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1 n (HSA), an abundant plasma protein, are non-esterified fatty acids.
2 y agents include insulin, prolactin, and non-esterified fatty acids.
3          PPARs and LXRs are activated by non-esterified fatty acids and cholesterol metabolites, resp
4 and the metabolites, triglycerides (TG), non-esterified fatty acids and glucose; (3) an increase in m
5    tCys correlated positively with serum non-esterified fatty acids and leptin, partly independent of
6 re is unique inside the cell, with a core of esterified fatty acids and sterols, mainly triglycerides
7  that primarily lowers concentrations of non-esterified fatty acids and thereby lowers VLDL triglycer
8                Diurnal concentrations of non-esterified fatty acid are often elevated in obesity, in
9 sulin, are significantly elevated, while non-esterified fatty acids are reduced.
10      Other methods, such as creamatocrit and esterified fatty acid assay (EFA), have also been used w
11 S-based formula had the lowest levels of non-esterified fatty acids at all time points, and glucose a
12  metabolic rate, fasting plasma glucose, non-esterified fatty acids, cholesterol, and triglycerides.
13 acity, LCFA-CoA acyl chain distribution, and esterified fatty acid distribution.
14                         Combining Pb and non-esterified fatty acids enhanced these effects.
15 es for its primary physiological ligand, non-esterified fatty acids (FA).
16 n high sugar diets impaired the synthesis of esterified fatty acids from dietary glucose.
17 le avoiding interferences from hydrolysis of esterified fatty acids from other lipid classes.
18 ose tissue releases increased amounts of non-esterified fatty acids, glycerol, hormones, pro-inflamma
19 -standing elevation of concentrations of non-esterified fatty acid in plasma.
20               Because DHA is the predominant esterified fatty acid in rod outer segment (ROS) phospho
21                    Levels of glucose and non-esterified fatty acid in the blood are reversed in DD an
22 xpression selectively altered the pattern of esterified fatty acids in favor of polyunsaturated fatty
23 ed through altered Wnt signaling, Pb and non-esterified fatty acids in MC3T3 cells increased in vitro
24                                          Non-esterified fatty acids in plasma originate from adipose
25  with increased glucose levels than with non-esterified fatty acid levels, thus supporting the import
26 s in adipocytes and thereby reduce serum non-esterified fatty acid levels.
27 body weight, plasma lipids, glucose, and non-esterified fatty acid levels.
28 , overburdened by high concentrations of non-esterified fatty acids, may develop resistance to insuli
29 onstrate that DHA uptake from the plasma non-esterified fatty acid (NEFA) pool predicts brain uptake
30              We hypothesized that plasma non-esterified fatty acids (NEFA) are trafficked directly to
31           While increases in circulating non-esterified fatty acids (NEFA) are well-described in diab
32               Elevated concentrations of non-esterified fatty acids (NEFA) in biological fluids are r
33 ed the ability of adrenaline to mobilize non-esterified fatty acids (NEFAs) in young lambs.
34                                          Non-esterified fatty acids or fatty acid metabolites bind to
35 ctin, pigment epithelial-derived factor, non-esterified fatty acids or noradrenaline (all P > 0.05).
36 ks, whereas neither plasma triglyceride, non-esterified fatty acid, or islet triglyceride levels were
37 lysis of membrane phospholipids to yield non-esterified fatty acids, such as AA, that facilitate Ca(2
38 icantly reduced plasma glucose, insulin, non-esterified fatty acids, triglycerides, and cholesterol a

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