ライフサイエンスコーパス: fatty acid oxidation

1 reas OXPHOS(low) BAP1 mutant UM cells employ fatty acid oxidation.

2 ignaling-dependent switch from glycolysis to fatty acid oxidation.

3 activate expression of the genes involved in fatty acid oxidation.

4 During fasting, the KO mice had a defect in fatty acid oxidation.

5 genes and downregulation of genes related to fatty acid oxidation.

6 e CoA in these animals, indicating increased fatty acid oxidation.

7 which produced interleukin-23 and increased fatty acid oxidation.

8 active oxygen species generated by increased fatty acid oxidation.

9 ype consisting of a reduction of glucose and fatty acid oxidation.

10 ings suggestive of a defect in mitochondrial fatty acid oxidation.

11 energetic lipid substrate for mitochondrial fatty acid oxidation.

12 f hepatic fatty acid synthesis and increased fatty acid oxidation.

13 a ubiquitously expressed enzyme involved in fatty acid oxidation.

14 supercomplex formation and elevated hepatic fatty acid oxidation.

15 ion of genes associated with lipogenesis and fatty acid oxidation.

16 can be uncoupled from the systemic effect on fatty acid oxidation.

17 vity in type 2 diabetes in part by promoting fatty acid oxidation.

18 ased expression of hepatic genes involved in fatty acid oxidation.

19 acid transport, resulting in a reduction of fatty acid oxidation.

20 ha, a PGC-1alpha binding partner, to promote fatty acid oxidation.

21 n deacetylates and dimerizes CPT2 to enhance fatty acid oxidation.

22 7 induction accelerates PPARalpha-stimulated fatty acid oxidation.

23 lls, enhanced glycolysis, and suppression of fatty acid oxidation.

24 l role for Nox4 in the regulation of cardiac fatty acid oxidation.

25 ested a potential beneficial effect on liver fatty acid oxidation.

26 ue in part by induction of thermogenesis and fatty acid oxidation.

27 a switch in energy metabolism-glycolysis to fatty acid oxidation.

28 g hepatic lipid infiltration through reduced fatty acid oxidation.

29 for lung injury in humans with dysfunctional fatty acid oxidation.

30 on of hormone-sensitive lipase and increased fatty acid oxidation.

31 d in cholesterol efflux, HDL biogenesis, and fatty acid oxidation.

32 toyltransferase-1B (CPT-1B), a key enzyme in fatty acid oxidation.

33 r TG lipolysis, and subsequent mitochondrial fatty acid oxidation.

34 he activation of energy-sensing pathways for fatty acid oxidation.

35 pathways: glucose oxidation, glycolysis, and fatty acid oxidation.

36 gy need is covered mostly from mitochondrial fatty acid oxidation.

37 ine acylation on several enzymes involved in fatty acid oxidation.

38 enriched in C18:1 fatty acid, and increases fatty acid oxidation.

39 d in potentiating mitochondrial function and fatty acid oxidation.

40 as fuel source but increased utilisation of fatty acid oxidation.

41 ely reduces acyl-CoA synthetase activity and fatty acid oxidation.

42 T1A, a rate-limiting enzyme of mitochondrial fatty acid oxidation.

43 peroxisomes, the two organelles that mediate fatty acid oxidation.

44 acids, and other byproducts of lipolysis and fatty acid oxidation.

45 current decrease in PPARalpha expression and fatty acid oxidation.

46 romote the brown fat thermogenic program and fatty acid oxidation, 2) stimulate uncoupling protein 1

47 resulting in glycolytic rates 30% lower, and fatty acid oxidation 36% higher, in hypoxic diabetic hea

48 nes Cpt1, Pparalpha and Pgc1alpha related to fatty acid oxidation; (5) increased hepatic total choles

49 te and FBA improved respiratory capacity and fatty acid oxidation, activated the AMPK-acetyl-CoA carb

50 Fatty acid oxidation activity and tricarboxylic acid (TC

51 valuated whether the loss of ACAD9 enzymatic fatty acid oxidation affects clinical severity in patien

52 in powdered infant milks and to evaluate the fatty acid oxidation after package opening.

53 ting autophagy-mediated lipid degradation or fatty acid oxidation alone was sufficient to cause defec

54 knockout in HEK293 cells affected long-chain fatty acid oxidation along with Cl, both of which were r

55 ells led to a marked increase of endothelial fatty acid oxidation, an increase of reactive oxygen spe

56 c respiration, driving cells to rely more on fatty acid oxidation, anaerobic respiration and fermenta

57 1.3+/-6.7% and 32.5+/-10.9% increase in free fatty acid oxidation and a 31.3+/-9.2% and 41.4+/-8.9% d

58 osphor-defective S164A-SIRT1 mutant promoted fatty acid oxidation and ameliorated liver steatosis and

59 and releases fumarate in a manner involving fatty acid oxidation and ATP-citrate lyase activity.

60 lained by compensatory increases in rates of fatty acid oxidation and by decreased de novo lipogenesi

61 xis mediated promotion of DNL, inhibition of fatty acid oxidation and cholesterol metabolism.

62 Furthermore, avocatin B inhibited fatty acid oxidation and decreased NADPH levels, resulti

63 uced autophagy in the liver while increasing fatty acid oxidation and decreasing lipogenesis in G6pc-

64 This switch disinhibited muscle fatty acid oxidation and drove Cori Cycling that contrib

65 they can switch between the active states of fatty acid oxidation and energy dissipation versus a mor

66 as partly mediated by increased hepatic beta-fatty acid oxidation and energy expenditure.

67 tly enhanced respiratory capacity, increased fatty acid oxidation and enhanced mitochondrial biogenes

68 to control key nutrient pathways, including fatty acid oxidation and gluconeogenesis in the fasted s

69 IRT5KO mice, including apparent decreases in fatty acid oxidation and glucose oxidation as well as an

70 which results in a compensatory increase in fatty acid oxidation and glycolysis.

71 function by decreased lipogenesis, increased fatty acid oxidation and improved insulin signaling.

72 d mitochondrial import, while downregulating fatty acid oxidation and inhibiting ATP5A (ATP synthase

73 ult, gain of hepatic CES2 function increases fatty acid oxidation and inhibits lipogenesis, whereas l

74 expression contribute to the coordination of fatty acid oxidation and insulin action in the fasting-r

75 ke the liver, expresses enzymes required for fatty acid oxidation and ketogenesis.

76 ange ratio, and increased gene expression of fatty acid oxidation and ketogenic pathways.

77 enes and overcomes defective fasting-induced fatty acid oxidation and lipid accumulation.

78 patic transcriptional regulators involved in fatty acid oxidation and lipolysis, and thus promoted he

79 tic studies reveal that uncoupling increases fatty acid oxidation and membrane phospholipid catabolis

80 gy substrates for the kidney, and defects in fatty acid oxidation and mitochondrial dysfunction are u

81 in response to high fat feeding, the rate of fatty acid oxidation and mitochondrial protein acetylati

82 gramming that preserves glycogen in favor of fatty acid oxidation and mitochondrial respiration.

83 as associated with further declines in liver fatty acid oxidation and mitochondrial respiratory capac

84 L6 regulates a core set of genes involved in fatty acid oxidation and mitochondrial uncoupling, which

85 ng sepsis and heart failure leads to reduced fatty acid oxidation and myocardial energy deficiency.

86 most forms of heart failure lead to altered fatty acid oxidation and often also to the accumulation

87 hospholipids and free fatty acids to sustain fatty acid oxidation and oxidative phosphorylation.

88 me alternatively (or, M2) activated increase fatty acid oxidation and oxidative phosphorylation; thes

89 ial functions in lipid metabolism, including fatty acid oxidation and plasmalogen synthesis.

90 enhances the expression of genes involved in fatty acid oxidation and reduces survival in response to

91 Ketone bodies (KB) are products of fatty acid oxidation and serve as essential fuels during

92 on engenders a metabolic state that requires fatty acid oxidation and shunting of tricarboxylic acid

93 gy among ILC2s impaired their ability to use fatty acid oxidation and strikingly promoted glycolysis,

94 nce of cold exposure, GPAT4 limits excessive fatty acid oxidation and the detrimental induction of a

95 esuccinylase known to regulate mitochondrial fatty acid oxidation and the urea cycle.

96 dipose expression of genes for mitochondrial fatty acid oxidation and thermogenesis, and overall ener

97 l muscle, findings consistent with increased fatty acid oxidation and thermogenesis.

98 with metabolic processes (ATP synthesis and fatty acid oxidation) and lack methylation at specific b

99 ed to increased ketogenesis, reduced cardiac fatty acid oxidation, and diminished cardiac oxygen cons

100 Whole-body VO2, fatty acid oxidation, and endurance running capacity wer

101 m signaling pathways regulating lipogenesis, fatty acid oxidation, and glucose homeostasis.

102 de novo lipogenesis, decreased intrahepatic fatty acid oxidation, and inadequate increases in IHTG e

103 art, hypoxia decreased PPARalpha expression, fatty acid oxidation, and mitochondrial uncoupling prote

104 Inflammatory biomarkers, fatty acid oxidation, and oral anticoagulation were inde

105 alone enhanced oxidative muscle expression, fatty acid oxidation, and reduced insulin levels.

106 pecific genes involved in TAG hydrolysis and fatty acid oxidation, and that PA relieves AHL4-mediated

107 Fasting diverts metabolism to fatty acid oxidation, and the fasted response occurs muc

108 diet increased cardiac PPARalpha expression, fatty acid oxidation, and UCP3 levels with decreased gly

109 al beta-oxidation, have an increased rate of fatty acid oxidation, and undergo marked remodelling of

110 eas that of genes implicated in lipogenesis, fatty acid oxidation, and VLDL secretion was unaltered.

111 lmost exclusively dependent on mitochondrial fatty acid oxidation as a consequence of mitochondrial c

112 function of TAMs and suggests targeting TAM fatty acid oxidation as a potential therapeutic modality

113 bit increased TG lipolysis, TG turnover, and fatty acid oxidation as compared with controls.

114 changes were associated with reduced cardiac fatty acid oxidation, ATP levels, increased triglyceride

115 dative capacity of the cells and ameliorates fatty acid oxidation avoiding the lipotoxicity that resu

116 and in vivo metastasis assays, inhibition of fatty acid oxidation blocks AKR1B10(High)-enhanced metas

117 plays an important role in the regulation of fatty acid oxidation both in the fasted state and in mic

118 hat elevated serum bile acids reduce cardiac fatty acid oxidation both in vivo and ex vivo.

119 MiR-30c had no effect on fatty acid oxidation but reduced lipid synthesis.

120 ac hypertrophy is closely linked to impaired fatty acid oxidation, but the molecular basis of this li

121 and cells with BMPR2 mutation have impaired fatty acid oxidation, but whether these findings affect

122 d the proportion of respiration supported by fatty acid oxidation by 18% (P < 0.001).

123 injury with standard techniques and measured fatty acid oxidation by the catabolism of (14)C-labeled

124 The mechanism of omega-6 polyunsaturated fatty acid oxidation by wild-type cyclooxygenase 2 and t

125 (e.g., glycolysis, glutamine metabolism, and fatty acid oxidation) can regulate immune responses and

126 tabolic effects, particularly an increase in fatty acid oxidation, cannot be explained by decarboxyla

127 enzymatic ACAD activity is required for full fatty acid oxidation capacity in cells expressing high l

128 Fatty acid oxidation capacity is decreased and there may

129 ific ablation of LSD1 impaired mitochondrial fatty acid oxidation capacity of the brown adipose tissu

130 heart and skeletal muscle, nitrate increases fatty acid oxidation capacity, and in the latter case, t

131 obligate enzyme in mitochondrial long-chain fatty acid oxidation, carnitine palmitoyltransferase 2 (

132 FGF19 induced metabolic gene expression, fatty acid oxidation, cell growth, and proliferation in

133 phosphate pathway deregulation and impaired fatty acid oxidation collectively contribute to the redo

134 This coincided with higher peroxisomal fatty acid oxidation compared with mitochondria fatty ac

135 MNADK facilitates fatty acid oxidation, counteracts oxidative damage, main

136 sed beta-oxidation but diminished incomplete fatty acid oxidation, decreased fat but increased protei

137 marked hepatic mitochondrial dysfunction and fatty acid oxidation deficiency, along with significant

138 tionally, UV-HSV-1 stimulates glycolysis and fatty acid oxidation-dependent oxygen consumption in NK

139 sis-dependent acute inflammatory response to fatty acid oxidation-dependent sepsis adaptation.

140 alk, which involves shifting from glucose to fatty acid oxidation, derived from adipose tissue lipoly

141 vance to pathophysiological conditions (e.g. fatty acid oxidation disorders and cardiac ischemia) whe

142 n related with a variety of diseases, termed fatty acid oxidation disorders.

143 h its effects to promote gluconeogenesis and fatty acid oxidation) drives ketogenesis, and working in

144 IMP2-deficient muscle exhibits reduced fatty acid oxidation, due to a reduced abundance of mRNA

145 ents should aim at counteracting both CI and fatty acid oxidation dysfunctions.

146 Consistent with Hsp10-Hsp60 regulation of fatty acid oxidation enzyme integrity, medium-chain acyl

147 ed reduced lung function in mice lacking the fatty acid oxidation enzyme long-chain acyl-CoA dehydrog

148 60 chaperone complex mediates folding of the fatty acid oxidation enzyme medium-chain acyl-CoA dehydr

149 -CoA dehydrogenase (LCAD) is a mitochondrial fatty acid oxidation enzyme whose expression in humans i

150 rdiac acyl-CoA profile paralleled changes in fatty acid oxidation enzymes and acyl-CoA thioesterases,

151 Increasing expression of fatty acid oxidation enzymes at Wk-4 supported the switc

152 secretion in vivo and ex vivo and decreased fatty acid oxidation ex vivo Remarkably, the gene expres

153 expression of key enzymes and regulators of fatty acid oxidation (FAO) and higher intracellular lipi

154 d that p16 modulates fasting-induced hepatic fatty acid oxidation (FAO) and lipid droplet accumulatio

155 llular metabolism characterized by increased fatty acid oxidation (FAO) and oxidative phosphorylation

156 sociation with reduced hepatic mitochondrial fatty acid oxidation (FAO) and respiratory capacity comp

157 Mitochondrial fatty acid oxidation (FAO) contributes to the proton mot

158 hagy-deficient cells to be more dependent on fatty acid oxidation (FAO) for energy production, leadin

159 Increased fatty acid oxidation (FAO) has long been considered a cu

160 phenotype, knowledge of pathways that drive fatty acid oxidation (FAO) in cancer is limited.

161 howed that PRDM16 transcriptionally controls fatty acid oxidation (FAO) in crypts.

162 ntial use of glucose to the up-regulation of fatty acid oxidation (FAO) in myeloid cells, including m

163 in this process through directly activating fatty acid oxidation (FAO) in the ground-state ESCs.

164 ) inhibitor diphenyleneiodonium (DPI), and a fatty acid oxidation (FAO) inhibitor perhexiline (PER).

165 sue of Blood, Ricciardi et al report a novel fatty acid oxidation (FAO) inhibitor, ST1326, that effec

166 receptor CD36, accumulated lipids, and used fatty acid oxidation (FAO) instead of glycolysis for ene

167 argeted metabolomics approach, we identified fatty acid oxidation (FAO) intermediates as being dramat

168 Fatty acid oxidation (FAO) is a key bioenergetic pathway

169 etic organ: lymph gland, we demonstrate that Fatty Acid Oxidation (FAO) is essential for the differen

170 We also show that fatty acid oxidation (FAO) is specifically induced by AM

171 Recent observations demonstrated that the fatty acid oxidation (FAO) pathway may represent an alte

172 erent expression of proteins involved in the fatty acid oxidation (FAO) pathway, and FAO activity was

173 , which is a key mitochondrial enzyme in the fatty acid oxidation (FAO) pathway.

174 and progressive repression of mitochondrial fatty acid oxidation (FAO) pathways.

175 lism involving oxidative phosphorylation and fatty acid oxidation (FAO) with substantial accumulation

176 these vesicles carry proteins implicated in fatty acid oxidation (FAO), a feature highly specific to

177 een intramyocellular lipid (IMCL), decreased fatty acid oxidation (FAO), and insulin resistance have

178 ial loss of CPT1A, a rate-limiting enzyme of fatty acid oxidation (FAO), causes vascular sprouting de

179 phosphorylation (OXPHOS) driven by elevated fatty acid oxidation (FAO), rendering GBM cells dependen

180 VEGF-A promoted glycolysis at the expense of fatty acid oxidation (FAO), whereas GW0742 reduced both

181 alterations in lipid transport and impaired fatty acid oxidation (FAO), which is exacerbated by a hi

182 roduction in MCF-7 cells appeared to involve fatty acid oxidation (FAO)-dependent mitochondrial metab

183 ch has recently been linked to high rates of fatty acid oxidation (FAO).

184 scued by Vitamin E through the activation of fatty acid oxidation (FAO).

185 T (TM) cells engage catabolic pathways, like fatty acid oxidation (FAO).

186 reduced mitochondrial oxidative capacity and fatty acid oxidation (FAO).

187 r sarcolipin, with an associated increase in fatty acid oxidation (FAO).

188 tumor cells undergo a metabolic shift toward fatty acid oxidation (FAO).

189 abolism away from aerobic glycolysis towards fatty acid oxidation (FAO).

190 enesis to concomitantly drive high levels of fatty-acid oxidation (FAO) and glycolysis and, consequen

191 colytic while Tconv cells used predominantly fatty-acid oxidation (FAO).

192 hypertriglyceridemia, and increased hepatic fatty acid oxidation; FAO), and extends lifespan by at l

193 ve redox signaling when 2-oxo-isocaproate or fatty acid oxidation formed superoxides through electron

194 CP1) in brown and beige adipocytes uncouples fatty acid oxidation from ATP generation in mitochondria

195 5C associate with high angiogenesis and AMPK/fatty acid oxidation gene expression, while CDKN2A/B and

196 ce, concomitant with increased expression of fatty acid oxidation genes and decreased Pparg expressio

197 ch1 signaling can regulate the expression of fatty acid oxidation genes and may provide therapeutic s

198 O mice fed an HFD, and the expression of key fatty acid oxidation genes was increased.

199 synthesis genes, and increased expression of fatty acid oxidation genes.

200 o rescue the bile acid-mediated reduction in fatty acid oxidation genes.

201 Expression levels of fatty acid oxidation, glucose metabolism, atrophy genes,

202 olism genes and increases direct measures of fatty acid oxidation, glucose oxidation and metabolic fl

203 and Nqo1, without changes in key enzymes for fatty acid oxidation, glucose utilization, or gluconeoge

204 The dysregulation of fatty acid oxidation has been related with a variety of

205 Defects in skeletal muscle fatty acid oxidation have been implicated in the etiolog

206 hondrial reactive oxygen species and promote fatty acid oxidation; however, the global impact of UCP3

207 ondrial mass, oxidative phosphorylation, and fatty acid oxidation; (ii) survival capacity; and (iii)

208 methanogenesis linked to short-chain alkane/fatty acid oxidation in a previously undescribed class o

209 Activation of PPARdelta stimulates fatty acid oxidation in adipose tissue and skeletal musc

210 and raise the possibility that inhibition of fatty acid oxidation in beta-cells is beneficial to diab

211 1-target genes involved in thermogenesis and fatty acid oxidation in brown fat.

212 Arkaitz has investigated the regulation of fatty acid oxidation in cancer cells and how these chang

213 Here we show that excess bile acids decrease fatty acid oxidation in cardiomyocytes and can cause hea

214 hat Cd evidently inhibited the mitochondrial fatty acid oxidation in hepatocytes and that SIRT1 signa

215 18, in regulating the expression of genes in fatty acid oxidation in humanized livers through its int

216 These mice also consistently showed elevated fatty acid oxidation in isolated skeletal muscle, wherea

217 GAT lipolysis fuels fatty acid oxidation in LSCs, especially within a subpop

218 fects of oxidative stress thereby sustaining fatty acid oxidation in metabolically challenging metast

219 BACKGROUND & AIMS: Inefficient fatty acid oxidation in mitochondria and increased oxida

220 Inefficient fatty acid oxidation in mitochondria and increased oxida

221 promotes anaerobic glycolysis and represses fatty acid oxidation in mouse embryonic fibroblasts (MEF

222 (AMPK) pathway mediates leptin's effects on fatty acid oxidation in muscle and also plays a role in

223 A preference for fatty acid oxidation in Nox4 hearts correlated with a be

224 gluconeogenesis, glycerolipid synthesis, and fatty acid oxidation in pancreatic islet beta-cells and

225 We measured rates of fatty acid oxidation in primary hepatocytes using radiol

226 balance of mitochondrial versus peroxisomal fatty acid oxidation in proximal tubular epithelial cell

227 on of genes associated with mitochondria and fatty acid oxidation in RYR1 mutants when compared with

228 s, Sherpas demonstrated a lower capacity for fatty acid oxidation in skeletal muscle biopsies, along

229 transcription factors and enzymes related to fatty acid oxidation in the heart were profoundly down-r

230 if nervonic acid alters markers of impaired fatty acid oxidation in the liver.

231 ty acid oxidation compared with mitochondria fatty acid oxidation in the Sirt5(-/-) proximal tubular

232 ed signaling and enhanced glucose uptake and fatty acid oxidation in vitro, which were augmented or a

233 the highly-tuned balance between glucose and fatty-acid oxidation in the two cell types.

234 glucose-fatty acid cycle in which increased fatty acid oxidation increases acetyl-CoA concentrations

235 nt in phenolic compounds and with the lowest fatty acids oxidation index.

236 suggest that a shift away from mitochondrial fatty acid oxidation initiates deleterious hypertrophic

237 so noted marked improvement in mitochondrial fatty acid oxidation, insulin sensitivity, dyslipidemia

238 of 237 DEGs involved in glucose metabolism, fatty acid oxidation, ion channels, exocytosis, homeosta

239 These results suggest that fatty acid oxidation is critical for normal skeletal mus

240 We also provide evidence that fatty acid oxidation is negatively regulated by miR-29 o

241 Fatty acid oxidation is transcriptionally regulated by p

242 ata suggest that ECHA, a protein involved in fatty acid oxidation, is a major enzyme that is regulate

243 Pathway analysis indicated downshifting of fatty acid oxidation, ketone body production and breakdo

244 rated the Maillard reaction, and alcohol and fatty acid oxidation, leading to wines with a volatile c

245 d that mitochondrial dysfunction and reduced fatty acid oxidation likely leads to the accumulation of

246 in MCSFA-HFD, accompanied by increased basal fatty acid oxidation, maintained glucose metabolic flexi

247 GRP78 control of fatty acid oxidation may represent a new homeostatic fun

248 Lower efficiency of mitochondrial fatty acid oxidation may represent a potential target in

249 Enhancing fatty acid oxidation might have an adaptive role in the

250 overexpression in chow-fed mice compromises fatty acid oxidation, mitochondrial respiration, and the

251 However, the effects of decreased fatty acid oxidation on skeletal muscle function, histol

252 de novo lipogenesis, decreased hepatic free fatty acid oxidation, or decreased very-low-density lipo

253 inhibition of pyruvate dehydrogenase kinase, fatty acid oxidation, or glutaminolysis.

254 s ER stress-induced inhibition on lipolysis, fatty acid oxidation, oxidative metabolism, and thermoge

255 Pathway analyses revealed an increase in fatty acid oxidation ( P = 3 x 10-04) but also triglycer

256 hway for IL-10 production, shifting from the fatty acid oxidation pathway conventionally utilized for

257 (peroxisome proliferator-activated receptor)-fatty acid oxidation pathway promotes expansion of Tie2(

258 BF infants had higher levels of fatty acid oxidation products (preference for fat metabo

259 Infants consuming EF had higher levels of fatty acid oxidation products compared to infants consum

260 cids triggered an accumulation of incomplete fatty acid oxidation products in skeletal muscle.

261 Tgr5(-/-) mice had increased hepatic fatty acid oxidation rate and decreased hepatic fatty ac

262 triglyceride levels as well as an increased fatty acid oxidation rate and greater mitochondrial enzy

263 te efflux and glycogen content and decreased fatty acid oxidation rates, with similar activation of H

264 in the rat stomach, indicated by compromised fatty acid oxidation, reduced complex I- associated elec

265 UCP3 activity affects metabolism well beyond fatty acid oxidation, regulating biochemical pathways as

266 model where the inhibition of mitochondrial fatty acid oxidation results in accumulation of lipid me

267 ns involved in oxidative phosphorylation and fatty acid oxidation, such as cytochrome c, medium-chain

268 pids and lipid storage, coupled to augmented fatty acid oxidation that sustains both ATP levels and R

269 sed fatty acid uptake and storage, decreased fatty acid oxidation that was associated with reduced co

270 s, to suppress oxidative phosphorylation and fatty acid oxidation, thereby attenuating energy expendi

271 event attenuates MCAD activity and inhibits fatty acid oxidation, thereby leading to the accumulatio

272 ndrial biogenesis and enhanced mitochondrial fatty acid oxidation, thereby preventing diet-induced ob

273 modest diet-induced fatty liver by impairing fatty acid oxidation through increased degradation of th

274 rt1/mTORC2/Akt pathway, whereas it increases fatty acid oxidation through LKB1/AMPK signaling.

275 tochondrial oxidative capacity programme and fatty acid oxidation through the AMPK/PGC1-alpha pathway

276 ich activates both amino acid metabolism and fatty acid oxidation to drive OXPHOS, thereby providing

277 tem cells experience a metabolic switch from fatty acid oxidation to glycolysis.

278 nvolved in autophagy, lysosomal function and fatty acid oxidation to support bacterial replication.

279 de novo fatty-acid synthesis and concurrent fatty-acid oxidation to generate ATP for cell survival.

280 bition of both oxidative phosphorylation and fatty acid oxidation using HK2 shRNA and small-molecule

281 D2 plays a dominant albeit indirect role in fatty acid oxidation via its sympathetic control of BAT

282 Mechanistically, Fas impairs fatty acid oxidation via the BH3 interacting-domain deat

283 ssion and acylcarnintine flux suggested that fatty acid oxidation was increased and fatty acid syntha

284 However, de novo lipogenesis was higher and fatty acid oxidation was lower in HI individuals compare

285 This switch away from fatty acid oxidation was reversed by nitrate treatment i

286 f fatty acid oxidative genes and the rate of fatty acid oxidation were also increased by inhibition o

287 Alterations to cardiac fatty acid oxidation were explored in primary cardiomyoc

288 Glycolysis and fatty acid oxidation were identified as the most enriche

289 We found that oxygen consumption and fatty acid oxidation were increased markedly in Sln(OE)

290 nance spectroscopy (MRS), and glycolysis and fatty acid oxidation were measured using [(3)H] labeling

291 pathways such as Sertoli cell signaling and fatty acid oxidation were specifically enriched in BA19

292 Mitochondrial oxygen consumption and fatty-acid oxidation were unaltered in primary HNKO hepa

293 sion of genes involved in TAG hydrolysis and fatty acid oxidation, whereas the opposite was observed

294 pressed, ACAD9 plays a physiological role in fatty acid oxidation, which contributes to the severity

295 ex III activities, suggesting an increase in fatty acid oxidation, which is supported by an increase

296 ondrial function but significantly increased fatty acid oxidation, which was localized to the peroxis

297 PPARalpha activation induces fatty acid oxidation, while FXR controls bile acid homeo

298 t of obesity by increasing thermogenesis and fatty acid oxidation, while inhibition of hormone-sensit

299 auses the most common inherited disorders of fatty acid oxidation, with syndromes that are exacerbate

300 n and enhancing mitochondrial biogenesis and fatty acid oxidation, without affecting T cell receptor-