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1                                              ZDF rats at 12 weeks of age showed a significant reducti
2                                              ZDF rats compared with ZCL rats have lower hepatic GK ac
3                                              ZDF rats were treated at various doses with an adenoviru
4                                              ZDF rats with global deletion of CB1R are protected from
5                                 Six lean and ZDF rats underwent small-animal PET at the age of 14 wk
6 vements in glucose tolerance in DIO mice and ZDF rats were observed after 2 weeks of q.d. dosing.
7 inistration of DM199 in obese db/db mice and ZDF rats, showed an acute, dose-dependent improvement in
8 nas obtained from the same groups of STZ and ZDF rats was significantly reduced at all time points ex
9 leptin by approximately 20 ng/ml in VMHL and ZDF rats but had no effect on their food intake, body we
10 hyperglycemia was reduced in both Wistar and ZDF rats after pioglitazone administration.
11 nsulin resistant and hyperinsulinemic ZF and ZDF rats, relative to the ZLC rat; 2) at 12 weeks of age
12 nesis and apoptosis is evident in the ZF and ZDF rats.
13 a control for mGPD, was normal in the ZL and ZDF rats.
14 pe 1 skeletal muscle of both lean Zucker and ZDF rats.
15                                      Because ZDF rats are homozygous for a mutation in their leptin r
16 n secretion, which was negligible in control ZDF rat islets, was improved in UCP-2-overexpressing isl
17 beta in a rat beta cell line and in cultured ZDF rat, mouse, and human islets.
18  glucose levels would prevent these defects, ZDF rats were treated with troglitazone beginning at 6 w
19              NAD did not develop in diabetic ZDF rat sympathetic ganglia and ileal mesenteric nerves
20 are high (>1 mM) in prediabetic and diabetic ZDF rats; therefore, we cultured prediabetic islets in 1
21 ce and insulin secretory defects in diabetic ZDF rats is inadequate.
22 red the UCP-2 gene to the islets of diabetic ZDF rats and lean (+/+) ZDF control rats.
23 ecause the fat content of islets of diabetic ZDF rats remains high unless they are treated with lepti
24                        Treatment of diabetic ZDF rats with losartan, an angiotensin II receptor-1 (Ag
25 ive UCP-2-underexpressing islets of diabetic ZDF rats, we transferred the UCP-2 gene to the islets of
26                                        Fa/fa ZDF rats had higher IMCL contents than controls througho
27                                        Fa/fa ZDF rats were studied at 3 different ages corresponding
28 at of wild-type (+/+) and homozygous (fa/fa) ZDF rats.
29 beta-actin mRNA ratio in heterozygous (fa/+) ZDF rats with that of wild-type (+/+) and homozygous (fa
30                         Zucker diabetic fat (ZDF) rats with the metabolic syndrome and hyperlipidemia
31 PD is abnormal in the Zucker diabetic fatty (ZDF) rat (ZDF/Gmi-fa/fa), an animal model of NIDDM in wh
32 duced model in type-2 Zucker diabetic fatty (ZDF) rat and normoglycemic littermates, we investigated
33  from the prediabetic Zucker diabetic fatty (ZDF) rat between 5-6 weeks and 12 weeks of age (after th
34                   The Zucker diabetic fatty (ZDF) rat is a model of type 2 diabetes and, like the hum
35 mozygous mutant (-/-) Zucker diabetic fatty (ZDF) rat is related more to chronic hyperglycemia or to
36 crocirculation of the Zucker diabetic fatty (ZDF) rat was quantified by intravital microscopy.
37                   The Zucker Diabetic Fatty (ZDF) rat, an animal model of type 2 diabetes, also devel
38  vivo, we studied the Zucker diabetic fatty (ZDF) rat, an animal model of type 2 diabetes.
39  diabetes, namely the Zucker diabetic fatty (ZDF) rat, and validated PET measurements of glucose upta
40 on of diabetes in the Zucker diabetic fatty (ZDF) rat, beta-cell mass and replication rates were dete
41 ic obesity, the fa/fa Zucker diabetic fatty (ZDF) rat, the mechanisms involved in the most common com
42 togenic mutation, the Zucker diabetic fatty (ZDF) rat, we cultured islets from 6-week-old obese (fa/f
43 bese hyperinsulinemic Zucker diabetic fatty (ZDF) rats 45 min after a single oral dose of pioglitazon
44 uced hyperglycemia in Zucker diabetic fatty (ZDF) rats after single oral doses ranging from 0.1 to 1.
45 e and triglyceride in Zucker diabetic fatty (ZDF) rats and db/db mice, decreased the expression of th
46 ic and nonprediabetic Zucker diabetic fatty (ZDF) rats and of lean Wistar and lean ZDF rats.
47          Ten-week-old Zucker diabetic fatty (ZDF) rats at an early stage of diabetes embody metabolic
48  skeletal muscle from Zucker diabetic fatty (ZDF) rats compared with lean controls and determined the
49 esistance arteries in Zucker diabetic fatty (ZDF) rats compared with lean Zucker (LZ) rats.
50                       Zucker diabetic fatty (ZDF) rats develop type 2 diabetic nephropathy with album
51    Like obese humans, Zucker diabetic fatty (ZDF) rats exhibit early beta cell compensation for insul
52 process replicated in Zucker Diabetic Fatty (ZDF) rats in which beta-cell loss has been linked to can
53 ed (SL) controls, and Zucker Diabetic Fatty (ZDF) rats in which the leptin receptor is mutated.
54 output in prediabetic Zucker diabetic fatty (ZDF) rats is mediated by NO.
55 sion in beta cells of Zucker diabetic fatty (ZDF) rats is profoundly reduced at the onset of beta-cel
56 nization of islets of Zucker diabetic fatty (ZDF) rats is the proximal cause of their inability to co
57 29 or troglitazone to Zucker diabetic fatty (ZDF) rats resulted in dose-dependent decreases in daily
58 islets of obese fa/fa Zucker Diabetic Fatty (ZDF) rats results from overproduction of ceramide, an in
59 rom pre-diabetic male Zucker diabetic fatty (ZDF) rats showed increased expression of hypoxia-related
60 tic genes from female Zucker diabetic fatty (ZDF) rats treated with the FXR agonist GW4064, we have i
61 nd fatty (fa/fa), and Zucker diabetic fatty (ZDF) rats were studied.
62                       Zucker Diabetic Fatty (ZDF) rats were subjected to temporary myocardial RI and
63 amined in 20-week-old Zucker diabetic fatty (ZDF) rats whether restoration of hepatic glucokinase (GK
64 ow that treating male Zucker diabetic fatty (ZDF) rats with E2 suppressed synthesis and accumulation
65 er early treatment of Zucker diabetic fatty (ZDF) rats with ebselen, an oral GPx mimetic, will preven
66              In obese Zucker diabetic fatty (ZDF) rats with mutant leptin receptors, pancreatic islet
67  in lipid dynamics in Zucker diabetic fatty (ZDF) rats, in response to 7 days of treatment with eithe
68 ic rings from BBd and Zucker diabetic fatty (ZDF) rats, models of human type I and type II diabetes,
69 from Lean control and Zucker Diabetic Fatty (ZDF) rats, using single-channel recording techniques.
70 in hyperglycemic male Zucker diabetic fatty (ZDF) rats, with an ED(50) for glucose normalization of 3
71 n Norway (FBN) and in Zucker Diabetic Fatty (ZDF) rats.
72  receptor agonist, in Zucker diabetic fatty (ZDF) rats.
73 e adipogenic NIDDM of Zucker diabetic fatty (ZDF) rats.
74 of type 2 diabetes in Zucker diabetic fatty (ZDF) rats.
75 amined in 14-week-old Zucker diabetic fatty (ZDF) rats.
76 ue-Dawley [S-D] rats, Zucker diabetic fatty [ZDF] rats, and rats expressing human islet amyloid polyp
77 impaired glucose homeostasis in high-fat fed ZDF rats.
78   In vivo administration of GW4064 to female ZDF rats promoted a dose-dependent and >6-fold increase
79 soyasaponin-1 (DHS-1) was lost in cells from ZDF rats.
80                                  Islets from ZDF rats failed to increase insulin secretion in respons
81                         Isolated islets from ZDF rats were completely resistant to the lipopenic acti
82  0.05, respectively) in skeletal muscle from ZDF rats compared with lean controls.
83         GLUT4 levels in skeletal muscle from ZDF rats were similar to those in lean control animals.
84 ts of 6-week-old heterozygous and homozygous ZDF rats lack the capacity for FFA-induced enhancement o
85                Three weeks prior to imaging, ZDF rats were randomized into a no-restriction (ZDF-ND)
86 ey feeding behavior and metabolic centers in ZDF rat brain or directly enhance glucose-stimulated ins
87                                           In ZDF rats, hyperphagia leads to hyperinsulinemia, which u
88         Alteration of hepatic GK activity in ZDF rats has profound effects on plasma glucose and hepa
89 for NF vessels, but this was not the case in ZDF rats.
90 er oral or intravenous glucose challenges in ZDF rats and db/db mice, without causing hypoglycemia or
91                 We found that BK channels in ZDF rats have impaired Ca(2+) sensitivity, including an
92 % to 32%) but was significantly decreased in ZDF rats after 2 to 5 months of diabetes (-9% to -16%).
93 erglycemia resulting from type 2 diabetes in ZDF rats is associated with loss of insulin and PDX-1 mR
94 the proximate cause of lipotoxic diabetes in ZDF rats.
95             Endothelium-mediated dilation in ZDF rats, which was lower than in LZ rats, was further d
96                                When dosed in ZDF rats, 25 showed both a robust pharmacodynamic effect
97 lexibility and glucose flux were examined in ZDF rats during fasting and near-normal postprandial ins
98 also attenuated urinary albumin excretion in ZDF rats.
99 ose-dependently reduced glucose excursion in ZDF rats.
100  in BK channel beta(1)-subunit expression in ZDF rats, compared with that of Lean rats.
101 nd the impaired beta-cell response to FFA in ZDF rats.
102 d oxidation and postprandial glucose flux in ZDF rats.
103 e parameters of peripheral nerve function in ZDF rats.
104 ed with impaired regulation of GK by GKRP in ZDF rats.
105                                  However, in ZDF rats and db/db mice, there was profound increase in
106 d glucose levels were significantly lower in ZDF rats during a drug wash-out period.
107 LUT-4 was significantly (P = 0.004) lower in ZDF rats.
108 ements of myocardial substrate metabolism in ZDF rats using small-animal PET are consistent with the
109                                      MGUp in ZDF rats at both week 14 (W14) and W19 (P < 0.006) was s
110              The level of adipose ob mRNA in ZDF rats was 3-fold greater than that detected in the Zu
111  Metanx on diabetic peripheral neuropathy in ZDF rats, a model of type 2 diabetes.
112 ion of normoglycemia and normoinsulinemia in ZDF rats with rosiglitazone (30 micromol/kg) normalized
113 ression in islets of normal rats, but not in ZDF rats, in which PPARalpha is very low.
114  was slightly increased in Wistar but not in ZDF rats.
115 ance of 3-nitrotyrosine-modified proteins in ZDF rats.
116 ndothelial cells is progressively rampant in ZDF rats and is associated with the signs of severe vasc
117  for HF-dependent remodeling, was reduced in ZDF rats compared with LZ rats and restored by ALT-711.
118 gen species reduction restored relaxation in ZDF rats but not in LZ or ALT-711-treated rats.
119 f nonesterified free fatty acids was seen in ZDF rats but not in db/db mice.
120 d nuclear magnetic resonance spectroscopy in ZDF rats during early and advanced diabetes.
121 glucose in an oral glucose tolerance test in ZDF rats.
122                   These results show that in ZDF rats, treatment with a synthetic insulin-receptor-ac
123 d at the mechanistic level, removal of VF in ZDF rats prevented the progressive decrease in insulin a
124               Sub-acute dosing for a week in ZDF rats improved glucose utilization, with a concomitan
125 fatty (ZDF) rats and of lean Wistar and lean ZDF rats.
126 esity and apparently normal islets from lean ZDF rats (fa/+) in 0, 1, or 2 mM FFA.
127  increased only slightly in islets from lean ZDF rats (not significant) and declined in islets from o
128 ated islets of ZDF rats or in islets of lean ZDF rats.
129  islets but not in islets from obese or lean ZDF rats.
130 despite a similar impact on glycemia in male ZDF rats.
131 us administration of NRTN to 8-week-old male ZDF rats prevented the development of hyperglycemia and
132 ncreased approximately twofold in young male ZDF rats by both morphometric analysis and quantifying m
133 gnificant) and declined in islets from obese ZDF rats (p < 0.05).
134  in the range of those found in the blood of ZDF rats increased albumin permeability in nondiabetic Z
135 the culture medium reduced the TG content of ZDF rats by 52%; this was reflected by decreased esterif
136 ramyocardial lipid overload in the hearts of ZDF rats was associated with contractile dysfunction and
137 lioration of beta cell function in islets of ZDF rats might be associated with a reduction in their e
138  rise in either the precompensated islets of ZDF rats or in islets of lean ZDF rats.
139 tin and is low in leptin-resistant islets of ZDF rats.
140            We conclude that lipoapoptosis of ZDF rats is mediated by enhanced ceramide synthesis from
141 sation of albumin in the microcirculation of ZDF rats was significantly increased when compared with
142                 Chronic ebselen treatment of ZDF rats restored renal tissue levels of glutathione and
143                                 Treatment of ZDF rats with different doses of AdvCMV-GKL, which resto
144                      Islets from 15-week-old ZDF rats did not induce migration; rather, they caused a
145 nts were performed in prediabetic 6-week-old ZDF rats in comparison with 12-week-old overtly hypergly
146                       Islets from 7-week-old ZDF rats showed a fivefold increase in migration score c
147               Islets from 7- and 12-week-old ZDF rats showed an approximate three- and twofold increa
148 ctron microscopy of normoglycemic 7-week-old ZDF rats showed thickened endothelial cells with loss of
149                         Treating 10-week-old ZDF rats with sustained hyperglycemia with liraglutide r
150 8% of normal in islets of 6- and 12-week-old ZDF rats, respectively (P < 0.001 by analysis of varianc
151 f normal in the islets of 6- and 12-week-old ZDF rats, respectively (P < 0.001).
152 As glycemia increased in 12- and 16-week-old ZDF rats, we observed decrements in glucose-induced insu
153 red with age-matched ZLC rats and 6-week-old ZDF rats.
154                Given orally in db/db mice or ZDF rats, 46a,b showed a significant glucose-lowering ef
155 al islets and in islets of obese prediabetic ZDF rats; in the latter, this correlated with improvemen
156 e or aminoguanidine treatment of prediabetic ZDF rats prevented the iNOS expression in islets and dec
157 ta-cell mass in 5- to 7-week-old prediabetic ZDF rats (4.3 +/- 0.06 mg) was similar to age-matched in
158 ly prevented in vivo by treating prediabetic ZDF rats with L-cycloserine for 2 weeks.
159                          Whereas prediabetic ZDF rats had a fourfold elevation in islet fat, in VMHL
160                       Troglitazone prevented ZDF rats from becoming hyperglycemic and preserved gluco
161 specific in vivo knockdown of Irf5 protected ZDF rats from beta-cell loss and hyperglycemia.
162 1 skeletal muscle from the insulin-resistant ZDF rats but not from insulin-sensitive lean Zucker rats
163                                        Since ZDF rats are euglycemic at 6 weeks of age and ZL animals
164                                In our study, ZDF rats maintained for 6 to 7 months in a severely diab
165                  These findings suggest that ZDF rats develop a progressive nephropathy with glomerul
166 re made between the activity observed in the ZDF rat and that seen in the ZDF lean control (ZLC) rat
167 s failure of beta-cell mass expansion in the ZDF rat does not appear to be from a reduction in the ra
168               These data suggest that in the ZDF rat model of type 2 diabetes, an inability of the is
169 nd chylomicrons (CM) was investigated in the ZDF rat model of type 2 diabetes, in order to define the
170     Accordingly, we can conclude that in the ZDF rat model, type 2 diabetes develops in the absence o
171  represent the primary genetic defect in the ZDF rat.
172             This study demonstrates that the ZDF rat carries a genetic defect in beta-cell transcript
173                                          The ZDF rats were allowed to recover for 2 h or 28 days.
174                                          The ZDF rats were treated for 6 weeks with either bezafibrat
175 ime points) was significantly greater in the ZDF rats (0.88 +/- 0.1%) compared with the ZF and ZLC ra
176 after diabetes onset), beta-cell mass in the ZDF rats (8.1 +/- 1.7 mg) was significantly lower than t
177 However, higher glucose plasma levels in the ZDF rats resulted in higher myocardial glucose utilizati
178 ificantly in db/db mice but increased in the ZDF rats.
179 doptive transfer of CB1R(-/-) bone marrow to ZDF rats also prevents beta-cell loss and hyperglycemia
180         AGEs were reduced in ALT-711-treated ZDF rats compared with ZDF rats.
181 sulin staining compared with vehicle-treated ZDF rats.
182 d blood glucose, compared with the untreated ZDF rats.
183 ed in ALT-711-treated ZDF rats compared with ZDF rats.
184                                    At 22 wk, ZDF rats developed focal and segmental sclerosis, protei
185                                     At 8 wk, ZDF rats showed hyperglycemia, no proteinuria or nephrop
186 0.62 +/- 0.07%, respectively, P < 0.05), yet ZDF rats have a lower beta-cell mass than the ZF rats de

 
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