ライフサイエンスコーパス: ketogenesis

1 ered TGD, and stimulated lipolysis, LOx, and ketogenesis.

2 stress hormones that stimulate lipolysis and ketogenesis.

3 blast growth factor 21 expression and intact ketogenesis.

4 with consequent diversion of acetyl-CoA into ketogenesis.

5 a-hydroxybutyryate, without evidence of true ketogenesis.

6 o-glucagon ratio) favors glucose release and ketogenesis.

7 ng liver and kidney, which was essential for ketogenesis.

8 amined whether OS phagocytosis was linked to ketogenesis.

9 pha target genes in fatty acid oxidation and ketogenesis.

10 ive hepatic fatty acid oxidation and fasting ketogenesis.

11 c fatty acid oxidation, gluconeogenesis, and ketogenesis.

12 ient to prevent the ageing-induced defect in ketogenesis.

13 glucose concentrations and rates of HGP and ketogenesis.

14 c gluconeogenesis, fatty acid oxidation, and ketogenesis.

15 d fast and have impaired gluconeogenesis and ketogenesis.

16 lglycerol synthesis and toward oxidation and ketogenesis.

17 riptional programmes of lipid metabolism and ketogenesis.

18 nzymes required for fatty acid oxidation and ketogenesis.

19 on of mitochondrial fatty acid oxidation and ketogenesis.

20 lipogenesis is energy wasteful and precludes ketogenesis.

21 rhagic shock has any salutary effects on gut ketogenesis.

22 iagenesis, ureagenesis, gluconeogenesis, and ketogenesis.

23 ycemia causes the increases in lipolysis and ketogenesis.

24 hepatic G0S2 knockdown also showed increased ketogenesis, accelerated gluconeogenesis, and decelerate

25 sis, which was sufficient to prevent rise in ketogenesis, also prevented a fall in leptin.

26 lic pathways including fatty acid oxidation, ketogenesis, amino acid catabolism, and the urea and tri

27 er and skeletal muscle, resulting in hepatic ketogenesis and glucocorticoid-driven muscle catabolism,

28 es encoding enzymes of fatty acid oxidation, ketogenesis and glycolysis.

29 ha agonist induced hepatic fat oxidation via ketogenesis and hepatic TCA cycle activity but failed to

30 regulator of PPARalpha function and hepatic ketogenesis and suggest a role for mTORC1 activity in pr

31 rn promotes hepatic fatty acid oxidation and ketogenesis and ultimately leads to increased energy exp

32 duced lipid droplet formation and subsequent ketogenesis and, ultimately, for maintaining systemic en

33 f genes involved in fatty acid oxidation and ketogenesis, and increased expression of genes that cont

34 etabolic alterations related to lipogenesis, ketogenesis, and inflammation in db/db mice.

35 HMG-CoA lyase (HMGCL) is crucial to ketogenesis, and inherited human mutations are potential

36 These studies suggest that FAO and ketogenesis are key to supporting the metabolism of the

37 wed fasting hepatic steatosis and diminished ketogenesis associated with decreased expression of gene

38 ne palmitoyltransferase (CPT I) over hepatic ketogenesis because its role in controlling this pathway

39 es are depleted, hepatic gluconeogenesis and ketogenesis become major energy sources.

40 was impaired twofold secondary to decreased ketogenesis, but tricarboxylic acid (TCA) cycle activity

41 epatic glucose production (HGP), and hepatic ketogenesis by 50% within 6 hours and were independent o

42 BP contributes to hepatic LCFA oxidation and ketogenesis by a nontranscriptional mechanism, whereas L

43 Ketogenesis can dispose of much of the fat that enters t

44 t these genes were significantly involved in ketogenesis, cardiovascular disease, apoptosis and other

45 ual flux control coefficients for CPT I over ketogenesis, CO2 production and total carbon flux (0.51

46 Patients with CFRD rarely develop ketogenesis, despite insulin deficiency.

47 Pentoxifylline promotes gut ketogenesis following trauma-hemorrhage and resuscitatio

48 e by the liver are similar, the rate of C(5) ketogenesis from heptanoate is much lower than the rate

49 ptanoate is much lower than the rate of C(4) ketogenesis from octanoate.

50 C(5) ketogenesis from propionate is virtually nil because ace

51 xidation (LOx; by indirect calorimetry), and ketogenesis (from circulating beta-hydroxybutyrate conce

52 1), a co-repressor of PPARalpha, reactivates ketogenesis in cells and livers with hyperactive mTORC1

53 tin-induced decreases in lipolysis, HGP, and ketogenesis in DKA were also nullified by relatively sma

54 CPT I exerts significantly less control over ketogenesis in hepatocytes isolated from suckling rats t

55 alpha can induce genes of beta-oxidation and ketogenesis in hepatocytes, but these effects do not req

56 ous FGF21 does not drive starvation-mediated ketogenesis in humans.

57 Here we show that mTORC1 controls ketogenesis in mice in response to fasting.

58 lysed starvation-induced gluconeogenesis and ketogenesis in mouse strains lacking autophagy in liver,

59 A synthase (HMGCS2) to determine the role of ketogenesis in preventing diet-induced steatohepatitis.

60 impairment of fatty acid beta-oxidation and ketogenesis in the liver under chronic fasting or ketoge

61 other specialized tissue functions, such as ketogenesis in the liver.

62 d the connection between OS phagocytosis and ketogenesis in wild-type mice and mice with defects in p

63 hydroxy-3-methylglutarate-CoA synthase 2 (in ketogenesis) in wild-type (Pxr(+/+)) mice only.

64 F21 induces hepatic fatty acid oxidation and ketogenesis, increases insulin sensitivity, blocks somat

65 ediates and gluconeogenesis in the livers of ketogenesis-insufficient animals.

66 Together, these findings indicate that ketogenesis is a critical regulator of hepatic acyl-CoA

67 ittle or no glycolytic reserve; (iii) marked ketogenesis; (iv) depletion of intracellular NTPs; (v) a

68 ion in the absorptive state and suggest that ketogenesis may modulate fatty liver disease.

69 nt, Ppar alpha-regulated increase in hepatic ketogenesis occurs, and myocardial metabolism is directe

70 In addition, CR reversed ketogenesis pathway enzymes and the enhanced autophagy,

71 Hepatic ketogenesis plays an important role in catabolism of fat

72 investigated the interrelations between C(4) ketogenesis (production of beta-hydroxybutyrate + acetoa

73 f beta-hydroxybutyrate + acetoacetate), C(5) ketogenesis (production of beta-hydroxypentanoate + beta

74 expression of lipogenic genes, and increased ketogenesis relative to controls.

75 al and extramitochondrial LCFA oxidation and ketogenesis remained at wild-type levels.

76 c (endogenous glucose production, lipolysis, ketogenesis) responses to exercise; 2) antecedent hypogl

77 h-fat diet feeding of mice with insufficient ketogenesis resulted in extensive hepatocyte injury and

78 ed acyl-CoA esters reveal that C(4) and C(5) ketogenesis share the same pool of acetyl-CoA.

79 the flux control coefficients for CPT I over ketogenesis specifically and over total carbon flux (< 0

80 bited decreased rates of lipolysis, HGP, and ketogenesis; these effects were reversed by corticostero

81 stimulating mitochondrial beta-oxidation and ketogenesis through the XBP1s-PPARalpha axis.

82 However, the capacity for ketogenesis was not reduced: BHB plasma levels were rest

83 No increase in ketogenesis was observed following ingestion of oxidized

84 e production (EGP), lipolytic responses, and ketogenesis were also significantly attenuated (P<0.01)

85 a3-adrenergic agonist, in vivo lipolysis and ketogenesis were decreased in G0S2 transgenic mice when

86 es participating in fatty acid oxidation and ketogenesis were induced more slowly (24 h), following a

87 le genes responsible for lipid oxidation and ketogenesis were up-regulated in HRFI group.

88 promote lipolysis, fatty acid oxidation, and ketogenesis, whereas refeeding suppresses its expression

89 ORC1, livers from aged mice have a defect in ketogenesis, which correlates with an increase in mTORC1