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1 rovascular O(2) delivery and skeletal muscle oxidative metabolism.
2 technique that might provide a biomarker of oxidative metabolism.
3 P-MRS data, acquired at rest, as a marker of oxidative metabolism.
4 o the apnoea, there was no change in the non-oxidative metabolism.
5 n in the brain depends almost exclusively on oxidative metabolism.
6 balance between glycolysis and mitochondrial oxidative metabolism.
7 the Z-line, and an incremental shift towards oxidative metabolism.
8 esis that is of heightened importance during oxidative metabolism.
9 tochondrial-encoded transcripts and enhances oxidative metabolism.
10 oea, although there was no change in the non-oxidative metabolism.
11 ying the BRAF V600E mutation, which promotes oxidative metabolism.
12 ts of H2O2 as a product of host and pathogen oxidative metabolism.
13 changes in the transcriptional regulation of oxidative metabolism.
14 a transcriptional modulator of mitochondrial oxidative metabolism.
15 urcation point between T cell glycolytic and oxidative metabolism.
16 tion to promote mitochondrial biogenesis and oxidative metabolism.
17 rapid in vivo hepatic clearance mediated by oxidative metabolism.
18 chondrial biogenesis and enzymes involved in oxidative metabolism.
19 ounts of energy, which is often generated by oxidative metabolism.
20 on to fatty acids in tissues with high lipid oxidative metabolism.
21 ameters critical for tissues with high lipid oxidative metabolism.
22 ing skeletal muscle mitochondrial number and oxidative metabolism.
23 tal glycolytic metabolism to a mitochondrial oxidative metabolism.
24 atty acids are the two primary substrates in oxidative metabolism.
25 d 25-fold upon a switch from fermentation to oxidative metabolism.
26 yed ALDH+/CD133+ and MET-like phenotype with oxidative metabolism.
27 abetes that are often linked with defects in oxidative metabolism.
28 sociated with an inhibition of mitochondrial oxidative metabolism.
29 s regulation of lipolysis, thermogenesis and oxidative metabolism.
30 otentially incapable of developing inducible oxidative metabolism.
31 e available source of radicals through their oxidative metabolism.
32 ply is significant and these cells engage in oxidative metabolism.
33 pment, concomitant with increased demand for oxidative metabolism.
34 d levels of MITF and PGC1alpha and decreased oxidative metabolism.
35 onstrated effects of diabetes medications on oxidative metabolism.
36 n about the mechanisms by which THs increase oxidative metabolism.
37 iated with an increase in glucose uptake and oxidative metabolism.
38 1 protects and preserves HSCs by restricting oxidative metabolism.
39 tophagy and help to explain how THs increase oxidative metabolism.
40 disturbed and presumably preserved cerebral oxidative metabolism.
41 entricular function and increased myocardial oxidative metabolism.
42 g this response may reflect the intensity of oxidative metabolism.
43 scription remodels mitochondria and enhances oxidative metabolism.
44 revalence of glycolysis and dysregulation of oxidative metabolism.
45 has been associated with aging and abnormal oxidative metabolism.
46 MEIS1 with age underlies a gradual switch to oxidative metabolism.
47 chondrial multienzyme complexes required for oxidative metabolism.
48 receptor alpha (PPARalpha) driven program of oxidative metabolism.
49 at exerts many of the pleiotropic effects of oxidative metabolism.
50 infusion on muscle force and skeletal muscle oxidative metabolism.
51 gnaling and transcription of genes promoting oxidative metabolism.
52 rvival in the context of profoundly impaired oxidative metabolism.
53 weakness, along with disruption of muscle's oxidative metabolism.
54 dase) involved in biological respiration and oxidative metabolism.
55 ed suppression of excessive inflammation and oxidative metabolism.
56 ritical role in mitochondrial biogenesis and oxidative metabolism.
57 ry high energy demands, largely satisfied by oxidative metabolism.
58 which ATP is generated via glycolysis and/or oxidative metabolism.
59 c contributes to heart failure by disrupting oxidative metabolism.
60 ide (FMN), are two key cofactors involved in oxidative metabolism.
61 s shifted to the pentose phosphate cycle and oxidative metabolism.
62 use through the pentose phosphate cycle and oxidative metabolism.
63 increased phospholipid species and decreased oxidative metabolism.
64 calculated to be 21, close to upper limit of oxidative metabolism.
65 r the non-invasive investigation of muscular oxidative metabolism.
66 fate reduction or a mixture of reductive and oxidative metabolisms.
67 cid beta-oxidation-mediated oxidative (glyco-oxidative) metabolism.
68 originally envisioned as a necessary evil of oxidative metabolism, a product of an imperfect system.
69 same species to investigate whether enhanced oxidative metabolism also confers clomazone resistance i
71 phis exhibited up to 2-fold-higher levels of oxidative metabolism and .NO production than SYL-infecte
72 the present study, we found that defects in oxidative metabolism and 2-HG production confer chemosen
73 as obesity, which is associated with reduced oxidative metabolism and a lower type I fiber content in
74 revealed impaired mitochondrial function and oxidative metabolism and a reliance on glycolytic metabo
75 s regulation may contribute to the increased oxidative metabolism and aberrant cell proliferation typ
76 utamine antagonism by markedly up-regulating oxidative metabolism and adopting a long-lived, highly a
78 del of tight calcium-dependent regulation of oxidative metabolism and ATP synthase-dependent respirat
79 ochondrial fusion dynamics, ensuring maximum oxidative metabolism and avoidance of FA toxicity in sta
80 de evidence for the novel role Lcn2 plays in oxidative metabolism and BAT activation via an adrenergi
82 igated the effect of human mHtt fragments on oxidative metabolism and Ca(2+) handling in isolated bra
85 creted factor that promotes muscle stem cell oxidative metabolism and differentiation, and suggests t
86 of the cell division cycle, suggesting that oxidative metabolism and DNA replication are not incompa
90 2 expression is crucial for CO modulation of oxidative metabolism and for conferring cytoprotection.
91 a fatty acid tracer, we have quantified BAT oxidative metabolism and glucose and nonesterified fatty
93 pathways is energetically backed by elevated oxidative metabolism and hence contributes to oxidative
94 of TLE3 in adipocytes promotes mitochondrial oxidative metabolism and increases energy expenditure, t
95 ) is a potent transcriptional coactivator of oxidative metabolism and is induced in response to a var
96 od, we demonstrate the detection of cerebral oxidative metabolism and its modulation by administratio
99 young healthy control subjects, cold-induced oxidative metabolism and NEFA uptake per BAT volume and
101 ic acid ((18)FTHA), a fatty acid tracer, BAT oxidative metabolism and perfusion and glucose and nones
102 has evolved a panoply of metalloproteins for oxidative metabolism and protection against reactive oxy
103 and nontoxic, it exhibited poor stability to oxidative metabolism and relatively poor selectivity aga
104 prehensive bioenergetic analyses to evaluate oxidative metabolism and respiratory kinetics in mouse m
105 ngs identify BCL6 as a negative regulator of oxidative metabolism and reveal that alternating recruit
106 ich SFRP5 inhibits WNT signaling to suppress oxidative metabolism and stimulate adipocyte growth duri
107 ocks traffic through the channel and reduces oxidative metabolism and that this requires the unstruct
108 Rgamma target genes, as well as the shift to oxidative metabolism and the increased mitochondrial bio
110 ide group to limit the potential for in vivo oxidative metabolism and to achieve an acceptable pharma
111 -intrinsic nutrient supply for mitochondrial oxidative metabolism and to maintain cellular homeostasi
113 60%), (ii) this energy demand is met through oxidative metabolism, and (iii) the CBF response is medi
114 inamide adenine dinucleotide, as a result of oxidative metabolism, and CCK by increasing cytosolic Ca
118 ulated transcriptional coactivators to drive oxidative metabolism, and increased their rates of FA ox
120 lved in genome stability, protein stability, oxidative metabolism, and other cellular mechanisms such
121 ift their reliance on glycolysis relative to oxidative metabolism, and studies in model systems have
122 , eosinophils, and monocytes), high rates of oxidative metabolism, and the activation of multiple oxy
123 hibition on lipolysis, fatty acid oxidation, oxidative metabolism, and thermogenesis in brown adipocy
124 ufficient to reduce mitochondrial Ca(2+) and oxidative metabolism, and to establish a pseudohypoxic s
125 chnique, complementary methods for assessing oxidative metabolism, and whether the P(i) --> ATP flux
126 l to test whether individuals with increased oxidative metabolism are be more sensitive to hepatotoxi
127 this argument is that animal models in which oxidative metabolism are completely abolished are not al
129 sulin-resistance and decreased mitochondrial oxidative metabolism are early metabolic changes in the
130 sults show that cold-induced NEFA uptake and oxidative metabolism are not defective in type 2 diabete
131 s important for mitochondrial biogenesis and oxidative metabolism are under the control of members of
132 can shift their metabolism toward increased oxidative metabolism as nutrients become depleted and/or
133 ependent reductive carboxylation rather than oxidative metabolism as the major pathway of citrate for
134 lucose also causes a very rapid elevation of oxidative metabolism as was followed by NAD(P)H autofluo
135 ype characterized by elevated glycolysis and oxidative metabolism as well as augmented size, granular
136 variant display increased mTOR activity and oxidative metabolism, as well as larger size, improved m
138 amma treatment resulted in the inhibition of oxidative metabolism at the gene expression and function
139 pharmacological inhibition of mitochondrial oxidative metabolism attenuates EMCV-mediated beta-cell
141 the ERRalpha coactivator PGC-1alpha enhanced oxidative metabolism but did not affect tumor growth.
142 mization led to compounds of type 2 with low oxidative metabolism but poor oral bioavailability.
143 tion of fatty acid delivery not only induced oxidative metabolism, but also amplified anaplerosis/cat
144 Ca(2+) flux into the mitochondria helps pace oxidative metabolism, but there is limited in vivo evide
145 that synapses can switch from glycolytic to oxidative metabolism, but to do so, they rely on activit
146 channels control global Ca(2+) signaling and oxidative metabolism by inducing Na(+) and Ca(2+) respon
147 for CD8(+) memory T cells, regulated SRC and oxidative metabolism by promoting mitochondrial biogenes
149 Carbon dioxide (CO2 ), a primary product of oxidative metabolism, can be sensed by eukaryotic cells
151 use of increased adipocyte thermogenesis and oxidative metabolism caused by upregulating key enzymes
152 ammatory genes (Mrc1, Tgfb1, Il10, Mgl2) and oxidative metabolism, characteristic of M2 macrophages.
153 ch in turn were used to calculate changes in oxidative metabolism (CMR(O2)) with calibrated fMRI.
154 We conclude that succinate can improve glial oxidative metabolism, consistent our previous findings i
157 These results suggest that stimulants of oxidative metabolism could have therapeutic potential in
158 crophages exhibited increased glycolytic and oxidative metabolism, coupled with increased ATP product
159 KCl) and preventing O2-induced increases in oxidative metabolism, cytosolic calcium, and ductal smoo
160 m is inhibited and support the inhibition of oxidative metabolism (decreased ATP) as one protective m
161 at 7% for 2 weeks, results in inhibition of oxidative metabolism, decreased reactive oxygen species
163 Here, we propose that the normal decline in oxidative metabolism during aging constitutes an early a
164 nd inflammation are associated with elevated oxidative metabolism during an obesogenic diet, and this
168 beta-Klotho pathway orchestrates a switch to oxidative metabolism during fasting and starvation and h
169 es that promote mitochondrial biogenesis and oxidative metabolism during terminal erythroid maturatio
170 interaction between insulin sensitivity and oxidative metabolism during the course of metabolic dise
171 led that migratory cells selectively utilize oxidative metabolism during the process of migration to
172 revealed a clear shift from fermentative to oxidative metabolism enabled by higher periplasmic super
174 ative species (ROS) oxidation, extracellular oxidative metabolism (EXOMET), and inorganic chemical re
178 ly when MEFs are forced to use mitochondrial oxidative metabolism for ATP generation that mitochondri
180 in melanoma cells led to broadening of their oxidative metabolism from mainly glutamine-dependent to
181 o primed pluripotency by directly repressing oxidative metabolism genes and metabolic intermediates i
184 have revealed that the metabolic pathways of oxidative metabolism, glycolysis, and glutaminolysis pre
185 ed CD8(+) T cells displayed greater rates of oxidative metabolism, higher bioenergetic capacity, diff
186 r repression of inflammation, maintenance of oxidative metabolism, IL-4-mediated induction of alterna
187 beta-cell lysis by attenuating mitochondrial oxidative metabolism in a nitric oxide-dependent manner.
188 roves exercise endurance and skeletal-muscle oxidative metabolism in animals and may enhance vascular
190 , we demonstrated cold-induced activation of oxidative metabolism in BAT, but not in adjoining skelet
191 ATM and p53 in the control of glycolysis and oxidative metabolism in cancer, but their involvement in
192 d increased glucose consumption with reduced oxidative metabolism in cell culture and increased respi
193 e PGC-1alpha/PPARalpha signaling and promote oxidative metabolism in cells and animal models in a SIR
200 ed the AMP-to-ATP ratio, thereby stimulating oxidative metabolism in liver and adipose tissue via AMP
201 udy describes the cerebral oxidative and non-oxidative metabolism in man during a prolonged apnoea (r
202 he ICC lineage and ICC dependence on glucose oxidative metabolism in mice with disruption of the succ
204 pecifies slow twitch fibers, suggesting that oxidative metabolism in muscle is selectively controlled
205 RC1 activity and dysregulated glycolytic and oxidative metabolism in response to IL-15 stimulation.
206 on of PGC-1alpha/PPAR-alpha target genes and oxidative metabolism in response to increased ATGL-media
207 a class II-selective HDAC inhibitor enhanced oxidative metabolism in skeletal muscle and adipose tiss
214 cells, demonstrated increased mitochondrial oxidative metabolism in the presence of exogenous FFAs;
216 that ectopic expression of ERRgamma enhanced oxidative metabolism in vitro and inhibited the growth o
219 activity-dependent NADH transients, neuronal oxidative metabolism increased first upon activation wit
222 As a consequence, in brain tissue where oxidative metabolism is disturbed, brain glucose concent
223 ling under conditions in which mitochondrial oxidative metabolism is inhibited and support the inhibi
224 re indicates that mitochondrial capacity for oxidative metabolism is lower in human obesity and type
228 commensurate with the dependence of cells on oxidative metabolism, is more frequent than mitophagy an
229 er regulator of mitochondrial biogenesis and oxidative metabolism, lipogenesis, and triglyceride (TG)
230 ycolytic metabolism to fatty acid and ketone oxidative metabolism may modulate metabolism, signal tra
232 ice was associated with decreases in cardiac oxidative metabolism, mitochondrial mass, and mitochondr
233 ic molecule that is important for oxygen and oxidative metabolism, most notably as the prosthetic gro
234 ultiple aspects of brain function, including oxidative metabolism, myelination, and neurotransmitter
235 ates that reprogramming from a glycolytic to oxidative metabolism occurs during cellular differentiat
236 reactions (ADRs), including hepatotoxicity; oxidative metabolism of 1 has been implicated in the pat
243 port the notion that ISO acutely accelerates oxidative metabolism of glucose to meet the ATP demand r
244 rmally functioning tumour cell mitochondria, oxidative metabolism of glucose- and glutamine-derived c
246 n for its inhibitory action, emphasizing the oxidative metabolism of NAEs as an important feature of
247 or-activated receptor-alpha, and products of oxidative metabolism of polyunsaturated fatty acids via
252 sociated with replication, transcription, or oxidative metabolism; other direct sources of endogenous
253 ganelles share fission machinery components, oxidative metabolism pathways, ROS scavenging activities
254 ted the M2 hallmark Ym-1 and genes promoting oxidative metabolism (PGC-1alpha) and adipogenesis (MMP-
255 ant increase in 2 transcriptional drivers of oxidative metabolism, PGC1alpha and PPARD, suggesting an
256 Together these results indicate that DHEA oxidative metabolism produces potent novel molecules wit
257 ness associated, but upregulated activation, oxidative metabolism, protein synthesis, and lineage ass
259 igated as an alternative approach to address oxidative metabolism, reduce lipophilicity, and improve
260 myotube mRNA expression of genes involved in oxidative metabolism, regardless of the donor and degree
263 hat alterations in cancer cell mitochondrial oxidative metabolism resulting in increased levels of O2
264 in the tumor microenvironment repress T cell oxidative metabolism, resulting in effector cells with m
265 oxygen species (ROS), the toxic products of oxidative metabolism seen as culprits in aging, neurodeg
268 drug that we have recently shown to silence oxidative metabolism, suppresses apoptotic cell death in
269 perfusion (increased anaerobic and decreased oxidative metabolism) that then normalize over the follo
270 ted by GPD2, which coordinates a shutdown of oxidative metabolism; this limits the availability of ac
272 , our data link Salmonella genes controlling oxidative metabolism to inflammasome activation and sugg
273 iosis, triggered a switch in host cells from oxidative metabolism to lactate fermentation, increasing
274 ive OXPHOS, reductive carboxylation replaces oxidative metabolism to maintain amounts of reducing equ
275 ates protein substrates involved in cellular oxidative metabolism to maintain mitochondrial energy pr
277 D8(+) TRM cells use exogenous FFAs and their oxidative metabolism to persist in tissue and to mediate
278 rt of a cell-adaptive response to high lipid oxidative metabolism to protect lipid droplet storage ag
279 t maturation into adult-like CMs with higher oxidative metabolism, transcriptional signatures closer
280 a key role for SIRT5 in maintaining cardiac oxidative metabolism under pressure overload to ensure s
282 olysis promotes mitochondrial biogenesis and oxidative metabolism via a SIRT1/PGC-1alpha/PPARalpha-de
283 ack of functional hyperemia, measurements of oxidative metabolism via flavoprotein fluorescence sugge
285 c defect at the level of both glycolysis and oxidative metabolism was apparent, which was restored af
286 The increase in DEE associated with BAT oxidative metabolism was highly variable in the high-BAT
290 scle contraction, and lipid and carbohydrate oxidative metabolism were also observed in cKO SOL.
292 olism, whereas DLST protein levels and hence oxidative metabolism were partially maintained in microR
293 through glycolysis with a downregulation of oxidative metabolism, whereas alternative activation is
294 d in wild-type mice, paralleling a decreased oxidative metabolism, whereas DLST protein levels and he
295 neurons, probably from DNA damage induced by oxidative metabolism, which kills nondividing cells in t
296 U-(13)C-palmitic acid) demonstrated enhanced oxidative metabolism, which was driven by FAO and suppor
297 o inhibits the expression of genes linked to oxidative metabolism while stimulating the expression of
298 Disruption of complex I assembly reduces oxidative metabolism with concomitant increase in mitoch