ライフサイエンスコーパス: chow

1 P = .015] and 1.0 for CD-TREAT [P = .044] vs chow).

2 to 20-mo-old male C57BL mice fed a standard chow.

3 but is normalized when mice consume standard chow.

4 s in Fgf13 heterozygous knockouts fed normal chow.

5 teatohepatitis; control mice were fed normal chow.

6 mpared with those of control mice fed normal chow.

7 t alterations in beta-cell mass with control chow.

8 eserve when compared with mice fed on normal chow.

9 the retina as compared with mice fed normal chow.

10 able from wild-type littermates on a regular chow.

11 atic steatosis in mice fed normal laboratory chow.

12 tion in the human population, posits Clement Chow.

13 undernourished rats were rehabilitated with chow.

14 d nondiabetic Nos3(-/-) mice received normal chow.

15 ed proteinuria than were animals on standard chow.

16 s of GLUT5 in adult wild-type mice consuming chow.

17 epatic insulin resistance in rats fed normal chow.

18 e of rejection compared with mice fed normal chow.

19 wder, while remaining rats were fed breeding chow.

20 f adipose tissue in adult animals fed normal chow.

21 g suckling (CO, OC) and weaned onto standard chow.

22 flux observed in rats fed carbohydrate rich chow (0.726 +/- 0.201).

23 ek-old C57BL/6 virgin female mice were fed a chow (21%) or high-fat (60%) diet and divided into four

24 C57BL/6 female mice were fed a chow (21%) or high-fat (60%) diet and further divided by

25 mproved glucose tolerance in aged mice fed a chow (~30% vs. saline) or HF (~50% vs. saline) diet and

26 Rats self-administered 60% high fat or chow 45 mg pellets and were then tested for incubation o

27 re fed a HFD (59% kcal from fat) or standard chow (9% Kcal from fat) for 8 weeks.

28 Allograft mice received normal chow, a high-fiber diet, or normal chow supplemented wit

29 KO mice only to the level in the WT mice fed chow and had no effect on aortic eNOS(Ser1177) phosphory

30 AJ mice consumed more of both standard chow and HCD than the other three strains tested when bo

31 Surprisingly, however, in both chow and HFD-fed mice, insulin-stimulated Akt phosphoryl

32 Finally, incubation of craving for chow and high fat was accompanied by an increase in calc

33 s the hypothesis, behavioral tests including chow and high-fat diet intake, meal patterns, conditione

34 Heterozygous Fgf13 knockouts fed normal chow and housed at 22 degrees C showed hyperactivity acc

35 GF13 in adipose of wild-type mice fed normal chow and no obesity in adipose-specific heterozygous kno

36 g, we tested the effects of memantine on the Chow and Palatable food groups' intake.

37 macrophages isolated from mice fed standard chow and supplemented with DHA in vitro.

38 istration potently reduced food intake (both chow and Western diet) and body weight, whereas HPFv GLP

39 ated fat, 30% sucrose solution, and standard chow and whether this was mediated by the Y1R.

40 PY increased intake of fat, but not sugar or chow, and this was mediated by the Y1R.

41 press endogenous glucose production (EGP) in chow- and HFD-fed mice.

42 nsulin sensitivity in insulin-resistant aged chow- and high-fat diet-fed (HFD-fed) mice.

43 played an adjuvant-free IgE-sensitization to chow antigens that was most pronounced for wheat and soy

44 a high-fat diet (HFD) to induce obesity, or chow as reference group.

45 eived ASK1 inhibitor (GS-444217 delivered in chow) as an early intervention (2-8 weeks after STZ) or

46 ly associated with high fat was greater than chow at both 1 and 30 days.

47 ce fed with a high-fat diet (HFD) or regular chow at weeks 1, 9, and 18.

48 g the transition from a milk-based diet to a chow-based diet after weaning.

49 ither atorvastatin (15 mg/kg; 7d) or control chow before sacrifice.

50 gnificant risk factors including breed (e.g. Chow Chow, Bulldog and French Bulldog), higher bodyweigh

51 In this model, rats in the control group (Chow/Chow) are provided a standard chow diet 7 days a we

52 fect food intake or body weight under normal chow consumption.

53 tion of LHA (GABA) neurons increased overall chow consumption.

54 old, female mdr2(-/-) mice were fed high-fat chow containing 0.006% SC-435, a minimally absorbed, pot

55 rabbits were placed on a normal chow diet or chow containing 0.14% (wt/wt) des-fluoro-anacetrapib for

56 When the Tg mice were fed chow containing IC3, plasma prolactin concentrations inc

57 olically labeled with a specially formulated chow containing nitrogen-15 ((15)N) with the absence of

58 le Sprague-Dawley rats were fed standard rat chow containing normal (0.25%) and low (0.025%) Na(+) fo

59 eased by 60% in the stomach of mice fed with chow containing Sub-A-mPEG-PLGA (0.2 mg Sub-A/g chow) (n

60 ) (n = 9) compared to 31.9% in mice fed with chow containing unmodified Sub-A (n = 9).

61 et (Palatable group) or a regular chow diet (Chow control group), for 1 h a day, under a fixed-ratio

62 nti-inflammatory agent sulindac vs mice on a chow (control) diet.

63 re(+/0) mice, respectively) were fed regular chow (control) or a high-fat diet supplemented with 30%

64 model of BE, called L2-IL1B mice) were fed a chow (control) or high-fat diet (HFD) or were crossbred

65 s were isolated from adult mice fed standard chow, control diets, or DHA supplemented diets.

66 blished rat MO model, female Wistar rats ate chow (controls (C)) or high energy, obesogenic diet to i

67 IC3 chow did not affect the WT mice.

68 nes were reared as control group on standard Chow diet (18% fat).

69 kout (WT/KO) dams were fed a control breeder chow diet (25% fat) or a semi-purified HFD (45% fat) 4 w

70 /6JRJ mice were fed with a short-term HFD or chow diet (CD) for 12 weeks.

71 In this work, we fed mice either a chow diet (CD), a 16 week high-fat diet (HFD), or a CR d

72 intake to match body weight to the mice on a chow diet (CD).

73 , sugary diet (Palatable group) or a regular chow diet (Chow control group), for 1 h a day, under a f

74 r tissues collected from mice fed a standard chow diet (controls) and 9 mouse models of NAFLD: mice o

75 pyridoxamine in drinking water, or a normal chow diet (controls) for 6 weeks.

76 chronic safety study in WT mice fed a normal chow diet (NCD +/- CAP, 0.01% in NCD) or HFD +/- CAP (0.

77 gh all UtxAKO mice grew normally on a normal chow diet (NCD), female UtxAKO mice on a high fat diet (

78 /SCD: six wild-type (WT) mice fed a standard chow diet (SCD); WT/HFD, six WT mice fed a HFD; NOX2(-/-

79 he intake of nutritionally balanced standard chow diet (SD) irrespective of age, sex, body mass accru

80 ol group (Chow/Chow) are provided a standard chow diet 7 days a week, while the experimental group (C

81 ine body weights compared with wild types on chow diet and attenuated weight gain when fed cafeteria

82 ed greater weight than animals fed a control chow diet and greater perirenal adiposity by the end of

83 Mice received chow diet and normal water (CDNW) or high fat western di

84 These mice gain more weight on chow diet and short-term as well as long-term high-fat d

85 asma cholesterol was lowered by switching to chow diet and treatment with LDLR sense oligonucleotides

86 ckground (n = 3-5/group) were fed a standard chow diet and water ad libitum.

87 ure monitored during 15 days of feeding with chow diet containing vehicle or resveratrol.

88 adipocyte-specific hRBP4 mice fed a standard chow diet display significantly elevated hepatic triglyc

89 reatic insulin content, MIP-CreERT mice on a chow diet exhibited normal ambient glycemia, glucose tol

90 ntrol group (143 mice maintained on standard chow diet for 20 weeks).

91 mice (5 weeks) were maintained on a standard chow diet for 6 weeks.

92 different CC lines were maintained on rodent chow diet for 8 weeks and were subsequently transferred

93 t loss resulting from conversion to a normal chow diet for 8 weeks resulted in more than a 25% decrea

94 Male DKO mice fed a chow diet had reduced liver lipid levels but increased s

95 and subsequent steatohepatitis on a regular chow diet in the absence of whole-body insulin resistanc

96 er of <=2.5 mum (PM(2.5)) in mice fed with a chow diet leads to similar metabolic effects caused by h

97 eficient and E85V knock-in mutant mice fed a chow diet manifested an increase in the length of their

98 C57BL6/J mice were fed a chow diet or a fast-food diet (FFD) with or without EGFR

99 leaved caspase 3 in mice fed either a normal chow diet or a high-fat diet.

100 NZW rabbits were placed on a normal chow diet or chow containing 0.14% (wt/wt) des-fluoro-an

101 BALB/c male mice were fed either standard chow diet or Western-type diet (characterized by high fa

102 nto 4 groups: control (chow diet), MCD diet, chow diet plus G49, and M+G49 (MCD diet plus G49).

103 betaPKD1KO mice under a chow diet presented no significant difference in glucose

104 Atp7b (-/-) mice fed a chow diet presented with blunted body-weight gain over t

105 s end mice received either regular chow or a chow diet supplemented with canola oil for 6 months.

106 liver of mice fed a high cholesterol diet or chow diet supplemented with the HMGCR inhibitor lovastat

107 e 1 receptor deficient (Glp-1r(-/-)) mice on chow diet were characterized following GB-IL.

108 ult male C57BL/6 mice maintained on a normal chow diet were subjected to a microbiome depletion/trans

109 Five noninjured rabbits fed a chow diet were used as controls.

110 1 week were divided into 4 groups: control (chow diet), MCD diet, chow diet plus G49, and M+G49 (MCD

111 enic mice were randomized to receive regular chow diet, a diet deficient in folate and B vitamins (Di

112 ct the response to damage of adult muscle in chow diet, and it determines the maintenance of muscle f

113 With mice on a standard chow diet, body weight and glucose homeostasis were not

114 On a standard chow diet, hep-LAL-ko mice exhibited increased hepatic C

115 s old mice were randomly assigned to receive chow diet, high fat diet with sugar in drinking water (W

116 in Apoe(-/-) and Ldlr(-/-) mice fed a normal chow diet, resulting in mildly increased plasma choleste

117 protein to young or aged mice fed a standard chow diet, short-term high-fat diet (HFD), or long-term

118 On chow diet, Sucnr1(-/-) mice had increased energy expendi

119 When fed a chow diet, these mice show an elevation in adipose total

120 e is seen in CX3CR1(+/GFP)/apoE(-/-) mice on chow diet, with a further 2- to 3-fold increase on Weste

121 t induced obese mice were lower than regular chow diet-fed mice challenged by the LPS.

122 To address this question, we treated regular chow diet-fed mice or high-fat diet induced obese mice w

123 larly, acute and chronic leptin treatment of chow diet-fed WT mice decreased MTP expression in the in

124 only lowered TG in LDLR WT mice fed a normal chow diet.

125 or(-/-) mice consuming a high-cholesterol or chow diet.

126 ozygous (Het), and wild type (WT) mice fed a chow diet.

127 e diet was evaluated and compared to mice on chow diet.

128 striction-induced overeating of the standard chow diet.

129 ice fed the HFD and both sexes of mice fed a chow diet.

130 All mice were fed a standard chow diet.

131 ein tolerance and lethal hyperammonemia on a chow diet.

132 aralpha(-/-)mice fed a Wy14,643-supplemented chow diet.

133 iver and serum, compared to mice on a normal chow diet.

134 sausage, control pork sausage or a standard chow diet.

135 lammation properties on a high-fat or normal chow diet.

136 ically fed with Mankai compared with control chow diet.

137 ated in the liver of Shp (Hep-/-) mice fed a chow diet.

138 mice had less preference for HFD over normal chow diet.

139 lates adiponectin but not leptin in mice fed chow diet.

140 /-) mice were glucose-intolerant even on the chow diet; HFD further increased fasting glucose and ins

141 with offspring always maintained on a normal chow diet; thus the only experience offspring had with h

142 in the presence of FCCP when compared to the chow-diet fed control mice.

143 Alcohol Abuse and Alcoholism binge model) or chow diets along with water containing 0.18% DL-homocyst

144 inbred ILSXISS strains were fed high-fat or chow diets and subjected to metabolic phenotyping and me

145 bonyl-1,4-dihydrocollidine (DDC) or standard chow diets to induce biliary injury or were given inject

146 oduced to HFD, similar to WT mice on regular chow during IU/L.

147 In this issue of Immunity, Chow et al. (2019) show that the CXCR3-CXCL9 axis is req

148 Wild-type mice fed normal chow exhibited dysbiosis after receiving a kidney allogr

149 After return to the same body weight as chow fed control mice, the fasting insulin, glucose, and

150 ty were obtained in high fat diet and normal chow fed male C57BL/6J mice.

151 d obese female C57BL6/J mice were mated with chow fed males.

152 Male offspring were chow fed, sedentary, and studied at 8, 12, 24, 36, and 5

153 ulin secretion or glucose tolerance in lean, chow-fed adult mice.

154 lic burden of overnutrition was tested using chow-fed and high-fat (HF)-fed SkM-specific AMPKalpha1al

155 Absent in chow-fed animals, PI-BMDCs account for 60% of the ATMs i

156 ma levels of inflammatory markers in regular chow-fed but not in high fat-fed mice.

157 Compared with chow-fed C57BL/6 mice, fasted or ketogenic diet-fed mice

158 study, we modeled early life exposure using chow-fed C57BL/6J male mice that were exposed to real-wo

159 signaling and ER stress markers under normal-chow-fed conditions, indicating chronic low-level ER str

160 Compared with a normoxic, chow-fed control mouse heart, hypoxia decreased PPARalph

161 Consistently, chow-fed CysC KO mice were more susceptible to lipopolys

162 Offspring from chow-fed dams that trained both before and during gestat

163 glucose tolerance compared with offspring of chow-fed dams throughout their first year of life, an ef

164 osis gene expression levels are increased in chow-fed DKO mice compared to WT mice and that the top r

165 Ex vivo cholesterol loading of chow-fed DKO SC recapitulated the effect, indicating tha

166 Chow-fed GLP-1RKD(DeltaNkx2.1cre) mice exhibited increas

167 liraglutide treatment reduced body weight in chow-fed GLP-1RKD(DeltaNkx2.1cre) mice, but this effect

168 cause ex vivo exposure of soleus muscle from chow-fed lean mice to compound A increased glucose trans

169 and diglyceride contents were normalized to chow-fed levels in HF-fed itga1(-/-) mice.

170 atic accumulation of hepatic BMP compared to chow-fed littermates.

171 Hepatic Fas overexpression in chow-fed mice compromises fatty acid oxidation, mitochon

172 In 5 mmol/L glucose, islets from C57BL/6J chow-fed mice cycled approximately 16% of net glucose up

173 Chow-fed mice lacking T39 (T39(-/-)) display increased h

174 GB-IL in wild-type, chow-fed mice prompted weight-independent improvements i

175 Furthermore, rm-resistin-injected normal chow-fed mice showed upregulated blood glucose level by

176 sis and causes hepatic insulin resistance in chow-fed mice while selectively conferring protection fr

177 nesis (DNL) was increased in male and female chow-fed mice, compared with GHR-intact littermate contr

178 Compared with chow-fed mice, HFD-fed mice had a rapid increase in body

179 Compared with IgG from control chow-fed mice, IgG from HFD-fed mice was hyposialylated,

180 D4CD25Foxp3 T regulatory cells compared with chow-fed mice, whereas PN + BBS assimilated chow levels.

181 s' effects on EGP in HFD-fed mice but not in chow-fed mice.

182 levels of Nrp1 in macrophages compared with chow-fed mice.

183 aximal respiration, when compared to control chow-fed mice.

184 ent to cause an impairment in BA function in chow-fed mice.

185 aximal respiration, when compared to control chow-fed mice.

186 ortic lymph nodes, and aortas, compared with chow-fed mice.

187 Transplantation of cecal microbiota from chow-fed Mttp-IKO mice into antibiotic-treated wild-type

188 elevated in perigonadal white AT (PGWAT) of chow-fed RBP4-overexpressing mice and in serum and PGWAT

189 food intake and worsens glucose tolerance in chow-fed rodents and causes excess weight gain during hi

190 Females were bred with chow-fed sedentary C57BL/6 males.

191 When implanted into normal chow-fed, or into high-fat diet (HFD)-fed, glucose-intol

192 nt did not affect performance of the control Chow food group.

193 with standard mouse chow or OLT1177-enriched chow for 3 mo.

194 d 6 weeks of CDAHFD and switched to standard chow for 3 weeks (n = 12); (f) were fed CDAHFD for 9 wee

195 Pde11a knockout mice (KO) given 0.4% lithium chow for 3+ weeks exhibit greater lithium responsivity r

196 rague-Dawley rats were fed either a standard chow for 4 weeks or a methionine- and choline-deficient

197 ammation received EEN, CD-TREAT, or standard chow for 4 weeks.

198 ey were fed a high-fat diet (HFD) or regular chow for 4 weeks.

199 erimental group (Chow/Palatable) is provided chow for 5 days a week ("C Phase"), followed by 2 days o

200 A BA overload, feeding 0.5% cholic acid chow for 6 days, resulted in adaptive responses of alter

201 driven Cre and maintained on standard rodent chow for 6 months.

202 randomized to 0.24% Li2CO(3) chow or normal chow from PND 49 to 77.

203 eterogeneous manifestations, and that animal chow has the potential to influence data reproducibility

204 BL/6JJcl mice fed with high fat-high sucrose chow (HFS), multifunctionality of CD8 + splenic and tumo

205 penditure, and improved glucose tolerance on chow, high-fat, and FFDs.

206 s a time- and dose-dependent accumulation of chow in the stomachs of mice fed ad libitum without chan

207 n both male and female mice fed with regular chow, increased susceptibility to diet-induced obesity (

208 sistance when compared with mice fed regular chow, indicating that the mice developed MetS.

209 Chow intake and meal size were significantly increased f

210 aserin significantly reduced both ad libitum chow intake and PR responding for chocolate pellets and

211 blood glucose levels and baseline water and chow intake in adulthood.

212 tum feeding of mice, affecting neither daily chow intake nor body weight or glucose tolerance.

213 In sham-lesioned rats, Ex4 reduced chow intake within 4 h of injection and sucrose intake w

214 ing neurons significantly reduced ad libitum chow intake, operant responding for chocolate pellets, a

215 ored sucrose pellets without affecting prior chow intake.

216 On normal chow, IRMOE mice have body weight similar to that of con

217 On chow, JAK2L mice had hepatic steatosis and severe whole-

218 was not activated in Fx-/- mice fed standard chow, leading to decreased expression of its target Hes1

219 propria) T cells, whereas PN-BBS assimilated chow levels.

220 4 memory B cells, whereas PN-BBS assimilated chow levels.

221 chow-fed mice, whereas PN + BBS assimilated chow levels.

222 In chow-maintained rats, systemic amylin and GLP-1 combine

223 MCK-Plin5 mice fed high-fat chow manifest lower expression of inflammatory markers i

224 cells, as well as in mice fed with high-fat chow; mechanistically, inflammasome-activating short int

225 onsisting of either pure rodent chow, rodent chow mixed to yield a content of either 20% glucose or 2

226 sured LTL by qPCR in pedigreed baboons fed a chow (n = 105) or HCHF (n = 106) diet for 2 years, teste

227 (b) weight-matched animals received standard chow (n = 12 per group); (c) received choline-deficient,

228 w containing Sub-A-mPEG-PLGA (0.2 mg Sub-A/g chow) (n = 9) compared to 31.9% in mice fed with chow co

229 Adult female mice were fed a normal chow (NC) or a high fat diet (HFD) for 5 weeks before ma

230 in mice consuming standard (normal) low-fat chow (NC) or a high-fat/high-sucrose Western diet (WD) i

231 left carotid artery in young and old, normal chow (NC) or WD fed male B6D2F1 mice.

232 When the Tg mice were fed normal chow (NC), plasma prolactin concentrations were comparab

233 eceived Ex4 (1 mug/kg) before 24 h home cage chow or 90 min 0.3 M sucrose access tests, and licking m

234 To this end mice received either regular chow or a chow diet supplemented with canola oil for 6 m

235 C57BL/6 mice were placed on chow or a diet high in fat, fructose, and cholesterol to

236 deficient (ILK(lox/lox)HSAcre) mice were fed chow or a high-fat (HF) diet for 16 weeks.

237 can model retinal disease, we weaned mice to chow or a high-fat diet and tested the hypothesis that d

238 ormed inhalation exposure of mice fed normal chow or a high-fat diet to airborne fine particulate mat

239 lucose metabolism in mice fed either regular chow or a high-fat diet, demonstrating that these metabo

240 full-length Il6 gene (controls), were fed a chow or a high-fat diet; some mice were given injections

241 ith normal senescence (n=15) were fed normal chow or a high-fat, high-salt diet (WD).

242 C57Bl/6 mice fed chow or a methionine and choline-deficient (MCD) diet fo

243 s compared with diabetic controls fed normal chow or a zero-fiber diet.

244 onditions: food-deprived rats given standard chow or ad libitum-fed rats given a palatable chocolate

245 metabolic characterization of these mice fed chow or after 6 wk of a high-fat diet.

246 nfusions did not alter the overall intake of chow or chocolate shake.

247 (WT) and Cyp2e1-null mice were fed standard chow or FF for 2, 12, and 24 weeks.

248 Mice were placed on standard chow or fucose-containing diet (equivalent to a control

249 ch were improved in ECIRS1 TG mice on normal chow or HF diet.

250 HCR and LCR rats were fed a chow or HFD for 3 days and received a single in vivo HT

251 protein (RIP) 3(-/-) mice were randomized to chow or HFD.

252 le mice were acutely fed a standard breeding chow or HFD.

253 CXCR3(-/-) and wild type (WT) mice were fed chow or high saturated fat, fructose, and cholesterol (F

254 Mice were cohoused for 8 or 13 weeks and fed chow or high-fat cholesterol-rich diet.

255 male Sik2(S587A) mice that were fed either a chow or high-fat diet showed similar weight gain as the

256 ta-cell function of these mice fed a control chow or high-fat diet.

257 e from 29 different inbred strains to normal chow or lithium diet (40 mmol/kg), we housed the animals

258 ND) 21 and were randomized to 0.24% Li2CO(3) chow or normal chow from PND 49 to 77.

259 nd APP/PS1 mice were fed with standard mouse chow or OLT1177-enriched chow for 3 mo.

260 PBNx rats did not show reduced chow or sucrose intake after Ex4 treatment, indicating t

261 C57Bl/6 J mice were fed chow or the GAN diet rich in saturated fat (40%), fructo

262 out and wild-type mice were fed either mouse chow or WD for 16 weeks.

263 and C57BL/6J wild type (WT) mice were fed a chow or WD for 8 weeks.

264 -HDL cholesterol levels in F2 mice on either chow or Western diet.

265 Following 10 wk on a chow or Western-type diet (40% kcal fat), parameters of

266 c mice were randomized to high-fiber, normal chow, or zero-fiber diets, or SCFAs in drinking water.

267 ic CES2 causes liver steatosis and damage in chow- or Western diet-fed C57BL/6 mice.

268 Chow/Palatable rats displayed blunted d-Amphetamine-indu

269 Furthermore, DAT mRNA was increased in Chow/Palatable rats during the P Phase.

270 We found that Chow/Palatable rats had blunted DA efflux following d-Am

271 xtracellular baseline DA and DAT function in Chow/Palatable rats.

272 7 days a week, while the experimental group (Chow/Palatable) is provided chow for 5 days a week ("C P

273 : Intravenously cannulated ICR mice received chow, PN, or PN + BBS injections for 5 days.

274 dy weight and glucose tolerance on a regular chow (RC) diet.

275 treatments consisting of either pure rodent chow, rodent chow mixed to yield a content of either 20%

276 We used Chow's test to confirm significant changes in expenditur

277 aving effect than those paired with standard chow (SC) pellets.

278 e compared with mice fed standard fiber-rich chow (SC).

279 d to mice fed a low-fat, high-fiber standard chow (SD) (100%).

280 In adult mice fed normal chow, skeletal muscle expression of insulin receptor bet

281 After surgery, animals were fed either a chow (standard) diet or a high-fat diet (HFD), and gluco

282 ed normal chow, a high-fiber diet, or normal chow supplemented with sodium acetate.

283 nd structural breakpoints were determined by Chow test.

284 Feeding chow that contains 5-HTP slow release (5-HTP SR) to TPH2

285 d by feeding rats a novel ketone ester diet: chow that is supplemented with (R)-3-hydroxybutyl (R)-3-

286 s were administered high fat diet or regular chow throughout 3 weeks gestation.

287 Offspring were fed regular chow throughout their life and tested for spatial learni

288 that inhalation exposure of mice fed normal chow to concentrated ambient PM2.5 repressed hepatic tra

289 , a finding confirmed by feeding Neu5Gc-rich chow to human-like Neu5Gc-deficient mice.

290 s, followed by a period of 2 weeks on normal chow to induce the formation of lesion foci in the foreb

291 n weeks followed by additional five weeks of chow, to identify HFD-mediated changes to the hepatic tr

292 WT) and Gipr(-/-) offspring received control chow until 25 weeks of age followed by 20 weeks of HFD.

293 In vivo, apigenin treatment mixed with chow was administered prenatally to the dams and fed to

294 The new chow was enriched in PPi, which increased plasma PPi, an

295 f hepatic steatosis in L-Them2(-/-) mice fed chow was explained by compensatory increases in rates of

296 oice condition where a low-value reward (lab chow) was freely available as an alternative to pressing

297 iang YB, Hosgood HD III, Ji BT, Hu W, Wen C, Chow WH, Cai Q, Yang G, Gao YT, Zheng W, Lan Q.

298 ed sated mice to pick up pellets of standard chow with latencies that varied based on stimulation int

299 d mesolimbic DA after alternating a standard chow with palatable diet, a model of compulsive eating.

300 We compared the effects of feeding chow, with or without 5-HTP SR, to mice with the TPH2-R4