ライフサイエンスコーパス: insulin-resistant

1 i) quartiles: Q1 = more sensitive; Q4 = more insulin resistant).

2 ivity) or a high-fat diet (HFD; for 2 weeks, insulin-resistant).

3 They were not, however, insulin resistant.

4 lucose challenge, and Fxr(-/-) mice are also insulin resistant.

5 d-type mice administered recombinant CRP are insulin resistant.

6 pose tissue that for unknown reasons becomes insulin resistant.

7 obese, hyperphagic, glucose intolerant, and insulin resistant.

8 in which the liver appears to be selectively insulin resistant.

9 in murine strains that are hyperglycemic and insulin resistant.

10 d pancreatic beta-cell activity and are more insulin resistant.

11 NPLA3 genotypes, but the obese subjects were insulin-resistant.

12 in high-fat diet-fed mice that are obese and insulin-resistant.

13 nce tests showed that male Znt7 KO mice were insulin-resistant.

14 eases in SOCS3 levels in a TNF-alpha-induced insulin-resistant 3T3-L1 adipocyte model.

15 several insulin resistance models, including insulin-resistant 3T3-L1 adipocytes and fat explants pre

16 elease of fatty acids from dysfunctional and insulin-resistant adipocytes results in lipotoxicity, ca

17 tion in lean and obese insulin-sensitive and insulin-resistant adolescents.

18 ATP stimulated 2-NBDG uptake in normal and insulin-resistant adult muscle fibers, resembling the re

19 adipose tissue lipolysis or inflammation in insulin-resistant adults.

20 2) with a placebo (4.2 g oleate/d; n = 9) in insulin-resistant adults.

21 of which subjects would be considered to be insulin resistant after 6 mo of weight maintenance [vali

22 drenergic receptor activation, and were more insulin resistant after a high-fat diet challenge.

23 ment showed that the TRPV1 KO mice were more insulin resistant after HFD because of the approximately

24 glucose tolerance and insulin sensitivity in insulin-resistant aged chow- and high-fat diet-fed (HFD-

25 airments in AS160 phosphorylation evident in insulin-resistant aged individuals.

26 quires unsuppressible hyperglucagonemia from insulin-resistant alpha cells and is prevented by glucag

27 on of Akt1 and Akt2 were glucose intolerant, insulin resistant and defective in their transcriptional

28 ive stress and inflammation were elevated in insulin resistant and diabetic rats.

29 Despite this, obese HXO mice became as insulin resistant and dyslipidemic as obese FLX mice.

30 RBP4-overexpressing mice (RBP4-Ox) are insulin resistant and glucose intolerant and have increa

31 e with those in YL, whereas OO were markedly insulin resistant and had more than twofold greater IMCL

32 677 NW individuals (20%) were classified as insulin resistant and normal weight (IR-NW), and 72 of 3

33 ng of mice exposed to HFD during IU/L became insulin resistant and obese and exhibited increased adip

34 ntify differentially expressed genes between insulin resistant and sensitive iPSC lines.

35 ost-microbe interactions that differ between insulin-resistant and insulin-sensitive individuals.

36 3 ligase, SCF(FBW7) In addition, genetically insulin-resistant and obese db/db mice in the fasted sta

37 HPAH animal models are insulin resistant, and cells with BMPR2 mutation have im

38 urn-injured adults remain hyperglycemic, are insulin resistant, and express defects in insulin secret

39 summary, BG4KO mice are glucose intolerant, insulin resistant, and have impaired glucose sensing, in

40 normal glucose tolerance, insulin sensitive, insulin resistant, and impaired glucose tolerance).

41 The diabetic CPCs were insulin-resistant, and they showed higher energetic reli

42 ids were determined among insulin-sensitive, insulin-resistant, and type 2 diabetic (T2DM) individual

43 We determined that in insulin-resistant animals, portal vagal afferents failed

44 The LBW men were more insulin resistant as determined by the HOMA-IR index.

45 l as distinct molecular patterns of aging in insulin-resistant as compared to insulin-sensitive indiv

46 without steatosis, patients with NAFLD were insulin resistant at the level of adipose tissue, liver,

47 Reduced inflammation in obese/insulin resistant B cell-null mice associates with an in

48 All patients were insulin resistant based on a Homeostasis Model Assessmen

49 Here we show that LIRKO mice are severely insulin resistant based on glucose, insulin and C-peptid

50 olution with those in the top quartile (most insulin resistant) being least likely to resolve (12%) v

51 ng and glucose-lowering pathways that become insulin-resistant but also lipogenic pathways that remai

52 Hearts of rats, rendered insulin resistant by high-sucrose feeding, were subjecte

53 Male adult Sprague-Dawley rats were rendered insulin-resistant by feeding high fat diet for 16 weeks.

54 In vivo administration of these compounds to insulin resistant C57Bl/6J mice fed a high fat diet redu

55 sue is an important etiological component in insulin-resistant cardiometabolic disease and highlight

56 hibits PTP and improves IFNalpha response in insulin-resistant cells.

57 This effect was attenuated in insulin-resistant cohorts, both those with IGT and those

58 found to be upregulated in the intestine of insulin-resistant compared to insulin-sensitive subjects

59 nd differently expressed in the intestine of insulin-resistant compared to insulin-sensitive subjects

60 factor/receptor expression were unchanged in insulin-resistant compared with control mice, indicating

61 te the effect of insulin to modulate GSIS in insulin-resistant compared with insulin-sensitive subjec

62 e heart and metabolic parameters under obese-insulin resistant condition is not known.

63 ity may contribute to anabolic resistance in insulin-resistant conditions by impairing translation in

64 Under insulin-resistant conditions such as obesity, pancreatic

65 The GLP-1 system is known to be impaired in insulin-resistant conditions, and we sought to understan

66 take in response to exercise is preserved in insulin-resistant conditions, but the signals involved a

67 Under insulin-resistant conditions, it is well known that insu

68 eletal muscle mass appears to be impaired in insulin-resistant conditions, such as type 2 diabetes, t

69 ole in altered hepatic apoB100 metabolism in insulin-resistant conditions.

70 Adipose tissue inflammation is present in insulin-resistant conditions.

71 that the brain of aged APP/PS1 mice was not insulin resistant, contrary to the current state of the

72 Both are commonly associated with insulin resistant diabetes, usually accompanied by dysli

73 tinopathy and neuropathy, whereas the severe insulin-resistant diabetes (SIRD) group had the highest

74 imizing ectopic fat accumulation that causes insulin-resistant diabetes and non-alcoholic fatty liver

75 db/db mice, a widely used model of insulin-resistant diabetes and obesity, were either pair

76 thiazolidinediones in patients in the severe insulin-resistant diabetes cluster and for sulfonylureas

77 the development of systemic inflammation and insulin-resistant diabetes mellitus type 2 (DM).

78 protected mice from diet-induced obesity and insulin-resistant diabetes.

79 efore be therapeutically useful for treating insulin-resistant diabetes.

80 in humans and experimental animal models of insulin-resistant diabetes.

81 ding cause of death of patients with type 2 (insulin-resistant) diabetes.

82 deficiency, glucose transporter aberrations, insulin-resistant diabetogenic responses, and distinct c

83 In addition, apoA-I injections in insulin-resistant diet-induced obese (DIO) mice lead to

84 ds were investigated in diabetic db/db mice, insulin-resistant diet-induced obese (DIO) mice, and rat

85 was increased by insulin and impaired in an insulin-resistant disease model.

86 d with a 40% fat diet, they become obese and insulin resistant, display increased serum cytokine leve

87 sk factor for T2DM, most individuals who are insulin resistant do not develop diabetes.

88 e cells, independent of donor Si, cells from insulin-resistant donors show markedly impaired GSV teth

89 strate-1 (IRS1-het) are hyperinsulinemic and insulin resistant during pregnancy, despite normal plasm

90 in association with basal hyperinsulinemia, insulin-resistant endogenous glucose production, and dow

91 of Nox2, which was specifically elevated in insulin-resistant endothelial cells, significantly reduc

92 demonstrated higher levels of superoxide in insulin-resistant endothelial cells, which could be phar

93 ranscriptome sequencing (RNA-seq) studies in insulin-resistant fat bodies revealed differential expre

94 it, with glucose uptake enhancing ability in insulin-resistant FL83B mouse hepatocytes, as shown in o

95 nd other genes distinguish adipose tissue of insulin resistant from insulin-sensitive individuals wit

96 noid receptor, appears to be up-regulated in insulin-resistant, glucose-intolerant mice.

97 mass index (BMI; in kg/m(2)): 23.2 +/- 1.5]; insulin-resistant, glucose-tolerant, obese humans (OBEs)

98 altered beta-cell-to-alpha-cell area in the insulin- resistant group.

99 vere obesity were compared indicate that the insulin-resistant group is also distinguished by increas

100 ed muscles from the insulin-sensitive versus insulin-resistant group.

101 Interestingly, fructose-fed, insulin-resistant hamsters showed a more pronounced resp

102 ty and increases virologic response rates in insulin-resistant HCV genotype 4 patients, but it is unc

103 was undertaken in a mouse model that has an insulin-resistant heart and is susceptible to AF.

104 an be manipulated to improve function of the insulin-resistant heart.

105 escue constrained glucose utilization in the insulin-resistant heart.

106 lating substrate uptake and oxidation in the insulin-resistant heart.

107 s from chow-fed rats recovered to 93%, while insulin-resistant hearts recovered only to 80% (P<0.001

108 In this study, we show that in insulin-resistant high-fat diet-fed mice, the enhanced i

109 mined insulin signaling factors in brains of insulin-resistant high-fat-fed mice, ob/ob mice, mice wi

110 f insulin-sensitive (HOMA-IR < 3, n = 9) and insulin-resistant (HOMA-IR > 7, n = 9) obese subjects we

111 decreased and PTEN activity is increased in insulin-resistant human subjects.

112 te that plasma betaine levels are reduced in insulin-resistant humans and correlate closely with insu

113 capillaries, and reduced MCP-1 expression in insulin-resistant humans and in macrophages and adipocyt

114 valine) are elevated in the blood of obese, insulin-resistant humans and rodents.

115 ios are increased in serum of lean and obese insulin-resistant humans compared to ratios in insulin-s

116 ransiently upregulated in the liver of obese insulin-resistant humans with or without fatty liver, gi

117 to determine whether the treatment of obese, insulin-resistant humans with the beta3-AR agonist mirab

118 n resistant male mice and increased in obese/insulin-resistant humans.

119 sphorus metabolites in insulin-sensitive and insulin-resistant humans.

120 d are reduced in adipose tissue and serum of insulin-resistant humans.

121 le measures of glucose homeostasis in obese, insulin-resistant humans.

122 lipid-overloaded hypertrophic adipocytes are insulin resistant independent of adipocyte inflammation.

123 levels in muscle, fat, and skin tissues from insulin resistant individuals, but similar data on liver

124 t seasonal patterns in insulin sensitive and insulin resistant individuals.

125 f insulin-sensitive individuals and those of insulin-resistant individuals (matched on BMI), trans-re

126 aring fat oxidation in insulin-sensitive and insulin-resistant individuals have shown that fat oxidat

127 indicating that the mitochondrial defect in insulin-resistant individuals is, at least in part, reve

128 idation is higher in T2DM patients and obese insulin-resistant individuals than in insulin-sensitive

129 patients with type 2 diabetes (T2DM), obese insulin-resistant individuals, and lean insulin-resistan

130 r the upregulation of triglyceride levels in insulin-resistant individuals, in addition to identifyin

131 n amino acids (BCAAs) are elevated in obese, insulin-resistant individuals.

132 In an insulin resistant, insulinopenic model of diabetes, XMet

133 d PAK activation was decreased in both acute insulin-resistant (intralipid infusion) and chronic insu

134 Insulin-resistant iPSC also showed reduced catalase acti

135 Insulin-resistant iPSC had increased mitochondrial numbe

136 proliferation were also potently reduced in insulin resistant iPSCs.

137 analysis revealed marked differences in both insulin-resistant iPSCs and corresponding fibroblasts co

138 yzed muscle biopsy samples from young, lean, insulin resistant (IR) offspring of parents with type 2

139 weight/obese individuals classified as IS or insulin resistant (IR).

140 Only obese AE-PCOS women were insulin resistant (IR).

141 egnant females on HF diet were segregated as insulin resistant (IR; HF+IR) or insulin sensitive (IS;

142 sified as insulin-sensitive [IS] [n = 64] or insulin-resistant [IR] [n = 79] by euglycemic clamp) rec

143 ive C57BL/6J mice; hyperglycemic, but mildly insulin-resistant, KK mice; and hyperglycemic and marked

144 ant, KK mice; and hyperglycemic and markedly insulin-resistant KKAy mice were used for ozone exposure

145 trial registry: TAYSIDE trial (Metformin in Insulin Resistant Left Ventricular [LV] Dysfunction).

146 ereby preventing the transformation into the insulin-resistant liver.

147 emoattractant protein-1 and VCAM-1 levels in insulin-resistant LMCs indicated activation of inflammat

148 ymphatic muscle contraction, was observed in insulin-resistant LMCs.

149 Additionally, insulin resistant lymphatic muscle cells exhibited eleva

150 OBEs and T2Ds were similarly insulin resistant (M value: 3.5 +/- 1.4 and 1.9 +/- 2.5

151 text of polymicrobial sepsis, mice harboring insulin-resistant macrophages exhibited reduced sepsis-i

152 protein kinase A thus offers a way to rescue insulin-resistant macrophages from excessive ER stress r

153 Insulin-resistant macrophages had increased basal mTORC1

154 eversed the increase in UPR and apoptosis of insulin-resistant macrophages in atherosclerotic lesions

155 element-binding protein (CREBP) signaling in insulin-resistant macrophages leads to decreased express

156 -like phenotype and suppressed glycolysis in insulin-resistant macrophages.

157 ssed by insulin in vitro, increased in obese/insulin resistant male mice and increased in obese/insul

158 n glucose transport in insulin-sensitive and insulin-resistant mature skeletal muscle has not previou

159 d that youths with type 1 diabetes were more insulin resistant (median glucose infusion rate 10.1 vs.

160 ry NR supplementation in middle-aged, obese, insulin-resistant men affects mitochondrial respiration,

161 -designed randomized controlled trial in 121 insulin-resistant men and women, we measured vascular fu

162 ingle-blind, randomized, crossover study, 10 insulin-resistant men consumed 3 high-fat mixed meals (2

163 es involved in lipid metabolism in 28 obese, insulin-resistant men.

164 on skeletal muscle mitochondria in obese and insulin-resistant men.

165 and of Sirt2 activators in the treatment of insulin-resistant metabolic disorders.

166 rison of the effects of hyperglycemic and/or insulin-resistant metabolic stress conditions on human a

167 Insulin-resistant MetS subjects with more metabolic comp

168 Insulin-resistant MetS subjects with the highest HOMA-IR

169 chemical parameters in HFD-induced obese and insulin resistant mice.

170 urthermore, C22:1-CoA was 2.3-fold higher in insulin-resistant mice and correlated significantly with

171 and signaling were investigated in muscle of insulin-resistant mice and humans.

172 ered in liver of both ob/ob and diet-induced insulin-resistant mice and improved by rosiglitazone tre

173 insulin in normal mice, increased basally in insulin-resistant mice and monkeys, and accompanied by d

174 bd2 was down-regulated in diet-induced obese insulin-resistant mice in a leptin-dependent manner.

175 Knockdown of FMO3 in insulin-resistant mice suppresses FoxO1, a central node

176 thological progression of NAFLD in obese and insulin-resistant mice through effects on immune cell re

177 High-fat diet (HFD)-induced obese and insulin-resistant mice treated by an apelin injection (0

178 Here, we report that treatment of obese insulin-resistant mice with an allosteric MK2/3 inhibito

179 tissue of ob/ob mice and diet-induced obese, insulin-resistant mice.

180 lates growth of pancreatic beta cell mass in insulin-resistant mice.

181 e tolerance and insulin sensitivity in obese insulin-resistant mice.

182 in skeletal muscle of diet induced obese and insulin resistant mouse models we generated mice express

183 muscle and PAK1/2 signalling is impaired in insulin-resistant mouse and human skeletal muscle.

184 naling is inappropriately activated in obese/insulin-resistant mouse models.

185 use mechanisms for exercise effects on GU in insulin-resistant muscle are unknown, our primary object

186 ucose uptake additively with insulin, and in insulin-resistant muscle, and alters the phosphorylation

187 ulin-sensitive muscle, in the basal state in insulin-resistant muscle, and if so, to determine whethe

188 In insulin-resistant muscle, caCaMKKalpha increased basal g

189 t target the vasculature in the treatment of insulin-resistant muscle.

190 vary in their properties between healthy and insulin-resistant muscle.

191 t alternative to stimulate glucose uptake in insulin-resistant muscle.

192 rotein, and phosphorylation are increased in insulin-resistant muscles.

193 m lean healthy control subjects (LCs), obese insulin-resistant nondiabetic control subjects (OCs), an

194 Insulin-resistant, nondiabetic subjects were treated wit

195 ta on the prognosis of insulin-sensitive and insulin-resistant normal-weight (NW) or obese individual

196 Primary macrophages from insulin-resistant ob/ob and insulin receptor (Insr)(-/-)

197 Insulin-resistant ob/ob mice have increased PTP-1B gene

198 diet-induced obese and genetically obese and insulin-resistant ob/ob mice.

199 n adipose tissue from metabolically abnormal insulin-resistant obese (MAO) subjects, metabolically no

200 n the use of aligned treatment strategies in insulin-resistant obese and lipodystrophic patients, the

201 imately 23 years) insulin-sensitive lean and insulin-resistant obese men and women were studied.

202 ctivity and improves response to IFNalpha in insulin-resistant obese mice.

203 insulin resistance were observed in healthy insulin-resistant obese subjects and obese type 2 diabet

204 y, in matched biopsies from "healthy" versus insulin-resistant obese subjects we find HO-1 to be amon

205 bese insulin-resistant individuals, and lean insulin-resistant offspring of parents with T2DM have ~3

206 e insulin resistance in healthy, young, lean insulin-resistant offspring of parents with type 2 diabe

207 denectomy from nondiabetic subjects who were insulin-resistant or insulin-sensitive.

208 reover, during respiratory viral infections, insulin-resistant participants respond differently than

209 sses were dampened and some were reversed in insulin-resistant participants.

210 The downstream mediators of insulin-resistant pathophysiology remain unclear.

211 Sequencing of ARL15 in 375 severely insulin resistant patients identified four rare heterozy

212 ges during an 8-wk LCD allowed us to predict insulin-resistant patients after 6 mo of weight maintena

213 Among insulin-resistant patients with a recent ischaemic strok

214 e liver and skeletal muscle were observed in insulin-resistant patients with NAFLD.

215 In obese, insulin-resistant patients with nonalcoholic fatty liver

216 hich adipose tissue of insulin-sensitive and insulin-resistant patients with severe obesity were comp

217 In chronically insulin-resistant patients with T2DM, hyperglycemic-hype

218 g in 13 normal subjects and in 6 chronically insulin-resistant patients with type 2 diabetes mellitus

219 months after RDN treatment in this group of insulin-resistant patients without diabetes and with res

220 a, a common pancreatic disorder in obese and insulin-resistant patients, is known to cause amylin oli

221 nce exercise improves insulin sensitivity in insulin-resistant patients, we hypothesized that it woul

222 hinery, is dramatically altered in obese and insulin-resistant patients.

223 PAHSA levels are reduced in insulin resistant people, and levels correlate highly wi

224 ulin secretion (GSIS) would be diminished in insulin-resistant persons.

225 -dependent activation of PKCtheta induces an insulin-resistant phenotype, limiting the access of tumo

226 sult in transgenerational inheritance of the insulin-resistant phenotype.

227 disorders and directing adipocytes to a more insulin-resistant phenotype.

228 us muscle of high sucrose diet (HSD) induced insulin resistant rats and TNF-alpha exposed cultured my

229 at VNS attenuates cognitive decline in obese-insulin resistant rats by attenuating brain mitochondria

230 rved cardiac mitochondrial function in obese-insulin resistant rats.

231 e variability (HRV) and LV function in obese-insulin resistant rats.

232 genetic model of spontaneously hypertensive, insulin-resistant rats (SHHF).

233 its target genes was enhanced in nondiabetic insulin-resistant rats and markedly reduced with diabete

234 High-fat diet (HFD)-fed, insulin-resistant rats show attenuated angiotensin (ANG)

235 were performed in normal rats, high fat-fed insulin-resistant rats, and insulin receptor 2'-O-methox

236 retina and systemic circulation of obese and insulin resistant rodents with and without diabetes.

237 e of human subjects with type-2 diabetes and insulin resistant rodents.

238 f lipolysis, whereas obese-derived ASCs were insulin-resistant, showing impaired insulin-stimulated g

239 hat 1) HA content is increased in the ECM of insulin-resistant skeletal muscle and 2) reduction of HA

240 rate many of the defects observed in vivo in insulin-resistant skeletal muscle and provide a new mode

241 trix (ECM) components is a characteristic of insulin-resistant skeletal muscle.

242 ctive stimulus to increase glucose uptake in insulin-resistant skeletal muscle.

243 control and insulin sensitivity in the obese insulin resistant state.

244 otes compensatory beta-cell expansion in the insulin-resistant state and in response to beta-cell str

245 ffects and mechanisms of action in the obese insulin-resistant state are unknown.

246 Sleep restriction results in an insulin-resistant state in human adipocytes.

247 The obese insulin-resistant state is characterized by impairments

248 hot of hepatic fat accumulation alongside an insulin-resistant state is that hepatic lipid enzymatic

249 Baf60c in glucose homeostasis in the severe insulin-resistant state remain unknown.

250 h to identify biomarkers of diabetes and the insulin-resistant state that precedes overt pathology.

251 rugs might accelerate the transition from an insulin-resistant state to overt diabetes.

252 ir wild type controls at 4 months of age (an insulin-resistant state) versus a 5-fold difference betw

253 asia and dysfunction that characterizes this insulin-resistant state.

254 IMCD could contribute to hypertension in the insulin-resistant state.

255 In insulin resistant states such as type 2 diabetes, there

256 -resistant (intralipid infusion) and chronic insulin-resistant states (obesity and diabetes).

257 ction by insulin is consistently abnormal in insulin-resistant states and diabetes.

258 e hepatic Tmem127 expression is increased in insulin-resistant states and is reversed by diet or the

259 a seen in common metabolic disorders such as insulin-resistant states and type 2 diabetes and likely

260 Obese, insulin-resistant states are characterized by a paradoxi

261 its levels are also abnormally increased in insulin-resistant states in rodents and humans.

262 treatment of type 2 diabetes and other human insulin-resistant states in the future.

263 Moreover, insulin-resistant states such as type 2 diabetes mellitu

264 ptor in the proximal tubule, which occurs in insulin-resistant states, may promote hyperglycemia thro

265 in adipocytes but not in skeletal muscle in insulin-resistant states, such as obesity and type 2 dia

266 y, type 2 diabetes mellitus (T2DM) and other insulin-resistant states.

267 to the development of hyperproinsulinemia in insulin-resistant states.

268 preserves WAT lipid homeostasis in obese and insulin-resistant states.

269 us impacts energy homeostasis in obesity and insulin-resistant states.

270 uman skeletal muscle and are dysregulated in insulin-resistant states.

271 l function, apoptosis and cognition in obese-insulin resistant subjects have never been investigated.

272 ably, in humans, we show that both obese and insulin-resistant subjects have elevated plasma concentr

273 ates glucose-stimulated insulin secretion in insulin-resistant subjects to a lesser degree than in no

274 redicted to be activated in the intestine of insulin-resistant subjects.

275 viously identified in the intestine of obese insulin-resistant subjects.

276 n improves insulin signalling in muscle from insulin-resistant subjects.

277 unting for a mild increase of iron stores in insulin-resistant subjects.

278 It can be a choice of drug for insulin resistant T2DM patients having dyslipidaemia, hy

279 ed ATP synthesis) also has been described in insulin-resistant T2DM and obese subjects.

280 d postexercise ATP resynthesis and were more insulin resistant than control subjects.

281 d that the TRPV1 KO mice were more obese and insulin resistant than the WT mice at 9 mo of age.

282 xposure, while APNko-DHT mice were even more insulin resistant than their DHT-exposed littermate WTs.

283 Migrant south Asians seem to be more insulin resistant than white Europeans across the life c

284 Although both strains were equally insulin resistant, the MUP-uPA mice exhibited more liver

285 in both groups were overweight or obese and insulin resistant; they displayed similar oGTT and STT p

286 and Ucp2(fl/fl) mice were rendered obese and insulin resistant through high-fat feeding.

287 Insulin-resistant type 2 diabetes mellitus is associated

288 d in macrophages from db/db and diet-induced insulin-resistant type 2 diabetic (T2D) mice, but not fr

289 e became obese but not glucose intolerant or insulin resistant, unlike B(1) (-/-)->B(1) (-/-) mice.

290 n (TNMD) is upregulated in adipose tissue of insulin-resistant versus insulin-sensitive individuals,

291 jects and further stratified the cohort into insulin-resistant versus insulin-sensitive subgroups bas

292 sease, patients with advanced NASH were more insulin-resistant, viscerally obese, and older, but ther

293 Y (NPY) was significantly down-regulated in insulin-resistant vs. insulin-sensitive mouse podocytes

294 sis and a unique M2-like phenotype, termed M-insulin resistant, which accounts for obesity-related ch

295 However, not all obese individuals are insulin resistant, which confounds our understanding of

296 on-alcoholic fatty liver disease and who are insulin resistant, will be randomised into either a Medi

297 bal androgen receptor (AR) knockout mice are insulin resistant with increased fat, but it is unclear

298 e determined whether obese (BMI 33 kg/m(2)), insulin-resistant women with polycystic ovary syndrome h

299 show that duodenal bypass surgery on obese, insulin-resistant Zucker fa/fa rats restored insulin sen

300 p-Tyr911 of IRS2 were observed in vessels of insulin-resistant Zucker fatty rats versus lean rats.