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1  that Pparg(P465L/+)Ins2(Akita/+) livers are insulin sensitive.
2 ts suggest that skeletal muscles are equally insulin sensitive.
3 ed normal amounts of adipose tissue and were insulin sensitive.
4 rably to Step II diets than do those who are insulin sensitive.
5 significantly decreased body fat, and remain insulin sensitive.
6 rtion of African-American NIDDM subjects are insulin sensitive.
7  of severely obese (BMI >40) individuals are insulin sensitive.
8 at hGLUT4 TG mice fed an HFD remained highly insulin sensitive.
9 nKO mice remained fully glucose tolerant and insulin sensitive.
10 ated intramyocellular lipids, yet are highly insulin sensitive.
11 e of the reasons that these tissues remained insulin sensitive.
12 e type 1 resist diet-induced obesity and are insulin-sensitive.
13 betic subjects who were insulin-resistant or insulin-sensitive.
14           Thus, HF/HS+INDO-fed mice remained insulin-sensitive.
15 mice with JNK-deficient macrophages remained insulin-sensitive.
16 tive (34.3 +/- 13.1 micro g/ml) or nonobese, insulin-sensitive (29.8 +/- 15.3 micro g/ml) subjects.
17 5 micro g/ml) as compared with either obese, insulin-sensitive (34.3 +/- 13.1 micro g/ml) or nonobese
18                         We show here that in insulin-sensitive 3T3-L1 adipocytes and other cultured c
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  advanced age, these clones are euglycaemic, insulin sensitive and normotensive.
27 0 obese individuals (22%) were classified as insulin sensitive and obese (IS-obese).
28  the hypothesis that B6-Ins2Akita/+ mice are insulin sensitive and provide an excellent model for isl
29 istinguish physiological differences between insulin-sensitive and -resistant individuals.
30  between (1) heavy and thin adolescents; (2) insulin-sensitive and insulin-resistant adolescents; and
31 esponses to dipyridamole were similar in the insulin-sensitive and insulin-resistant groups.
32 ly affects hepatic phosphorus metabolites in insulin-sensitive and insulin-resistant humans.
33 st of the studies comparing fat oxidation in insulin-sensitive and insulin-resistant individuals have
34 downstream signaling in glucose transport in insulin-sensitive and insulin-resistant mature skeletal
35                                         Both insulin-sensitive and insulin-resistant nondiabetic subg
36 or UCP2, UCP3S, or UCP3L mRNA levels between insulin-sensitive and insulin-resistant nondiabetic subg
37 are few prospective data on the prognosis of insulin-sensitive and insulin-resistant normal-weight (N
38    Recent studies in which adipose tissue of insulin-sensitive and insulin-resistant patients with se
39  were 0.4%, 6.3%, and 3.3%, respectively, in insulin-sensitive and normal-weight (IS-NW) individuals
40                                         Lean insulin-sensitive and obese insulin-resistant subjects (
41                                Podocytes are insulin-sensitive and take up glucose in response to ins
42 rence of > or = 600% exists between the most insulin-sensitive and the most insulin-resistant persons
43    The IPGR group remained lean, euglycemic, insulin sensitive, and active while maintaining metaboli
44                   Acsl1(M-/-) mice were more insulin sensitive, and, during an overnight fast, their
45 ay be normalized by transfusion of APCs from insulin-sensitive animals but not from insulin-resistant
46                                          The insulin-sensitive, anti-inflammatory phenotype of KO-DIO
47 utes, showing that the output of leptin- and insulin-sensitive ARH neurons that ordinarily stimulate
48                   The SRA(-/-) mice are more insulin sensitive, as evidenced by reduced fasting insul
49 ately 50% less fat mass and were 2-fold more insulin sensitive, as measured by hyperinsulinemic-eugly
50 n obese insulin-resistant compared with lean insulin-sensitive baboons.
51 ses an increase in the production of EDNO in insulin-sensitive but not insulin-resistant subjects.
52 % sucrose fraction by 2.8-fold over basal in insulin-sensitive but only by 1.5-fold in both insulin-r
53              SCD1(-/-) mice on an HFD remain insulin-sensitive, but develop glucose intolerance and i
54 valuated their biological effects in several insulin sensitive cell lines.
55  whether increased expression of PTP1B in an insulin-sensitive cell type could contribute to insulin
56 NA appears as a 9-kb transcript, enriched in insulin-sensitive cells and tissues, likely transcribed
57 ing molecules that mediate insulin action in insulin-sensitive cells.
58 enic signaling similar to that described for insulin-sensitive cells.
59 roposed for this proinflammatory cytokine in insulin-sensitive cells.
60  insulin-receptor mechanism as described for insulin-sensitive cells.
61 tection of insulin was accomplished using an insulin-sensitive chemically modified electrode.
62    In this study, we found smokers were less insulin sensitive compared with controls, which increase
63 bited better glucose tolerance and were more insulin sensitive compared with wild-type controls.
64 zed IRAP protein traffics to the perinuclear insulin-sensitive compartment and acquires insulin sensi
65 SP rat model compared with the normotensive, insulin-sensitive control strain, Wistar-Kyoto (WKY).
66 l x g(-1) x min(-1), P = 0.02) compared with insulin-sensitive control subjects (96.1 +/- 16.3 nmol x
67 n the insulin-resistant subjects than in the insulin-sensitive control subjects (P<0.001) and was ass
68 fspring of patients with type 2 diabetes and insulin-sensitive control subjects matched for age, heig
69 nt offspring of type 2 diabetic patients and insulin-sensitive control subjects underwent (13)C MRS s
70  obese insulin-resistant individuals than in insulin-sensitive control subjects.
71 age-weight-body mass index-activity-matched, insulin-sensitive, control subjects.
72 and bottom pellet in diabetics compared with insulin-sensitive controls, without any differences in m
73 oted in the men, whereas the women were more insulin sensitive, demonstrating further dissociation be
74 trated abdominal lipodystrophy, and remained insulin-sensitive despite having a marked impairment in
75 rd diet, mice overexpressing ChREBP remained insulin sensitive, despite increased expression of genes
76         A mouse that spontaneously developed insulin-sensitive diabetes without beta-cell autoimmunit
77     Using this definition, the proportion of insulin-sensitive diabetic subjects was very low in all
78 P-I-KO mice remain more glucose tolerant and insulin sensitive during high-fat-diet feeding.
79                The lean, hypermetabolic, and insulin-sensitive E2+/p- phenotype appears to result fro
80 rtment model of GLUT1 recycling involving an insulin sensitive endocytosis step in common with the GL
81      Adipose tissue lipoprotein lipase is an insulin-sensitive enzyme.
82         We demonstrate that DZ regulates key insulin-sensitive enzymes involved in regulation of adip
83 d us to investigate the effects of DZ on key insulin-sensitive enzymes regulating adipose tissue meta
84                       This corresponded with insulin-sensitive expression changes in enzymes of EC me
85  variance), but not in FH+, as even the most insulin-sensitive FH+ offspring had diminished endotheli
86                         We sought to examine insulin-sensitive food intake behavior and neuroendocrin
87            Here, we report that SIN3A is the insulin-sensitive FOXO1 corepressor of glucokinase.
88  and beta3-adrenergic receptor), other novel insulin-sensitive genes were also identified (e.g. Egr-1
89 3T3-J2 murine embryonic fibroblasts maintain insulin-sensitive glucose metabolism for several weeks.
90 th liver an important site of alterations in insulin-sensitive glucose production.
91 vestigate the ability of PPARgamma to confer insulin-sensitive glucose transport to a variety of muri
92  C/EBPalpha is required for establishment of insulin-sensitive glucose transport.
93 ivo, due primarily to the recruitment of the insulin-sensitive glucose transporter (GLUT4) to the pla
94 onavir were investigated in mice lacking the insulin-sensitive glucose transporter GLUT4 (G4KO).
95 bGAP AS160/TBC1D4 controls exocytosis of the insulin-sensitive glucose transporter Glut4 in adipocyte
96 ulin signaling is that they both express the insulin-sensitive glucose transporter Glut4.
97  transport by promoting translocation of the insulin-sensitive glucose transporter isoform 4 (GLUT4)
98  the regional and cellular expression of the insulin-sensitive glucose transporter, GLUT4, in rodent
99                        The expression of the insulin-sensitive glucose transporter, GLUT4, is signifi
100  led to the transcriptional induction of the insulin-sensitive glucose transporter, GLUT4.
101 particularly in the regulation of GLUT4, the insulin-sensitive glucose transporter, in the AT of PCOS
102                       Evidence suggests that insulin-sensitive glucose transporters (GLUTs) other tha
103 6 h) resulted in a substantial inhibition of insulin-sensitive glucose uptake.
104 them to the adipocyte phenotype and restores insulin-sensitive glucose uptake.
105 stigate whether GLUT12 may represent another insulin-sensitive GLUT, transgenic (TG) mice that overex
106 dence that GLUT12 represents a novel, second insulin-sensitive GLUT.
107 alpha(i2) regulates the translocation of the insulin-sensitive GLUT4 glucose transporter in skeletal
108                                          The insulin-sensitive GLUT4 isoform was localized to vascula
109  translocation, probably by way of tethering insulin-sensitive Glut4 vesicles at an as yet unknown in
110                                              Insulin-sensitive Glut4 vesicles did not contain either
111 nes, confirming that Vti1a is a component of insulin-sensitive GLUT4-containing vesicles.
112 groups, as well as reasons for believing the insulin-sensitive group will be less disease prone.
113 differences between insulin-resistant versus insulin-sensitive groups than the expression of genes in
114 (T-IS), thin insulin-resistant (T-IR), heavy insulin-sensitive (H-IS), and heavy insulin-resistant (H
115                       Obese Tg mice remained insulin sensitive, had increased glucose uptake by adipo
116 ed a high-fat diet, although obese, remained insulin sensitive, had lower free fatty acid in plasma,
117 nerates a burst of intracellular H(2)O(2) in insulin-sensitive hepatoma and adipose cells that is ass
118         Transcripts from duodenal samples of insulin-sensitive (HOMA-IR < 3, n = 9) and insulin-resis
119 ucose positron emission tomography, in seven insulin-sensitive (homeostasis model assessment of insul
120  insulin-resistant (HR 1.50, P=0.01) but not insulin-sensitive (HR 1.02, P=0.9) participants.
121                                 Young, lean, insulin-sensitive humans (CONs) [mean +/- SD body mass i
122 sulin-resistant humans compared to ratios in insulin-sensitive humans, indicating that higher apo-RBP
123  insulin resistance, skeletal muscle is more insulin sensitive in BKS-db than in B6-db mice.
124 besity to wild-type littermates but remained insulin sensitive in skeletal muscle.
125                      HFD mice rapidly become insulin-sensitive in all major insulin-target tissues, i
126 pothesis that some signaling pathways remain insulin-sensitive in metabolically insulin-resistant adi
127                       One gene that remained insulin-sensitive in the insulin-resistant adipocytes is
128 fat (P < 0.0002) while remaining euglycemic, insulin sensitive, inactive, and exhibiting metabolic in
129 d from vastus lateralis muscle from lean and insulin-sensitive individuals and from obese and insulin
130 R < 0.05) between muscle or adipose cells of insulin-sensitive individuals and those of insulin-resis
131 ry markers and non-HDL cholesterol levels in insulin-sensitive individuals but not in lean or obese i
132 ish adipose tissue of insulin resistant from insulin-sensitive individuals with severe obesity.
133 rsus 1.68 mg/L [1.13 to 2.49]; P=0.018) than insulin-sensitive individuals, but individuals with decr
134 n adipose tissue of insulin-resistant versus insulin-sensitive individuals, who were matched for body
135 a of diabetic patients compared with that of insulin-sensitive individuals.
136 itochondrial physiology toward that of lean, insulin-sensitive individuals.
137 s do type II diabetic patients compared with insulin-sensitive individuals.
138 nd this effect is particularly manifested in insulin-sensitive individuals.
139 asured in liver biopsy samples obtained from insulin sensitive, insulin resistant, and untreated T2DM
140  and serum amino acids were determined among insulin-sensitive, insulin-resistant, and type 2 diabeti
141                                          The insulin-sensitive intracellular Ca2+ pool differs pharma
142         Recently, we purified three distinct insulin-sensitive intracellular GLUT4 compartments (G4T(
143             It was found in all of the three insulin-sensitive intracellular GLUT4 compartments, and
144 tantial number of overweight persons who are insulin sensitive is relatively minimal.
145  muscle Rad expression in well-characterized insulin sensitive (IS) and insulin resistant (IR) subjec
146 gregated as insulin resistant (IR; HF+IR) or insulin sensitive (IS; HF+IS) compared with control (CON
147 e (GDR) during hyperinsulinemic clamps in 56 insulin sensitive (IS; mean +/- SD: GDR 15.8 +/- 2.0 mg.
148           To test the hypothesis that obese, insulin-sensitive (IS) individuals possess adaptive adip
149  type 2 diabetes mellitus (DM) compared with insulin-sensitive (IS) individuals.
150 ssified as insulin-resistant (IR; n = 12) or insulin-sensitive (IS; n = 10), determined by hyperinsul
151 d order, nondiabetic subjects (classified as insulin-sensitive [IS] [n = 64] or insulin-resistant [IR
152                                          The insulin-sensitive isoform of the glucose transporting pr
153              Young ( approximately 23 years) insulin-sensitive lean and insulin-resistant obese men a
154  the insulin-resistant ZDF rats but not from insulin-sensitive lean Zucker rats.
155 MI) and insulin sensitivity index (SI): lean insulin sensitive (LIS), mean+/-SEM BMI, 23.2+/-0.3 kg/m
156     The rise in LDL with egg feeding in lean insulin-sensitive (LIS) participants is 2- and 3-fold gr
157 men, 101 women), a priori classified as lean insulin-sensitive (LIS, n = 56), lean insulin-resistant
158                                     Using an insulin-sensitive liver cell line, we show that localiza
159                 These data indicate that the insulin-sensitive membrane compartment that sequesters G
160 tion of different fatty acid sources between insulin-sensitive men and women.
161 r in the insulin-resistant compared with the insulin-sensitive men are those derived from splanchnic
162                        Insulin-resistant and insulin-sensitive men had similar postprandial chylomicr
163 atidylinositol 3-kinase and regulate various insulin-sensitive metabolic processes.
164 g of a novel PI 3-kinase, p170, from cDNA of insulin-sensitive mouse 3T3-L1 adipocytes.
165  of oral administration of ACE inhibitors on insulin-sensitive muscle glucose transport activity.
166                                           In insulin-sensitive muscle, caCaMKKalpha increased basal i
167 te glucose uptake additively with insulin in insulin-sensitive muscle, in the basal state in insulin-
168 oxical, this phenomenon is characteristic of insulin-sensitive myofibers and suggests that DGAT1 play
169 ose homeostasis in the face of fewer type I (insulin-sensitive) myofibres.
170 their insulin sensitivity index (S(I)): lean insulin sensitive (n = 65), lean insulin resistant (n =
171               Insulin-resistant (n = 11) and insulin-sensitive (n = 11) men and women (n = 6) were gi
172       Postmenopausal women were divided into insulin-sensitive (n = 15) and insulin-resistant (n = 15
173 cipants into insulin-resistant (IR, n=20) or insulin-sensitive (n=18) groups, similar in terms of mea
174               We conclude that the number of insulin-sensitive NIDDM subjects is low and similar amon
175 t obese (MAO) subjects, metabolically normal insulin-sensitive obese (MNO) subjects, and lean subject
176 ce deficient in CB1R or SCD1 remain lean and insulin-sensitive on an HFD, suggesting a functional lin
177 KI), and patients were further classified as insulin sensitive or insulin resistant.
178 2 and impaired mTorc2/Akt signaling in other insulin-sensitive organs, leading to insulin resistance
179                                              Insulin-sensitive organs, overburdened by high concentra
180          These mice are also leaner and more insulin-sensitive owing to increased energy expenditure.
181 12 randomly selected, nonobese, nondiabetic, insulin-sensitive participants in a population-based stu
182 nic groups and between insulin-resistant and insulin-sensitive participants individually and using ge
183  These findings suggest that modification of insulin-sensitive pathways can be therapeutically benefi
184 ynaptic plasticity through the impairment of insulin-sensitive pathways regulating neuronal survival,
185 sis (proteostasis) due to hyperactivation of insulin-sensitive pathways such as protein synthesis.
186 st increased by 47.6% from resting values in insulin-sensitive patients and by 14.4% in insulin-resis
187  were relatively overexpressed in adipose of insulin-sensitive patients.
188 ulin-stimulated glucose clearance rates into insulin-sensitive peripheral tissues were measured using
189 egulated isoform in these cells, as it is in insulin-sensitive peripheral tissues, such as muscle.
190 al Sorbs1-null macrophages, we show that the insulin-sensitive phenotype can be transferred to wild-t
191  mechanism for the in vivo anti-inflammatory insulin-sensitive phenotype observed in mice with macrop
192 hepatic overexpression of TRB-3 reversed the insulin-sensitive phenotype of PGC-1-deficient mice.
193       Together, our data identify Sac3 as an insulin-sensitive phosphatase whose down-regulation incr
194                             To determine the insulin-sensitive phosphorylation sites, phosphocalmodul
195  gene, termed PDK4, in insulin-resistant and insulin-sensitive Pima Indians, and detected five DNA va
196                            Incubation of the insulin-sensitive rat hepatoma Fao cells with bacterial
197          These studies demonstrate a chronic insulin-sensitive regulation of GLUT4 in rodent brain an
198 hus diabetic gastropathy in mice reflects an insulin-sensitive reversible loss of nNOS.
199                                          The insulin-sensitive rise in [Ca2+]i moves into the distal
200                            Smokers were less insulin sensitive (S(i)) compared with nonsmokers (S(i)
201                 We defined the proportion of insulin-sensitive (S(I)) subjects as > or =1.61 min-1 x
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 ole-body glucose metabolism by acting on the insulin-sensitive skeletal muscle glucose transport syst
207                                           In insulin-sensitive skeletal muscle, the expression of con
208 )) or nonobese (<27.0 kg/m(2)) and as either insulin sensitive (SSPG <100 mg/dl) or insulin resistant
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 ects (with BMI <30 kg/m2), the proportion of insulin-sensitive subjects (S(I) > or =1.61 min-1 x micr
212                         Using this approach, insulin-sensitive subjects demonstrated a twofold higher
213  = 0.60, P < 0.02), suggesting that the most insulin-sensitive subjects had the greatest enhancement
214                           Two groups of lean insulin-sensitive subjects underwent euglycemic-hyperins
215               Finally, adiponectin levels in insulin-sensitive subjects varied to a significantly gre
216 late GSIS in insulin-resistant compared with insulin-sensitive subjects, 10 participants with impaire
217  adipose tissue lipin expression is found in insulin-sensitive subjects, and lipin-beta expression in
218                                In cells from insulin-sensitive subjects, insulin augmented GSV tether
219  +/- 1.1 micro g/ml in insulin-resistant and insulin-sensitive subjects, respectively; P < 0.0005).
220 ssion levels of both lipin isoforms in lean, insulin-sensitive subjects.
221 d approximately threefold above those of the insulin-sensitive subjects.
222 ng muscle mRNA from insulin-resistant versus insulin-sensitive subjects.
223 s have greater amounts of body fat than lean insulin-sensitive subjects.
224 e intestine of insulin-resistant compared to insulin-sensitive subjects.
225 higher in insulin-resistant subjects than in insulin-sensitive subjects.
226 e intestine of insulin-resistant compared to insulin-sensitive subjects: the transcripts of the insul
227 lin sensitivity (31 insulin-resistant and 31 insulin-sensitive subjects; 40 were European American an
228 port process features characteristics of the insulin-sensitive system Nm transporter.
229  insulin-resistant adolescents; and (3) thin insulin-sensitive (T-IS), thin insulin-resistant (T-IR),
230 Wnt10b-Ay mice are more glucose tolerant and insulin sensitive than A(y) controls, perhaps due to red
231  mice have lower plasma insulin and are more insulin sensitive than AKR mice.
232 mass, Txnip knockout mice were markedly more insulin sensitive than controls, and augmented glucose t
233  standard chow and HFD, SINKO mice were more insulin sensitive than Sirt1(f/f) mice.
234                Adults born preterm were less insulin sensitive than those born at term (19.0 +/- 2.5
235 sponse to intravenous glucose, and were more insulin sensitive than those with type 2 diabetes.
236 iet (HFD), Chga-KO mice (KO-DIO) remain more insulin sensitive than wild-type DIO (WT-DIO) mice.
237 e, MacT3 mice were more glucose tolerant and insulin sensitive than wild-type mice in both in vitro a
238 rations were significantly lower in the lean insulin-sensitive than in the lean insulin-resistant men
239 nsulin-sensitive than SC adipocytes and more insulin-sensitive than male adipocytes from either depot
240 ales, intra-abdominal PG adipocytes are more insulin-sensitive than SC adipocytes and more insulin-se
241 ransgenic mice are more glucose-tolerant and insulin-sensitive than wild type mice.
242 disrupt the rhythmic internal environment of insulin sensitive tissue, thereby predisposing the anima
243 ears, it has been established that VSM is an insulin-sensitive tissue like skeletal muscle and adipoc
244 e yet concerning the localization of PDK1 in insulin-sensitive tissue.
245  are e, f, g, diabetes-associated protein in insulin-sensitive tissues (DAPIT), and the 6.8-kDa prote
246 ities of intracellular calcium metabolism in insulin-sensitive tissues (liver, skeletal muscle, and a
247 which enhances glucose utilization among the insulin-sensitive tissues (skeletal muscle, liver, heart
248 inistration regulated key metabolic genes in insulin-sensitive tissues and conferred a strong protect
249 2 influences insulin-mediated GU in multiple insulin-sensitive tissues and may explain, at least in p
250 e body weight through targeting pancreas and insulin-sensitive tissues and organs via site-specific m
251  regulators of inflammation and autophagy in insulin-sensitive tissues and postulate sEH as a druggab
252 etabolic effects of an inflammatory state in insulin-sensitive tissues appear essential for permanent
253 cial for energy homeostasis control, and key insulin-sensitive tissues are still unknown.
254 ggest that the delivery of insulin itself to insulin-sensitive tissues could be a mechanism of insuli
255 lin signaling cascade that modulates mTOR in insulin-sensitive tissues has been a major focus of inve
256 emonstrated that decreased lipid delivery to insulin-sensitive tissues improves insulin sensitivity a
257 esis that the deposition of triglycerides in insulin-sensitive tissues other than adipocytes causes i
258         In addition to p85alpha and p85beta, insulin-sensitive tissues such as fat, muscle, and liver
259  by pp185 tyrosine phosphorylation status in insulin-sensitive tissues using the Western blotting met
260 n regulates CREB transcriptional activity in insulin-sensitive tissues via the Raf --> MEK pathway an
261 40-75% in TG compared with wild-type mice in insulin-sensitive tissues with no change in GLUT4 conten
262  f, g, DAPIT (diabetes-associated protein in insulin-sensitive tissues), and 6.8PL (6.8-kDa proteolip
263     LAR, a transmembrane PTPase expressed in insulin-sensitive tissues, acts as a negative regulator
264 d 19,20-epoxydocosapentaenoic (19,20-EDP) in insulin-sensitive tissues, especially liver, as determin
265 feedback loop including islet beta cells and insulin-sensitive tissues, in which tissue sensitivity t
266    GLUT4, the glucose transporter present in insulin-sensitive tissues, resides in intracellular vesi
267 nd type II isozymes of hexokinase coexist in insulin-sensitive tissues, such as cardiac and skeletal
268 nover is regulated differently than in other insulin-sensitive tissues, such as skeletal muscle.
269 nism/antagonism influences insulin action in insulin-sensitive tissues.
270 mus, innate and adaptive immune systems, and insulin-sensitive tissues.
271 ty acids (LCFAs) and is expressed in several insulin-sensitive tissues.
272  p110beta catalytic subunits was observed in insulin-sensitive tissues.
273 viously less intensively perfused regions of insulin-sensitive tissues.
274 both the expression and activity of PTP1B in insulin-sensitive tissues.
275 glycemia and so-called "glucose toxicity" in insulin-sensitive tissues.
276 attern of expression of the MEF2 isoforms in insulin-sensitive tissues.
277 on in HepG2 and 3T3-L1 cell lines, models of insulin-sensitive tissues.
278           PTG was expressed predominantly in insulin-sensitive tissues.
279 ating free fatty acids and thus causes IR in insulin-sensitive tissues.
280 the induction of LCN2 varied among different insulin-sensitive tissues.
281 e for this methyltransferase in signaling in insulin-sensitive tissues.
282  and 3) insulin signal transduction (IST) in insulin-sensitive tissues.
283 kin-6 in the hypothalamus and key peripheral insulin-sensitive tissues.
284 ites contributes to a better redox status in insulin-sensitive tissues.
285 tion and metabolic processes in a variety of insulin-sensitive tissues; however, its role in regulati
286 nes Scd-1 and Fas is regulated partly by the insulin-sensitive transcription factor SREBP-1c and live
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).

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