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1 itochondrial tricarboxylic acid (TCA) cycle (anaplerosis).
2  to fill the tricarboxylic acid (TCA) cycle (anaplerosis).
3 aloacetate for continued TCA cycle function (anaplerosis).
4 nt manner, thereby promoting glutamine-based anaplerosis.
5 ve from replacement of oxidized glutamate by anaplerosis.
6 d entry into the tricarboxylic acid cycle by anaplerosis.
7 s a glucose store, glycogen may also furnish anaplerosis.
8 ther cancers in vivo depend on glutamine for anaplerosis.
9 as, both for oxidative stress management and anaplerosis.
10 A cycle in HEK293 T cells, confirming direct anaplerosis.
11 ogen facilitates cardiac betaHB oxidation by anaplerosis.
12 ty for amino acid biosynthesis and TCA cycle anaplerosis.
13 nd S. aureus instead has a critical need for anaplerosis.
14 s, with no compensation from glucose-derived anaplerosis.
15 use differential dependence on glutamine for anaplerosis.
16 reliance on glutamate to fuel energetics and anaplerosis.
17  in cancer cells that lack glucose-dependent anaplerosis.
18 sis, suggesting a metabolic reprogramming to anaplerosis.
19 ucose and other substrates generate TCAs via anaplerosis.
20 ired glutamine-derived carbon utilization in anaplerosis.
21 pecially in the context of citric acid cycle anaplerosis.
22  decreased FAO with increased glycolysis and anaplerosis.
23       Many tumor cells use glutamine to feed anaplerosis.
24 e-derived pyruvate rather than glutamine for anaplerosis.
25 ylglyceride (TAG) was linked to ME-catalyzed anaplerosis.
26 , very little is known about the products of anaplerosis.
27  cTnI-G203S hearts consistent with increased anaplerosis.
28         Thus, PC-mediated, glucose-dependent anaplerosis allows cells to achieve glutamine independen
29 abolism and enhanced carbon fixation through anaplerosis and accumulates massive intracellular inclus
30 g and (13)C-flux analyses revealed TCA cycle anaplerosis and altered metabolism in OPA1-deficient NP
31                                    Together, anaplerosis and cataplerosis help regulate rates of bios
32            This article reviews the roles of anaplerosis and cataplerosis in various tissues and disc
33 ements for PC- and GLS-mediated pathways for anaplerosis and cell proliferation.
34 cate ZFP36 and ZFP36L1 in limiting glutamine anaplerosis and differentiation of activated CD4(+) T ce
35                                              Anaplerosis and gluconeogenesis from heptanoate are inhi
36 defining important determinants of glutamine anaplerosis and glutaminase dependence in cancer.
37 veal a fundamental role of CA5b in TCA cycle anaplerosis and insulin secretion in beta cells.
38 K(ATP)-independent mechanisms involving both anaplerosis and mitochondrial GTP (mtGTP).
39 he specific inability to cope with glutamate anaplerosis and nitroxidative stress.
40 rt, glucose and glycolysis are important for anaplerosis and potentially therefore for d-beta-hydroxy
41 t a substantial fraction of palmitate toward anaplerosis and re-release of bioenergetic carbons into
42 gy and glutaminolysis can provide carbon for anaplerosis and reductive carboxylation to citrate.
43 rease in the expression of genes involved in anaplerosis and reverse cholesterol transport.
44 uantities of glutamine to maintain TCA cycle anaplerosis and support cell survival.
45 vailable MPC1/2 inhibitor, inhibits pyruvate anaplerosis and targets imatinib-resistant CML LSCs in r
46 pha-ketoglutarate to maintain the TCA cycle (anaplerosis) and ATP production.
47 tabolic flux through pyruvate carboxylation (anaplerosis) and phosphoenolpyruvate carboxykinase (cata
48  Citric acid cycle fluxes, pyruvate cycling, anaplerosis, and cataplerosis were also elevated during
49 elerated oxidative mitochondrial metabolism, anaplerosis, and malonyl-CoA/lipid signaling in beta-cel
50 through YAP/TAZ-dependent glutaminolysis and anaplerosis, and thereby link mechanical stimuli to dysr
51 STAT5 inhibition and disruption of TCA cycle anaplerosis are associated with reduced IL-2 production,
52  increased, even though pyruvate cycling and anaplerosis are decreased; 4) the liver is unable to syn
53 ollectively these results highlight pyruvate anaplerosis as a persistent and therapeutically targetab
54 d metformin-induced glycolysis and glutamine anaplerosis, both of which are survival responses of cel
55 Here, we show that mTORC1 promotes glutamine anaplerosis by activating glutamate dehydrogenase (GDH).
56 enzyme A production toward carbon influx via anaplerosis bypasses energy, yielding reactions contribu
57 ic markers were associated with decreases in anaplerosis, CAC flux, and oxygen consumption.
58 tures of beta-cell metabolism, such as leak, anaplerosis, cataplerosis, and NADPH production that sub
59 ced oxidative metabolism, but also amplified anaplerosis/cataplerosis and caused a proportional rise
60 olism with metformin also normalized hepatic anaplerosis/cataplerosis and reduced markers of inflamma
61                              Second, loss of anaplerosis/cataplerosis via genetic knockdown of phosph
62 catabolism and reduced reliance on glutamine anaplerosis compared to cells cultured in standard tissu
63 vel findings include that aspartate used for anaplerosis does not derive from the glucose fuel added
64 s of the tricarboxylic acid cycle, balancing anaplerosis from amino acid breakdown.
65 mediates, less pentose shunt flux, increased anaplerosis from glutamine, and decreased fatty acid bet
66 rt the hypothesis that a signal generated by anaplerosis from increased pyruvate carboxylase flux is
67      As part of a study on the regulation of anaplerosis from propionyl-CoA precursors in rat livers
68 yl-CoA pathway explains the effectiveness of anaplerosis from propionyl-CoA precursors such as heptan
69     We hypothesized that increased glutamine anaplerosis fuels elevations in CAC flux and oxidative s
70                Because different pathways of anaplerosis generate distinct products, they may differe
71 hetase 1 (urea cycle), pyruvate carboxylase (anaplerosis, gluconeogenesis), propionyl-CoA carboxylase
72 ntrol on the balance between respiration and anaplerosis/gluconeogenesis.
73           We postulate that the high rate of anaplerosis in awake brain is linked to brain activity b
74 er, some cell lines that depend on glutamine anaplerosis in culture rely less on glutamine catabolism
75  that lipotoxic palmitate treatments enhance anaplerosis in cultured rat hepatocytes, causing a shift
76     These findings indicate that PC-mediated anaplerosis in early-stage NSCLC is required for tumor s
77 ow that rates of mitochondrial oxidation and anaplerosis in human liver can be directly determined no
78      Increasing competition from PDH reduced anaplerosis in HYP+DCA by 18%.
79                       Interestingly, reduced anaplerosis in HYP+DCA corresponded with normalized TAG
80 etermined partial reversibility of increased anaplerosis in HYP.
81 ydroxypentanoate + beta-ketopentanoate), and anaplerosis in isolated rat livers perfused with (13)C-l
82 wever, studies designed to lower the rate of anaplerosis in the beta cell have been inconclusive.
83 ruvate carboxylase (PC), the major enzyme of anaplerosis in the beta cell.
84                      Inhibition of glutamine anaplerosis in the presence of metformin further attenua
85  nucleotide synthesis and leverage glutamine anaplerosis in the tricarboxylic acid (TCA) cycle to sup
86 be learned about the sites and regulation of anaplerosis in these tissues.
87 nsulin secretion by the beta cell depends on anaplerosis in which insulin secretagogues are metaboliz
88 stain membrane potential, ATP synthesis, and anaplerosis, in response to varying degrees of O2 limita
89  new mechanism of insulin secretion in which anaplerosis increases short chain acyl-CoAs that have ro
90 and increases GAC levels, enhances glutamine anaplerosis into the TCA cycle, and drives cells towards
91                  To test the hypothesis that anaplerosis is important for insulin secretion, we lower
92               Tricarboxylic acid (TCA) cycle anaplerosis is maintained primarily by glutamine.
93 tabolomics reveals that deregulated pyruvate anaplerosis is not affected by imatinib.
94                In inborn metabolic diseases, anaplerosis is often affected, leading to impaired TCA c
95 nish tricarboxylic acid cycle intermediates (anaplerosis) is primarily used for amino acid biosynthes
96   Refilling the pool of precursor molecules (anaplerosis) is therefore crucial to maintain cell growt
97 arboxylic acid (TCA) cycle intermediates, or anaplerosis, is crucial to ensure optimal TCA cycle acti
98  but impaired tricarboxylic acid (TCA) cycle anaplerosis, macromolecule production, and redox homeost
99 e reduced, whereas compensatory increases in anaplerosis maintain tricarboxylic acid cycle flux and a
100 t NADH production from pyruvate fueling this anaplerosis, ME also consumes NADPH necessary for lipoge
101 emonstrate that LSCs have increased pyruvate anaplerosis, mediated by increased mitochondrial pyruvat
102 xes in the TCA cycle and the gluconeogenesis-anaplerosis nodes, despite decrease in several proteins
103 mitate oxidation, preventing the increase in anaplerosis observed in nontransgenic TAC hearts.
104 was driven by FAO and supported by increased anaplerosis of glucose carbons.
105 etoglutarate to glutamate, with impaired TCA anaplerosis of glutamate carbon.
106 er of the coenzyme A derivatives involved in anaplerosis of the citric acid cycle via precursors of p
107 , DODA contributes a substantial fraction to anaplerosis of the citric acid cycle.
108 g of the propionyl moiety of heptanoate into anaplerosis of the citric acid cycle.
109 an catalyze the reverse reaction, supporting anaplerosis of the tricarboxylic acid cycle, under condi
110 ans also increased longevity suggesting that anaplerosis of tricarboxylic acid (TCA) cycle substrates
111 evated ME expression with a 90% elevation in anaplerosis over SHAM.
112                                       As the anaplerosis pathways are implicated in glucose-induced i
113 light the potential importance of PC and the anaplerosis pathways in the enhanced insulin secretion a
114 (3)] propionate was used to quantify hepatic anaplerosis, pyruvate cycling, and TCA cycle flux.
115  of PC expression that prevent impairment of anaplerosis, pyruvate cycling, NAPDH production, and GSI
116 2 expression rescued cell proliferation, TCA anaplerosis, redox balance, and mitochondrial function a
117  Encouragingly, genetic ablation of pyruvate anaplerosis sensitises CML cells to imatinib.
118 alyzes the first step in glutamine-dependent anaplerosis, suppressed but did not eliminate the growth
119           Hyperoxia induces glutamine-fueled anaplerosis that reverses basal Muller cell metabolism f
120 tabolism and demonstrated a unique marker of anaplerosis, the level of which was significantly increa
121                     Also, we find defects in anaplerosis, the metabolic process involved in replenish
122 rbon recycling to the TCA cycle via enhanced anaplerosis, the metabolism of gluconeogenic substrates
123                                              Anaplerosis, the net synthesis in mitochondria of citric
124 esses include neuronal alanine synthesis and anaplerosis, the replenishment of tricarboxylic acid (TC
125                                              Anaplerosis, the synthesis of citric acid cycle intermed
126 mate dehydrogenase (GDH) and thereby enables anaplerosis-the entry of glutamine-derived carbon into t
127 ted insulin secretion in beta-cells and that anaplerosis through GDH does not play a major role in th
128                         The findings suggest anaplerosis through NADPH-dependent, cytosolic ME limits
129 iazides significantly attenuated Krebs cycle anaplerosis through reduction of mitochondrial oxaloacet
130 lts confirm the central importance of PC and anaplerosis to generate metabolites from glucose that su
131 d by the Krebs cycle, which in turn requires anaplerosis to replenish precursor intermediates.
132 nd (v) the uptake of amino acids rather than anaplerosis via PEP carboxylase determines carbon flow i
133 r analysis of liver glutamate confirmed that anaplerosis was sevenfold greater than flux through PDH.
134 g of TCA cycle flux through glutamine-driven anaplerosis while maintaining oxidative phosphorylation.
135 tions in mitochondrial energy production and anaplerosis with glycolytic oscillations, which in the b

 
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