ライフサイエンスコーパス: fatty acid oxidation

1 hways (i.e. the tricarboxylic acid cycle and fatty acid oxidation).

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

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

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

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

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

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

8 7 induction accelerates PPARalpha-stimulated fatty acid oxidation.

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

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

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

12 g hepatic lipid infiltration through reduced fatty acid oxidation.

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

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

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

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

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

18 tion, glutamine metabolism, Krebs cycle, and fatty acid oxidation.

19 mitochondrial energy transduction, including fatty acid oxidation.

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

21 n of malonyl-CoA, a metabolite that inhibits fatty acid oxidation.

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

23 rimetry consistent with increased whole-body fatty acid oxidation.

24 d levels of M2 markers and genes involved in fatty acid oxidation.

25 volved in processes such as lipid uptake and fatty acid oxidation.

26 e 1 and PGC-1alpha mRNA/proteins and hepatic fatty acid oxidation.

27 n in muscle of HFD-fed mice without changing fatty acid oxidation.

28 y seen in many cancers, but also glucose and fatty acid oxidation.

29 ormone that modulates glucose metabolism and fatty acid oxidation.

30 tes, and an inability of insulin to suppress fatty acid oxidation.

31 n at Lys-318/Lys-322 is a mode of regulating fatty acid oxidation.

32 ffecting hepatic triglyceride production and fatty acid oxidation.

33 ssociated with both inflammation and reduced fatty acid oxidation.

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

35 al for suppressing mitochondrial H2O2 during fatty acid oxidation.

36 transcriptional complex to modulate rates of fatty acid oxidation.

37 tty acid synthesis, lipolysis, or hepatocyte fatty acid oxidation.

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

39 nd plays a crucial role in the regulation of fatty acid oxidation.

40 itant with reduced LCAD activity and reduced fatty acid oxidation.

41 active oxygen species generated by increased fatty acid oxidation.

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

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

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

45 energetic lipid substrate for mitochondrial fatty acid oxidation.

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

47 a ubiquitously expressed enzyme involved in fatty acid oxidation.

48 supercomplex formation and elevated hepatic fatty acid oxidation.

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

50 a key regulator of mitochondrial long-chain fatty-acid oxidation.

51 n index of the VOO autoxidation state before fatty acids oxidation.

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

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

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

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

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

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

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

59 electron transport chain, citric acid cycle, fatty acid oxidation, amino acid synthesis and cellular

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

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

62 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

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

64 Despite a reduction in PPARalpha, fatty acid oxidation and associated genes were not decre

65 e found increased acetylation of proteins in fatty acid oxidation and branched-chain amino acid metab

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

67 d hepatic steatosis resulting from increased fatty acid oxidation and decreased lipogenesis.

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

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

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

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

72 KO mice also exhibited defective hepatic fatty acid oxidation and fasting ketogenesis.

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

74 epatocytes each exhibited decreased rates of fatty acid oxidation and gluconeogenesis.

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

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

77 In addition, hepatic fatty acid oxidation and hepatic insulin action were ass

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

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

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

81 ion of FGF21, which in turn promotes hepatic fatty acid oxidation and ketogenesis and ultimately lead

82 uced hepatic expression of genes involved in fatty acid oxidation and ketogenesis, and increased expr

83 tor-activated receptor alpha target genes in fatty acid oxidation and ketogenesis.

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

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

86 ow that Cdc2-like kinase 2 (Clk2) suppresses fatty acid oxidation and ketone body production during d

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

88 mented ethanol-induced impairment of hepatic fatty acid oxidation and lipoprotein production, likely

89 In addition to polyunsaturated fatty acid oxidation and lysine degradation, NADPH also

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

91 Thus, in addition to eliciting fatty acid oxidation and metabolic signals, PPARalpha in

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

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

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

95 ype) induced cardiac dysfunction and reduced fatty acid oxidation and mRNA levels of peroxisome proli

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

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

98 n carrier linking dehydrogenases involved in fatty acid oxidation and one-carbon metabolism to the me

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

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

101 D2-generated T3 in BAT accelerates fatty acid oxidation and protects against diet-induced o

102 transcript levels for enzymes that catalyze fatty acid oxidation and pyruvate metabolism and for key

103 sm in normal dogs, whereas they enhance free fatty acid oxidation and reduce glucose oxidation in HF

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

105 ealed decreases in products of dysfunctional fatty acid oxidation and ROS, prompting us to explore th

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

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

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

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

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

111 se 1A (CPT1A), which increases mitochondrial fatty acid oxidation and ultimately enhances the express

112 ice reduced hepatic steatosis and normalized fatty acid oxidation and VLDL-TG secretion.

113 activity of CES1, with subsequent changes in fatty acid oxidation and/or de novo lipogenesis.

114 tor alpha (PPARalpha), a master regulator of fatty acid oxidation, and activation of the JNK signalin

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

116 ha) protein content, mitochondrial capacity, fatty acid oxidation, and glycogen synthesis in wild-typ

117 an increase in mitochondrial respiration and fatty acid oxidation, and in cellular accumulation of tr

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

119 oreover, EPO increased oxidative metabolism, fatty acid oxidation, and key metabolic genes in adipocy

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

121 c lipid droplet formation, increases cardiac fatty acid oxidation, and promotes cardiac dysfunction;

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

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

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

125 ficiency of these genes increased intestinal fatty acid oxidation as a consequence of increased expre

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

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

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

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

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

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

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

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

134 s identify a role of VASP to enhance hepatic fatty acid oxidation by activating AMPK and to promote V

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

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

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

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

139 Fatty acid oxidation capacity is decreased and there may

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

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

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

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

144 idation and ATP production without affecting fatty acid oxidation, confirming in vivo and ex vivo eff

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

146 reased the expression of genes that regulate fatty acid oxidation, decreased fasting-induced steatosi

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

148 nditure and induces inactivity in long-chain fatty acid oxidation-deficient mouse models.

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

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

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

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

153 tes mitochondrial biogenesis and glucose and fatty acid oxidation during differentiation in skeletal

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

155 These data, coupled with the fact that fatty acid oxidation enhances mitochondrial H(2)O(2) pro

156 PPARalpha and fatty acid oxidation enzyme inhibitors increased DEX-med

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

158 blished study of wild type and mitochondrial fatty acid oxidation enzyme knockdown mutants of human h

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

160 60 chaperone complex mediates folding of the fatty acid oxidation enzyme medium-chain acyl-CoA dehydr

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

162 dehydrogenase (LCAD) is a key mitochondrial fatty acid oxidation enzyme.

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

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

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

166 m by orchestrating mitochondrial biogenesis, fatty acid oxidation (FAO) and oxidative phosphorylation

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

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

169 Mitochondrial fatty acid oxidation (FAO) in human unactivated CD4 T(me

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

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

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

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

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

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

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

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

178 y an important role in regulating myocardial fatty acid oxidation (FAO) via its phosphorylation and i

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

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

181 M2 polarization is dependent on fatty acid oxidation (FAO), but the source of the fatty

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

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

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

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

186 perature, energy expenditure, and whole-body fatty acid oxidation (FAO).

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

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

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

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

191 t is characterized by enhanced mitochondrial fatty-acid oxidation (FAO).

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

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

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

195 oactivator-1alpha, whereas the expression of fatty acid oxidation genes was either preserved or unreg

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

197 vator PGC-1alpha and increased mitochondrial fatty acid oxidation genes.

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

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

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

201 Impaired skeletal muscle fatty acid oxidation has been suggested to contribute to

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

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

204 nt as a function of RV mutant Bmpr2 in mice; fatty acid oxidation impairment in human HPAH RVs may un

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

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

207 1-target genes involved in thermogenesis and fatty acid oxidation in brown fat.

208 tulating the phenotype of reduced long chain fatty acid oxidation in cardiac hypertrophy.

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

210 with this, overexpression of miR-33* reduces fatty acid oxidation in human hepatic cells.

211 Microarray analysis demonstrated defects in fatty acid oxidation in human HPAH RVs.

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

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

214 Inefficient fatty acid oxidation in mitochondria and increased oxida

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

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

217 Conversely, overexpression of G0S2 inhibited fatty acid oxidation in mouse primary hepatocytes and ca

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

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

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

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

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

223 e UCP3 as a critical regulator of long-chain fatty acid oxidation in the stressed heart postischemia

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

225 aller adipocytes, and elevated indicators of fatty acid oxidation in white adipose tissue (WAT) compa

226 Fatty-acid oxidation in response to S6K1 inactivation re

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

228 tive PCR analyses revealed that key genes of fatty acid oxidation, including carnitine palmitoyl tran

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

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

231 nto lipids), FB treatment markedly increased fatty acid oxidation (indicated by induction of ACOX1, p

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

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

234 We also found that fatty acid oxidation is needed for TM cells to rapidly r

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

236 Fatty acid oxidation is transcriptionally regulated by p

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

238 across several metabolic pathways including fatty acid oxidation, ketogenesis, amino acid catabolism

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

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

241 However, increasing muscle fatty acid oxidation may cause a reciprocal decrease in

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

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

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

245 AMPK regulates liver cell proliferation and fatty acid oxidation, most likely as a downstream effect

246 ccumulation, such as increased mitochondrial fatty acid oxidation (mtFAO).

247 o exploit tumor cell metabolic dependencies (fatty acid oxidation, nicotinamide adenine dinucleotide

248 The enhanced fatty acid oxidation observed in SIRT4 KO hepatocytes re

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

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

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

252 ese findings for the first time identify the fatty acid oxidation pathway and LCAD in particular as f

253 The physiological role of LCAD and the fatty acid oxidation pathway in lung was subsequently st

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

255 d undergoes intracellular metabolism via the fatty acid oxidation pathway.

256 the PPARalpha agonist (WY-14643), increased fatty acid oxidation, prevented LPS-mediated reduction o

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

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

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

260 atocytes, and SIRT4 overexpression decreases fatty acid oxidation rates.

261 In addition to fatty acid oxidation reactions, an oxidation of endogeno

262 Ex5 cardiomyocytes had reduced fatty acid oxidation, reduced oxygen consumption and res

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

264 ar glucose utilization in DKO mice decreased fatty acid oxidation, resulting in increased reesterific

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

266 Finally, addition of an inhibitor of fatty-acid oxidation significantly enhanced cytotoxicity

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

268 4 knockout (KO) mice exhibit higher rates of fatty acid oxidation than wild-type hepatocytes, and SIR

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

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

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

272 lower diurnal RQ and greater contribution of fatty acid oxidation to energy expenditure, but no diffe

273 the sarcolemma, associated with a shift from fatty acid oxidation to glycolysis, while intramyocardia

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

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

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

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

278 malonyl CoA in the heart regulate long chain fatty acid oxidation via L-CPT1.

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

280 sis as a result of significant impairment of fatty acid oxidation, VLDL-triglyceride (TG) secretion,

281 M-ERRgamma(-/-) myotubes, while medium-chain fatty acid oxidation was increased by 34% in M-ERRgamma(

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

283 Lung fatty acid oxidation was reduced in LCAD(-/-) mice.

284 coactivator-1alpha target genes required for fatty acid oxidation was similarly decreased.

285 receptor alpha (PPARalpha), which regulates fatty acid oxidation, was also increased by DEX, and adi

286 itions that increase blood triglycerides and fatty acid oxidation, we measured changes in antioxidant

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

288 asmic reticulum stress, lipid synthesis, and fatty acid oxidation were down-regulated at baseline in

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

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

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

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

293 In addition, key enzymes in fatty acid oxidation were suppressed following MCD induc

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 suggest that polarizing cells are reliant on fatty acid oxidation, which is supported by pharmacologi

297 The treatment increased fatty acid oxidation while decreased lipogenesis in both

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

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

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