis, but these benefi

89 lipolysis was inhibited, the stress-induced insulin resistance and hyperglycemia were largely abolis

90 early baroreflex dysfunction, likely due to insulin resistance and hyperglycemia, albeit without pro

91 ocyte lipolysis and simultaneously triggered insulin resistance and hyperglycemia.

92 in both adipose tissue and ileum, leading to insulin resistance and impaired glucose and lipid metabo

93 llitus (T2DM) is a disorder characterized by insulin resistance and impaired glucose metabolism.

94 In line, HFD-induced hepatic insulin resistance and impairment of glucose tolerance w

95 Adipose tissue dysfunction, insulin resistance and inflammation are recognized as im

96 of diabetes because hyperinsulinemia causes insulin resistance and insulin hypersecretion is an inde

97 iabetes onset, HbA(1c), BMI, and measures of insulin resistance and insulin secretion) to cluster adu

98 Obesity is linked with insulin resistance and is characterized by excessive acc

99 trogenic hyperinsulinemia-principally drives insulin resistance and its consequences in this populati

100 llular signalling and its effect on obesity, insulin resistance and lipotoxicity.

101 ated type 2 diabetes mellitus (T2DM) entails insulin resistance and loss of beta-cell mass.

102 e of the major drivers of obesity-associated insulin resistance and metabolic abnormalities.

103 ation and AT inflammation and contributes to insulin resistance and metabolic dysfunctions in obese m

104 loci for many key AT transcripts influencing insulin resistance and obesity.

105 aintenance haemodialysis are associated with insulin resistance and protein metabolism dysfunction.

106 Muscle atrophy, insulin resistance and reduced muscle phosphoinositide 3

107 n of which was associated with a reversal of insulin resistance and restoration of chromatin accessib

108 rus' inflammatory surge, resulting in severe insulin resistance and severe hyperglycemia.

109 eneration by HIF-1 contributes to IH-induced insulin resistance and T2D as well as disrupted NMDA rec

110 e former was attributed to decreased hepatic insulin resistance and the latter to increased hepatic m

111 ity is closely related to the development of insulin resistance and type 2 diabetes (T2D).

112 ty-linked metabolic dysfunctions, leading to insulin resistance and type 2 diabetes mellitus.

113 n-for example, in obesity-is associated with insulin resistance and type 2 diabetes(5,6).

114 Adipocyte dysfunction links obesity to insulin resistance and type 2 diabetes.

115 ogenesis and thus hepatosteatosis leading to insulin resistance and type 2 diabetes.

116 ial therapeutic targets for the treatment of insulin resistance and type 2 diabetes.

117 thought to be related to the development of insulin resistance and type 2 diabetes.

118 lipid accumulation in the liver, leading to insulin resistance and type 2 diabetes.

119 hed-chain amino acids (BCAAs) associate with insulin resistance and type 2 diabetes.

120 Insulin resistance and uric acid concentrations were ben

121 ith low-grade chronic inflammation promoting insulin-resistance and diabetes.

122 raditional risk factors (such as obesity and insulin resistance) and improvements in vascular health

123 tance in vivo (euglycemic clamps and HOMA of insulin resistance), and the presence of nonalcoholic fa

124 on but impairs beta-cell function, 2) causes insulin resistance, and 3) reduces metabolic clearance r

125 ntly, CD81 loss causes diet-induced obesity, insulin resistance, and adipose tissue inflammation.

126 DEX offspring had glucose, insulin resistance, and adiposity and also displayed col

127 y processes, including fatty acid synthesis, insulin resistance, and adiposity.

128 ovale after cryptogenic stroke, treatment of insulin resistance, and best medical treatment of intrac

129 bolic syndrome, including obesity, diabetes, insulin resistance, and cardiovascular complications.

130 loped Alzheimer's like pathologies, cerebral insulin resistance, and cognitive impairments.

131 for the development of NAFLD: hyperglycemia, insulin resistance, and dyslipidemia.

132 The effects of excess adiposity, insulin resistance, and hepatic steatosis on the complex

133 ine, leucine, valine) metabolism in obesity, insulin resistance, and immunity; thus, we hypothesized

134 with protection from cardiovascular disease, insulin resistance, and inflammation.

135 clusion of participants with relatively mild insulin resistance, and lack of concurrent dietary inter

136 -specific ablation of Sh2b1 develop obesity, insulin resistance, and liver steatosis.

137 ecific functions strongly linked to obesity, insulin resistance, and type 2 diabetes.

138 improve metabolic health and reduce obesity, insulin resistance, and type II diabetes.

139 Stress hyperglycemia and insulin resistance are evolutionarily conserved metaboli

140 eased C-reactive protein (CRP), reduced HDL, insulin resistance as well as increased androgens compar

141 This leads to insulin resistance as well as lung and endothelial damag

142 rculating 3-HIB concentrations with HOMA2 of insulin resistance, as well as a transient increase in 3

143 in adipose tissue and its potential role in insulin resistance associated with obesity.

144 increased energy expenditure and ameliorated insulin resistance, associated with a smaller adipocyte

145 reduces cardiac DFA partitioning and hepatic insulin resistance at least in part through increased in

146 ial for whole-body glucose homeostasis, with insulin resistance being a major risk factor for metabol

147 pe 2 diabetes (T2D) via pathways involved in insulin resistance, beta-cell dysfunction, and inflammat

148 y primary drivers with subsequent adiposity, insulin resistance, beta-cell dysfunction, and metabolic

149 5-11.5 years) with fasting glucose, insulin, insulin resistance, beta-cell function, and adiponectin

150 There was no difference in insulin or insulin resistance between the two PCOS cohorts.

151 not provide evidence for resistin increasing insulin resistance, body mass index, or type 2 diabetes

152 -cell adaptation to compensate for increased insulin resistance, but deregulation of miRNA expression

153 y, this metabolic remodeling did not improve insulin resistance, but induced fibrogenic genes and inf

154 igh-fat diet-induced glucose intolerance and insulin resistance by increasing AKT (protein kinase B)

155 n in individuals with obesity contributes to insulin resistance by increasing plasma PAI-1 concentrat

156 LDN improves hyperinsulinemia-induced insulin resistance by reorienting macrophages toward ant

157 bese subjects may cause hepatic and systemic insulin resistance by stimulating basal lipolysis and by

158 t deregulated insulin activities or cerebral insulin resistance contributes to neuroinflammation and

159 in other groups, and the magnitude of their insulin resistance correlated positively with the insula

160 We found that insulin resistance correlates significantly with a shift

161 KD rapidly reverses NAFLD and insulin resistance despite increasing circulating nonest

162 Insulin resistance did not differ between the two PCOS p

163 Insulin secretion/insulin resistance (disposition) index declined by 60% (

164 Insulin resistance due to overnutrition places a burden

165 ot increase with lipolysis or correlate with insulin resistance during acute stress.

166 contributes to stage-dependent increases in insulin resistance during human pregnancy and its elevat

167 arly impactful, as they elicit the selective insulin resistance, dyslipidemia, and ultimately cell de

168 ides, higher homeostatic model assessment of insulin resistance (e.g. NH white men, 1.45 +/- 0.07 com

169 yndrome is characterized by central obesity, insulin resistance, elevated blood pressure, and dyslipi

170 with obesity, arrhythmias, cardiac ischemia, insulin resistance, etc.

171 gh inflammatory and oxidative mechanisms and insulin resistance, even in the absence of weight gain.

172 s must precede the insulin stimulus to cause insulin resistance, explaining why short-term, insulin-d

173 d fatty liver, emphasizing the importance of insulin resistance for DKD and hepatosteatosis in T2D.

174 as when treated with other agents that cause insulin resistance, glucose-dependent mitochondrial oxid

175 uded reductions in metabolites implicated in insulin resistance (glutamate, -29%; P=1.5x10(-55); dime

176 lipid metabolites leading to skeletal muscle insulin resistance has not been investigated.

177 Further, improvements in fasting insulin and insulin resistance have also been reported.

178 dministration of UAB126 ameliorated obesity, insulin resistance, hepatic steatosis, and hyperlipidemi

179 (eGFR), and homeostasis model assessment of insulin resistance (HOMA-IR) and beta-cell function (HOM

180 reduction in homeostasis model assessment of insulin resistance (HOMA-IR) at 24 weeks.

181 insulin and homeostasis model of assessment-insulin resistance (HOMA-IR) index, cognitive performanc

182 ary outcome, homeostatic model assessment of insulin resistance (HOMA-IR), and secondary outcomes (in

183 parameters, homeostatic model assessment of insulin resistance (HOMA-IR), and total energy and macro

184 sessments of beta-cell function (HOMA-B) and insulin resistance (HOMA-IR), as well as incident diabet

185 g glucose (FG), glycated hemoglobin (HbA1c), insulin resistance (HOMA-IR), uric acid, C-reactive prot

186 resistance (homeostatic model assessment of insulin resistance [HOMA-IR] between 2.0 and 8.0) to wee

187 resistance (homeostatic model assessment of insulin resistance [HOMA-IR]), trunk-to-leg fat ratio, r

188 zed 24 adults with obesity and mild-moderate insulin resistance (homeostatic model assessment of insu

189 Body weight, insulin resistance (homeostatic model assessment of insu

190 metabolic flexibility, resulting in systemic insulin resistance, hyperglycemia, and hepatic inflammat

191 omonas gingivalis (Pg) to WT mice results in insulin resistance, hyperinsulinemia, and glucose intole

192 iber have been associated with lower risk of insulin resistance, hyperinsulinemia, and inflammation,

193 fests from inadequate glucose control due to insulin resistance, hypoinsulinemia, and deteriorating p

194 Collectively, these data demonstrate that insulin resistance impairs this PKB-SPEG-SERCA2a signal

195 g and postprandial TRLP subfractions despite insulin resistance in black compared with white pre- and

196 schemic stroke, septic shock, lung injuries, insulin resistance in diabetic patients, and cancer.

197 ight gain, liver fat, serum cholesterol, and insulin resistance in female mice on a high-fat, high-ca

198 ously linked to fasting glycaemic traits and insulin resistance in genome wide association studies.

199 reduced phenylalanine flux without affecting insulin resistance in haemodialysis patients.

200 reduced phenylalanine flux without affecting insulin resistance in haemodialysis patients.

201 tribute to reduced amino acid metabolism and insulin resistance in haemodialysis.

202 d exacerbates tissue-specific and whole-body insulin resistance in high-fat-diet-induced obese mice.

203 We evaluated whether telmisartan reduces insulin resistance in human immunodeficiency virus (HIV)

204 e, lipid species known to be associated with insulin resistance in humans.

205 whether this mechanism explains RBP4-induced insulin resistance in humans.

206 a critical role of SIRT1 in inflammation and insulin resistance in hyperinsulinemia.

207 sis, hyperglycemia, glucose intolerance, and insulin resistance in liver and skeletal muscle of obese

208 SP8 rs2334499 risk variant with hypothalamic insulin resistance in men.

209 tribute to reduced amino acid metabolism and insulin resistance in MHD patients.

210 otected against obesity-associated NAFLD and insulin resistance in mice.

211 ction may involve a transient development of insulin resistance in nonmammary tissues to support redi

212 ated insulin secretion (GSIS) and peripheral insulin resistance in nonpregnant mice and that sEVs fro

213 ide approaches to reduce AT inflammation and insulin resistance in obesity and diabetes.

214 tes programmed susceptibility to obesity and insulin resistance in offspring of mothers on a high-fat

215 mulation), further supporting the concept of insulin resistance in olfactory neuronal cells from SZ p

216 ed induction by activated ProINS-Tf overcame insulin resistance in palmitate-treated HepG2 cells.

217 infection and other stresses and can promote insulin resistance in target tissues.

218 ta cell dysfunction, lipid dysregulation and insulin resistance in the pathogenesis of diabetes melli

219 sive increase in fasting glycemia induced by insulin resistance in the prediabetic state.

220 vels also correlate with body mass index and insulin resistance in the same individuals and are incre

221 els were strongly associated with markers of insulin resistance in vivo (euglycemic clamps and HOMA o

222 may become therapeutic targets for treating insulin resistance, in particular, the transforming grow

223 ompanied by an elevation of serum markers of insulin resistance, including increases in total cholest

224 Features of insulin resistance increased significantly in the HIV+ p

225 Insulin resistance increases patients' risk of developin

226 on analyses for homeostatic modeling-derived insulin resistance index, body mass index, and type 2 di

227 igated whether dietary MCFAs protect against insulin resistance induced by a hypercaloric high-fat di

228 uces inflammasome activation in diabetic and insulin resistance-induced human cells, as well as in mi

229 , LPL, USF1), gene-pregnancy (LPL), and gene-insulin resistance interactions (APOE, LPL).

230 obesity and one of its chief complications, insulin resistance, involves the participation of multip

231 Obesity is a major risk factor for insulin resistance (IR) and its attendant complications.

232 n insulin receptor gene (INSR) cause extreme insulin resistance (IR) and usually death in childhood,

233 have identified genetic loci associated with insulin resistance (IR) but pinpointing the causal genes

234 Insulin resistance (IR) is an important risk factor for

235 BACKGROUNDPostreceptor insulin resistance (IR) is associated with hyperglycemia

236 aired brain insulin signaling with resultant insulin resistance (IR) modulates synaptic plasticity an

237 Insulin resistance (IR) precedes the development of type

238 pment of a range of metabolic disorders from insulin resistance (IR) to hepatic steatosis.

239 With the development of insulin resistance (IR), there is a compensatory increas

240 mated; HOMA-IR values >= 2.6 were considered insulin resistance (IR).

241 Insulin resistance is a common link in the development o

242 Skeletal muscle insulin resistance is a prominent early feature in the p

243 Insulin resistance is an underappreciated facet of type

244 ody of evidence demonstrates obesity-induced insulin resistance is associated with the development of

245 ever, how hyperinsulinemia leads to systemic insulin resistance is less clear.

246 the hypothesis that obesity, independent of insulin resistance, is associated with increased insulin

247 bese subjects is widely recognized to induce insulin resistance, leading to the development of type 2

248 ycerides, HDL cholesterol, glucose, insulin, insulin resistance, leptin, adiponectin, resistin, liver

249 etabolic dysregulation, with higher insulin, insulin resistance, leptin, CRP, IL-1RA, and IL-6, and l

250 In patients with NASH and diabetes or insulin resistance, low AGER1 levels were associated wit

251 Lipoprotein subparticles, lipoprotein-insulin resistance (LP-IR), and GlycA were measured usin

252 ter amplification processes that encompasses insulin resistance, lysosomal defects, decreased surviva

253 d with development of metabolic syndrome and insulin resistance, manifests when triglyceride (TG) inp

254 hypothesized that molecules associated with insulin resistance might be such common mediators, and t

255 in white and brown adipose tissues, causing insulin resistance, moderate rather than severe hypergly

256 e for the development of compounds to reduce insulin resistance, obesity, and nonalcoholic fatty live

257 ed sensitivity analyses for the influence of insulin resistance on the results.

258 ffects of diabetic milieu (hyperglycemia and insulin resistance) on lipotoxic-mediated injury.

259 liorates glucose tolerance, protects against insulin-resistance onset and remarkably reverses already

260 nsulin hypersecretion is a primary driver of insulin resistance or a consequence of the progressive i

261 anges in markers of inflammation, adiposity, insulin resistance, or predictors of diabetes, were obse

262 inflammatory markers (WBC and CRP), HDL and insulin resistance (p < 0.001).

263 d higher waist-hip ratio, triglycerides, and insulin resistance (P <= .03).

264 STAT1 (a-KO) reduced WAT inflammation, but insulin resistance persisted in obese mice.

265 patients with polycystic ovary syndrome and insulin resistance, pioglitazone-induced improvement of

266 entiation: Wolbachia feminizes males through insulin resistance, presumably through defunct insulin r

267 e irisin lacking mice had hyperlipidemia and insulin resistance, reduced HDL-cholesterol level, incre

268 These mice also exhibited insulin resistance-related abnormalities of energy metab

269 in subcutaneous adipose tissue (SAT) and an insulin resistance-related phenotype (e.g. higher waist-

270 is unable to compensate for the increase in insulin resistance, resulting in impaired glucose homeos

271 ial oxidants as a unifying driver of adipose insulin resistance, serving as a signal of nutrient exce

272 , 6.3%; P = 0.09) or biological mediators of insulin resistance, such as plasma adiponectin (2.3%; 95

273 injections, in non-obese diabetic mice with insulin resistance symptoms.

274 pose tissue (WAT) that may contribute to the insulin resistance that characterizes type 2 diabetes.

275 All HF/HC-fed mice developed insulin resistance, the magnitude being lower in ALR-H-K

276 Hypomagnesemia has been linked to insulin resistance through reduced tyrosine kinase activ

277 We propose that insulin resistance, through a reduction in GLP-1r densit

278 inhibit the expression of PEMT by increased insulin resistance, thus potentially suggesting a functi

279 hibited the release of cytokines involved in insulin resistance - TNF, IL-1beta, and CCL2 - by lipopo

280 were associated with higher blood pressure, insulin resistance, total cholesterol, triglycerides, an

281 creases risk for many diseases, particularly insulin resistance, type 2 diabetes mellitus, and cardio

282 ic steatosis is linked to increased risk for insulin resistance, type 2 diabetes, and cardiovascular

283 pathophysiological mediators associated with insulin resistance underlying these mental and physical

284 ced AT MDC polarization and inflammation and insulin resistance using mice with specific knockout of

285 olecular mechanism underlying improvement of insulin resistance, using a type 2 diabetic rat model.

286 ifferences in adipose tissue inflammation or insulin resistance was found between the two genotypes,

287 A contradictory role of CD36 in insulin resistance was found to be related to the nutrie

288 Adipocyte-extrinsic insulin resistance was observed in liver and muscle.

289 Hepatic insulin resistance was significantly reduced in close as

290 In complementary cohorts with measures of insulin resistance, we found positive correlates for cir

291 Weight loss and alleviation of insulin resistance were consistently associated with imp

292 Lipotoxic factors and insulin resistance were evaluated by reverse transcripta

293 lipoprotein characterization, adiposity, or insulin resistance were observed with secukinumab treatm

294 a-cells to self-check hypothetically induces insulin resistance when it is absent.

295 asal conditions, and glucose intolerance and insulin resistance when raised on a high-fat diet, compa

296 s suggest a race-specific pathophysiology of insulin resistance, which has implications for the preve

297 e, could be a new insulin analog to overcome insulin resistance, which is associated with several dis

298 ty to ensure euglycemia improves, iatrogenic insulin resistance will become the final barrier to over

299 causes the teeny phenotype, characterized by insulin resistance with late failure of insulin producti

300 T) prevents ectopic lipid deposition-induced insulin resistance, yet the underlying mechanism remains