ライフサイエンスコーパス: NEFA

1 NEFA elevation during consumption of the SFA-rich drinks

2 NEFA levels early in pregnancy were independently associ

3 NEFAs purified from lipoproteins hydrolyzed by hGIIF wer

4 drink, KE reduced glucose (-11%, P = 0.002), NEFA (-21%, P = 0.009), and glucagon-like peptide 1 (-31

5 FA species and accurate quantification of 36 NEFA species in human plasma is described, the highest n

6 Detection of 50 NEFA species and accurate quantification of 36 NEFA spec

7 he impact of KE on nonesterified fatty acid (NEFA) concentration and glucoregulatory hormones.

8 Nonesterified (free) fatty acid (NEFA) concentrations increased with declining glucose to

9 greater serum nonesterified free fatty acid (NEFA) concentrations than controls, whereas the HF-SPI p

10 sol, glucagon, and nonesterified fatty acid (NEFA) concentrations were not or were only marginally af

11 t of reductions in nonesterified fatty acid (NEFA) concentrations.

12 port rates, plasma nonesterified fatty acid (NEFA) flux, and sources of fatty acids used for the asse

13 vestigate systemic nonesterified fatty acid (NEFA) incorporation into VLDL TGs.

14 th decreased non-esterified free fatty acid (NEFA) levels and increased alkaline phosphatase activity

15 increase in plasma nonesterified fatty acid (NEFA) levels and is mediated transcriptionally by the pe

16 (-1)) to clamp the nonesterified fatty acid (NEFA) levels during hyperinsulinemia; the other group (I

17 levation of plasma nonesterified fatty acid (NEFA) levels has been shown in various studies to induce

18 s of intracellular nonesterified fatty acid (NEFA) levels.

19 e from the plasma non-esterified fatty acid (NEFA) pool predicts brain uptake of DHA upon oral admini

20 ne-stimulated nonesterified free fatty acid (NEFA) release and plasma levels of NEFA are similar in S

21 Nonesterified fatty acid (NEFA) release was suppressed after the meal in both depo

22 r determination of nonesterified fatty acid (NEFA) species are still missing.

23 nsitivity based on nonesterified fatty acid (NEFA) suppression after oral glucose administration [ISI

24 sm and glucose and nonesterified fatty acid (NEFA) turnover in 6 healthy men under controlled cold ex

25 on and glucose and nonesterified fatty acid (NEFA) turnover were determined in men with well-controll

26 crease in plasma non-esterified fatty acids (NEFA) and beta-hydroxybutyrate (BHB).

27 ized that plasma non-esterified fatty acids (NEFA) are trafficked directly to intramyocellular long-c

28 s in circulating non-esterified fatty acids (NEFA) are well-described in diabetes, effects on signali

29 Plasma nonesterified fatty acids (NEFA) at elevated concentrations antagonize insulin acti

30 Although nonesterified fatty acids (NEFA) have been positively associated with coronary hear

31 oncentrations of non-esterified fatty acids (NEFA) in biological fluids are recognized as critical bi

32 Nonesterified fatty acids (NEFA) in urine are bound to albumin and reabsorbed in th

33 ative analysis of nonesterified fatty acids (NEFA) species in biofluids is a challenging task because

34 uces glycerol and nonesterified fatty acids (NEFA) that serve as energy sources during nutrient scarc

35 es of delivery of nonesterified fatty acids (NEFA) were downregulated, resulting in normal systemic N

36 he association of nonesterified fatty acids (NEFA) with dysglycemia in older adults, NEFA levels were

37 asing circulating nonesterified fatty acids (NEFA), the main substrate for synthesis of intrahepatic

38 of albumin-bound nonesterified fatty acids (NEFAs) across the damaged glomerular filtration barrier

39 ression of plasma nonesterified fatty acids (NEFAs) after glucose ingestion may contribute to glucose

40 ed the effects of nonesterified fatty acids (NEFAs) and adipokines on acinar cells in culture.

41 ssociation between fasting free fatty acids (NEFAs) and insulin secretion.

42 tic generation of nonesterified fatty acids (NEFAs) from circulating triglycerides (TGs) could worsen

43 ntal elevation of nonesterified fatty acids (NEFAs) impairs endothelial function, but the effect of N

44 riglycerides; and nonesterified fatty acids (NEFAs) in a total of 139 OT1DM and 48 control subjects a

45 ulation of nonesterified (free) fatty acids (NEFAs) in the first trimester of pregnancy would mark wo

46 and the entry of nonesterified fatty acids (NEFAs) in the liver, whereas IR-associated hyperinsuline

47 uptake of plasma nonesterified fatty acids (NEFAs) in the postprandial but not the fasting state.

48 line to mobilize non-esterified fatty acids (NEFAs) in young lambs.

49 adiponectin, and nonesterified fatty acids (NEFAs) may be involved in amino acid-mediated insulin re

50 ine the effect of nonesterified fatty acids (NEFAs) on net hepatic glucose uptake (NHGU).

51 levels with their nonesterified fatty acids (NEFAs) precursors during alcohol intoxication and clinic

52 ggest that plasma nonesterified fatty acids (NEFAs) raise plasma ANGPTL4 concentrations in humans.

53 lipid oxidation, nonesterified fatty acids (NEFAs), and glycerol responses were equivalent between m

54 l and track serum nonesterified fatty acids (NEFAs), dietary fatty acids, and those derived from the

55 concentrations of nonesterified fatty acids (NEFAs), transported bound to serum albumin, are associat

56 cerides (TGs) and nonesterified fatty acids (NEFAs), ultimately leading to insulin resistance.

57 generated excess nonesterified fatty acids (NEFAs), which caused organ failure in the absence of acu

58 s, which include non-esterified fatty acids (NEFAs).

59 lower quantity of nonesterified fatty acids (NEFAs).

60 d plasma free FA [nonesterified fatty acids (NEFAs)] were analyzed by using gas chromatography for th

61 Adipo-IR (fasting nonesterified fatty acids [NEFAs] x fasting insulin) was calculated at baseline and

62 shunted the utilization of exogenously added NEFA from triglycerides to phospholipids.

63 ids (NEFA) with dysglycemia in older adults, NEFA levels were measured among participants in the Card

64 d pancreatic acinar injury without affecting NEFA signaling or acute pancreatitis induction.

65 IGF-I was inversely related only to age, NEFA, and Pakistani ethnicity.

66 alphaR-cis-4alphaH-fluoren-++ +4alpha-amine (NEFA), a structural analog of phencyclidine (PCP).

67 SH1C locus by the sequencing of an amplified NEFA cDNA from an USH1C patient; however, no mutations w

68 - 0.19 mmol/l, respectively; P < 0.001), and NEFA (median 0.17 [interquartile range 2.30-2.95] and 0.

69 genous fatty acids on PPARalpha activity and NEFA pool composition in rat primary hepatocytes.

70 l, and plasma 3-HIB, FGF21, adiponectin, and NEFA concentrations, under basal conditions and during a

71 comparison of the uptake rate of LPC-DHA and NEFA-DHA demonstrates that uptake of NEFA-DHA into the b

72 Nevertheless, systemic NEFA fluxes and NEFA spillover remained similar, suggesting that increas

73 consumed before an OGTT lowered glucose and NEFA AUCs with no increase in circulating insulin.

74 in vitro treatment of AML12 with glucose and NEFA lead to higher Let-7 expression.

75 itively related to age, fasting glucose, and NEFA.

76 gated glucose removal, lactate, glycerol and NEFA accumulation in media, and metabolic gene expressio

77 ssed by indirect calorimetry), glycerol, and NEFA responses were increased (P<0.01) in type 1 diabeti

78 y correlated with serum glucose, insulin and NEFA, and in vitro treatment of AML12 with glucose and N

79 jects, cold-induced oxidative metabolism and NEFA uptake per BAT volume and an increase in total body

80 Plasma ANGPTL4, NEFA, and triglyceride concentrations were measured.

81 ssive lipolysis causes hepatic steatosis, as NEFA released from adipose tissue constitutes a major so

82 obesity-related morbidity is interesting as NEFAs constitute a reservoir of metabolic energy, are pr

83 nd Preeclampsia Prevention Study, we assayed NEFA levels in nonfasting serum collected at a mean gest

84 al spectrum extends beyond readily available NEFA standard compounds by a regression model predicting

85 Because NEFAs stimulate secretion through FFAR1, we examined the

86 t data are available on the relation between NEFA and sudden cardiac death.

87 th (sPTB) and examined the interplay between NEFAs, lipids, and other markers to explore pathways to

88 sfection with Let-7a inhibitor impaired both NEFA-mediated reduction of Prkaa2 levels and the fat acc

89 A computational model of antagonism by NEFA was developed and constrained using kinetic measure

90 a2 levels and the fat accumulation driven by NEFA.

91 peri-fat acinar necrosis (PFAN, indicated by NEFA spillage) contributed to most of the necrosis obser

92 HC caused NEFA accumulation in media to decrease by 30% relative t

93 this study we measure changes in circulating NEFA species in plasma samples taken from 25 obese indiv

94 entage weight of LC n-3 PUFAs in circulating NEFAs and change in FMD response [Spearman's rho (r(s))

95 Once the channel has closed, NEFA is unable to dissociate until the channel reopens.

96 ivity are important determinants controlling NEFA pool composition and PPARalpha activity.

97 increased insulin sensitivity, and decreased NEFA, after the Cap treatment.

98 VLDL-TG extraction and direct NEFA uptake were similar in the two depots.

99 In the men, elevated NEFA levels decreased insulin-stimulated glucose R(d) du

100 ited increased serum triglycerides, elevated NEFA and impaired glucose tolerance.

101 f the high-insulin dose clamps with elevated NEFA, glucose oxidation was decreased by 33% in the men

102 ia and relative insulin deficiency, elevated NEFAs reduce NHGU by stimulating hepatic glucose release

103 asal cellular energy uptake, but can enhance NEFA uptake and divert glucose from glycogen synthesis t

104 g adipose triglyceride and generating excess NEFAs.

105 ) storage and/or increased nonesterified FA (NEFA) flux from adipose tissue intracellular lipolysis.

106 centrations of circulating nonesterified FA (NEFA) with the development of graft failure in RTR.

107 ) uptake of most sources of postprandial FA (NEFA + DFA uptake) integrated over 6 h was higher in IGT

108 A prospective blinded study compared FAEEs, NEFAs, and ethanol blood levels on hospitalization for a

109 found an inverse association between fasting NEFA concentrations and risk for development of graft fa

110 onfidence interval: 1.08, 1.29), but fasting NEFA were not (hazard ratio = 1.12, 95% confidence inter

111 ssociations, which were stronger for fasting NEFA with DM in men but were accentuated for postload NE

112 ermediates, and after adjustment for fasting NEFA.

113 -GO) is proposed as a biosensor platform for NEFA detection.

114 the production of redox active species from NEFA.

115 r in liver, 59.0% +/- 9.9% of TAG arose from NEFAs; 26.1% +/- 6.7%, from DNL; and 14.9% +/- 7.0%, fro

116 a previously characterized but unmapped gene NEFA (DNA binding/EF hand/acidic amino-acid-rich).

117 ited negative effects on ADG, blood glucose, NEFA, and AA profile.

118 ncreased (P < 0.05) levels of blood glucose, NEFA, and AAs (lysine and glutamic acid) compared to LP

119 evels decreased the levels of blood glucose, NEFA, and amino acids (AAs) (lysine and glutamic acid) c

120 In the INS group, NEFA levels dropped from 700 +/- 90 (basal) to 230 +/- 6

121 /- 1.0 micromol.kg(-1).min(-1)), net hepatic NEFA uptakes (0.1 +/- 0.1 and 1.8 +/- 0.2 micromol.kg(-1

122 was particularly high among women with high NEFA levels (odds ratio = 3.73, 95% confidence interval:

123 Lower glucose utilization and higher NEFA levels, correlated with CAC volume (r = -0.42, P <

124 levels during fasting, likely due to higher NEFA availability, suggesting that the metabolic respons

125 However, NEFA - TGFA x lipase correlations became stronger with T

126 However, NEFAs, but not adipokines, caused acinar cell necrosis.

127 Diabetic albumin showed impaired NEFA binding capacity, and both structural and functiona

128 imTG NEFA storage was correlated only with NEFA concentration

129 TL4 positively correlated with the change in NEFA concentrations (beta = 0.048, P < 0.001) and negati

130 Changes in NEFA pool 20:5n-3 mass correlated with dynamic changes i

131 etes and strongly correlated with changes in NEFA, consistent with their liberation during adipose li

132 The fall in NEFA levels brings about a redirection of glycogenolytic

133 lin resistance (-58%) despite an increase in NEFA concentrations (+35%).

134 between the two cell types were observed in NEFA uptake or lipolysis.

135 ith the SCD1(1)(6) index, and the pattern in NEFAs echoed that of VLDL-triacylglycerols.

136 synthesis can inhibit NEFA release, increase NEFA uptake, and promote insulin-mediated glucose utiliz

137 ious nutritional interventions that increase NEFA concentrations in healthy subjects and in patients

138 remained similar, suggesting that increased NEFA storage capacity per volume of adipose tissue exact

139 concentrations, concomitantly with increased NEFA concentrations.

140 d 2 were associated with sPTB: 1) increasing NEFA and HDL cholesterol levels and 2) family history of

141 These results show that cold-induced NEFA uptake and oxidative metabolism are not defective i

142 Insulin-induced NEFA suppression was also lower in type 1 diabetic compa

143 function, but variation in FFAR1 influences NEFA effects on insulin secretion and therefore could af

144 c flow to triglyceride synthesis can inhibit NEFA release, increase NEFA uptake, and promote insulin-

145 Additional study into NEFA metabolism could uncover novel potential targets fo

146 lthough the composition of the intracellular NEFA pool is likely an important factor controlling PPAR

147 ISI(NEFA) was related to ATBF response (r(s) = 0.73, P < 0.0

148 ssion after oral glucose administration [ISI(NEFA)] were higher in the top tertile ATBF response grou

149 elationship between increase in ATBF and ISI(NEFA) was independent of BMI (P = 0.015) in multivariate

150 Separation of isotopologic NEFA is achieved using ultrahigh-performance liquid chro

151 ed SEM = 0.23] or for lipid metabolism [Kitt(NEFA) (the rate constant for the decline in blood fatty

152 ter-mediated uptake of fluorescently labeled NEFA in cultured proximal tubule cells and microperfused

153 e and with the product of TGFA serum lipase (NEFAs - TGFAs x lipase).

154 al proximal tubule transporter that mediates NEFA uptake and cytotoxicity.

155 The ability of adrenaline to mobilize NEFA was 55 +/- 15% lower (P < 0.05) in IUGRs than contr

156 We estimated that approximately 11% of NEFA were stored in imTG.

157 The inverse association of NEFA and secretion was modulated by rs1573611 and became

158 Median (IQR) fasting concentrations of NEFA were 373 (270-521) muM/L.

159 Plasma concentrations of NEFA were measured using established enzymatic methods,

160 whereas in HTG subjects, the contribution of NEFA was somewhat lower overall and was reduced further

161 airs endothelial function, but the effect of NEFA composition is unknown.

162 otective rather than a tubulotoxic effect of NEFA.

163 appear comparable, the inhibitory effects of NEFA on peripheral tissue insulin sensitivity are observ

164 n was measured at baseline and at the end of NEFA elevation; venous blood was collected for measureme

165 , ion path settings, and response factor) of NEFA species based on chain length and number of double

166 tty acid (NEFA) release and plasma levels of NEFA are similar in SHRSP and WKY.

167 predictions and experimental measurements of NEFA action at a high NMDA concentration, we determined

168 (0.60-1.38) across consecutive quartiles of NEFA concentration.

169 cross increasing gender-specific tertiles of NEFA (P=0.04).

170 ion models were used to evaluate tertiles of NEFA levels and sPTB at <34 weeks and 34-36 weeks; facto

171 er studies on the role of different types of NEFA in the progression of renal disease are warranted.

172 and hepatic total postprandial FA uptake of NEFA+DFA has, however, never been reported in prediabete

173 DHA and NEFA-DHA demonstrates that uptake of NEFA-DHA into the brain is 10-fold greater than LPC-DHA.

174 The composition of NEFAs can acutely affect FMD.

175 lopment and modeling; high concentrations of NEFAs and insulin resistance occurring with high fat int

176 was to test the effect of acute elevation of NEFAs enriched with either saturated fatty acids (SFAs)

177 The role of NEFAs in obesity-related morbidity is interesting as NEF

178 In summary, 1) impaired suppression of NEFAs after oral glucose impairs insulin's ability to su

179 ugh the addition of 18:1n-9 had no effect on NEFA pool composition, 20:5n-3 mass increased >15-fold w

180 Only NEFA concentration and stearic acid were influenced by p

181 cine ingestion altered plasma adiponectin or NEFA concentrations.

182 mirrors the 2- to 4-fold increase in parent NEFA.

183 FAEEs comprised 0.1% to 2% of the parent NEFA concentrations.

184 Plasma NEFA and glucose concentrations are regulated, in part,

185 Plasma NEFA levels were elevated in one study for 3 h before an

186 by the sum of de novo lipogenesis and plasma NEFA input in HTG subjects.

187 cally significant association between plasma NEFA and sudden cardiac death.

188 ) to evaluate the association between plasma NEFA and the risk of sudden cardiac death in older adult

189 e evidence for an association between plasma NEFA measured late in life and the risk of sudden cardia

190 In conclusion, plasma NEFA-DHA is the major plasma pool supplying the brain.

191 We compared the effects of elevated plasma NEFA levels on basal and insulin-stimulated glucose meta

192 Despite the elevated plasma NEFA levels, ex vivo mitochondrial respiration in skelet

193 o link diabetes-associated changes in plasma NEFA and signaling lipids, we quantitatively targeted >1

194 es not only results in an increase in plasma NEFA, but shifts the plasma lipidomic profiles in ways t

195 thy men, concomitantly with increased plasma NEFA concentrations.

196 Acipimox treatment increased plasma NEFA levels (759 +/- 44 vs. 1,135 +/- 97 mumol/L for pla

197 -(13)C]oleate (0800-1400 h) labelling plasma NEFA, imTG, imLCAC and im-non-esterified FA (imNEFA).

198 ystemic NEFA delivery with maintained plasma NEFA concentrations.

199 suggests that impaired suppression of plasma NEFA after glucose ingestion would impair HGO suppressio

200 al EGP was unaffected by elevation of plasma NEFA levels in both groups.

201 ere provides unbiased quantitation of plasma NEFA species by liquid chromatography-tandem mass spectr

202 At rest, plasma NEFA are trafficked largely to imTG before they enter LC

203 output (HGO), in part by suppressing plasma NEFA levels, suggests that impaired suppression of plasm

204 racting fatty acids directly from the plasma NEFA and VLDL-TG pools compared with chylomicron-TG.

205 oral administration, which enters the plasma NEFA pool as well as multiple plasma esterified pools.

206 ain is similar to the uptake from the plasma NEFA pool.

207 Factors relating to plasma NEFA storage into imTG differ in men and women.

208 When plasma NEFA levels were prevented from falling during a selecti

209 interventions significantly increased plasma NEFAs in both healthy men and patients with diabetes.

210 In one study, plasma NEFAs were prevented from falling by infusion of 20% Lip

211 ke of these fatty acids compared with plasma NEFAs.

212 Postload NEFA were associated with risk of DM (per standard devia

213 Fasting and postload NEFA showed significant associations with lower insulin

214 Fasting and postload NEFA were related to lower insulin sensitivity and pancr

215 DM in men but were accentuated for postload NEFA in women and among leaner individuals.

216 The association for postload NEFA persisted after adjustment for putative intermediat

217 reatic beta-cell function, but only postload NEFA were associated with increased DM.

218 lesterol, reduced triglycerides, and reduced NEFA, with a minimum effective dose of 30 mg/kg/day.

219 erular injury revealed significantly reduced NEFA uptake and palmitate-induced apoptosis in microperf

220 liferation and blocked significantly reduced NEFA-induced insulin resistance.

221 ative feedback loop in which CREBH regulates NEFA flux from adipose tissue to the liver via FGF21.

222 Diabetes related NEFA patterns indicated approximately 60% increase in st

223 Lipidomic analyses of released NEFAs from lipoproteins demonstrate that sPLA2s with ant

224 well as a positive correlation between serum NEFA levels and Ezh2 expression, were observed.

225 RESULTSPatients with HTG-AP had higher serum NEFA and TG levels and more severe AP (19% vs. 7%; P < 0

226 Serum NEFAs were correlated with serum TG fatty acids (TGFAs)

227 Alcoholic pancreatitis increased serum NEFAs.

228 Concentrations of seven NEFAs were found to decrease 9 months after surgery comp

229 tion with various concentrations of standard NEFA and serum samples.

230 diabetic compared with nondiabetic subjects: NEFA levels (muM) during 8 mU/m(2)/min insulin infusion

231 All subjects displayed substantial NEFA and glucose uptake upon cold exposure.

232 were associated with an increase in systemic NEFA turnover.

233 Nevertheless, systemic NEFA fluxes and NEFA spillover remained similar, suggest

234 downregulated, resulting in normal systemic NEFA concentrations over a 24-h period.

235 to an appropriate downregulation of systemic NEFA delivery with maintained plasma NEFA concentrations

236 tion of fatty acids from endogenous systemic NEFAs was similar across the groups, as were dietary fat

237 linical outcomes.METHODSAdmission serum TGs, NEFA composition, and concentrations were analyzed prosp

238 tidylcholine (LPC)-DHA enters the brain than NEFA-DHA, this is due to the longer plasma half-life and

239 ll recording technique, we demonstrated that NEFA inhibits NMDA responses with an IC50 of 0.51 microM

240 high NMDA concentration, we determined that NEFA affects receptor operation through an influence on

241 We determined that NEFA binds to the open channel, and subsequently the cha

242 Single-channel recordings revealed that NEFA reduces the mean open time of single NMDA-activated

243 etected a novel risk pattern suggesting that NEFAs together with HDL cholesterol may be related to sP

244 The NEFA gene was assessed as the USH1C locus by the sequenc

245 The NEFA pool contributed the great majority of fatty acids

246 suggest that basal fatty acid levels in the NEFA pool coupled with rates of fatty acid esterificatio

247 undance of putative PPARalpha ligands in the NEFA pool is 20:4n-6 = 18:2n-6 = 18:1n-9 > 22:6n-3 > 18:

248 a significant accumulation of 20:5n-3 in the NEFA pool through a process that requires peroxisomal be

249 olysis in organ failure and to interpret the NEFA-TGFA correlations.RESULTSPatients with HTG-AP had h

250 of active metabolites in platelets when the NEFA binding capacity of albumin is blunted by glycoxida

251 tion.CONCLUSIONSHTG-AP is made severe by the NEFAs generated from intravascular lipolysis of circulat

252 ications on biological mechanisms related to NEFA handling were investigated.

253 dents caused lipolysis of circulating TGs to NEFAs.

254 ted Cox-regression analysis, log-transformed NEFA level was inversely associated with the development

255 12 wk of intervention, plasma triglyceride, NEFA, and glucose concentrations were significantly high

256 is12-CLA group, whereas plasma triglyceride, NEFA, glucose, and insulin concentrations were significa

257 that FATP2 is a major apical proximal tubule NEFA transporter that regulates lipoapoptosis and may be

258 Correlations of long-chain unsaturated NEFAs with corresponding TGFAs increased with TG concent

259 specific ATP6AP2 knockout increases urinary NEFA excretion in the setting of impaired receptor-media

260 ized that ATP6AP2 knockout increases urinary NEFA excretion through a reduction in megalin.

261 h ND and HFD fed mice while normalized urine NEFA concentration increased 489% and 259% in ND and HFD

262 microperfusion and in vitro experiments with NEFA-bound albumin at concentrations that mimic apical p

263 teraction of genetic variation in FFAR1 with NEFA and insulin secretion.

264 imTG NEFA storage was correlated only with NEFA concentrations (r = 0.52, P = 0.004) in women and w

265 Women with NEFA levels in the highest tertile versus the lowest wer

266 blasts or mesenchymal stromal ST2 cells with NEFAs significantly decreased insulin signaling.

267 FAEES correlated strongly with NEFAs independent of ethanol levels in alcoholic pancrea