ライフサイエンスコーパス: nonesterified

1 with the secondary hydroxyl group remaining nonesterified.

2 at 2-12(S)-HETE-lysophospholipids as well as nonesterified 12(S)-HETE are potent lipid mediators that

3 Here we demonstrate that nonesterified AA regulates the biophysical activity of t

4 Nonesterified ACP was not an inhibitor.

5 th PGF2 alpha, 11-deoxy-PGE1, or PhXA85 (the nonesterified analogue of PhXA41) for 12 to 72 hours.

6 ith PGF2alpha, 11-deoxy-PGE1, or PhXA85 (the nonesterified analogue of PhXA41) for 12 to 72 hours.

7 ture was two-thirds esterified and one-third nonesterified and consisted of beta-sitosterol (48%), ca

8 Arabidopsis cell wall, the pectins have both nonesterified and highly esterified regions.

9 IL-1 does enhance release of nonesterified arachidonate from islets, as measured by i

10 Accumulation of nonesterified arachidonate in islet membranes may influe

11 IL-1 also induces accumulation of nonesterified arachidonic acid in islets by an NO-depend

12 novel action of NO is to increase levels of nonesterified arachidonic acid in islets.

13 terol and heme-supplemented media accumulate nonesterified carboxylic acid sterols such as 4beta, 14a

14 acic aorta, with concentrations of total and nonesterified cholesterol 17% and 25% (both P<.05) great

15 holesterol turnover, causing accumulation of nonesterified cholesterol in lysosomes/autolysosomes, it

16 ks, concentrations of total, esterified, and nonesterified cholesterol were similar for the pulmonary

17 ar cholesterol levels nor the cellular free (nonesterified) cholesterol pool.

18 his influences whether DHA is metabolized to nonesterified DHA (free DHA) or a phospholipid form call

19 ed dietary FA (DFA) storage and/or increased nonesterified FA (NEFA) flux from adipose tissue intrace

20 ion of fasting concentrations of circulating nonesterified FA (NEFA) with the development of graft fa

21 cytes is associated with marked increases in nonesterified FAHFA levels, demonstrating that FAHFA-TGs

22 tions are greater than 100-fold than that of nonesterified FAHFAs, indicating that FAHFA-TGs are a ma

23 ood mutual agreement was demonstrated for 12 nonesterified FAs consistently measured in 50 serum samp

24 ration platform for analysis of more than 20 nonesterified FAs in human serum or plasma.

25 erol (12 +/- 3 to 258 +/- 47 micromol/l) and nonesterified fatty acid (194 +/- 10 to 540 +/- 80 micro

26 andial responses in plasma concentrations of nonesterified fatty acid (meal x time, P = 0.00014), tri

27 ctives were to determine the impact of KE on nonesterified fatty acid (NEFA) concentration and glucor

28 opic hormone (ACTH), cortisol, glucagon, and nonesterified fatty acid (NEFA) concentrations were not

29 ndrial function independent of reductions in nonesterified fatty acid (NEFA) concentrations.

30 VLDL particle and TG transport rates, plasma nonesterified fatty acid (NEFA) flux, and sources of fat

31 2)H(2)]palmitic acid to investigate systemic nonesterified fatty acid (NEFA) incorporation into VLDL

32 f various hormones and an increase in plasma nonesterified fatty acid (NEFA) levels and is mediated t

33 arin (0.5 U x kg(-1) x min(-1)) to clamp the nonesterified fatty acid (NEFA) levels during hyperinsul

34 Elevation of plasma nonesterified fatty acid (NEFA) levels has been shown in

35 widely regarded as monitors of intracellular nonesterified fatty acid (NEFA) levels.

36 Nonesterified fatty acid (NEFA) release was suppressed a

37 rd quantitative methods for determination of nonesterified fatty acid (NEFA) species are still missin

38 Determinants of insulin sensitivity based on nonesterified fatty acid (NEFA) suppression after oral g

39 ied BAT oxidative metabolism and glucose and nonesterified fatty acid (NEFA) turnover in 6 healthy me

40 ive metabolism and perfusion and glucose and nonesterified fatty acid (NEFA) turnover were determined

41 fasting plasma insulin (r = 0.60, P < 0.05), nonesterified fatty acid (r = 0.63, P < 0.02), and gluco

42 The d31-palmitate appearance in nonesterified fatty acid and very-low-density lipoprotei

43 Blood nonesterified fatty acid concentration was not affected

44 The nonesterified fatty acid concentration was significantly

45 ion, it increased lipid oxidation and plasma nonesterified fatty acid concentrations compared with HF

46 Nonesterified fatty acid concentrations were lower up to

47 serum insulin, glucose, triacylglycerol, and nonesterified fatty acid concentrations were measured, a

48 eficient mice cleared blood triglyceride and nonesterified fatty acid less efficiently than wild-type

49 n of glucagon secretion, reduction in plasma nonesterified fatty acid level, decrease in the load of

50 ratio (P = 0.013), and, surprisingly, higher nonesterified fatty acid levels (P = 0.01).

51 ion decreases serum triacylglycerol (TG) and nonesterified fatty acid levels and improves insulin sen

52 rization associated with reduced circulating nonesterified fatty acid levels and normal glucose homeo

53 Fasting increased plasma nonesterified fatty acid levels in both lean and obese r

54 olysis but did not result in increased serum nonesterified fatty acid levels or ectopic TAG storage.

55 nd beta cell volume without affecting plasma nonesterified fatty acid levels, strongly suggesting tha

56 ks, without significant alteration of plasma nonesterified fatty acid levels.

57 ution exerts a major influence on endogenous nonesterified fatty acid metabolism, which may in turn m

58 This fall in nonesterified fatty acid was accompanied by a fall in th

59 pid, triacylglycerol, cholesteryl ester, and nonesterified fatty acid) were extracted from fasting ba

60 ous glucose production, lipolysis (glycerol, nonesterified fatty acid), and glycogenolysis (lactate)

61 tion into triglyceride-rich lipoproteins and nonesterified fatty acid, AEE, and muscle markers were s

62 i on exercise capacity, oxygen uptake, serum nonesterified fatty acid, and glucose were measured duri

63 ome in db mice contributed high-glucose- and nonesterified fatty acid-induced osteoblast apoptosis th

64 y deplete [Ca(2+)](m) and thus contribute to nonesterified fatty acid-responsive mitochondrial dysfun

65 essing harmful intracellular accumulation of nonesterified fatty acid.

66 iators, lysophosphatidylcholine and oxidized nonesterified fatty acid.

67 Plasma nonesterified fatty acids (NEFA) at elevated concentrati

68 Although nonesterified fatty acids (NEFA) have been positively as

69 Nonesterified fatty acids (NEFA) in urine are bound to a

70 gy for simultaneous quantitative analysis of nonesterified fatty acids (NEFA) species in biofluids is

71 ipose tissue lipolysis produces glycerol and nonesterified fatty acids (NEFA) that serve as energy so

72 ntrol subjects, but the rates of delivery of nonesterified fatty acids (NEFA) were downregulated, res

73 To evaluate the association of nonesterified fatty acids (NEFA) with dysglycemia in old

74 in resistance despite increasing circulating nonesterified fatty acids (NEFA), the main substrate for

75 mechanism involves leakage of albumin-bound nonesterified fatty acids (NEFAs) across the damaged glo

76 Impaired suppression of plasma nonesterified fatty acids (NEFAs) after glucose ingestio

77 We studied the effects of nonesterified fatty acids (NEFAs) and adipokines on acin

78 hus examined whether lipolytic generation of nonesterified fatty acids (NEFAs) from circulating trigl

79 Experimental elevation of nonesterified fatty acids (NEFAs) impairs endothelial fu

80 HDL, and LDL cholesterol; triglycerides; and nonesterified fatty acids (NEFAs) in a total of 139 OT1D

81 tissue increases lipolysis and the entry of nonesterified fatty acids (NEFAs) in the liver, whereas

82 issue there was significant uptake of plasma nonesterified fatty acids (NEFAs) in the postprandial bu

83 t growth factor 21 (FGF21), adiponectin, and nonesterified fatty acids (NEFAs) may be involved in ami

84 in conscious dogs to determine the effect of nonesterified fatty acids (NEFAs) on net hepatic glucose

85 We compared FAEEs levels with their nonesterified fatty acids (NEFAs) precursors during alco

86 Preliminary data suggest that plasma nonesterified fatty acids (NEFAs) raise plasma ANGPTL4 c

87 Autonomic symptom scores, lipid oxidation, nonesterified fatty acids (NEFAs), and glycerol response

88 isotopes for 4 days to label and track serum nonesterified fatty acids (NEFAs), dietary fatty acids,

89 High plasma concentrations of nonesterified fatty acids (NEFAs), transported bound to

90 rgans to circulating triglycerides (TGs) and nonesterified fatty acids (NEFAs), ultimately leading to

91 ed adipose triglyceride and generated excess nonesterified fatty acids (NEFAs), which caused organ fa

92 ic than hGV but releases a lower quantity of nonesterified fatty acids (NEFAs).

93 (VLDL)-triacylglycerols and plasma free FA [nonesterified fatty acids (NEFAs)] were analyzed by usin

94 r (P < 0.05), whereas glucose (P < 0.05) and nonesterified fatty acids (P < 0.0001) were higher.

95 Adipo-IR (fasting nonesterified fatty acids [NEFAs] x fasting insulin) was

96 racteristic decrease from baseline in plasma nonesterified fatty acids after a mixed meal was inhibit

97 had a lower concentration of fasting plasma nonesterified fatty acids and less hepatic steatosis.

98 Nonesterified fatty acids and lipid peroxidation were in

99 atty acyl chains from phospholipids to yield nonesterified fatty acids and lysophospholipids.

100 ease plasma concentrations of both TGRLs and nonesterified fatty acids and meal 2 to increase TGRLs o

101 In contrast, the liver pool sizes of nonesterified fatty acids and triglycerides were not alt

102 r epididymal fat pads, lower blood levels of nonesterified fatty acids and triglycerides, and higher

103 Nonesterified fatty acids are key intermediates in cellu

104 ese results also suggest that esterified and nonesterified fatty acids can bind to and regulate prote

105 zed de novo in the liver from carbohydrates, nonesterified fatty acids derived from adipose tissue, n

106 ied fatty acids derived from adipose tissue, nonesterified fatty acids derived from the spillover of

107 ucagon-like peptide 1, insulin, glucose, and nonesterified fatty acids determined for 4 h.

108 Metabolic profiling of plasma nonesterified fatty acids discovered that palmitic acid

109 Pathologically increased nonesterified fatty acids have widely been viewed as a k

110 Adipose release of nonesterified fatty acids into plasma decreased by 53% a

111 Nonesterified fatty acids may influence mitochondrial fu

112 occurred with elevated glucose, insulin, and nonesterified fatty acids peak after lunch.

113 ction similarly in all groups and suppressed nonesterified fatty acids similarly between control subj

114 of glucose, lactate, and ketones and higher nonesterified fatty acids than wild type (WT) littermate

115 es results in the liberation of glycerol and nonesterified fatty acids that are released into the vas

116 n the dose-response curve for suppression of nonesterified fatty acids versus insulin levels in the N

117 Neither lipolysis nor flux of plasma nonesterified fatty acids were altered compared with bas

118 Lipolysis (glycerol, nonesterified fatty acids) and endogenous glucose produc

119 line, triglycerides, cholesteryl esters, and nonesterified fatty acids).

120 ty lipoproteins, cholesterol, triglycerides, nonesterified fatty acids, and leptin, whereas adiponect

121 plasma glucose, branched chain amino acids, nonesterified fatty acids, beta-hydroxybutyrate, and uri

122 ts in increased serum levels of glycerol and nonesterified fatty acids, consistent with increased lip

123 to a meal produced TGRL that was enriched in nonesterified fatty acids, decreased IRF-1 expression, i

124 Plasma concentrations of triglycerides, nonesterified fatty acids, glucose, and insulin were mon

125 ed at 10-min intervals; blood triglycerides, nonesterified fatty acids, glucose, lactate, inflammator

126 beta-cell membrane phospholipids to release nonesterified fatty acids, including AA, and inhibiting

127 fied non-HDL-cholesterol, triglycerides, and nonesterified fatty acids, with a minimum effective dose

128 was accounted for by MAP, triglycerides, and nonesterified fatty acids.

129 creases cholesterol synthesis and release of nonesterified fatty acids.

130 orary storage site for energy in the form of nonesterified fatty acids.

131 ercise elicit an immediate increase in serum nonesterified fatty acids.

132 nge in the pattern of total, esterified, and nonesterified fatty acids.

133 rations, and were negatively associated with nonesterified fatty acids.

134 ators, lyso-phosphatidylcholine and oxidized nonesterified fatty acids.

135 is likely due to decreased beta-oxidation of nonesterified fatty acids.

136 ced physical activity; increased circulating nonesterified fatty acids; and increased IMCLs, diacylgl

137 the percentage of small dense LDL; glucose; nonesterified fatty acids; insulin; and the homeostasis

138 mass spectrometry was used to analyze free (nonesterified) fatty acid (FFA) and triacylglycerol flux

139 HF-Cas group had significantly greater serum nonesterified free fatty acid (NEFA) concentrations than

140 st, basal levels of catecholamine-stimulated nonesterified free fatty acid (NEFA) release and plasma

141 sk factors in the onset of type II diabetes, nonesterified free fatty acid and triglyceride content i

142 In summary, we have described a novel nonesterified free fatty acid-stimulated pathway that se

143 ulinemia coexists with increased circulating nonesterified free fatty acids and increased adiposity i

144 uman islets and is stimulated by exposure to nonesterified free fatty acids at concentrations observe

145 d the plasma level and net hepatic uptake of nonesterified free fatty acids increased, whereas during

146 A dose-dependent decrease of nonesterified free fatty acids was seen in ZDF rats but

147 ose, insulin, triglyceride, cholesterol, and nonesterified free fatty acids) than could be accounted

148 , as indicated by measurements of C-peptide, nonesterified free fatty acids, and glycerol, were also

149 t increase in fasting levels of cholesterol, nonesterified free fatty acids, and triacylglycerol.

150 S) in pancreatic islets that is activated by nonesterified free fatty acids, the major fuel used by b

151 Nonesterified (free) fatty acid (NEFA) concentrations in

152 We considered that accumulation of nonesterified (free) fatty acids (NEFAs) in the first tr

153 hanism in planta, a benzyl etherification of nonesterified hydroxyl groups of glycerol and hydroxy fa

154 observations suggest an inherent efficacy of nonesterified long-chain fatty acids (LCFA) in suppressi

155 Nonesterified long-chain fatty acids may enter cells by

156 ds was 3-fold higher than the ratio of their nonesterified moieties.

157 -acylceramides and led to an accumulation of nonesterified omega-hydroxy-ceramides.

158 eceptors that recognize and are activated by nonesterified or "free" fatty acids (FFAs).

159 strongly hydrated almost exclusively at the nonesterified oxygen atoms, and that the hydration of th

160 ntrations of polyunsaturated fatty acids and nonesterified polyunsaturated fatty acids in hypothalami

161 s were observed in the cholesteryl ester and nonesterified pools.

162 ition of fatty acids to primary hepatocytes, nonesterified unsaturated fatty acid levels are very low

163 ed two sources of PPARalpha activators (i.e. nonesterified unsaturated fatty acids and chylomicron re

164 bile acids were additive with the effects of nonesterified unsaturated fatty acids in regulating FGF2