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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

47 lower quantity of nonesterified fatty acids (NEFAs).

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

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

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

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

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

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

54 - 0.19 mmol/l, respectively; P < 0.001), and NEFA (median 0.17 [interquartile range 2.30-2.95] and 0.

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

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

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

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

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

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

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

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

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

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

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

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

67 Because NEFAs stimulate secretion through FFAR1, we examined the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

84 the production of redox active species from NEFA.

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

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

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

88 /- 1.0 micromol.kg(-1).min(-1)), net hepatic NEFA uptakes (0.1 +/- 0.1 and 1.8 +/- 0.2 micromol.kg(-1

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

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

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

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

93 imTG NEFA storage was correlated only with NEFA concentration

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

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

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

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

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

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

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

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

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

103 concentrations, concomitantly with increased NEFA concentrations.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124 otective rather than a tubulotoxic effect of NEFA.

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

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

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

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

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

130 (0.60-1.38) across consecutive quartiles of NEFA concentration.

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

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

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

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

135 The composition of NEFAs can acutely affect FMD.

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

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

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

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

140 cine ingestion altered plasma adiponectin or NEFA concentrations.

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

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

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

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

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

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

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

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

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

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

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

152 thy men, concomitantly with increased plasma NEFA concentrations.

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

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

155 ystemic NEFA delivery with maintained plasma NEFA concentrations.

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

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

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

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

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

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

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

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

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

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

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

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

168 ke of these fatty acids compared with plasma NEFAs.

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

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

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

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

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

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

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

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

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

178 were associated with an increase in systemic NEFA turnover.

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

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

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

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

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

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

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

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

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

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

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

190 The NEFA pool contributed the great majority of fatty acids

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

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

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

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

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

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

197 12 wk of intervention, plasma triglyceride, NEFA, and glucose concentrations were significantly high

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

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

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

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

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

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

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