ライフサイエンスコーパス: palmitate

1 than those of cells not exposed to elevated palmitate.

2 rotene, lycopene, phylloquinone, and retinyl palmitate.

3 omoting sugars and unusually large stores of palmitate.

4 is responsible for the de novo synthesis of palmitate.

5 n, which is rescued by addition of exogenous palmitate.

6 monoesterification and diesterification with palmitate.

7 ived macrophages to the saturated fatty acid palmitate.

8 l laurate (ML), methyl myristate, and methyl palmitate.

9 cultures elongated laurate to myristate and palmitate.

10 starch-palmitate, sucrose-oleate and sucrose-palmitate.

11 starch-palmitate < sucrose-oleate < sucrose-palmitate.

12 ed an autophagic response to oleate, but not palmitate.

13 iolaxanthin laurate and (all-E)-violaxanthin palmitate.

14 etal muscle cells treated with saturated FA, palmitate.

15 w-density lipoprotein triglyceride (VLDL-TG) palmitate.

16 eractions of human leukemia cells exposed to palmitate.

17 that negated the pro-inflammatory effects of palmitate.

18 treated with mixtures of oleate and the SFA palmitate.

19 ed ER stress and inflammation in response to palmitate.

20 docyte apoptosis induced by high glucose and palmitate.

21 circadian clocks by the proinflammatory SFA, palmitate.

22 ha expression in IRPTCs by high glucose plus palmitate.

23 ariations in the 13C:12C ratio (delta13C) of palmitate (16:0) and linoleate (18:2n-6) were measured b

24 FA levels (R(2) = 0.99, P < 0.0001), whereas palmitate (16:0) was negatively correlated (R(2) = 0.83,

25 rated fatty acids (SFA), stearate (18:0) and palmitate (16:0), respectively.

26 Finally, LPS (0.5-2 ng.ml(-1) ) and palmitate (20 and 30 mum) acted synergistically to induc

27 se (HG, 27.5 mmol/L) medium and treated with palmitate (50 mumol/L) or bovine serum albumin (BSA) for

28 oneogenesis from fructose), blood VLDL-(13)C palmitate (a marker of hepatic de novo lipogenesis), and

29 Palmitate (a) induced the accumulation of sphingomyelin

30 Short-term treatments of myotubes with palmitate, a ceramide precursor, or directly with cerami

31 microscopy, we discovered that metabolism of palmitate, a prevalent saturated fatty acid (SFA), could

32 Importantly, mice fed MCD starch-palmitate accumulated as much hepatic palmitate as mice

33 atalytic effect on lipid oxidation: ascorbyl palmitate addition and co-spray-drying of heme iron with

34 nthophyll esters: (all-E)-antheraxanthin 3-O-palmitate, (all-E)-violaxanthin laurate and (all-E)-viol

35 s quantification of retinyl acetate, retinyl palmitate, alpha-tocopherol and gamma-tocopherol, revers

36 re isolated and extracted, and alpha-retinyl palmitate (alphaRP) and retinyl palmitate were measured

37 Intriguingly, the palmitate anchor of Hedgehog occupies a similar site in

38 and glucose uptake were measured with (11)C-palmitate and (18)F-fluorodeoxyglucose positron emission

39 ry islets with glucolipotoxicity (0.5 mmol/L palmitate and 25 mmol/L glucose) increases LC3 II, a mar

40 esence of its naturally occurring acyl donor palmitate and a nonhydrolyzable palmitoyl-CoA analog.

41 against the membrane rigidifying effects of palmitate and acts as a suppressor of AdipoR2 knockdown,

42 (SHH), is highly hydrophobic because of dual palmitate and cholesterol modification, and thus, its re

43 we found an increase in the uptake of (14)C-palmitate and fatty acid transporter CD36 that was furth

44 e treated with physiologic concentrations of palmitate and glucose and assessed for alterations in mi

45 e found differential bioenergetic effects of palmitate and glucose on resting and energetically chall

46 Myocardial palmitate and glucose uptake were measured with (11)C-pa

47 3 was reduced in cardiomyocytes treated with palmitate and in hearts of mice fed with a high-fat, hig

48 on in primary hepatocytes using radiolabeled palmitate and in mice using indirect calorimetry.

49 c neurodegeneration requires the presence of palmitate and may be a result of enhanced NO production.

50 l, diacylglycerol, and monoacylglycerol with palmitate and myristate acyl chains.

51 aturated and unsaturated fatty acids such as palmitate and oleate, respectively, triggered autophagy,

52 Using a dual pulse-chase strategy comparing palmitate and protein half-lives, we found knockdown or

53 entified two approved drugs, ascorbic acid 6-palmitate and salmon sperm protamine, that effectively i

54 ed that it was modified with the fatty acids palmitate and stearate.

55 could be rapidly restored by the addition of palmitate and substantially reduced production of oxidiz

56 ux analysis of H4IIEC3 cells co-treated with palmitate and the pan-transaminase inhibitor aminooxyace

57 In contrast, palmitate and tocopherol-conjugated ASOs showed enhanced

58 asis of delta(34)S, Y, U, Cu, Rb, zeaxanthin palmitate and total carotenoid content, discriminant ana

59 n of (pro)vitamins (beta-carotene or retinyl palmitate) and the digestion of triglyceride oils (trica

60 ured on-chip by exposure to lipotoxic agent (palmitate), and then connected to the bioanalysis module

61 lpxL2 mutant lacked the 2-hydroxymyristate, palmitate, and 4-aminoarabinose decorations found in the

62 Kupffer cells were stimulated with oleate or palmitate, and levels of M1/M2 polarization markers and

63 version into blood (13)C glucose, VLDL-(13)C palmitate, and postprandial plasma lactate concentration

64 is synergistically induced by high glucose, palmitate, and TNF-alpha via NF-kappaB and PKA pathways.

65 alis L.) (ROSM) (200-1500mg/kg) and ascorbyl palmitate (AP) (100-300mg/kg) were tested for 18hopen pa

66 Ascorbyl palmitate (AP) and ascorbyl stearate (AS) are examples o

67 Electrooxidation of ascorbyl palmitate (AP) over gold screen-printed electrode (AuSPE

68 he most suitable matrix polymer for ascorbyl palmitate (AP).

69 All of these effects of palmitate are fatty acid specific because oleate (C18:1,

70 bjects fasting levels of the free fatty acid palmitate are raised.

71 de production in HEK293 cells incubated with palmitate as a direct substrate for SPT reaction.

72 starch-palmitate accumulated as much hepatic palmitate as mice fed MCD sucrose-oleate, yet their degr

73 ng alpha-tocopherol, beta-carotene, ascorbyl palmitate, ascorbic acid, citric acid, and their combina

74 to the triacylglycerol class and containing palmitate at the first position) were significantly gene

75 methyl laurate, methyl myristate, and methyl palmitate, attracting healthy flies, which in turn becom

76 Dietary palmitate becomes toxic when combined with dietary sugar

77 ardiac triglyceride accumulation and ex vivo palmitate beta-oxidation.

78 These lipids likely bind in the palmitate binding cavity as observed in tablysin-15, sin

79 of binding affinity as tablysin-15, a known palmitate-binding protein.

80 diated dimerization of the TLR4-MD2 complex, palmitate binds a monomeric TLR4-MD2 complex that trigge

81 Conversely, autophagy triggered by palmitate, but not oleate, required AMPK, PKR and JNK1 a

82 ic nalmefene derivatives were evaluated: the palmitate (C16), the octadecyl glutarate diester (C18-C5

83 nversion in anaerobic bioreactors results in palmitate (C16:0) accumulation.

84 We report that palmitate (C16:0, 200 muM) significantly modulates the m

85 The fatty acid palmitate can activate death receptor 5 (DR5) on hepatoc

86 and beta-adrenergic stimulation conditions, palmitate can, at least in part, offset left ventricle (

87 from RAW 264.7 or Kupffer cells loaded with palmitate (CM-P), phosphorylation of stress kinases and

88 ffects of high concentrations of glucose and palmitate combined for 48 h (glucolipotoxicity) on the t

89 Therefore, pathologic palmitate concentrations promote the acquisition of a sp

90 of v-ATPase in cardiomyocytes exposed to low palmitate concentrations reduced insulin sensitivity and

91 e the expression of CCL19 and TRIB3 Besides, palmitate conditions macrophages for exacerbated proinfl

92 rtially share genetic basis of T2D; and c) 1-palmitate containing TAGs may provide additional insight

93 ECs glucose stimulates PFKFB3 expression and palmitate contributes to increased proinflammatory respo

94 Interestingly, palmitate decreased PFKFB3 expression and increased proi

95 ction of oleate, but not of the saturated FA palmitate, decreased food intake and increased locomotor

96 mice and chronic exposure of human islets to palmitate decreases endogenous sorcin expression while l

97 onstrate that Sonic Hedgehog signals via the palmitate-dependent arm of a two-pronged contact with Pa

98 The palmitate-dependent interaction is also abolished in con

99 The palmitate-dependent interaction with Patched1 is specifi

100 ate Patched1 inhibition is caused by direct, palmitate-dependent interaction with the Sonic Hedgehog

101 Investigation of palmitate-dependent respiration in mutant fibroblasts sh

102 By contrast, mice fed MCD sucrose-palmitate developed severe liver injury, worse than that

103 cific deletion of Sptlc2 is not required for palmitate-driven Nlrp3 inflammasome activation.

104 to knock out the Sms2 gene recapitulated the palmitate effects by inducing the accumulation of SM pre

105 intermediates accounting for the deleterious palmitate effects.

106 In general, ascorbyl palmitate, either alone or in combination with the co-sp

107 In conclusion, oleate and palmitate elicit an opposite cross-talk between macropha

108 We have demonstrated that palmitate enhances glucose-stimulated insulin secretion

109 ssion apparently affects the partitioning of palmitate-enriched diacylglycerol between the phosphatid

110 s hypothesis, C57BL/6 mice were either fed a palmitate-enriched high fat diet or administered with ch

111 e might be explained by the observation that palmitate esterification influenced the cis-trans equili

112 Unlike LPS, palmitate exposure does not activate STAT1, and its tran

113 omethoxyphenylhydrazone (FCCP), we show that palmitate exposure induced comparable peak OCR and highe

114 Palmitate exposure to neonatal rat ventricular cardiomyo

115 here were no significant changes in the IC50(palmitate)f (19 +/- 2 compared with 24 +/- 3 muIU/mL), a

116 eded to suppress palmitate flux by 50% (IC50(palmitate)f).In the omega-3 group, the EPA and DHA contr

117 Under these conditions, palmitate failed to alter levels of SMs, which are the m

118 the insulin concentration needed to suppress palmitate flux by 50% (IC50(palmitate)f).In the omega-3

119 conditioned medium from myotubes exposed to palmitate for 4 h significantly reduced apoptosis of mur

120 Treatment of myotubes with 0.5 mmol/L palmitate for 4 h, but not with oleate, promoted an incr

121 copherols in salad vegetables and 2) retinyl palmitate formed from the provitamin A carotenoids.Women

122 The enzyme then transfers palmitate from itself onto substrate proteins.

123 he response to membrane aberrancy induced by palmitate from unfolded protein stress, our analysis sho

124 ith an oral dose of either VA (6 mug retinyl palmitate/g body weight) or canola oil (control), both c

125 However, long-term exposure to palmitate (>8 hours) enhances ROS generation, which is a

126 Ascorbyl palmitate had less inhibitory effect than erythorbic aci

127 According to the literature, retinyl palmitate has been found to be the most abundant vitamin

128 eading to restored redox balance imparted by palmitate helps explain maintained LV function and may c

129 duced in human and mouse plaque VSMCs and by palmitate in a p38- and c-Jun N-terminal kinase-dependen

130 lso correlated positively with the amount of palmitate in the liver, but the relationship was weak.

131 ative stress in cultured myotubes exposed to palmitate in the presence of a beta-oxidation inhibitor.

132 HUVECs were treated with and without palmitate in the presence or absence of EMPs.

133 Using a control probe, DDAO palmitate, in addition to cPLA2alpha inhibition and gene

134 tes, namely glutamine, pyruvate, glucose, or palmitate, in mitochondria.

135 meC18SO was synthesized from anteiso-methyl-palmitate, in turn synthesized from a precursor metaboli

136 isingly, this was not due to lower exogenous palmitate incorporation into cellular PCs.

137 e of macrophages to the saturated fatty acid palmitate increased glycolysis and HIF-1alpha expression

138 Treatment with 1 mm palmitate increases de novo ceramide synthesis in both c

139 L from healthy humans and lean mice inhibits palmitate-induced adipocyte inflammation; however, the e

140 vealed significantly reduced NEFA uptake and palmitate-induced apoptosis in microperfused Slc27a2(-/-

141 Although palmitate-induced endoplasmic reticulum stress and nucle

142 BBR treatment also caused a decrease in palmitate-induced fat deposition in primary mouse hepato

143 yme expression and glucose output and blunts palmitate-induced hepatocyte fat deposition in an Akt-de

144 ditioned medium led to a 20-fold increase in palmitate-induced IL-8 expression by hepatocytes.

145 sed JNK and NF-kappaB activation and blocked palmitate-induced IL-8 expression in hepatocytes.

146 ced JNK and NF-kappaB activity and increased palmitate-induced IL-8 secretion.

147 3, thereby releasing the brake and enhancing palmitate-induced IL-8 synthesis and secretion.

148 the ability of SAA-containing HDL to inhibit palmitate-induced inflammation and cholesterol efflux.

149 om mice injected with AgNO3 fails to inhibit palmitate-induced inflammation and reduces cholesterol e

150 In contrast, palmitate-induced lipid droplet formation is significant

151 in a PGC1alpha-dependent manner and reduced palmitate-induced lipotoxicity.

152 e and rat hepatocytes, and protected against palmitate-induced lipotoxicity.

153 ncreasing FAO by knockdown of ACC2 prevented palmitate-induced mitochondria dysfunction and cardiomyo

154 th normoxia, hypoxia significantly increased palmitate-induced mRNA expression and protein secretion

155 Additional studies showed increased palmitate-induced oxidative stress, mitochondrial and ly

156 function in a model of free fatty acid (FFA) palmitate-induced oxidative stress.

157 Palmitate-induced p52Shc binding to p47(phox) , activati

158 -6- or TNFalpha-mediated signaling repressed palmitate-induced phase shifts of the fibroblast clock.

159 Palmitate-induced ROS generation in human CD68(low)CD14(

160 ed from plaques or undergoing replicative or palmitate-induced senescence versus healthy aortic VSMCs

161 Here, we demonstrate that palmitate-induced sorcin downregulation and subsequent i

162 ospholipids was studied in HepG2 cells under palmitate-induced steatosis.

163 m torpid squirrel brain show a high level of palmitate-induced uncoupling.

164 The mechanism of palmitate-induced v-ATPase inhibition involved its disso

165 Together, these results suggest that palmitate induces DRG neuron mitochondrial depolarizatio

166 ring 1 h of exercise at 50% VO2max ([U-(13)C]palmitate infusion combined with electron microscopy of

167 a 2-step pancreatic clamping with a [U-(13)C]palmitate infusion to determine the insulin concentratio

168 mitate storage was assessed using a [U-(13)C]palmitate infusion to measure palmitate kinetics and an

169 Palmitate inhibited IGFBP-3 secretion by THP-1 macrophag

170 Under lipotoxic conditions, palmitate inhibits hepatic macrophage secretion of IGFBP

171 over under different conditions (glucose +/- palmitate +/- insulin +/- dichloroacetate).

172 3D switch; however, FASN's synthetic product palmitate is dispensable for this process since cells sa

173 boxylase involved in de novo biosynthesis of palmitate is reduced by cell density in an Nf2/Merlin-de

174 the modification of proteins with the lipid palmitate, is a key regulator of protein targeting and t

175 In the case of palmitate, its accelerated uptake ultimately precipitate

176 patocytes and Huh7 cells were incubated with palmitate, its metabolite lysophosphatidylcholine, or di

177 ing a [U-(13)C]palmitate infusion to measure palmitate kinetics and an intravenous palmitate radiotra

178 cells, lipid stress by exposure to elevated palmitate leaves unchanged the rate by which MC4R and tr

179 wer FASN activity in PINK1 mutants decreases palmitate levels and increases the levels of cardiolipin

180 The ability of chronically elevated palmitate levels to simultaneously increase basal secret

181 n the WD-fed BMPR2-mutant RV showed impaired palmitate-linked oxygen consumption, and metabolomics an

182 ne, glutamate, or dimethyl-alphaKG increased palmitate lipotoxicity compared with media that lacked t

183 amate dehydrogenase (Glud1) had no effect on palmitate lipotoxicity.

184 patitis, in the order starch-oleate < starch-palmitate < sucrose-oleate < sucrose-palmitate.

185 at, upon exposure to a saturated fatty acid, palmitate, macrophages release nucleotides that attract

186 erexpressing SNRK have decreased glucose and palmitate metabolism and oxygen consumption, but maintai

187 The hydrophobic palmitate moiety is covalently attached to a cysteine re

188 fference between these two, the less complex palmitate monoester was chosen to demonstrate that dog p

189 Agonist-induced turnover of palmitate occurs predominantly on Cys-265.

190 te, and monitoring (13) C incorporation into palmitate of circulating very low-density lipoprotein tr

191 Compared with palmitate, oleate more effectively stimulated both autop

192 d, catechin, alpha tocopherol, ascorbic acid palmitate) on the physical and chemical stability of lut

193 the enzyme responsible for the attachment of palmitate onto Shh, is a novel target for inhibition of

194 The contribution of labeled palmitate or acetate to the TCA cycle was reduced in org

195 duodenal crypts, incubated them with labeled palmitate or acetate, and measured production of TCA cyc

196 12 or human muscle cells were incubated with palmitate or directly with ceramide for short or long pe

197 loss and increased ER stress in response to palmitate or lipopolysaccharide (LPS).

198 ytes (PMHs) and Huh7 cells were treated with palmitate or lysophosphatidylcholine (LPC).

199 n of primary hepatocytes and Huh7 cells with palmitate or lysophosphatidylcholine increased their rel

200 this study, we have evaluated the impact of palmitate or oleate overload of macrophage/Kupffer cells

201 ells and mouse islets for 8-48 h with either palmitate or oleate, and then monitored autophagic flux,

202 ern diet (WD) (35% kcal from fat enriched in palmitate) or a purified regular diet (16.9% kcal from f

203 thweight neonates to NVAS (50 000 IU retinyl palmitate) or placebo together with their Bacillus Calme

204 tyl-CoA (e.g. [(13)C6]glucose or [1,2-(13)C2]palmitate) or/and M1 acetyl-CoA (e.g. [1-(13)C]octanoate

205 otubes to either high glucose concentration, palmitate, or H2O2 decreases insulin-induced Akt phospho

206 and in rodent and human cardiomyocytes upon palmitate overexposure, and appeared as an early lipid-i

207 human myotubes, ACSL6 overexpression reduced palmitate oxidation and PGC-1alpha mRNA.

208 kout mouse hearts have increased glucose and palmitate oxidation and UCP3.

209 mpanied by significantly diminished rates of palmitate oxidation by isolated hepatocytes and liver mi

210 rfusions demonstrated a profound increase in palmitate oxidation relative to wild-type hearts (3.6 ti

211 Furthermore, palmitate oxidation was elevated in the white adipose ti

212 ered by small interfering RNA against DAPK3, palmitate oxidation was increased.

213 content, mitochondrial respiratory rates and palmitate oxidation.

214 2.16s(-1), respectively, when p-nitrophenyl palmitate (p-NPP) was used as the substrate.

215 re to HFD, cultured EGCs were incubated with palmitate (PA) and/or lipopolysaccharide (LPS).

216 BMDM from low fat-fed mice exposed to palmitate (PA) for 18 h ex vivo also showed elevated exp

217 tty acids (SFAs) (the "bad" fat), especially palmitate (PA), in the human diet are blamed for potenti

218 GSIS and abolished the stimulation of sodium palmitate (PA)-BSA on Nox2 gene expression.

219 Palmitate (PA)-induced changes in intracellular hydrogen

220 Previous data showed that palmitate (Palm) or glutathione preserved heart mitochon

221 brane lipid saturation following exposure to palmitate, phenocopying cells with perturbed SCD1 activi

222 In cultured EGCs, co-incubation with palmitate plus LPS led to a significant increase in both

223 ability is confirmed by lipase p-nitrophenyl palmitate (PNP) assay.

224 These actions were recapitulated in vitro in palmitate-primed hepatocytes and adipocytes incubated wi

225 Suppression of IGF binding protein-3 by palmitate promotes hepatic inflammatory responses.

226 The addition of ascorbyl palmitate provided protection against oxidation and loss

227 Maternal insulin value at 50% palmitate Ra suppression (IC50) for palmitate suppressio

228 easure palmitate kinetics and an intravenous palmitate radiotracer bolus/timed biopsy.

229 erases APT1 and APT2 - are known to catalyze palmitate removal from cytosolic cysteine residues.

230 from the saturated fatty acids stearate and palmitate, respectively.

231 A palmitate-rich diet, which increases serum 27OHC, or APP

232 here show that cereal bran protects retinyl palmitate (RP) during simmering and storage.

233 tes lipotoxicity by the saturated fatty acid palmitate: silencing ACSL1 protects against the membrane

234 -secreting alpha-cells, we hypothesized that palmitate simultaneously stimulates secretion of glucago

235 Here, we show that palmitate-stimulated CD11b(+)F4/80(low) hepatic infiltra

236 phate (S1P) levels are not only increased in palmitate-stimulated pancreatic beta-cells but also regu

237 cells to saturated fatty acids (FAs) such as palmitate stimulates ER stress and modulates autophagy,

238 Direct palmitate storage was assessed using a [U-(13)C]palmitat

239 rate-fat combinations: starch-oleate, starch-palmitate, sucrose-oleate and sucrose-palmitate.

240 However, lipid deprivation or palmitate supplementation has no effect on NF-kappaB exp

241 1 expression, which is able to be rescued by palmitate supplementation.

242 e at 50% palmitate Ra suppression (IC50) for palmitate suppression with insulinemia was higher in OB+

243 ell adhesion molecule (EPCAM), and carbamoyl palmitate synthase-1] also had the most cells expressing

244 ion of fatty acid synthase (FASN), the major palmitate-synthesizing enzyme.

245 ible for de novo synthesis of the fatty acid palmitate; the building block for protein palmitoylation

246 iabetic hearts show that, in the presence of palmitate, there is a metabolic remodelling involving tr

247 oxidation by the catabolism of (14)C-labeled palmitate to (14)CO(2).

248 the reversible posttranslational addition of palmitate to cysteines and promotes membrane binding and

249 ultured C2C12 myotubes, using BSA-conjugated palmitate to increase synthesis of endogenous sphingolip

250 ferences in the cell fluxes from glucose and palmitate to produce Acetyl-CoA, and secretion of hepara

251 rotein S-palmitoylation which adds 16-carbon palmitate to specific cysteines and contributes to vario

252 alent attachment of the 16-carbon fatty acid palmitate to the N-terminal cysteine of Sonic Hedgehog (

253 an liver and lung carcinomas that desaturate palmitate to the unusual fatty acid sapienate to support

254 Addition of a C16 fatty acid (palmitate) to lipid A by the outer membrane acyltransfer

255 We determined the effect of attaching palmitate, tocopherol or cholesterol to PS ASOs and thei

256 oxytoluene, tert-butylhydroquinone, ascorbyl palmitate, tocopherol, grape seed extract, olive extract

257 mp procedure in conjunction with glucose and palmitate tracer infusions and positron emission tomogra

258 [(14)C]Choline and [(3)H]palmitate tracking shows that SMS1 overexpression appare

259 In palmitate-treated C2C12 skeletal myotubes, GLP-1(32-36)a

260 itogen-activated protein kinase signaling in palmitate-treated cells.

261 Palmitate-treated DRG neurons also exhibited a reduction

262 related with mitochondrial depolarization in palmitate-treated DRG neurons.

263 the endoplasmic reticulum to mitochondria of palmitate-treated hepatocytes activates anaplerotic flux

264 ted ProINS-Tf overcame insulin resistance in palmitate-treated HepG2 cells.

265 vels of p62 were elevated in comparison with palmitate-treated hLrp1(+/+) hepatocytes, suggesting tha

266 Palmitate-treated hLrp1(-/-) hepatocytes displayed simil

267 modestly reduced IL-1beta gene expression in palmitate-treated hypoxic macrophages.

268 The secretome of hypoxic palmitate-treated macrophages promoted IL-6 and macropha

269 beta and reduced the hypoxic potentiation in palmitate-treated macrophages.

270 elevated ROS generation are also observed in palmitate-treated neonatal rat ventricular cardiomyocyte

271 Exposure of palmitate-treated THP-1 macrophages to IGFBP-3-deficient

272 Luc fibroblast cultures was increased during palmitate treatment although the time course and amplitu

273 ion from human islets, to be enhanced during palmitate treatment at normoglycemia.

274 s of endoplasmic reticulum (ER) stress after palmitate treatment compared with similarly treated hLrp

275 Palmitate treatment increased saturated glycerolipids, a

276 Palmitate treatment significantly reduced the number of

277 r ATP levels, prevented apoptosis induced by palmitate treatment, and promoted lipid droplet formatio

278 After palmitate treatment, triacylglycerol accumulation, insul

279 s in CAC flux and oxidative stress following palmitate treatment.

280 pendent phase shifts observed in response to palmitate, treatment with IL-6 or with the low dose (0.1

281 er, these results demonstrate that lipotoxic palmitate treatments enhance anaplerosis in cultured rat

282 itoylation of Huntingtin, but did not affect palmitate turnover on postsynaptic density protein 95 (P

283 Moreover, we found that palmitate up-regulates pannexin-1 channels in macrophage

284 ment of labeled very low-density lipoprotein palmitate via gas chromatography mass spectometry.

285 equire modification of DLK by the fatty acid palmitate, via a process called palmitoylation.

286 SULTSThe contribution of hepatic DNL to IHTG-palmitate was 11%, 19%, and 38% in the lean, obese, and

287 ed a high-fat diet or hepatocytes exposed to palmitate was accompanied by reduced PPARbeta/delta and

288 The spontaneous curvature of palmitate was calculated by molecular dynamic simulation

289 Tissue retinyl palmitate was inversely and significantly correlated wit

290 lutamine, whereas the capacity for oxidizing palmitate was limited to human hepatocarcinoma Huh7 cell

291 Exogenous palmitate was partitioned to different pools from endoge

292 oxia-potentiated inflammation induced by SFA palmitate, we found that the AMP-mimetic AMPK activator

293 lpha-retinyl palmitate (alphaRP) and retinyl palmitate were measured over 12 h postprandially via hig

294 sters, beta-carotene, and beta-cryptoxanthin palmitate were the most abundant in peels and pulp of al

295 gnificantly reduced the lipotoxic effects of palmitate, whereas knockdown of glutamate dehydrogenase

296 cells were treated with lipotoxic levels of palmitate while modulating anaplerotic pathways leading

297 es suggest that BTA121 binds lipids, notably palmitate with a similar order of binding affinity as ta

298 observed in tablysin-15, since MpPR-1i binds palmitate with comparable affinity as tablysin-15.

299 was a weak downward trend of tissue retinyl palmitate with increasing fibrosis stage.

300 ason why oleate is continuously converted to palmitate without further degradation via beta-oxidation