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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
19 cells, Glut4 is predominantly found in small insulin-sensitive 60-70 S membrane vesicles that may or
21 in resistant high fat diet (HFD) mice become insulin-sensitive after switching from HFD to normal cho
23 Our results show that miR-155KO animals are insulin sensitive and glucose tolerant compared to contr
25 adipocyte triglyceride levels typically are insulin sensitive and have normal or low liver and circu
28 the hypothesis that B6-Ins2Akita/+ mice are insulin sensitive and provide an excellent model for isl
30 between (1) heavy and thin adolescents; (2) insulin-sensitive and insulin-resistant adolescents; and
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
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
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
45 ay be normalized by transfusion of APCs from insulin-sensitive animals but not from insulin-resistant
47 utes, showing that the output of leptin- and insulin-sensitive ARH neurons that ordinarily stimulate
49 ately 50% less fat mass and were 2-fold more insulin sensitive, as measured by hyperinsulinemic-eugly
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
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
62 In this study, we found smokers were less insulin sensitive compared with controls, which increase
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
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
80 rtment model of GLUT1 recycling involving an insulin sensitive endocytosis step in common with the GL
83 d us to investigate the effects of DZ on key insulin-sensitive enzymes regulating adipose tissue meta
85 variance), but not in FH+, as even the most insulin-sensitive FH+ offspring had diminished endotheli
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.
91 vestigate the ability of PPARgamma to confer insulin-sensitive glucose transport to a variety of muri
93 ivo, due primarily to the recruitment of the insulin-sensitive glucose transporter (GLUT4) to the pla
95 bGAP AS160/TBC1D4 controls exocytosis of the insulin-sensitive glucose transporter Glut4 in adipocyte
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
101 particularly in the regulation of GLUT4, the insulin-sensitive glucose transporter, in the AT of PCOS
105 stigate whether GLUT12 may represent another insulin-sensitive GLUT, transgenic (TG) mice that overex
107 alpha(i2) regulates the translocation of the insulin-sensitive GLUT4 glucose transporter in skeletal
109 translocation, probably by way of tethering insulin-sensitive Glut4 vesicles at an as yet unknown in
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
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
119 ucose positron emission tomography, in seven insulin-sensitive (homeostasis model assessment of insul
122 sulin-resistant humans compared to ratios in insulin-sensitive humans, indicating that higher apo-RBP
126 pothesis that some signaling pathways remain insulin-sensitive in metabolically insulin-resistant adi
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
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
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
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.
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
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
161 r in the insulin-resistant compared with the insulin-sensitive men are those derived from splanchnic
165 of oral administration of ACE inhibitors on insulin-sensitive muscle glucose transport activity.
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
170 their insulin sensitivity index (S(I)): lean insulin sensitive (n = 65), lean insulin resistant (n =
173 cipants into insulin-resistant (IR, n=20) or insulin-sensitive (n=18) groups, similar in terms of mea
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
178 2 and impaired mTorc2/Akt signaling in other insulin-sensitive organs, leading to insulin resistance
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
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.
195 gene, termed PDK4, in insulin-resistant and insulin-sensitive Pima Indians, and detected five DNA va
203 Surprisingly, CGI-58 knockdown mice remain insulin-sensitive, seemingly dissociating DAG from the d
206 ole-body glucose metabolism by acting on the insulin-sensitive skeletal muscle glucose transport syst
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
211 ects (with BMI <30 kg/m2), the proportion of insulin-sensitive subjects (S(I) > or =1.61 min-1 x micr
213 = 0.60, P < 0.02), suggesting that the most insulin-sensitive subjects had the greatest enhancement
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
219 +/- 1.1 micro g/ml in insulin-resistant and insulin-sensitive subjects, respectively; P < 0.0005).
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
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
232 mass, Txnip knockout mice were markedly more insulin sensitive than controls, and augmented glucose t
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
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
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
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
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.
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
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
294 iet, the Pten-deleted mice remained markedly insulin sensitive, which correlated with massive subcuta
296 ination, bilirubin-treated DIO mice remained insulin sensitive with lower leptin and higher adiponect
298 state plasma glucose concentrations than did insulin-sensitive women (10.8 +/- 0.5 compared with 4.1
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