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1 line, triglycerides, cholesteryl esters, and nonesterified fatty acids).
2 essing harmful intracellular accumulation of nonesterified fatty acid.
3 iators, lysophosphatidylcholine and oxidized nonesterified fatty acid.
4 orary storage site for energy in the form of nonesterified fatty acids.
5 ercise elicit an immediate increase in serum nonesterified fatty acids.
6 nge in the pattern of total, esterified, and nonesterified fatty acids.
7 rations, and were negatively associated with nonesterified fatty acids.
8 ators, lyso-phosphatidylcholine and oxidized nonesterified fatty acids.
9 is likely due to decreased beta-oxidation of nonesterified fatty acids.
10 was accounted for by MAP, triglycerides, and nonesterified fatty acids.
11 creases cholesterol synthesis and release of nonesterified fatty acids.
12 erol (12 +/- 3 to 258 +/- 47 micromol/l) and nonesterified fatty acid (194 +/- 10 to 540 +/- 80 micro
13 tion into triglyceride-rich lipoproteins and nonesterified fatty acid, AEE, and muscle markers were s
14 racteristic decrease from baseline in plasma nonesterified fatty acids after a mixed meal was inhibit
16 had a lower concentration of fasting plasma nonesterified fatty acids and less hepatic steatosis.
19 ease plasma concentrations of both TGRLs and nonesterified fatty acids and meal 2 to increase TGRLs o
21 r epididymal fat pads, lower blood levels of nonesterified fatty acids and triglycerides, and higher
23 ous glucose production, lipolysis (glycerol, nonesterified fatty acid), and glycogenolysis (lactate)
24 i on exercise capacity, oxygen uptake, serum nonesterified fatty acid, and glucose were measured duri
25 ty lipoproteins, cholesterol, triglycerides, nonesterified fatty acids, and leptin, whereas adiponect
26 ced physical activity; increased circulating nonesterified fatty acids; and increased IMCLs, diacylgl
28 plasma glucose, branched chain amino acids, nonesterified fatty acids, beta-hydroxybutyrate, and uri
29 ese results also suggest that esterified and nonesterified fatty acids can bind to and regulate prote
32 ion, it increased lipid oxidation and plasma nonesterified fatty acid concentrations compared with HF
34 serum insulin, glucose, triacylglycerol, and nonesterified fatty acid concentrations were measured, a
35 ts in increased serum levels of glycerol and nonesterified fatty acids, consistent with increased lip
36 to a meal produced TGRL that was enriched in nonesterified fatty acids, decreased IRF-1 expression, i
37 zed de novo in the liver from carbohydrates, nonesterified fatty acids derived from adipose tissue, n
38 ied fatty acids derived from adipose tissue, nonesterified fatty acids derived from the spillover of
41 mass spectrometry was used to analyze free (nonesterified) fatty acid (FFA) and triacylglycerol flux
43 ed at 10-min intervals; blood triglycerides, nonesterified fatty acids, glucose, lactate, inflammator
45 beta-cell membrane phospholipids to release nonesterified fatty acids, including AA, and inhibiting
46 ome in db mice contributed high-glucose- and nonesterified fatty acid-induced osteoblast apoptosis th
47 the percentage of small dense LDL; glucose; nonesterified fatty acids; insulin; and the homeostasis
49 eficient mice cleared blood triglyceride and nonesterified fatty acid less efficiently than wild-type
50 n of glucagon secretion, reduction in plasma nonesterified fatty acid level, decrease in the load of
52 ion decreases serum triacylglycerol (TG) and nonesterified fatty acid levels and improves insulin sen
53 rization associated with reduced circulating nonesterified fatty acid levels and normal glucose homeo
55 olysis but did not result in increased serum nonesterified fatty acid levels or ectopic TAG storage.
56 nd beta cell volume without affecting plasma nonesterified fatty acid levels, strongly suggesting tha
59 andial responses in plasma concentrations of nonesterified fatty acid (meal x time, P = 0.00014), tri
60 ution exerts a major influence on endogenous nonesterified fatty acid metabolism, which may in turn m
61 ctives were to determine the impact of KE on nonesterified fatty acid (NEFA) concentration and glucor
62 opic hormone (ACTH), cortisol, glucagon, and nonesterified fatty acid (NEFA) concentrations were not
64 VLDL particle and TG transport rates, plasma nonesterified fatty acid (NEFA) flux, and sources of fat
65 2)H(2)]palmitic acid to investigate systemic nonesterified fatty acid (NEFA) incorporation into VLDL
66 f various hormones and an increase in plasma nonesterified fatty acid (NEFA) levels and is mediated t
67 arin (0.5 U x kg(-1) x min(-1)) to clamp the nonesterified fatty acid (NEFA) levels during hyperinsul
71 rd quantitative methods for determination of nonesterified fatty acid (NEFA) species are still missin
72 Determinants of insulin sensitivity based on nonesterified fatty acid (NEFA) suppression after oral g
73 ied BAT oxidative metabolism and glucose and nonesterified fatty acid (NEFA) turnover in 6 healthy me
74 ive metabolism and perfusion and glucose and nonesterified fatty acid (NEFA) turnover were determined
78 gy for simultaneous quantitative analysis of nonesterified fatty acids (NEFA) species in biofluids is
79 ipose tissue lipolysis produces glycerol and nonesterified fatty acids (NEFA) that serve as energy so
80 ntrol subjects, but the rates of delivery of nonesterified fatty acids (NEFA) were downregulated, res
82 in resistance despite increasing circulating nonesterified fatty acids (NEFA), the main substrate for
83 mechanism involves leakage of albumin-bound nonesterified fatty acids (NEFAs) across the damaged glo
86 hus examined whether lipolytic generation of nonesterified fatty acids (NEFAs) from circulating trigl
88 HDL, and LDL cholesterol; triglycerides; and nonesterified fatty acids (NEFAs) in a total of 139 OT1D
89 tissue increases lipolysis and the entry of nonesterified fatty acids (NEFAs) in the liver, whereas
90 issue there was significant uptake of plasma nonesterified fatty acids (NEFAs) in the postprandial bu
91 t growth factor 21 (FGF21), adiponectin, and nonesterified fatty acids (NEFAs) may be involved in ami
92 in conscious dogs to determine the effect of nonesterified fatty acids (NEFAs) on net hepatic glucose
95 Autonomic symptom scores, lipid oxidation, nonesterified fatty acids (NEFAs), and glycerol response
96 isotopes for 4 days to label and track serum nonesterified fatty acids (NEFAs), dietary fatty acids,
98 rgans to circulating triglycerides (TGs) and nonesterified fatty acids (NEFAs), ultimately leading to
99 ed adipose triglyceride and generated excess nonesterified fatty acids (NEFAs), which caused organ fa
101 (VLDL)-triacylglycerols and plasma free FA [nonesterified fatty acids (NEFAs)] were analyzed by usin
103 r (P < 0.05), whereas glucose (P < 0.05) and nonesterified fatty acids (P < 0.0001) were higher.
105 fasting plasma insulin (r = 0.60, P < 0.05), nonesterified fatty acid (r = 0.63, P < 0.02), and gluco
106 y deplete [Ca(2+)](m) and thus contribute to nonesterified fatty acid-responsive mitochondrial dysfun
107 ction similarly in all groups and suppressed nonesterified fatty acids similarly between control subj
108 of glucose, lactate, and ketones and higher nonesterified fatty acids than wild type (WT) littermate
109 es results in the liberation of glycerol and nonesterified fatty acids that are released into the vas
110 n the dose-response curve for suppression of nonesterified fatty acids versus insulin levels in the N
113 pid, triacylglycerol, cholesteryl ester, and nonesterified fatty acid) were extracted from fasting ba
114 fied non-HDL-cholesterol, triglycerides, and nonesterified fatty acids, with a minimum effective dose