ライフサイエンスコーパス: insulin-sensitive

1 ated intramyocellular lipids, yet are highly insulin sensitive.

2 e of the reasons that these tissues remained insulin sensitive.

3 that Pparg(P465L/+)Ins2(Akita/+) livers are insulin sensitive.

4 ocyte loss of MHC class II (MHC II) are more insulin sensitive.

5 ts suggest that skeletal muscles are equally insulin sensitive.

6 ed normal amounts of adipose tissue and were insulin sensitive.

7 rably to Step II diets than do those who are insulin sensitive.

8 significantly decreased body fat, and remain insulin sensitive.

9 Paradoxically, mdKO mice were more insulin sensitive.

10 of severely obese (BMI >40) individuals are insulin sensitive.

11 at hGLUT4 TG mice fed an HFD remained highly insulin sensitive.

12 nKO mice remained fully glucose tolerant and insulin sensitive.

13 e type 1 resist diet-induced obesity and are insulin-sensitive.

14 betic subjects who were insulin-resistant or insulin-sensitive.

15 Thus, HF/HS+INDO-fed mice remained insulin-sensitive.

16 mice with JNK-deficient macrophages remained insulin-sensitive.

17 tive (34.3 +/- 13.1 micro g/ml) or nonobese, insulin-sensitive (29.8 +/- 15.3 micro g/ml) subjects.

18 5 micro g/ml) as compared with either obese, insulin-sensitive (34.3 +/- 13.1 micro g/ml) or nonobese

19 cells, Glut4 is predominantly found in small insulin-sensitive 60-70 S membrane vesicles that may or

20 talytic subunit, is prominently expressed in insulin-sensitive adipose cells.

21 in resistant high fat diet (HFD) mice become insulin-sensitive after switching from HFD to normal cho

22 hiPSC-derived adipocytes are insulin sensitive and display beige-specific markers and

23 Our results show that miR-155KO animals are insulin sensitive and glucose tolerant compared to contr

24 They were also leaner and more insulin sensitive and had lower liver fat contents.

25 adipocyte triglyceride levels typically are insulin sensitive and have normal or low liver and circu

26 t demonstrate different seasonal patterns in insulin sensitive and insulin resistant individuals.

27 advanced age, these clones are euglycaemic, insulin sensitive and normotensive.

28 0 obese individuals (22%) were classified as insulin sensitive and obese (IS-obese).

29 the hypothesis that B6-Ins2Akita/+ mice are insulin sensitive and provide an excellent model for isl

30 y controlled by protein abundance changes in insulin-sensitive and -resistance states.

31 istinguish physiological differences between insulin-sensitive and -resistant individuals.

32 ance on beta-cell function in lean and obese insulin-sensitive and insulin-resistant adolescents.

33 between (1) heavy and thin adolescents; (2) insulin-sensitive and insulin-resistant adolescents; and

34 esponses to dipyridamole were similar in the insulin-sensitive and insulin-resistant groups.

35 ly affects hepatic phosphorus metabolites in insulin-sensitive and insulin-resistant humans.

36 st of the studies comparing fat oxidation in insulin-sensitive and insulin-resistant individuals have

37 downstream signaling in glucose transport in insulin-sensitive and insulin-resistant mature skeletal

38 Both insulin-sensitive and insulin-resistant nondiabetic subg

39 are few prospective data on the prognosis of insulin-sensitive and insulin-resistant normal-weight (N

40 Recent studies in which adipose tissue of insulin-sensitive and insulin-resistant patients with se

41 were 0.4%, 6.3%, and 3.3%, respectively, in insulin-sensitive and normal-weight (IS-NW) individuals

42 Lean insulin-sensitive and obese insulin-resistant subjects (

43 Podocytes are insulin-sensitive and take up glucose in response to ins

44 rence of > or = 600% exists between the most insulin-sensitive and the most insulin-resistant persons

45 The IPGR group remained lean, euglycemic, insulin sensitive, and active while maintaining metaboli

46 Acsl1(M-/-) mice were more insulin sensitive, and, during an overnight fast, their

47 ay be normalized by transfusion of APCs from insulin-sensitive animals but not from insulin-resistant

48 The insulin-sensitive, anti-inflammatory phenotype of KO-DIO

49 utes, showing that the output of leptin- and insulin-sensitive ARH neurons that ordinarily stimulate

50 The SRA(-/-) mice are more insulin sensitive, as evidenced by reduced fasting insul

51 ately 50% less fat mass and were 2-fold more insulin sensitive, as measured by hyperinsulinemic-eugly

52 n obese insulin-resistant compared with lean insulin-sensitive baboons.

53 lin-insensitive corneal epithelial cells and insulin-sensitive bronchial epithelial cells.

54 % sucrose fraction by 2.8-fold over basal in insulin-sensitive but only by 1.5-fold in both insulin-r

55 SCD1(-/-) mice on an HFD remain insulin-sensitive, but develop glucose intolerance and i

56 Normoglycemic and insulin-sensitive C57BL/6J mice; hyperglycemic, but mild

57 valuated their biological effects in several insulin sensitive cell lines.

58 whether increased expression of PTP1B in an insulin-sensitive cell type could contribute to insulin

59 NA appears as a 9-kb transcript, enriched in insulin-sensitive cells and tissues, likely transcribed

60 yrase interact, and colocalise with GLUT4 in insulin-sensitive cells.

61 ing molecules that mediate insulin action in insulin-sensitive cells.

62 enic signaling similar to that described for insulin-sensitive cells.

63 roposed for this proinflammatory cytokine in insulin-sensitive cells.

64 tection of insulin was accomplished using an insulin-sensitive chemically modified electrode.

65 y syndrome (PCOS) have been shown to be less insulin sensitive compared with control (CON) women, ind

66 In this study, we found smokers were less insulin sensitive compared with controls, which increase

67 bited better glucose tolerance and were more insulin sensitive compared with wild-type controls.

68 zed IRAP protein traffics to the perinuclear insulin-sensitive compartment and acquires insulin sensi

69 SP rat model compared with the normotensive, insulin-sensitive control strain, Wistar-Kyoto (WKY).

70 l x g(-1) x min(-1), P = 0.02) compared with insulin-sensitive control subjects (96.1 +/- 16.3 nmol x

71 n the insulin-resistant subjects than in the insulin-sensitive control subjects (P<0.001) and was ass

72 fspring of patients with type 2 diabetes and insulin-sensitive control subjects matched for age, heig

73 nt offspring of type 2 diabetic patients and insulin-sensitive control subjects underwent (13)C MRS s

74 obese insulin-resistant individuals than in insulin-sensitive control subjects.

75 age-weight-body mass index-activity-matched, insulin-sensitive, control subjects.

76 and bottom pellet in diabetics compared with insulin-sensitive controls, without any differences in m

77 oted in the men, whereas the women were more insulin sensitive, demonstrating further dissociation be

78 trated abdominal lipodystrophy, and remained insulin-sensitive despite having a marked impairment in

79 rd diet, mice overexpressing ChREBP remained insulin sensitive, despite increased expression of genes

80 A mouse that spontaneously developed insulin-sensitive diabetes without beta-cell autoimmunit

81 P-I-KO mice remain more glucose tolerant and insulin sensitive during high-fat-diet feeding.

82 The lean, hypermetabolic, and insulin-sensitive E2+/p- phenotype appears to result fro

83 rtment model of GLUT1 recycling involving an insulin sensitive endocytosis step in common with the GL

84 Adipose tissue lipoprotein lipase is an insulin-sensitive enzyme.

85 We demonstrate that DZ regulates key insulin-sensitive enzymes involved in regulation of adip

86 d us to investigate the effects of DZ on key insulin-sensitive enzymes regulating adipose tissue meta

87 This corresponded with insulin-sensitive expression changes in enzymes of EC me

88 variance), but not in FH+, as even the most insulin-sensitive FH+ offspring had diminished endotheli

89 We sought to examine insulin-sensitive food intake behavior and neuroendocrin

90 Here, we report that SIN3A is the insulin-sensitive FOXO1 corepressor of glucokinase.

91 and beta3-adrenergic receptor), other novel insulin-sensitive genes were also identified (e.g. Egr-1

92 3T3-J2 murine embryonic fibroblasts maintain insulin-sensitive glucose metabolism for several weeks.

93 Our objectives were to measure insulin-sensitive glucose metabolism in neonatal lambs w

94 th liver an important site of alterations in insulin-sensitive glucose production.

95 vestigate the ability of PPARgamma to confer insulin-sensitive glucose transport to a variety of muri

96 C/EBPalpha is required for establishment of insulin-sensitive glucose transport.

97 ivo, due primarily to the recruitment of the insulin-sensitive glucose transporter (GLUT4) to the pla

98 onavir were investigated in mice lacking the insulin-sensitive glucose transporter GLUT4 (G4KO).

99 bGAP AS160/TBC1D4 controls exocytosis of the insulin-sensitive glucose transporter Glut4 in adipocyte

100 ulin signaling is that they both express the insulin-sensitive glucose transporter Glut4.

101 transport by promoting translocation of the insulin-sensitive glucose transporter isoform 4 (GLUT4)

102 the regional and cellular expression of the insulin-sensitive glucose transporter, GLUT4, in rodent

103 The expression of the insulin-sensitive glucose transporter, GLUT4, is signifi

104 led to the transcriptional induction of the insulin-sensitive glucose transporter, GLUT4.

105 particularly in the regulation of GLUT4, the insulin-sensitive glucose transporter, in the AT of PCOS

106 Evidence suggests that insulin-sensitive glucose transporters (GLUTs) other tha

107 6 h) resulted in a substantial inhibition of insulin-sensitive glucose uptake.

108 them to the adipocyte phenotype and restores insulin-sensitive glucose uptake.

109 stigate whether GLUT12 may represent another insulin-sensitive GLUT, transgenic (TG) mice that overex

110 dence that GLUT12 represents a novel, second insulin-sensitive GLUT.

111 alpha(i2) regulates the translocation of the insulin-sensitive GLUT4 glucose transporter in skeletal

112 The insulin-sensitive GLUT4 isoform was localized to vascula

113 translocation, probably by way of tethering insulin-sensitive Glut4 vesicles at an as yet unknown in

114 Insulin-sensitive Glut4 vesicles did not contain either

115 nes, confirming that Vti1a is a component of insulin-sensitive GLUT4-containing vesicles.

116 groups, as well as reasons for believing the insulin-sensitive group will be less disease prone.

117 differences between insulin-resistant versus insulin-sensitive groups than the expression of genes in

118 (T-IS), thin insulin-resistant (T-IR), heavy insulin-sensitive (H-IS), and heavy insulin-resistant (H

119 Obese Tg mice remained insulin sensitive, had increased glucose uptake by adipo

120 ed a high-fat diet, although obese, remained insulin sensitive, had lower free fatty acid in plasma,

121 nerates a burst of intracellular H(2)O(2) in insulin-sensitive hepatoma and adipose cells that is ass

122 cebo-controlled trial in 126 overweight, non-insulin sensitive (HOMA-IR >=1.30), Chinese, Malay, and

123 Transcripts from duodenal samples of insulin-sensitive (HOMA-IR < 3, n = 9) and insulin-resis

124 ucose positron emission tomography, in seven insulin-sensitive (homeostasis model assessment of insul

125 insulin-resistant (HR 1.50, P=0.01) but not insulin-sensitive (HR 1.02, P=0.9) participants.

126 Young, lean, insulin-sensitive humans (CONs) [mean +/- SD body mass i

127 sulin-resistant humans compared to ratios in insulin-sensitive humans, indicating that higher apo-RBP

128 insulin resistance, skeletal muscle is more insulin sensitive in BKS-db than in B6-db mice.

129 besity to wild-type littermates but remained insulin sensitive in skeletal muscle.

130 HFD mice rapidly become insulin-sensitive in all major insulin-target tissues, i

131 pothesis that some signaling pathways remain insulin-sensitive in metabolically insulin-resistant adi

132 One gene that remained insulin-sensitive in the insulin-resistant adipocytes is

133 fat (P < 0.0002) while remaining euglycemic, insulin sensitive, inactive, and exhibiting metabolic in

134 d from vastus lateralis muscle from lean and insulin-sensitive individuals and from obese and insulin

135 R < 0.05) between muscle or adipose cells of insulin-sensitive individuals and those of insulin-resis

136 ry markers and non-HDL cholesterol levels in insulin-sensitive individuals but not in lean or obese i

137 ish adipose tissue of insulin resistant from insulin-sensitive individuals with severe obesity.

138 rsus 1.68 mg/L [1.13 to 2.49]; P=0.018) than insulin-sensitive individuals, but individuals with decr

139 n adipose tissue of insulin-resistant versus insulin-sensitive individuals, who were matched for body

140 of aging in insulin-resistant as compared to insulin-sensitive individuals.

141 a of diabetic patients compared with that of insulin-sensitive individuals.

142 ns that differ between insulin-resistant and insulin-sensitive individuals.

143 s do type II diabetic patients compared with insulin-sensitive individuals.

144 itochondrial physiology toward that of lean, insulin-sensitive individuals.

145 ps (lean and obese normal glucose tolerance, insulin sensitive, insulin resistant, and impaired gluco

146 asured in liver biopsy samples obtained from insulin sensitive, insulin resistant, and untreated T2DM

147 and serum amino acids were determined among insulin-sensitive, insulin-resistant, and type 2 diabeti

148 Recently, we purified three distinct insulin-sensitive intracellular GLUT4 compartments (G4T(

149 It was found in all of the three insulin-sensitive intracellular GLUT4 compartments, and

150 tantial number of overweight persons who are insulin sensitive is relatively minimal.

151 gregated as insulin resistant (IR; HF+IR) or insulin sensitive (IS; HF+IS) compared with control (CON

152 e (GDR) during hyperinsulinemic clamps in 56 insulin sensitive (IS; mean +/- SD: GDR 15.8 +/- 2.0 mg.

153 To test the hypothesis that obese, insulin-sensitive (IS) individuals possess adaptive adip

154 type 2 diabetes mellitus (DM) compared with insulin-sensitive (IS) individuals.

155 ssified as insulin-resistant (IR; n = 12) or insulin-sensitive (IS; n = 10), determined by hyperinsul

156 d order, nondiabetic subjects (classified as insulin-sensitive [IS] [n = 64] or insulin-resistant [IR

157 The insulin-sensitive isoform of the glucose transporting pr

158 Young ( approximately 23 years) insulin-sensitive lean and insulin-resistant obese men a

159 the insulin-resistant ZDF rats but not from insulin-sensitive lean Zucker rats.

160 MI) and insulin sensitivity index (SI): lean insulin sensitive (LIS), mean+/-SEM BMI, 23.2+/-0.3 kg/m

161 The rise in LDL with egg feeding in lean insulin-sensitive (LIS) participants is 2- and 3-fold gr

162 men, 101 women), a priori classified as lean insulin-sensitive (LIS, n = 56), lean insulin-resistant

163 Using an insulin-sensitive liver cell line, we show that localiza

164 These data indicate that the insulin-sensitive membrane compartment that sequesters G

165 tion of different fatty acid sources between insulin-sensitive men and women.

166 r in the insulin-resistant compared with the insulin-sensitive men are those derived from splanchnic

167 Insulin-resistant and insulin-sensitive men had similar postprandial chylomicr

168 atidylinositol 3-kinase and regulate various insulin-sensitive metabolic processes.

169 ntly down-regulated in insulin-resistant vs. insulin-sensitive mouse podocytes and in human glomeruli

170 In insulin-sensitive muscle, caCaMKKalpha increased basal i

171 te glucose uptake additively with insulin in insulin-sensitive muscle, in the basal state in insulin-

172 oxical, this phenomenon is characteristic of insulin-sensitive myofibers and suggests that DGAT1 play

173 ose homeostasis in the face of fewer type I (insulin-sensitive) myofibres.

174 their insulin sensitivity index (S(I)): lean insulin sensitive (n = 65), lean insulin resistant (n =

175 Insulin-resistant (n = 11) and insulin-sensitive (n = 11) men and women (n = 6) were gi

176 Postmenopausal women were divided into insulin-sensitive (n = 15) and insulin-resistant (n = 15

177 cipants into insulin-resistant (IR, n=20) or insulin-sensitive (n=18) groups, similar in terms of mea

178 t obese (MAO) subjects, metabolically normal insulin-sensitive obese (MNO) subjects, and lean subject

179 ce deficient in CB1R or SCD1 remain lean and insulin-sensitive on an HFD, suggesting a functional lin

180 KI), and patients were further classified as insulin sensitive or insulin resistant.

181 2 and impaired mTorc2/Akt signaling in other insulin-sensitive organs, leading to insulin resistance

182 Insulin-sensitive organs, overburdened by high concentra

183 These mice are also leaner and more insulin-sensitive owing to increased energy expenditure.

184 Lean and obese insulin-sensitive participants did not differ with respe

185 12 randomly selected, nonobese, nondiabetic, insulin-sensitive participants in a population-based stu

186 nic groups and between insulin-resistant and insulin-sensitive participants individually and using ge

187 istant participants respond differently than insulin-sensitive participants.

188 These findings suggest that modification of insulin-sensitive pathways can be therapeutically benefi

189 ynaptic plasticity through the impairment of insulin-sensitive pathways regulating neuronal survival,

190 sis (proteostasis) due to hyperactivation of insulin-sensitive pathways such as protein synthesis.

191 st increased by 47.6% from resting values in insulin-sensitive patients and by 14.4% in insulin-resis

192 were relatively overexpressed in adipose of insulin-sensitive patients.

193 ulin-stimulated glucose clearance rates into insulin-sensitive peripheral tissues were measured using

194 egulated isoform in these cells, as it is in insulin-sensitive peripheral tissues, such as muscle.

195 al Sorbs1-null macrophages, we show that the insulin-sensitive phenotype can be transferred to wild-t

196 mechanism for the in vivo anti-inflammatory insulin-sensitive phenotype observed in mice with macrop

197 hepatic overexpression of TRB-3 reversed the insulin-sensitive phenotype of PGC-1-deficient mice.

198 Together, our data identify Sac3 as an insulin-sensitive phosphatase whose down-regulation incr

199 These studies demonstrate a chronic insulin-sensitive regulation of GLUT4 in rodent brain an

200 hus diabetic gastropathy in mice reflects an insulin-sensitive reversible loss of nNOS.

201 Smokers were less insulin sensitive (S(i)) compared with nonsmokers (S(i)

202 The insulin-sensitive Sac3 pool likely controls a discrete P

203 Surprisingly, CGI-58 knockdown mice remain insulin-sensitive, seemingly dissociating DAG from the d

204 The PNGR group was insulin sensitive, similar to IPGR, but less active whil

205 Studies to identify the insulin-sensitive sites of phosphorylation reveal that a

206 In insulin-sensitive skeletal muscle, the expression of con

207 )) or nonobese (<27.0 kg/m(2)) and as either insulin sensitive (SSPG <100 mg/dl) or insulin resistant

208 ort our model that sorting of GLUT4 into its insulin-sensitive store involves a cycle of ubiquitinati

209 ied the cohort into insulin-resistant versus insulin-sensitive subgroups based on homeostasis model a

210 rom insulin-resistant subjects compared with insulin-sensitive subjects (all P < 0.05).

211 Using this approach, insulin-sensitive subjects demonstrated a twofold higher

212 = 0.60, P < 0.02), suggesting that the most insulin-sensitive subjects had the greatest enhancement

213 Two groups of lean insulin-sensitive subjects underwent euglycemic-hyperins

214 Finally, adiponectin levels in insulin-sensitive subjects varied to a significantly gre

215 late GSIS in insulin-resistant compared with insulin-sensitive subjects, 10 participants with impaire

216 adipose tissue lipin expression is found in insulin-sensitive subjects, and lipin-beta expression in

217 In cells from insulin-sensitive subjects, insulin augmented GSV tether

218 +/- 1.1 micro g/ml in insulin-resistant and insulin-sensitive subjects, respectively; P < 0.0005).

219 ssion levels of both lipin isoforms in lean, insulin-sensitive subjects.

220 d approximately threefold above those of the insulin-sensitive subjects.

221 ng muscle mRNA from insulin-resistant versus insulin-sensitive subjects.

222 s have greater amounts of body fat than lean insulin-sensitive subjects.

223 e intestine of insulin-resistant compared to insulin-sensitive subjects.

224 e intestine of insulin-resistant compared to insulin-sensitive subjects: the transcripts of the insul

225 lin sensitivity (31 insulin-resistant and 31 insulin-sensitive subjects; 40 were European American an

226 Moreover, healthy (i.e., insulin-sensitive) subjects with obesity had significant

227 insulin-resistant adolescents; and (3) thin insulin-sensitive (T-IS), thin insulin-resistant (T-IR),

228 Wnt10b-Ay mice are more glucose tolerant and insulin sensitive than A(y) controls, perhaps due to red

229 mice have lower plasma insulin and are more insulin sensitive than AKR mice.

230 mass, Txnip knockout mice were markedly more insulin sensitive than controls, and augmented glucose t

231 standard chow and HFD, SINKO mice were more insulin sensitive than Sirt1(f/f) mice.

232 Adults born preterm were less insulin sensitive than those born at term (19.0 +/- 2.5

233 sponse to intravenous glucose, and were more insulin sensitive than those with type 2 diabetes.

234 iet (HFD), Chga-KO mice (KO-DIO) remain more insulin sensitive than wild-type DIO (WT-DIO) mice.

235 e, MacT3 mice were more glucose tolerant and insulin sensitive than wild-type mice in both in vitro a

236 Atp7b (-/-) mice fed either diet were more insulin sensitive than WT controls; however, fasted Atp7

237 nsulin-sensitive than SC adipocytes and more insulin-sensitive than male adipocytes from either depot

238 ales, intra-abdominal PG adipocytes are more insulin-sensitive than SC adipocytes and more insulin-se

239 ransgenic mice are more glucose-tolerant and insulin-sensitive than wild type mice.

240 ion of DAPIT (diabetes-associated protein in insulin sensitive tissue) possibly influences oligomeriz

241 disrupt the rhythmic internal environment of insulin sensitive tissue, thereby predisposing the anima

242 e yet concerning the localization of PDK1 in insulin-sensitive tissue.

243 are e, f, g, diabetes-associated protein in insulin-sensitive tissues (DAPIT), and the 6.8-kDa prote

244 ities of intracellular calcium metabolism in insulin-sensitive tissues (liver, skeletal muscle, and a

245 which enhances glucose utilization among the insulin-sensitive tissues (skeletal muscle, liver, heart

246 inistration regulated key metabolic genes in insulin-sensitive tissues and conferred a strong protect

247 2 influences insulin-mediated GU in multiple insulin-sensitive tissues and may explain, at least in p

248 e body weight through targeting pancreas and insulin-sensitive tissues and organs via site-specific m

249 regulators of inflammation and autophagy in insulin-sensitive tissues and postulate sEH as a druggab

250 ereby counteracts inflammation of peripheral insulin-sensitive tissues and, thus, obesity-associated

251 etabolic effects of an inflammatory state in insulin-sensitive tissues appear essential for permanent

252 cial for energy homeostasis control, and key insulin-sensitive tissues are still unknown.

253 ggest that the delivery of insulin itself to insulin-sensitive tissues could be a mechanism of insuli

254 lin signaling cascade that modulates mTOR in insulin-sensitive tissues has been a major focus of inve

255 emonstrated that decreased lipid delivery to insulin-sensitive tissues improves insulin sensitivity a

256 esis that the deposition of triglycerides in insulin-sensitive tissues other than adipocytes causes i

257 In addition to p85alpha and p85beta, insulin-sensitive tissues such as fat, muscle, and liver

258 by pp185 tyrosine phosphorylation status in insulin-sensitive tissues using the Western blotting met

259 n regulates CREB transcriptional activity in insulin-sensitive tissues via the Raf --> MEK pathway an

260 40-75% in TG compared with wild-type mice in insulin-sensitive tissues with no change in GLUT4 conten

261 f, g, DAPIT (diabetes-associated protein in insulin-sensitive tissues), and 6.8PL (6.8-kDa proteolip

262 LAR, a transmembrane PTPase expressed in insulin-sensitive tissues, acts as a negative regulator

263 d 19,20-epoxydocosapentaenoic (19,20-EDP) in insulin-sensitive tissues, especially liver, as determin

264 feedback loop including islet beta cells and insulin-sensitive tissues, in which tissue sensitivity t

265 GLUT4, the glucose transporter present in insulin-sensitive tissues, resides in intracellular vesi

266 nd type II isozymes of hexokinase coexist in insulin-sensitive tissues, such as cardiac and skeletal

267 nover is regulated differently than in other insulin-sensitive tissues, such as skeletal muscle.

268 kin-6 in the hypothalamus and key peripheral insulin-sensitive tissues.

269 ites contributes to a better redox status in insulin-sensitive tissues.

270 regulates delivery of insulin and glucose to insulin-sensitive tissues.

271 nism/antagonism influences insulin action in insulin-sensitive tissues.

272 ty acids (LCFAs) and is expressed in several insulin-sensitive tissues.

273 p110beta catalytic subunits was observed in insulin-sensitive tissues.

274 viously less intensively perfused regions of insulin-sensitive tissues.

275 both the expression and activity of PTP1B in insulin-sensitive tissues.

276 glycemia and so-called "glucose toxicity" in insulin-sensitive tissues.

277 attern of expression of the MEF2 isoforms in insulin-sensitive tissues.

278 on in HepG2 and 3T3-L1 cell lines, models of insulin-sensitive tissues.

279 mus, innate and adaptive immune systems, and insulin-sensitive tissues.

280 ating free fatty acids and thus causes IR in insulin-sensitive tissues.

281 the induction of LCN2 varied among different insulin-sensitive tissues.

282 e for this methyltransferase in signaling in insulin-sensitive tissues.

283 and 3) insulin signal transduction (IST) in insulin-sensitive tissues.

284 tion and metabolic processes in a variety of insulin-sensitive tissues; however, its role in regulati

285 nes Scd-1 and Fas is regulated partly by the insulin-sensitive transcription factor SREBP-1c and live

286 Forkhead box protein O1 (FoxO1) is an insulin-sensitive transcription factor that is also regu

287 These novel data indicate that the insulin-sensitive transporter GLUT4 transports DHA in bo

288 AKO/cTg mice were highly insulin sensitive under hyperinsulinemic-euglycemic clam

289 se GU of insulin-stimulated muscles from the insulin-sensitive versus insulin-resistant group.

290 e consistent with the notion that a distinct insulin-sensitive vesicular cargo compartment forms earl

291 The differentiated cells possess a large insulin-sensitive vesicular compartment with negligible

292 They also express components of the insulin-sensitive vesicular transport machinery, namely,

293 Sixteen lean insulin-sensitive volunteers received intravenous fat (i

294 iet, the Pten-deleted mice remained markedly insulin sensitive, which correlated with massive subcuta

295 SCID mice were also more insulin sensitive with increased muscle glucose metaboli

296 ination, bilirubin-treated DIO mice remained insulin sensitive with lower leptin and higher adiponect

297 We have recently shown this cell to be insulin sensitive with respect to glucose uptake, with k

298 state plasma glucose concentrations than did insulin-sensitive women (10.8 +/- 0.5 compared with 4.1

299 mitochondrial physiology compared with lean, insulin-sensitive women (BMI 23 kg/m(2)).

300 icantly greater in insulin-resistant than in insulin-sensitive women (P < 0.001).