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1 ion and contractile dysfunction of the obese Zucker rat.
2 insulin resistance in the genetically obese Zucker rat.
3 se pathway) in the vascular tissues of obese Zucker rats.
4 ected from fatty (ZF) and lean (ZL, control) Zucker rats.
5 t increased glucose disposal by 88% in obese Zucker rats.
6 or body weight in either Long-Evans or fatty Zucker rats.
7 vely correlated with creatinine clearance in Zucker rats.
8 bular abnormalities are accelerated in obese Zucker rats.
9 ntake, and extended the observation to fatty Zucker rats.
10 n NPY receptor subtypes in obese versus lean Zucker rats.
11 mildly hyperglycemic hyperinsulinemic obese/Zucker rats.
12 ot significantly different in lean and obese Zucker rats.
13 ance of single fibers from obese versus lean Zucker rats.
14 Spontaneously breathing male Zucker rats.
15 as absent in leptin receptor-deficient obese Zucker rats.
16 sly breathing lean (n = 9) and obese (n = 9) Zucker rats.
17 ryngeal wall tissue strain in lean and obese Zucker rats.
18 served in neurones from lean, but not obese, Zucker rats.
19 ions after an oral glucose challenge in male Zucker rats.
20 ed in isoflurane-anesthetized lean and obese Zucker rats.
21 d hyperinsulinemia in leptin-resistant obese Zucker rats.
22 ZDF rats but not from insulin-sensitive lean Zucker rats.
23 h fasting or in free-feeding Wistar or obese Zucker rats.
24 on metabolism was investigated in male obese Zucker rats.
25 fusion rates were then examined in the obese Zucker rats.
26 e Zucker rats (type II diabetes) versus lean Zucker rats.
27 opment of muscle insulin resistance in obese Zucker rats.
28 take and body weight in lean, but not obese, Zucker rats.
29 thetized, 10-14 week old male lean and obese Zucker rats.
30 in target tissues of insulin-resistant obese Zucker rats.
31 sensitivity and reduced body weight in obese Zucker rats.
32 fold in obese Zucker rats compared with lean Zucker rats (0.21+/-0.06 versus 0.08+/-0.03 mm(2), P<0.0
35 rsisted through day 14 in the obese and lean Zucker rats (202.27+/-98.86 versus 35.71+/-20.54 bromode
36 mal area was markedly increased in the obese Zucker rats 7 days after injury (0.058+/-0.024 versus 0.
37 enes in untreated and losartan-treated obese Zucker rats, a model of obesity, insulin resistance, and
39 in the diet (50 micromol/kg of diet) to male Zucker rats ages 6-7 weeks for 9 months (prevention grou
41 ficantly lower in the obese relative to lean Zucker rats and ARC proNeuropeptide Y (proNPY) mRNA leve
42 on was examined in the kidney of young adult Zucker rats and compared with age-related changes in ren
46 d the oxidative stress in fatty livers of Ob Zucker rats and improved survival following lethal ische
47 channel is specific to GR neurones of obese Zucker rats and that the presence of this channel couple
48 eek-old fa/fa rats compared with age-matched Zucker (+/+) rats, and hepatic glycogen was dramatically
49 and food intake in Sprague-Dawley and obese Zucker rats, and enabled us to study the role that NT pl
51 a model of 70% hepatectomy in obese and lean Zucker rats, and obese Zucker rats pretreated with recom
53 lining cells (SLCs) in fatty livers of obese Zucker rats are more susceptible to ischemia/reperfusion
54 hypothesized that fatty livers of obese (Ob) Zucker rats are oxidatively stressed and oxidative stres
55 ncreases in longevity, suggesting that obese Zucker rats are particularly sensitive to energy restric
59 lucose tolerance of obese, insulin resistant Zucker rats at the 20 mg/kg dose level and had no effect
61 e measured in the livers of Ob and lean (Ln) Zucker rats before and after treatment with high-dose TO
64 othalamic neurons of lean Sprague-Dawley and Zucker rats, but is ineffective on neurons of obese Zuck
65 a highfat diet), and genetically obese fa/fa Zucker rats by quantifying the permeability coefficient
67 on decreases with advancing age in the obese Zucker rat, clusterin mRNA expression was examined in th
68 ointimal area was increased >2-fold in obese Zucker rats compared with lean Zucker rats (0.21+/-0.06
69 o release 5-HT at the MH is reduced in obese Zucker rats, consistent with their blunted responsivenes
72 hat glucose-receptive (GR) neurones of obese Zucker rats exhibit abnormal electrophysiological respon
79 in lean Zucker rat hearts, whereas, in obese Zucker rat hearts, muscle carnitine palmitoyltransferase
80 n of all PPAR-alpha -regulated genes in lean Zucker rat hearts, whereas, in obese Zucker rat hearts,
81 se in alpha-MSH in the PVN seen in the obese Zucker rat in the present study suggest that reduced act
82 obese insulin-resistant and type 2 diabetic Zucker rats, in streptozotocin-induced type 1 diabetic S
84 t the enhanced energetic efficiency of obese Zucker rats involves blunted serotonergic release within
85 t the enhanced energetic efficiency of obese Zucker rats is associated with a reduced capacity of act
86 dy suggests that insulin resistance in obese Zucker rats is tissue specific and that signaling from a
87 as increased in select nephrons of the obese Zucker rat kidney and in 24-mo-old F344 rat kidney as as
89 wo potentially pathogenic forces, we studied Zucker rats (leptin receptor wild type, +/+; heterozygou
91 endothelial cell necrapoptosis in steatotic Zucker rat liver isografts, which is prevented by in vit
94 istered through the portal vein of steatotic Zucker rat livers before and after cold ischemic storage
95 muscle of obese Zucker rats (OZR; with lean Zucker rats (LZR) as controls), we determined indices of
96 a obtained from gastrocnemius muscle of lean Zucker rats (LZRs) and obese Zucker rats (OZRs) were ana
98 e enhanced energetic efficiency of the obese Zucker rats may not be associated with attenuated seroto
100 1 overexpression in a well-established fatty Zucker rat model of I/R followed by orthotopic liver tra
104 Using the in situ cremaster muscle of obese Zucker rats (OZR; with lean Zucker rats (LZR) as control
106 muscle of lean Zucker rats (LZRs) and obese Zucker rats (OZRs) were analysed to investigate flow dis
107 sed regenerative capacity compared with lean Zucker rats (PCNA, BrdU, mitotic index, regenerated live
108 omy in obese and lean Zucker rats, and obese Zucker rats pretreated with recombinant interleukin 6 (r
111 of MC4-R with food restriction and in obese Zucker rats reflects receptor upregulation secondary to
115 performed on obese (fa/fa) and lean (Fa/fa) Zucker rats that had been treated orally with BWA1433 or
116 keletal muscle insulin resistance, the obese Zucker rat, to test the effect of oral administration of
118 omics analysis of fasting plasma from obese, Zucker rats treated with XN revealed decreases in produc
119 us regular Sprague-Dawley rats and (2) obese Zucker rats (type II diabetes) versus lean Zucker rats.
121 nd GVSK degraded collagen I when perfused in Zucker rat ventral skin and formed higher molecular weig
122 clamp, whole body glucose disposal in obese Zucker rats was only 22% of that observed in lean animal
124 Renal clusterin mRNA levels in the obese Zucker rat were 2.5-fold higher by 3 mo of age and fourf
127 In two experiments in which diabetic fatty Zucker rats were injected subcutaneously twice daily for
129 (30 min or 24 hr) livers from obese and lean Zucker rats were perfused ex vivo for 90 min with oxygen
134 d in diabetes, aorta and carotid arteries of Zucker rats were used for immunostaining, Western blotti
135 neuropeptide Y (NPY) receptors in the obese Zucker rat which has an increased synthesis and release
136 ation in Y5 'feeding' receptors in the obese Zucker rat which is known to possess a hyperactive arcua
137 othelial function in insulin-resistant fatty Zucker rats, which display hypertension and abnormal end
138 om normal rats but not in corneas from fa/fa Zucker rats, which lack functional leptin receptors.
139 s studies have shown that treatment of obese Zucker rats with the adenosine receptor antagonist 1,3-d
140 ed perfusion, treatment of genetically obese Zucker rats with the HO-1 inducer cobalt protoporphyrin
142 mproved hepatic insulin sensitivity in obese Zucker rats without altering the tyrosine phosphorylatio
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