ライフサイエンスコーパス: anaplerosis

1 to fill the tricarboxylic acid (TCA) cycle (anaplerosis).

2 aloacetate for continued TCA cycle function (anaplerosis).

3 in cancer cells that lack glucose-dependent anaplerosis.

4 s, with no compensation from glucose-derived anaplerosis.

5 sis, suggesting a metabolic reprogramming to anaplerosis.

6 ucose and other substrates generate TCAs via anaplerosis.

7 ired glutamine-derived carbon utilization in anaplerosis.

8 pecially in the context of citric acid cycle anaplerosis.

9 decreased FAO with increased glycolysis and anaplerosis.

10 Many tumor cells use glutamine to feed anaplerosis.

11 e-derived pyruvate rather than glutamine for anaplerosis.

12 ylglyceride (TAG) was linked to ME-catalyzed anaplerosis.

13 use differential dependence on glutamine for anaplerosis.

14 , very little is known about the products of anaplerosis.

15 ve from replacement of oxidized glutamate by anaplerosis.

16 d entry into the tricarboxylic acid cycle by anaplerosis.

17 reliance on glutamate to fuel energetics and anaplerosis.

18 Thus, PC-mediated, glucose-dependent anaplerosis allows cells to achieve glutamine independen

19 ements for PC- and GLS-mediated pathways for anaplerosis and cell proliferation.

20 Anaplerosis and gluconeogenesis from heptanoate are inhi

21 defining important determinants of glutamine anaplerosis and glutaminase dependence in cancer.

22 K(ATP)-independent mechanisms involving both anaplerosis and mitochondrial GTP (mtGTP).

23 he specific inability to cope with glutamate anaplerosis and nitroxidative stress.

24 gy and glutaminolysis can provide carbon for anaplerosis and reductive carboxylation to citrate.

25 rease in the expression of genes involved in anaplerosis and reverse cholesterol transport.

26 uantities of glutamine to maintain TCA cycle anaplerosis and support cell survival.

27 pha-ketoglutarate to maintain the TCA cycle (anaplerosis) and ATP production.

28 Citric acid cycle fluxes, pyruvate cycling, anaplerosis, and cataplerosis were also elevated during

29 elerated oxidative mitochondrial metabolism, anaplerosis, and malonyl-CoA/lipid signaling in beta-cel

30 through YAP/TAZ-dependent glutaminolysis and anaplerosis, and thereby link mechanical stimuli to dysr

31 increased, even though pyruvate cycling and anaplerosis are decreased; 4) the liver is unable to syn

32 d metformin-induced glycolysis and glutamine anaplerosis, both of which are survival responses of cel

33 Here, we show that mTORC1 promotes glutamine anaplerosis by activating glutamate dehydrogenase (GDH).

34 enzyme A production toward carbon influx via anaplerosis bypasses energy, yielding reactions contribu

35 ced oxidative metabolism, but also amplified anaplerosis/cataplerosis and caused a proportional rise

36 olism with metformin also normalized hepatic anaplerosis/cataplerosis and reduced markers of inflamma

37 Second, loss of anaplerosis/cataplerosis via genetic knockdown of phosph

38 catabolism and reduced reliance on glutamine anaplerosis compared to cells cultured in standard tissu

39 vel findings include that aspartate used for anaplerosis does not derive from the glucose fuel added

40 rt the hypothesis that a signal generated by anaplerosis from increased pyruvate carboxylase flux is

41 As part of a study on the regulation of anaplerosis from propionyl-CoA precursors in rat livers

42 yl-CoA pathway explains the effectiveness of anaplerosis from propionyl-CoA precursors such as heptan

43 Because different pathways of anaplerosis generate distinct products, they may differe

44 hetase 1 (urea cycle), pyruvate carboxylase (anaplerosis, gluconeogenesis), propionyl-CoA carboxylase

45 We postulate that the high rate of anaplerosis in awake brain is linked to brain activity b

46 er, some cell lines that depend on glutamine anaplerosis in culture rely less on glutamine catabolism

47 These findings indicate that PC-mediated anaplerosis in early-stage NSCLC is required for tumor s

48 ow that rates of mitochondrial oxidation and anaplerosis in human liver can be directly determined no

49 Increasing competition from PDH reduced anaplerosis in HYP+DCA by 18%.

50 Interestingly, reduced anaplerosis in HYP+DCA corresponded with normalized TAG

51 etermined partial reversibility of increased anaplerosis in HYP.

52 ydroxypentanoate + beta-ketopentanoate), and anaplerosis in isolated rat livers perfused with (13)C-l

53 wever, studies designed to lower the rate of anaplerosis in the beta cell have been inconclusive.

54 ruvate carboxylase (PC), the major enzyme of anaplerosis in the beta cell.

55 Inhibition of glutamine anaplerosis in the presence of metformin further attenua

56 be learned about the sites and regulation of anaplerosis in these tissues.

57 nsulin secretion by the beta cell depends on anaplerosis in which insulin secretagogues are metaboliz

58 stain membrane potential, ATP synthesis, and anaplerosis, in response to varying degrees of O2 limita

59 new mechanism of insulin secretion in which anaplerosis increases short chain acyl-CoAs that have ro

60 To test the hypothesis that anaplerosis is important for insulin secretion, we lower

61 Tricarboxylic acid (TCA) cycle anaplerosis is maintained primarily by glutamine.

62 nish tricarboxylic acid cycle intermediates (anaplerosis) is primarily used for amino acid biosynthes

63 Refilling the pool of precursor molecules (anaplerosis) is therefore crucial to maintain cell growt

64 but impaired tricarboxylic acid (TCA) cycle anaplerosis, macromolecule production, and redox homeost

65 e reduced, whereas compensatory increases in anaplerosis maintain tricarboxylic acid cycle flux and a

66 t NADH production from pyruvate fueling this anaplerosis, ME also consumes NADPH necessary for lipoge

67 mitate oxidation, preventing the increase in anaplerosis observed in nontransgenic TAC hearts.

68 etoglutarate to glutamate, with impaired TCA anaplerosis of glutamate carbon.

69 er of the coenzyme A derivatives involved in anaplerosis of the citric acid cycle via precursors of p

70 , DODA contributes a substantial fraction to anaplerosis of the citric acid cycle.

71 g of the propionyl moiety of heptanoate into anaplerosis of the citric acid cycle.

72 an catalyze the reverse reaction, supporting anaplerosis of the tricarboxylic acid cycle, under condi

73 ans also increased longevity suggesting that anaplerosis of tricarboxylic acid (TCA) cycle substrates

74 evated ME expression with a 90% elevation in anaplerosis over SHAM.

75 As the anaplerosis pathways are implicated in glucose-induced i

76 light the potential importance of PC and the anaplerosis pathways in the enhanced insulin secretion a

77 (3)] propionate was used to quantify hepatic anaplerosis, pyruvate cycling, and TCA cycle flux.

78 of PC expression that prevent impairment of anaplerosis, pyruvate cycling, NAPDH production, and GSI

79 alyzes the first step in glutamine-dependent anaplerosis, suppressed but did not eliminate the growth

80 tabolism and demonstrated a unique marker of anaplerosis, the level of which was significantly increa

81 Also, we find defects in anaplerosis, the metabolic process involved in replenish

82 Anaplerosis, the net synthesis in mitochondria of citric

83 Anaplerosis, the synthesis of citric acid cycle intermed

84 ted insulin secretion in beta-cells and that anaplerosis through GDH does not play a major role in th

85 The findings suggest anaplerosis through NADPH-dependent, cytosolic ME limits

86 lts confirm the central importance of PC and anaplerosis to generate metabolites from glucose that su

87 d by the Krebs cycle, which in turn requires anaplerosis to replenish precursor intermediates.

88 nd (v) the uptake of amino acids rather than anaplerosis via PEP carboxylase determines carbon flow i

89 r analysis of liver glutamate confirmed that anaplerosis was sevenfold greater than flux through PDH.

90 tions in mitochondrial energy production and anaplerosis with glycolytic oscillations, which in the b