ライフサイエンスコーパス: esterified fatty acid

1 n (HSA), an abundant plasma protein, are non-esterified fatty acids.

2 y agents include insulin, prolactin, and non-esterified fatty acids.

3 ld thicknesses (13 amino acid-related, 4 non-esterified fatty acids, 6 xenobiotics, and 5 unknown com

4 ine is best known for its ability to shuttle esterified fatty acids across mitochondrial membranes fo

5 d significantly higher concentrations of non-esterified fatty acids and beta-hydroxybutyrate than mid

6 PPARs and LXRs are activated by non-esterified fatty acids and cholesterol metabolites, resp

7 and the metabolites, triglycerides (TG), non-esterified fatty acids and glucose; (3) an increase in m

8 tCys correlated positively with serum non-esterified fatty acids and leptin, partly independent of

9 Concentrations of esterified and non-esterified fatty acids and oxylipins in TGRL were quanti

10 re is unique inside the cell, with a core of esterified fatty acids and sterols, mainly triglycerides

11 that primarily lowers concentrations of non-esterified fatty acids and thereby lowers VLDL triglycer

12 fasting on the concentration of insulin, non-esterified fatty acid, and ketones.

13 Diurnal concentrations of non-esterified fatty acid are often elevated in obesity, in

14 sulin, are significantly elevated, while non-esterified fatty acids are reduced.

15 Other methods, such as creamatocrit and esterified fatty acid assay (EFA), have also been used w

16 S-based formula had the lowest levels of non-esterified fatty acids at all time points, and glucose a

17 metabolic rate, fasting plasma glucose, non-esterified fatty acids, cholesterol, and triglycerides.

18 Fat oxidation and plasma non-esterified fatty acid concentrations were both lower in

19 acity, LCFA-CoA acyl chain distribution, and esterified fatty acid distribution.

20 Combining Pb and non-esterified fatty acids enhanced these effects.

21 es for its primary physiological ligand, non-esterified fatty acids (FA).

22 n high sugar diets impaired the synthesis of esterified fatty acids from dietary glucose.

23 le avoiding interferences from hydrolysis of esterified fatty acids from other lipid classes.

24 ose tissue releases increased amounts of non-esterified fatty acids, glycerol, hormones, pro-inflamma

25 -standing elevation of concentrations of non-esterified fatty acid in plasma.

26 Because DHA is the predominant esterified fatty acid in rod outer segment (ROS) phospho

27 Levels of glucose and non-esterified fatty acid in the blood are reversed in DD an

28 xpression selectively altered the pattern of esterified fatty acids in favor of polyunsaturated fatty

29 ed through altered Wnt signaling, Pb and non-esterified fatty acids in MC3T3 cells increased in vitro

30 Non-esterified fatty acids in plasma originate from adipose

31 estigate hepatic lipid profiles, focusing on esterified fatty acids in two mouse models of metabolic

32 control, including postprandial glucose, non-esterified fatty acids, insulin or triglycerides, were f

33 Interestingly, circulating non-esterified fatty acid levels did not increase with lipol

34 with increased glucose levels than with non-esterified fatty acid levels, thus supporting the import

35 s in adipocytes and thereby reduce serum non-esterified fatty acid levels.

36 body weight, plasma lipids, glucose, and non-esterified fatty acid levels.

37 , overburdened by high concentrations of non-esterified fatty acids, may develop resistance to insuli

38 onstrate that DHA uptake from the plasma non-esterified fatty acid (NEFA) pool predicts brain uptake

39 pose tissue led to an increase in plasma non-esterified fatty acids (NEFA) and beta-hydroxybutyrate (

40 We hypothesized that plasma non-esterified fatty acids (NEFA) are trafficked directly to

41 While increases in circulating non-esterified fatty acids (NEFA) are well-described in diab

42 Elevated concentrations of non-esterified fatty acids (NEFA) in biological fluids are r

43 ed the ability of adrenaline to mobilize non-esterified fatty acids (NEFAs) in young lambs.

44 d levels of plasma lipids, which include non-esterified fatty acids (NEFAs).

45 Non-esterified fatty acids or fatty acid metabolites bind to

46 ctin, pigment epithelial-derived factor, non-esterified fatty acids or noradrenaline (all P > 0.05).

47 ks, whereas neither plasma triglyceride, non-esterified fatty acid, or islet triglyceride levels were

48 lysis of membrane phospholipids to yield non-esterified fatty acids, such as AA, that facilitate Ca(2

49 icantly reduced plasma glucose, insulin, non-esterified fatty acids, triglycerides, and cholesterol a

50 vs. 750 (665, 835) ng/mL x min], whereas non-esterified fatty acids were increased [AUC 135 (117, 153

51 insulin resistance, diacylglycerols and non-esterified fatty acids, were distinct for healthy and im