ライフサイエンスコーパス: nonesterified

1 with the secondary hydroxyl group remaining nonesterified.

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

3 Nonesterified ACP was not an inhibitor.

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

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

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

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

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

9 Accumulation of nonesterified arachidonate in islet membranes may influe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

25 Nonesterified fatty acid (NEFA) release was suppressed a

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

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

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

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

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

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

32 The nonesterified fatty acid concentration was significantly

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

34 Nonesterified fatty acid concentrations were lower up to

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 iators, lysophosphatidylcholine and oxidized nonesterified fatty acid.

51 Plasma nonesterified fatty acids (NEFA) at elevated concentrati

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

75 Nonesterified fatty acids and lipid peroxidation were in

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

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

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

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

80 Nonesterified fatty acids are key intermediates in cellu

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

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

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

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

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

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

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

88 Nonesterified fatty acids may influence mitochondrial fu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 creases cholesterol synthesis and release of nonesterified fatty acids.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 Nonesterified long-chain fatty acids may enter cells by

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

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

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

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

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

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

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

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