ライフサイエンスコーパス: HFD

1 HFD causes steatosis, and both SAP and 1866 reduced it.

2 HFD disrupted the intestinal Mmp7/alpha-defensin axis, w

3 HFD feeding of CysC-deficient (CysC knockout [KO]) mice

4 HFD induced increased body weight gain, circulating leve

5 HFD mice displayed an increase in colonic IL-1beta and M

6 HFD treatment of control mice induced release of L13a fr

7 HFD worsened glucose tolerance test results and caused i

8 HFD-fed control and LIMP2 KO mice maintained a similar g

9 HFD-fed mice had increased circulating thrombomodulin, a

10 HFD-fed mice with depletion of the gamma1 subunit are re

11 HFD-fed rats exhibited prediabetes, cognitive decline, a

12 HFD-induced obesity is characterized by a hyperactivatio

13 HFD-induced obesity potentiates food-induced allergic re

14 HFD-induces GSH deficiency and epigenetically alters VD-

15 About 60% HFD-fed mice were treated intragastrically with CO-EtOAc

16 signs of metabolic dysfunction following 60% HFD feeding for 20 weeks +/- NR supplementation and foun

17 ) HFD + CA (CA), (b) HFD + PA (PA), or (c) a HFD-control group.

18 (~50% vs. saline) diet and young mice fed a HFD (~30%).

19 r 8 weeks to induce obesity and, then, fed a HFD during pregnancy and lactation with or without MFGM-

20 Female SD rats were fed a HFD for 8 weeks to induce obesity and, then, fed a HFD d

21 re weaned at postnatal Day 21 and then fed a HFD for 9 weeks.

22 was significantly increased in WT mice fed a HFD, but remained unchanged in GCN5L1 cKO mice relative

23 itochondrial protein acetylation following a HFD relative to wildtype (WT) mice.

24 aled that the most reproducible signals of a HFD are Lactococcus species, which we experimentally dem

25 was increased in WT (but not cKO mice) on a HFD.

26 t diet (LFD, 10% kcal), HFD (45% kcal), or a HFD administered with 0.5 g/kg bodyweight of 4-phenyl bu

27 In contrast, nSIRT1OE prevented a HFD-induced neuropathy despite the animals remaining hyp

28 increased GCN5L1 expression in response to a HFD promotes increased lysine acetylation, and that this

29 in ex vivo cardiac workload in response to a HFD.

30 ases hypothalamic inflammation, similar to a HFD.

31 exposure was lower than that observed with a HFD, the degree of alteration in chromatin accessibility

32 HFD-fed mice were treated 12 weeks with (a) HFD + CA (CA), (b) HFD + PA (PA), or (c) a HFD-control g

33 at diet rich in polyunsaturated fatty acids (HFD-P) present a higher frequency of neutrophils in bone

34 high-fat diet rich in saturated fatty acids (HFD-S).

35 ominantly expressed in macrophages but after HFD feeding PU.1 expression is also significantly increa

36 exerted long-term beneficial effects against HFD-induced obesity in later life.

37 brown/beige adipogenesis and protect against HFD-induced adiposity in offspring.

38 In addition, we also observed that allergic HFD female mice presented a robust lung remodelling in c

39 An HFD-associated microbiome was transmissible to germ-free

40 During an HFD time course, progressive adipose tissue expansion an

41 ed with littermate controls, cKO mice fed an HFD (16 weeks) had reductions in MDC (mainly CD11c(+) ma

42 e downregulated in the livers of mice fed an HFD (GSH- deficient) compared with control diet-fed grou

43 Our data showed that YAP( KO) mice fed an HFD exhibited lower serum alanine aminotransferase (ALT)

44 (TLR4; TLR4( KO) ), and animals were fed an HFD or treated with lipopolysaccharide (LPS).

45 no obvious phenotype, NNMT(-/-) males fed an HFD showed strongly improved insulin sensitivity (IS).

46 e results strongly suggest consumption of an HFD results in vascular changes in placenta reflected by

47 allergy and uncouple a pathogenic role of an HFD-associated microbiome from obesity.

48 Mice on an HFD had elevated serum levels of IL-1beta, IL-23, interf

49 This report shows that for mice on an HFD, injections of the sialidase inhibitor N-acetyl-2,3-

50 sed increased adipocyte size; for mice on an HFD, SAP improved glucose tolerance test results and red

51 is; and these effects were exacerbated on an HFD.

52 When stressed with an HFD, myonectin-knockout male mice had significantly elev

53 ND-fed rats were given a vehicle (n = 8) and HFD-fed rats were randomly assigned into three subgroups

54 s taxonomic redistribution under both CD and HFD conditions.

55 Surprisingly, however, in both chow and HFD-fed mice, insulin-stimulated Akt phosphorylation is

56 Both HFD female and HFD male mice treated with oestradiol also displayed str

57 The effects of fenugreek and HFD on gut microbiota were comprehensively mapped and th

58 ssels, reverted cerebral vasoreactivity, and HFD-induced effects in microstructural gray and white ma

59 As previously reported, fenugreek attenuated HFD-induced hyperlipidemia and stabilized glucose tolera

60 treated 12 weeks with (a) HFD + CA (CA), (b) HFD + PA (PA), or (c) a HFD-control group.

61 Both HFD female and HFD male mice treated with oestradiol als

62 quency power, low-frequency power), and both HFD groups had higher sympathovagal balance (SD of all p

63 When metabolic stress was induced by HFD, beta cells in control mice with intact Akt1 prolife

64 to external stressors, an effect mimicked by HFD feeding.

65 lized parkin was severely reduced in control HFD-fed mouse heart, which was restored, in part, in ACC

66 ine with multiple targets, ameliorated CXCL1/HFD-induced NASH or methionine-choline deficient diet-in

67 associated with high-fat high-caloric diet (HFD) feeding, ageing and obesity; however, the neural ba

68 hat in comparison with males, high-fat diet (HFD) allergic female mice exhibit a reduction in the num

69 ted in the mechanism by which high fat diet (HFD) and saturated fatty acids (SFA) modulate fundamenta

70 ups fed either a control or a high-fat diet (HFD) and then the mice on each diet were further divided

71 the effects of a prototypical high-fat diet (HFD) as well as cessation of exposure on phenotype rever

72 Mice fed a high-fat diet (HFD) become obese and develop osteoarthritis (OA)-like l

73 udies showed that 12 weeks of high-fat diet (HFD) consumption caused not only prediabetes but also co

74 that feeding maternal mice a high-fat diet (HFD) during lactation attenuated the activity of dopamin

75 in offspring of mothers on a high-fat diet (HFD) during pregnancy.

76 e prostate cancer model, that high-fat diet (HFD) enhances the MYC transcriptional program through me

77 macological intervention in a high-fat diet (HFD) fed mouse model, capable of recapitulating key aspe

78 Here, we showed that maternal high-fat diet (HFD) feeding during lactation in mice elicits long-lasti

79 C2 iKO mice were subjected to high-fat diet (HFD) feeding for 24 weeks to induce obesity.

80 In response to high fat diet (HFD) feeding for 6 or 18 weeks, WT and AIF1L deficient m

81 High-fat diet (HFD) feeding further exacerbates the K2KO metabolic dise

82 e intolerance after long-term high-fat diet (HFD) feeding.

83 (KO) were fed with high (60% kcal) fat diet (HFD) for 16 weeks.

84 We have previously shown that high fat diet (HFD) for 2 weeks increases airway hyperresponsiveness (A

85 e fed a normal chow (NC) or a high fat diet (HFD) for 5 weeks before mating, then also during the ges

86 in resistance with short-term high-fat diet (HFD) in young mice.

87 As high-fat diet (HFD) is a potent inducer of gut dysbiosis, we investigat

88 , we analyzed the impact of a high-fat diet (HFD) on Abcc8 knockout mice.

89 we explored the effects of a high-fat diet (HFD) on energy balance, gut microbiota, and risk factors

90 The influence of maternal high-fat diet (HFD) on metabolic response to ozone was examined in Long

91 However, mice fed a high-fat diet (HFD) only develop fatty liver without significant neutro

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

93 (MFGM-PL) supplementation to high-fat diet (HFD) rats during pregnancy and lactation could promote b

94 We demonstrate that a high-fat diet (HFD) reproducibly changes gut microbial community struct

95 Chronic high-fat diet (HFD) results in the accumulation of a monocyte-derived C

96 diet, plasmas from mice fed a high-fat diet (HFD) showed delayed PG and reduced PG velocity.

97 gm, we found that exposure to high-fat diet (HFD) suppresses the intake of nutritionally balanced sta

98 heterozygote (lean) mice fed high-fat diet (HFD) that received either 17beta-Estradiol (E2) or vehic

99 ce received 16 weeks either a high-fat diet (HFD) to induce obesity, or chow as reference group.

100 tribution in adult mice fed a high-fat diet (HFD) were examined.

101 ed in NT(+/+) mice fed with a high-fat diet (HFD) which were improved in NT-deficient mice.

102 ous study demonstrated that a high-fat diet (HFD), administered for one-three-days, induces hypothala

103 Obesity was induced by high-fat diet (HFD), and blood pressure (BP) was measured by radiotelem

104 When challenged with high-fat diet (HFD), IRMOE mice are protected from diet-induced obesity

105 Under an obesogenic high-fat diet (HFD), male offspring of exercised C57BL/6J-mouse dams we

106 tandard chow diet, short-term high-fat diet (HFD), or long-term HFD.

107 When mice were fed a high-fat diet (HFD), we found that fatty liver and dyslipidemia are pro

108 hesis that Nod2 protects from high fat diet (HFD)-dependent hepatic cancer.

109 aspects of atherosclerosis in high-fat diet (HFD)-fed L13a KO and intact (control) mice.

110 Furthermore, high-fat diet (HFD)-fed mice exhibit the downregulation of FABP5 and ST

111 rs in obese individuals or in high-fat diet (HFD)-fed mice.

112 tomy [UniNx]) in mice reduced high-fat diet (HFD)-induced adipose tissue inflammation, thereby improv

113 neurovascular dysfunction in high-fat diet (HFD)-induced cognitive impairment.

114 Normal diet (ND) and high-fat diet (HFD)-induced DM mice were randomized into control and SF

115 on factor A (TFAM) attenuates high-fat diet (HFD)-induced fat gain and IR in mice in conjunction with

116 High-fat diet (HFD)-induced inflammation and steatosis of adipose tissu

117 of evidence illustrating that high fat diet (HFD)-induced maternal obesity can regulate fetal bone de

118 TP synthesis, and aggravating high-fat diet (HFD)-induced NAFLD.

119 Here, we demonstrate that high-fat diet (HFD)-induced obesity impairs CD8(+) T cell function in t

120 functions in a mouse model of high-fat diet (HFD)-induced obesity.

121 ubfamily 1 (TRPV1) to counter high-fat diet (HFD)-induced obesity.

122 cemia, and liver steatosis in high-fat diet (HFD)-treated male mice.

123 MDCs of wild-type mice fed a high-fat diet (HFD).

124 her increases with fasting or high-fat diet (HFD).

125 n also found in rodents fed a high-fat diet (HFD).

126 n KCs of wild-type mice fed a high-fat diet (HFD).

127 n sensitivity when exposed to high-fat diet (HFD).

128 ring in response to a chronic high fat diet (HFD).

129 lic proteins in response to a high fat diet (HFD).

130 Wistar rats were fed either a high-fat diet (HFD; 35% fat) or a standard diet (3.5% fat) for 7 wk and

131 4; PCSK9-normal diet, n=6) or high-fat diet (HFD; WT-HFD, n=3; PCSK9-HFD, n=6).

132 We find that short-term high-fat-diet (HFD) feeding of mice activates prepronociceptin (PNOC)-e

133 ardiac dysfunction induced by high-fat-diet (HFD) persists for two subsequent generations in Drosophi

134 previous reports showed that high-fat-diet (HFD)-fed mice with liver-specific knockout of both AMPK

135 owed that AKT1 is involved in high-fat-diet (HFD)-induced growth and survival of beta cells but is un

136 obese mice (after 7 months of high-fat diet [HFD]) and age-matched controls.

137 ion (HFE) of the Cenp-T histone fold domain (HFD) combining with alpha-helix H3 of Cenp-K to create a

138 and 15.93+/-1.76 in atg7 cKO; P<0.05) during HFD feeding.

139 chanism for mitochondria in the heart during HFD consumption.

140 Microinjection of sperm tsRNAs from the F1-HFD male into normal zygotes reproduces obesogenic pheno

141 e were fed control/low fat (CD) or high fat (HFD) diets each supplemented with or without 2% (w/w) fe

142 ong with TCA cycle intermediates in females (HFD > CD).

143 f fatty acid-supported respiration following HFD.

144 ted that MGL-KO mice had less preference for HFD over normal chow diet.

145 ed insulin secretion response of islets from HFD-fed beta cell-specific Galpha(z)-null mice is signif

146 transcriptomics analyses reveal islets from HFD-fed Galpha(z) KO mice have a dramatically altered ge

147 cantly improved as compared with islets from HFD-fed WT controls, which, along with no impact of Galp

148 The protection of Galpha(z)-null mice from HFD-induced diabetes is beta-cell autonomous, as beta ce

149 xpression of myeloid KLF2 protects mice from HFD-induced obesity and insulin resistance.

150 Offspring from HFD dams had increased body fat and weight relative to C

151 ntiation of EOCCs to mature osteoblasts from HFD obese dams.

152 Atherosclerotic plaques from HFD-treated KO mice showed increased infiltration of M1

153 Nod2 and demonstrate that Nod2 protects from HFD-dependent liver malignancy and this protection is ac

154 Furthermore, HFD altered lipid metabolism and HDL oxidation and also

155 Furthermore, HFD suppressed mitophagy activity and caused damaged mit

156 opamine levels compared to early gestational HFD.

157 Late gestational HFD exposure leads to more prominent addictive-like beha

158 h several hypercaloric diets, including HFD, HFD supplemented with fructose, high trans-fat diet (HTF

159 branched-chain amino acids in the Glyco(Hi) HFD group.

160 However, HFD elevated plasma alanine aminotransferase and creatin

161 These findings identify HFD-induced microbial alterations as risk factors for ex

162 rt, which was restored, in part, in ACC2 iKO HFD-fed mice.

163 of CAP was observed at doses above 0.003% in HFD.

164 induced NASH and stress kinase activation in HFD-fed mice.

165 in and insulin, and increased adiponectin in HFD offspring.

166 rmalizing IgG sialylation were determined in HFD-fed mice administered the sialic acid precursor N-ac

167 achykininergic contractions were enhanced in HFD mice after 2 or 8 weeks, and they were blunted by FC

168 sed adipose tissue leptin mRNA expression in HFD-treated recipient mice.

169 eneficial effect of enhancing cardiac FAO in HFD-induced obesity is mediated, in part, by the mainten

170 In contrast, ex vivo cardiac function in HFD-fed WT mice dropped ~ 50% relative to low fat diet (

171 with obesity in humans and as shown here in HFD-fed mice.

172 atic insulin response was ~10-fold higher in HFD-fed Ad-GcR(-/-) mice.

173 ocytes rescues the effect of HuR knockout in HFD-induced NAFLD.

174 ulmonary CD11b(+) DCs were markedly lower in HFD-fed compared to CD-fed mice, which was associated in

175 amines, and metabolites of gut microbiota in HFD female offspring indicating gut microbiome alteratio

176 CXCL1 itself in the liver can induce NASH in HFD-fed mice and to test the therapeutic potential of IL

177 d hyperphosphorylated Tau and necroptosis in HFD-fed rats.

178 ast, hepatocyte-specific deletion of p38a in HFD-induced fatty liver where p38alpha activation is rel

179 and improved serum biochemical parameters in HFD-induced obese and insulin resistant mice.

180 s lead to altered fatty acid partitioning in HFD tumors, impairing CD8(+) T cell infiltration and fun

181 ntly increased cardiac lipid peroxidation in HFD-fed WT mice relative to GCN5L1 cKO animals under the

182 e collective impact of abnormal TG and PG in HFD-fed mice produced normal fibrin formation kinetics b

183 eomic analyses determined that delayed PG in HFD-fed mice was not due to altered levels of plasminoge

184 et shift toward a prothrombotic phenotype in HFD-fed mice.

185 -8 promoted steatosis-to-NASH progression in HFD-fed mice by inducing liver inflammation, injury, and

186 ne promotes steatosis-to-NASH progression in HFD-fed mice by inducing neutrophil infiltration, oxidat

187 nt to drive steatosis-to-NASH progression in HFD-fed mice through neutrophil-derived reactive oxygen

188 ment index, and adipose tissue remodeling in HFD rats.

189 esity, hyperglycemia, and liver steatosis in HFD-treated male mice.

190 s with several hypercaloric diets, including HFD, HFD supplemented with fructose, high trans-fat diet

191 ened cardiovascular risk in the SIV-infected HFD-receiving nonhuman primates.

192 data on the dose-response for CAP to inhibit HFD-induced obesity.

193 np-ANuc to the outer kinetochore through its HFD and N-terminal Ndc80-binding motif, respectively.

194 ice were fed a low-fat diet (LFD, 10% kcal), HFD (45% kcal), or a HFD administered with 0.5 g/kg body

195 nriched with saturated long-chain FAs (LCSFA-HFD), while the other group (n = 9) ingested a matched d

196 In LCSFA-HFD, whole-body insulin sensitivity and peripheral insul

197 In line, HFD-induced hepatic insulin resistance and impairment of

198 Male HFD-Hhip +/+ mice had more large islets in which insulin

199 Maternal HFD increased free fatty acids and decreased phospholipi

200 llectively, these data suggest that maternal HFD increases offspring susceptibility to metabolic alte

201 We tested our hypothesis that maternal HFD-induced inflammation contributes to metabolic diseas

202 These findings indicate that maternal HFD-induced obesity may be associated with decreasing fe

203 These impairments were prevented in MCSFA-HFD, accompanied by increased basal fatty acid oxidation

204 but with ~30 g (5E%) saturated MCFAs (MCSFA-HFD) in substitution for a corresponding fraction of the

205 light of these data, we designed a modified HFD in which BCAA dietary supply was reduced by half.

206 NAC treatment normalized HFD-induced maternal weight gain and oxidative stress, i

207 Next, obese HFD-fed mice were treated 12 weeks with (a) HFD + CA (CA

208 m fetuses at gestational day 18.5 (E18.5) of HFD-induced obese rat dams.

209 C administration resulted in amelioration of HFD-induced decidual vasculopathy independent of offspri

210 tabolic dysfunction caused by consumption of HFD.

211 ent with BAT thermogenesis in the context of HFD-induced obesity.

212 iency had no influence on the development of HFD-induced obesity and adipose tissue remodeling, where

213 The effect of HFD was more pronounced in female mice after VDR deletio

214 ut dysbiosis, we investigated the effects of HFD on bacterial flora in the small intestine and NSAID-

215 ecifically reversed the dysbiotic effects of HFD on numerous taxa in a manner tightly correlated with

216 re protected from the suppressive effects of HFD, a phenomenon associated with relatively increased c

217 and S100beta density in myenteric ganglia of HFD mice were increased at week 8, but not at week 1 or

218 min D (VD) metabolism genes in the livers of HFD-fed mice.

219 ties of food discovery even after periods of HFD abstinence.

220 White adipose tissue of HFD-fed Asxl2DeltaLysM mice also exhibited none of the p

221 e expression profiling of adipose tissues of HFD-fed UtxAKO female mice revealed decreased expression

222 Treatment of HFD-fed mice with verteporfin inhibited KC activation, r

223 clerosis formation (4, 8, 16 and 20 weeks of HFD).

224 s, ME may offer protection against offspring HFD-induced NAFLD by shaping hepatic proteomics signatur

225 /-) mice treated with DMBA and maintained on HFD gain significantly more weight and develop more live

226 ylbenz[a]anthracene (DMBA) and maintained on HFD.

227 Mice on HFD also showed higher percentage of chondrocyte death,

228 were acutely fed a standard breeding chow or HFD.

229 e fed control diet (CD; 10%kcal from fat) or HFD (60%kcal from fat) starting at post-natal day (PND)

230 h, along with no impact of Galpha(z) loss or HFD feeding on beta-cell proliferation or surrogates of

231 32) were fed with either normal diet (ND) or HFD for 20 weeks.

232 st hepatic steatosis caused by starvation or HFD due to induction of autophagic degradation of lipid

233 nd serum exosomes from elafin-overexpressing HFD-treated donor mice reduced food consumption and fat

234 Elafin-overexpressing HFD-treated male mice had increased serum leptin levels,

235 6) or high-fat diet (HFD; WT-HFD, n=3; PCSK9-HFD, n=6).

236 diet completion, hypercholesterolemic PCSK9-HFD had significantly (P<0.05 versus baseline) depressed

237 NF-alpha expression was upregulated in PCSK9-HFD, colocalized with nerve fibers, and correlated inver

238 Concurrent to impaired PG, HFD also enhanced thrombin generation (TG).

239 MFGM-PL+HFD offspring showed promoted thermogenic function in BA

240 FAO oxidation by deletion of ACC2 prevented HFD-induced cardiac dysfunction, pathological remodeling

241 nanoparticle-based siRNA delivery, prevented HFD-induced obesity.

242 Mechanistically, ACC2 iKO prevented HFD-induced downregulation of parkin.

243 Prior HFD consumption vastly diminished the capacity of SD to

244 The presumably protective HFD-induced hepatic expression of the metabolic regulato

245 lowered fasting insulin levels, and reduced HFD-induced liver macrovesicular steatosis, hypertrophy,

246 g the sialidase neuraminidase 3 have reduced HFD-induced adipose tissue and liver inflammation.

247 After stroke, we replaced HFD with standard diet for 8 weeks to mimic the poststro

248 Asxl2DeltaLysM mice resisted HFD-induced adipose tissue macrophage infiltration and i

249 Deficiency in BCAAs failed to reverse HFD-induced metabolic impairments while producing antide

250 hanced PGC1alpha and PPARbeta, and reversing HFD-induced GLUT4 and pAKT reductions.

251 PA and CA also reverted HFD-induced effects in functional connectivity between v

252 free animals were colonized with a signature HFD or lean microbiota for 8 weeks before induction of f

253 Similarly, HFD female mice express lower levels of EpCAM in lung ti

254 intained on normal diet while others started HFD later in life.

255 We also studied HFD male mice treated with oestradiol or vehicle.

256 rogenitors (FAPs) proliferate with long-term HFD feeding while giving rise to adipocytes and type I c

257 nduced a full spectrum of NAFLD in long-term HFD-fed mice including steatosis, inflammation, fibrosis

258 short-term high-fat diet (HFD), or long-term HFD.

259 Thus, short-term HFD feeding and associated metabolic alterations may hav

260 ANCE: These findings suggest that short-term HFD feeding attenuates the development of AHR, airway in

261 e C57BL/6JRJ mice were fed with a short-term HFD or chow diet (CD) for 12 weeks.

262 s from 1-year-old mice fed with a short-term HFD, impairing both Myc recruitment to cell cycle regula

263 T repeat domain of Cenp-IHead and C-terminal HFD of Cenp-T of the Cenp-HIKHead-TW sub-module interact

264 expression in lung tissue demonstrated that HFD female mice express lower levels of these regulatory

265 Our study demonstrated that HFD induces ER stress to promote chondrocyte death and s

266 Our results indicated that HFD-fed mice displayed impairment in the electrical acti

267 Analysis of fecal samples revealed that HFD-fed mice exhibited a reduction in fecal species rich

268 The HFD had a negative impact on SIV disease progression in

269 sues from dysplasias of L2-IL1B mice fed the HFD contained increased levels of cytokines that are pro

270 Immunostaining of joints from the HFD group showed increased expression of ER stress and a

271 attenuated liver injury and fibrosis in the HFD(+Cxcl1) -induced NASH model that is associated with

272 l-associated SIV DNA and RNA occurred in the HFD-receiving nonhuman primates, indicating a potential

273 y, hyperglycemia, and liver steatosis in the HFD-treated mice.

274 Administration of PBA alleviated all of the HFD-induced symptoms.

275 monstrate that the adipocyte responds to the HFD by adopting a fibroblast-like phenotype, characteriz

276 NT contributes to the HFD-induced disruption of gut microbiota composition and

277 Thus, HFD-induced microbial dysbiosis in small intestine cause

278 of neutralizing antibodies against IL-17A to HFD-fed mice reduced intestinal permeability and prevent

279 obesity or impaired glucose handling due to HFD, and advance understanding of this little-studied ge

280 n neurons, offspring from mothers exposed to HFD feeding exhibited a sexually dimorphic expression of

281 To mimic exposure to HFD, cultured EGCs were incubated with palmitate (PA) an

282 lencing of inflammatory genes in response to HFD as an endogenous defense against atherosclerosis in

283 /-0.018 in Parkin KO, P<0.05) in response to HFD feeding.

284 caused beta-cells to be more susceptible to HFD-induced impairment of glucose homeostasis, and these

285 MFGM-PL treatment to HFD dams decreased the body weight gain and WAT mass as

286 s SD devaluation and subsequent shift toward HFD consumption is encoded at the level of hypothalamic

287 besity; however, the neural basis underlying HFD effects on diurnal metabolism remains elusive.

288 promotes the activation of POMC neurons upon HFD exposure, reduces feeding, and protects from obesity

289 Thus, upon HFD feeding, Utx regulates lipid metabolism in adipose t

290 ing of mothers who consume a typical Western HFD.

291 However, the mechanism by which HFD/obesity induces chondrocyte apoptosis is not clearly

292 approaches, we demonstrate that, along with HFD, TCS induces hepatic steatosis and steatohepatitis j

293 a robust lung remodelling in comparison with HFD males, evidenced by higher deposition of collagen in

294 the development of obesity in mice fed with HFD and is also capable of stimulating glucose uptake.

295 C57BL/6J mice were fed with HFD or standard diet (SD) for 1, 2, or 8 weeks.

296 Tumor cells increase fat uptake with HFD, whereas tumor-infiltrating CD8(+) T cells do not.

297 were fed a well-defined high fat diet, with (HFD/ATI) or without (HFD) nutritionally irrelevant amoun

298 ed high fat diet, with (HFD/ATI) or without (HFD) nutritionally irrelevant amounts of ATI.

299 gene expression pattern as compared with WT HFD-fed mice, with entire gene pathways not only being m

300 -normal diet, n=6) or high-fat diet (HFD; WT-HFD, n=3; PCSK9-HFD, n=6).