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2 in fortified ethanol-containing liquid diet, pair fed a calorically equivalent sucrose-containing die
3 nd the control animals in each instance were pair fed a diet containing the basal requirement of thes
5 ment, transgenic and nontransgenic mice were pair fed a nutritionally complete liquid diet for 16 wee
9 (<1 mg Zn/kg) or zinc-adequate (35 mg Zn/kg, pair-fed) adult male rats, and zinc levels were manipula
11 i liquid diets, with matched control animals pair fed an isocaloric alcohol-free diet to ensure equal
16 nein-knockout and wild-type 129/Sv mice were pair-fed an ethanol-containing liquid diet for 12 weeks,
17 dam's diet, whereas control rats were either pair-fed an iso-caloric diet or given food ad libitum.
18 ion, respectively), as compared with animals pair-fed an isocaloric control diet containing the same
23 ortin 4 receptor knockout mice (MC4RKO) were pair-fed and received continuous hexarelin (10.56 ug/day
28 eight changes were also monitored and yoked, pair-fed animals were used to control for possible chang
29 ntake and weight gain in hyperleptinemic and pair-fed animals, identifiable fat tissue was completely
30 measuring percent HbA1c in BDNF-treated and pair-fed animals, we show that the effects of BDNF on no
31 libitum-fed exercise (AL+Exe), exercise but pair-fed at the amount as controls (PF+Exe), 20% DCR, an
33 ntrations in ethanol-fed cells compared with pair-fed cells, without significant differences in total
34 Western blots of renal membrane protein from pair-fed CON and OVX revealed bands at 129-135 kD, but t
35 back in a nonrestricted manner (N) or under pair-fed conditions (A+) to yield weight-matched rats.
39 ere fed an ethanol-containing liquid diet or pair-fed control diet for 4 (11% total kcal;early respon
40 were fed an ethanol-containing or isocaloric pair-fed control diet for 8 weeks, followed by DC isolat
43 ss to 2% (vol/vol) ethanol (11% calories) or pair-fed control diets for 2 days, 2 weeks or 5 weeks an
53 s increased susceptibility was reproduced in pair-fed control mitochondria pretreated with diethylmal
55 red saline) for 12-14 days (VEH; n = 10); 3) pair-fed control rats given a daily food ration matching
57 as evaluated in muscles of acidotic, CKD and pair-fed control rats under physiologic conditions and i
60 content was 0, compared with 14 ng/islet in pair-fed control rats, we coperfused a 2:1 oleate:palmit
66 5% ethanol (EtOH)-containing liquid diet or paired-fed control diet for 10 days followed by a single
69 inhibitor diethyldithiocarbamate to that of pair-fed controls abolished APAP toxicity in the 10-day
70 levation of ubiquitin above that in cells of pair-fed controls and this difference exceeded the relat
71 et-induced obese C57BL/6J mice compared with pair-fed controls and was associated with suppressed exp
72 s of adipose tissue inflammation relative to pair-fed controls independent of increased body weight o
74 r S-nitrosylated mitochondrial proteins from pair-fed controls or alcohol-fed rat livers were subsequ
77 atocytes from long-term ethanol-fed rats and pair-fed controls were stimulated with EGF (0.5-20 nmol/
78 egradation in ethanol-fed rats compared with pair-fed controls with no effect of ethanol on triglycer
81 ignificantly lower in hyperleptinemic versus pair-fed controls, while fatty acid and glucose levels w
97 cocaine HCl daily on gestational Days 8-20, pair-fed dams injected with saline, or nontreated contro
103 nd OVX rats fed ad libitum for 6 and 9 wk or pair-fed for 9 wk were processed for transmission electr
104 y weight and food intake were examined and a pair-fed group was included to determine if fluoxetine-i
107 +/- 8% of saline control; P < 0.01) and AGRP pair-fed groups (24 +/- 7% of saline control; P < 0.01).
108 ols in both the AGRP ad libitum fed and AGRP pair-fed groups (3.5 +/- 0.3 [saline] vs. 2.7 +/- 0.4 [A
110 cids were elevated in both tumor-bearing and pair-fed groups, while circulating levels of triglycerid
114 ts, 12 months of age, were fed an ethanol or pair-fed liquid diet, or rat chow for a period of 10, 20
118 cient ones in these experiments, even though pair fed, makes it difficult to isolate effects of zinc
119 nd were either allowed to feed ad libitum or pair-fed matched (PF SAL) to COC subjects to control for
126 xposed to CIH for 12 weeks and compared with pair-fed mice exposed to intermittent air (IA, n = 15).
129 x15) treatment of CNTF(Ax15)-treated but not pair-fed mice, followed by a gradual regain in body weig
130 attenuated in ethanol-fed mice compared with pair-fed mice, which was due to reduced natural killer g
139 icarboxylic acid (TCA) cycle flux, rats were pair-fed on diets consisting of 1) 59% safflower oil, 2)
140 -resistant diabetes and obesity, were either pair fed or treated with the Sglt inhibitor phloridzin,
143 murine C2C12 myotubes, skeletal muscle from pair-fed or ethanol-treated mice, and human patients wit
145 eated with TNF-alpha or leptin or in animals pair-fed over a 7-day time course using 11,000-gene micr
147 ncreased the available amount of ACh in both pair-fed (PF) and PTD rats, it did so to a greater exten
148 pocampus and the amygdala of PTD-treated and pair-fed (PF) control rats while they were tested on a s
149 12 wk: 1) control (Con), continuous HFD, 2) pair-fed (PF) to ketone ester (KE); and 3) KE: HFD+30% e
150 Zucker rats were studied: RYGB, sham surgery pair-fed (PF), and sham surgery ad libitum (AL) fed rats
154 f the study, body weights of the hypoxic and pair-fed pups were significantly lower than the weights
156 r) in vitro compared with Kupffer cells from pair-fed rats (< 150 pg/10(6) Kupffer cells/24 hr).
160 ease in oxygen consumption compared with the pair-fed rats, but there were no changes in oxygen consu
162 effects were greater than those observed in pair-fed rats, suggesting that although Rb1's antihyperg
167 rate (HR) were evaluated in radiotelemetered pair-fed sham-operated (SO), ovariectomized (OVX), and O
171 kDa protein increased 1.9-fold compared with pair-fed, sham-operated rats, whereas the 51- and 39-kDa
172 ortacaval anastomosis rat and sham-operated, pair-fed Sprague-Dawley rats treated with ammonia-loweri
174 e housed at 27 degrees C or 22 degrees C and pair fed the same diet for 21 weeks (95% of ad libitum i
176 red these with saline-infused rats that were pair-fed the amount of food consumed by the leptin-treat
177 Additionally, a group of inactive rats was pair-fed the amount of food consumed on the previous day
178 containing 5 ppm total zinc; and group 3 was pair-fed the control diet but restricted in amount to th
179 lated mitochondria from mice brain that were pair-fed the ethanol (4% v/v) and control liquid diets f
182 ietary AGEs promote AD, we evaluated WT mice pair-fed three diets throughout life: low-AGE (MG(-)), M
187 er, when corticosterone-treated animals were pair-fed to control intake, aiming to prevent the cortic
193 libitum, Fat/Sucrose ad libitum, Fat/Sucrose pair-fed to the caloric intake of CHO, or Fat/Sucrose at
194 d either BCD ad libitum, HPD ad libitum, HPD pair-fed to the caloric intake of the BCD, or the HPD at
195 n hyperleptinemic rats, whereas control rats pair-fed to the hyperleptinemic rats retained approximat
196 ntrols were either fed ad libitum (n = 8) or pair-fed to the intake of the leptin-treated group (n =
201 RYGB or VSG compared with rats fed ad lib or pair-fed, whereas glucose clearance was similar in all g
204 e and littermate loxP control (WT) mice were pair-fed with either an ethanol-containing diet or an et
205 Results were compared to control groups pair-fed with ethanol-free liquid diet and trained to se
207 C57BL/6J mice (n = 12/group) were isocaloric pair-fed with Lieber-DeCarli liquid diet containing eith
208 disease-free) and the MTX-treated group were pair-fed with positive controls (i.e., untreated AIA rat
209 ther caused by hyperphagia because they were pair-fed with the control group nor caused by increased
211 sham-operated rats, fed either ad libitum or pair-fed with the VSG group, were used as controls.
213 lamic NPY levels by nearly 50% compared with pair-fed young rats, whereas there were no changes in th