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1 iver glycogen and newly synthesized glucose (gluconeogenesis).
2 oactivator 1 alpha (PGC1alpha), resulting in gluconeogenesis.
3 promoted both hepatic insulin resistance and gluconeogenesis.
4 sulin resistance, hepatic triglycerides, and gluconeogenesis.
5 regulator that promotes FOXO1-driven hepatic gluconeogenesis.
6 ic FBP1 complex, the rate-limiting enzyme in gluconeogenesis.
7 chondrial dysfunctions, and enhanced hepatic gluconeogenesis.
8  activity may play an important role in cell gluconeogenesis.
9 -1 (Pck1) expression, suggesting a link with gluconeogenesis.
10 y for mitochondrial respiration and reducing gluconeogenesis.
11 ze its transcriptional activities in hepatic gluconeogenesis.
12 affected many metabolic processes, including gluconeogenesis.
13 cetyl coenzyme A (acetyl-CoA) production and gluconeogenesis.
14 ases FOXO1 protein but also enhances hepatic gluconeogenesis.
15 -phosphatase (G6Pase) and suppressed hepatic gluconeogenesis.
16 of glucose and the large sugar phosphates is gluconeogenesis.
17 s ER stress, insulin resistance, and hepatic gluconeogenesis.
18  balance between respiration and anaplerosis/gluconeogenesis.
19 ts of hypoxia and iron deficiency on hepatic gluconeogenesis.
20 uvate and decreased pyruvate utilization for gluconeogenesis.
21 al coactivator PGC-1alpha to control hepatic gluconeogenesis.
22 kinase (PEPCK) is well known for its role in gluconeogenesis.
23 rve a beneficial role in suppressing hepatic gluconeogenesis.
24 ntain glucose balance by stimulating hepatic gluconeogenesis.
25 enes in human liver cells, thereby enhancing gluconeogenesis.
26 the pathogenesis of diabetes by upregulating gluconeogenesis.
27 iminished substrate availability for hepatic gluconeogenesis.
28 thway has now been characterized for hepatic gluconeogenesis.
29 ) ratio diverts glucose precursors away from gluconeogenesis.
30 stimulation of Pck1 expression and increased gluconeogenesis.
31 in which statin treatment suppresses hepatic gluconeogenesis.
32 d after GBP and bile acids are inhibitors of gluconeogenesis.
33 atty acid oxidation, glucose utilization, or gluconeogenesis.
34 sed the effects of dietary iron on circadian gluconeogenesis.
35 s, and loss of Wnt-3a-mediated repression of gluconeogenesis.
36 slation regulation, DNA damage response, and gluconeogenesis.
37 iption factors form a complex that regulates gluconeogenesis.
38 glucose production to an enhanced intestinal gluconeogenesis.
39 trate would stimulate glycolysis and inhibit gluconeogenesis.
40 ediated hepatic inflammation, steatosis, and gluconeogenesis.
41  organs and provides necessary substrate for gluconeogenesis.
42 ing enzyme requirements of glycolysis versus gluconeogenesis.
43  showed increased inflammatory responses and gluconeogenesis.
44 n sensitivity and enhanced pyruvate-mediated gluconeogenesis.
45 ng pyruvate injections, indicating increased gluconeogenesis.
46 ible to genetic disruption of glycolysis and gluconeogenesis.
47 protein O1 and subsequently promoted hepatic gluconeogenesis.
48  male mice, which indicated impaired hepatic gluconeogenesis.
49 o1 plays a central role in the regulation of gluconeogenesis.
50 ncluding cardiolipin (CL)], lipogenesis, and gluconeogenesis.
51 low or absent glucose, cells make it through gluconeogenesis.
52 s to irregular feeding patterns and constant gluconeogenesis.
53  octanoate, two sources of energy to support gluconeogenesis.
54 sulin resistance via FoxO1-dependent hepatic gluconeogenesis.
55  in the fly brain is capable of carrying out gluconeogenesis.
56 quired for E(2) action on the suppression of gluconeogenesis.
57 /threonine kinase signalling, glycolysis and gluconeogenesis.
58 ted a repressive effect of TCF7L2 on hepatic gluconeogenesis, a recent study using liver-specific Tcf
59 es favorable fluxes in the TCA cycle and the gluconeogenesis-anaplerosis nodes, despite decrease in s
60                               In particular, gluconeogenesis and amino acid catabolism are affected b
61 ssical Warburg effect, the downregulation of gluconeogenesis and amino acid metabolism, and the upreg
62  GLPX and GPM2 is required for disruption of gluconeogenesis and attenuation of Mtb in a mouse model
63    Liver-specific deletion of MKP-1 enhances gluconeogenesis and causes hepatic insulin resistance in
64 st-translational control of FoxO1, regulates gluconeogenesis and controls metabolic pathways via mito
65 ular processes such as glucose reabsorption, gluconeogenesis and cytoskeletal remodelling.
66 F4A), a transcription factor associated with gluconeogenesis and diabetes, as a central regulatory hu
67 ion of SIRT1 (through its effects to promote gluconeogenesis and fatty acid oxidation) drives ketogen
68 b-3p, and -92b-3p co-regulate the glycolysis/gluconeogenesis and focal adhesion in cancers of kidney,
69 CF7L2DN, but not wild-type TCF7L2, increased gluconeogenesis and gluconeogenic gene expression.
70 rosis complex 1 (Tsc1) in the liver promotes gluconeogenesis and glucose intolerance.
71 o fuel high energy-demanding pathways (e.g., gluconeogenesis and glyceroneogenesis), whereas opposite
72  was no association with the contribution of gluconeogenesis and glycogenolysis to EGP.
73  an enzyme which catalyses the final step of gluconeogenesis and glycogenolysis.
74 ater hepatic glycogen synthesis and impaired gluconeogenesis and glycolysis related to low cytosolic
75 r fructose-6-P, which likely influences both gluconeogenesis and glycolysis.
76 te pathway, substrate-level phosphorylation, gluconeogenesis and glycolysis.
77 owed reduced expression of genes involved in gluconeogenesis and glycolysis.
78 sis, mitochondrial electron chain functions, gluconeogenesis and glycolytic processes while transcrip
79  in postreceptor IR, FFA contributes to both gluconeogenesis and hepatic steatosis.TRIAL REGISTRATION
80 Tmem127 loss: liver Tmem127 promotes hepatic gluconeogenesis and inhibits peripheral glucose uptake,
81  derangement that is associated with greater gluconeogenesis and insulin resistance.
82 carbon flux through the glyoxylate shunt and gluconeogenesis and into synthesis of trehalose, a disac
83  mechanisms of transcriptional regulation of gluconeogenesis and into the roles of chromatin readers
84       In Aspergillus fumigatus, AcuM governs gluconeogenesis and iron acquisition in vitro and virule
85 taacuK DeltaacuM double mutants had impaired gluconeogenesis and iron acquisition, similar to the Del
86 sphatase (FBP1) is a rate-limiting enzyme in gluconeogenesis and is frequently lost in various types
87 kinase 1 (PEPCK1) is the critical enzyme for gluconeogenesis and is linked with type II diabetes.
88 n this study, we analysed starvation-induced gluconeogenesis and ketogenesis in mouse strains lacking
89          The principal molecular stimulus to gluconeogenesis and ketogenesis is activation of SIRT1 (
90 tations of this fasting mimicry are enhanced gluconeogenesis and ketogenesis, which are not seen with
91 aling plays a key role in the maintenance of gluconeogenesis and lipid metabolism in males.
92  the hepatic expression of genes involved in gluconeogenesis and lipogenesis, attenuated ER stress re
93 glucocorticoid excess, and increased hepatic gluconeogenesis and lipogenesis.
94   These findings reveal that PRMT1 modulates gluconeogenesis and mediates glucose homeostasis under p
95 ts the hepatic TGF-beta pathway, influencing gluconeogenesis and mitochondrial bioenergetics in the U
96 /cataplerotic pathways that are essential to gluconeogenesis and other biosynthetic activities.
97 erate independent of glucose due to enhanced gluconeogenesis and oxidations of glutamine and branched
98 ment of intrahepatic glucose due to enhanced gluconeogenesis and reduced glucose use through the pent
99 ol reactions being essential for glycolysis, gluconeogenesis and related processes.
100 ression, skin androgenisation, disruption of gluconeogenesis and reproductive performance.
101 el; 2.70% dietary arginine level upregulated gluconeogenesis and resulted in high plasma glucose cont
102 on of baseline and 1-y changes in glycolysis/gluconeogenesis and TCA cycle metabolites with insulin r
103 ns of baseline and 1-y changes in glycolysis/gluconeogenesis and TCA cycle metabolites with subsequen
104 ied cytosolic isoform (PEPCK-C) potentiating gluconeogenesis and TCA flux.
105 y of glucose leads to the down-regulation of gluconeogenesis and the activation of glycolysis, leadin
106 also participates in the reverse reaction in gluconeogenesis and the Calvin-Benson cycle.
107 e microbiome functional potential identified gluconeogenesis and the putrefaction and fermentation pa
108  fatty acids like acetic acid, which induces gluconeogenesis and thereby accounts for glucose intoler
109 ysis and amino acid release to sustain liver gluconeogenesis and tissue protein synthesis.
110 es away from the energy-consuming process of gluconeogenesis and toward the anabolic process of growt
111                                   Glycolysis/gluconeogenesis and tricarboxylic acid (TCA) cycle metab
112  PPARalpha near genes involved in glycolysis/gluconeogenesis and uncovered a role for this factor in
113 y rat hepatocytes with amino acids increased gluconeogenesis and ureagenesis and, despite nutrient ex
114  the opposing effects of atRA and insulin on gluconeogenesis, and also suggest an interaction between
115 posite effects from metformin on glycolysis, gluconeogenesis, and cell G6P.
116 ssociated with lipid accumulation, abolished gluconeogenesis, and extensive liver damage.
117 rmentation, and altered hepatic lipogenesis, gluconeogenesis, and glycogenolysis in an AHR-dependent
118  systemic glucose tolerance, reduced hepatic gluconeogenesis, and increased insulin sensitivity.
119 eted metabolite profiling to the glycolysis, gluconeogenesis, and Krebs cycle (n = 48) and an explora
120 ed browning of the adipose tissue, decreased gluconeogenesis, and less hepatic steatosis.
121 ayed elevated gluconeogenic gene expression, gluconeogenesis, and loss of Wnt-3a-mediated repression
122  meiosis, cholesterol metabolism, glycolysis/gluconeogenesis, and MAPK, PI3K-AKT, HIPPO and calcium s
123 including the citrate acid cycle, glycolysis/gluconeogenesis, and metabolism of branched chain amino
124 e autophagy, preserve triglycerides, enhance gluconeogenesis, and prevent hypoglycemia in calorie-res
125 rate the dependence of key metabolic fluxes, gluconeogenesis, and signaling on the cytosolic or mitoc
126 inct pathways including inositide signaling, gluconeogenesis, and sulfur assimilation.
127 ssion, whereas mRNAs involved in glycolysis, gluconeogenesis, and T cell activation were unaffected.
128 pregulated blood glucose level by increasing gluconeogenesis, and upregulated the hepatic inflammator
129 hosphoenolpyruvate carboxykinase to initiate gluconeogenesis; and (v) (13)C-MFA together with RNA-seq
130 tabolism at the level of both glycolysis and gluconeogenesis are mostly unknown.
131 ltiple genes/proteins involved in glycolysis/gluconeogenesis are upregulated, whereas those involved
132 the effects of various signaling pathways on gluconeogenesis are well established, the downstream sig
133          Collectively, our results implicate gluconeogenesis as the key mechanism behind organophosph
134  and hyperglucagonemia and stimulate hepatic gluconeogenesis as well as their beneficial effects in c
135 e had reduced expression of liver markers of gluconeogenesis associated with increased glucose tolera
136 nto insulin resistance and increased hepatic gluconeogenesis associated with obesity and type 2 diabe
137 tformin (dimethylbiguanide) inhibits hepatic gluconeogenesis at concentrations relevant for type 2 di
138 kinase 1 (PCK1), the rate-limiting enzyme in gluconeogenesis, at Ser90.
139 nt with the inhibitory role of bile acids on gluconeogenesis, bile diversions promote a blunting in h
140 role of TGF-beta1/Smad3 signaling in hepatic gluconeogenesis, both in normal physiology and in the pa
141 ta1/Smad3 signaling pathway promotes hepatic gluconeogenesis, both upon prolonged fasting and during
142  mass, and increased hepatic ureagenesis and gluconeogenesis but decreased glycolysis.
143 icarboxylic acid (TCA) cycle, glycolysis and gluconeogenesis by conversion of mitochondrial oxaloacet
144 ), and pyruvate phosphate dikinase (PPDK) in gluconeogenesis by generating the respective Leishmania
145 ere we show that glucagon stimulates hepatic gluconeogenesis by increasing the activity of hepatic ad
146 ease in hepatic NADH, which inhibits hepatic gluconeogenesis by reducing the conversion of lactate to
147 e, which is likely due to the suppression of gluconeogenesis by salidroside as the protein levels of
148 nhibiting phosphofructokinase-1 and activate gluconeogenesis by stimulating fructose-1,6-bisphophatas
149   Mechanistically, CS and SULT2B1b inhibited gluconeogenesis by suppressing the expression of acetyl
150  hepatic glycogenolysis but similar rates of gluconeogenesis compared to those on the mixed diet.
151 understanding of the role of mitochondria in gluconeogenesis control.Hepatic gluconeogenesis is tight
152 emical modification known to inhibit hepatic gluconeogenesis, could be potentially used for treatment
153 turnover), hepatic glucose production (HGP), gluconeogenesis (deuterium incorporation from body water
154 h fat (LCHF) diet would have higher rates of gluconeogenesis during exercise compared to those who fo
155  in response to stress by increasing hepatic gluconeogenesis during fasting.
156 gy-deficiency in any tissue had no effect on gluconeogenesis during starvation.
157 ich PGC1A plays dual roles in the control of gluconeogenesis during the fasting-to-fed transition thr
158 a key transcriptional coactivator regulating gluconeogenesis, enhancing its activity via arginine met
159 sugar as well as metabolites associated with gluconeogenesis, entailing a critical nodal role of PEPC
160 tasis outcomes, reveal the exploitation of a gluconeogenesis enzyme for pyrimidine biosynthesis under
161 n gluconeogenic organs and reexpression of a gluconeogenesis enzyme, fructose-1,6-bisphosphatase (FBP
162 ndent carboxylases catalyze key reactions in gluconeogenesis, fatty acid synthesis, and amino acid ca
163             The low metformin dose inhibited gluconeogenesis from both oxidized (dihydroxyacetone) an
164 ructose conversion into blood (13)C glucose (gluconeogenesis from fructose), blood VLDL-(13)C palmita
165 cited by HFD feeding is linked with enhanced gluconeogenesis from glycerol and with alterations in BA
166 ase (G6pc) expression in liver and increased gluconeogenesis from glycerol.
167 of enhanced glycolysis, but it also enhances gluconeogenesis from lactate in the liver that contribut
168 nous glucose production, glycogenolysis, and gluconeogenesis from phosphoenolpyruvate.
169 vate ratio and redox-dependent inhibition of gluconeogenesis from reduced but not oxidized substrates
170 -(13)C3]glucose in equal proportions through gluconeogenesis from the level of trioses.
171 ate that Tup11/12 repress transcription of a gluconeogenesis gene, fbp1(+), by three distinct mechani
172 cortisol led to stronger upregulation of the gluconeogenesis genes g6pca and pepck1.
173 ealed that transcriptional regulation of the gluconeogenesis genes PCK1 and G6PC and the fatty acid s
174                            The expression of gluconeogenesis genes was evaluated in both the liver an
175                   Both the expression of two gluconeogenesis genes, G6PC and PCK1, and the inhibitory
176 iRNAs encoded by the Dlk1-Dio3 locus reduced gluconeogenesis, glucose intolerance, and fasting blood
177  including amino acid metabolism, TCA cycle, gluconeogenesis, glutathione metabolism, pantothenate an
178 xidation, cellular redox and ATP production, gluconeogenesis, glycerolipid synthesis, and fatty acid
179  activation of the cytoskeletal motility and gluconeogenesis/glycolysis pathways was most prominent i
180 eferential carbohydrate metabolism including gluconeogenesis, glyoxylate cycle and succinate producti
181  occurs via hepatic glycogenolysis (GLY) and gluconeogenesis (GNG) and plays an important role in mai
182                                              Gluconeogenesis (GNG) is de novo production of glucose f
183  degradation of hepatic glycogen stores, and gluconeogenesis (GNG).
184 egulating the balance between glycolysis and gluconeogenesis; however, in vivo regulation of PK flux
185  improved insulin sensitivity and suppressed gluconeogenesis; however, these effects of E(2) were abo
186 ional changes of biomarker genes involved in gluconeogenesis, immune response and circadian rhythm in
187 e, a single oral dose of shizukaol F reduced gluconeogenesis in C57BL/6 J mice.
188                           Still, the role of gluconeogenesis in cancer is unknown.
189 ed hepatic miR-22-3p expression and impaired gluconeogenesis in diabetic db/db mice via the regulatio
190 primary hepatocytes, E(2) suppressed HGP and gluconeogenesis in hepatocytes from control mice but fai
191 revious data suggest that adropin suppresses gluconeogenesis in hepatocytes.
192 uantitate the contribution and regulation of gluconeogenesis in humans.
193              Glucagon receptor signaling and gluconeogenesis in Mgat5(-/-) cultured hepatocytes was i
194 nt in the control of cell fate in cancer and gluconeogenesis in models of type 2 diabetes.
195                  Our work affirms a role for gluconeogenesis in Mtb virulence and reveals previously
196 ether, our analysis reveals a novel role for gluconeogenesis in neuronal signaling.
197 c nutrients and needs the ability to perform gluconeogenesis in order to colonize mice precolonized w
198 levels during fasting, and decreased hepatic gluconeogenesis in response to a pyruvate challenge.
199 oposed to inhibit anabolic processes such as gluconeogenesis in response to cellular energy stress.
200  was essential for suppression of hepatocyte gluconeogenesis in response to insulin in vitro.
201 tive FBPase (GPM2, Rv3214) that can maintain gluconeogenesis in the absence of GLPX.
202 pathways, including fatty acid oxidation and gluconeogenesis in the fasted state and lipogenesis and
203 d the expression levels of genes involved in gluconeogenesis in the liver and the kidney and signific
204 hat otherwise induce free radicals impacting gluconeogenesis in the liver.
205 riant 2 (PRMT1V2), is critical in regulating gluconeogenesis in the liver.
206 ific Ddb1 deletion leads to impaired hepatic gluconeogenesis in the mouse liver but protects mice fro
207 a transcriptome signature of more pronounced gluconeogenesis in tolerant accessions, a response that
208 ects of sirtinol, a SIRT2 inhibitor, on cell gluconeogenesis in vivo and in vitro.
209 only used stable isotopes methods to measure gluconeogenesis in vivo.
210 ependent transcriptional defects and blunted gluconeogenesis in Vps15 mutant cells.
211  to suppress expression of genes involved in gluconeogenesis, in the process improving glucose handli
212 ptake, although all genes for glycolysis and gluconeogenesis, including bifunctional unidirectional f
213 rate-limiting enzymes for glycogenolysis and gluconeogenesis, including liver glycogen phosphorylase
214  the current understanding of carbon flux in gluconeogenesis, including substrate contribution of var
215                                      Hepatic gluconeogenesis increased by 70%, and net glycogenolysis
216 ch from lactate to glycerol as substrate for gluconeogenesis, indicating an intricate balance of exac
217 rated significant upregulation of glycolysis/gluconeogenesis intermediates (e.g., glucose/fructose, C
218    The chronic effects of metformin on liver gluconeogenesis involve repression of the G6pc gene, whi
219                                              Gluconeogenesis is a complex metabolic process that invo
220                                              Gluconeogenesis is a fundamental metabolic process that
221                                    Increased gluconeogenesis is a major contributor to the hyperglyce
222                   Failure to inhibit hepatic gluconeogenesis is a major mechanism contributing to fas
223                                              Gluconeogenesis is a well-established metabolic process
224                            However, enhanced gluconeogenesis is also a signature feature of type 2 di
225                                              Gluconeogenesis is also increased in primary cultured he
226  most widely accepted technique to determine gluconeogenesis is by measuring the incorporation of deu
227                                              Gluconeogenesis is critical to fuel the transition from
228                                              Gluconeogenesis is essential for the conversion of fatty
229               Appropriate control of hepatic gluconeogenesis is essential for the organismal survival
230                                              Gluconeogenesis is frequently suppressed in tumors arisi
231 patic glucose production, whereas intestinal gluconeogenesis is increased in the gut segments devoid
232  that under fasting conditions, when hepatic gluconeogenesis is stimulated, pyruvate recycling is rel
233                      A rate-limiting step in gluconeogenesis is the conversion of fructose 1,6-bispho
234                        Inhibition of hepatic gluconeogenesis is the primary contributor to its anti-d
235 ochondria in gluconeogenesis control.Hepatic gluconeogenesis is tightly regulated at transcriptional
236 ncluding metabolites involved in glycolysis, gluconeogenesis, lipid metabolism, citric acid cycle, an
237               Transcripts of key pathways of gluconeogenesis, lipogenesis, and inflammatory cytokines
238 es often target biochemical pathways such as gluconeogenesis, lipogenesis, or the metabolic response
239                                      Hepatic gluconeogenesis makes a significant contribution to the
240                               Revealing that gluconeogenesis may be of nonenzymatic origin, our resul
241                  A comprehensive analysis of gluconeogenesis may enable a better understanding of T2D
242  brain metastasis and suggest that targeting gluconeogenesis may help eradicate this deadly feature i
243 the existing trunk pathway of glycolysis and gluconeogenesis may represent a maximal flux solution.
244 ne pathways controlling lipid metabolism and gluconeogenesis.METHODSCross-sectional study of severe r
245           Further, alterations in glycolysis/gluconeogenesis, mitochondrial function and lipid biosyn
246  to fuel Glu and glutathione synthesis while gluconeogenesis occurs in the PDTX.
247 tives to the trunk pathway of glycolysis and gluconeogenesis, one of the most highly conserved pathwa
248 lance by slowing down glycolysis, activating gluconeogenesis or depleting oxygen enables L-form growt
249 rol in the tricarboxylic acid cycle prior to gluconeogenesis or glyceroneogenesis.
250 rack the conversion of metabolites along the gluconeogenesis pathway, lung cancer cell lines were inc
251 ression of the rate-limiting enzymes in both gluconeogenesis (Pck1) and glycogenesis (Gys2), consiste
252  data suggest that RDN downregulated hepatic gluconeogenesis primarily by upregulating liver X recept
253             Lastly, we observe that neuronal gluconeogenesis promotes anterograde neuropeptide distri
254 nduced WAT lipolysis also stimulates hepatic gluconeogenesis, promoting fasting and postprandial hype
255 a the targeting of key regulators of hepatic gluconeogenesis, protein phosphatase 2A (PP2A), AMP-acti
256                                      Hepatic gluconeogenesis provides fuel during starvation, and is
257 vate and its major determinants (glycolysis, gluconeogenesis, pyruvate dehydrogenase [PDH], and H2O2
258   In receptor-level IR, FFA oxidation drives gluconeogenesis rather than being reesterified to trigly
259 ondrial (Pgc1a, Cox5b and Cox7a) and hepatic gluconeogenesis related genes (Pepck) in liver.
260 ition of IRS-1 mRNA levels and activation of gluconeogenesis-related gene expression.
261          We identified a panel of glycolysis/gluconeogenesis-related metabolites that was significant
262 ion of circulating fatty acids, amino acids, gluconeogenesis-related metabolites, and many other mole
263 MT2-specific pathways include glycolysis and gluconeogenesis-related processes, while HSP-specific pa
264                                              Gluconeogenesis results in the generation of glucose fro
265 e metabolism and PGC-1alpha-mediated hepatic gluconeogenesis, suggesting that influencing methionine
266 rate-limiting enzymes in both glycolysis and gluconeogenesis, supporting the formation of multienzyme
267 hydroxyisobutyrylation, including glycolysis/gluconeogenesis, TCA cycle, starch biosynthesis, lipid m
268 ars to be involved in suppression of hepatic gluconeogenesis, the molecular mechanism is not thorough
269 al metabolic pathways, including glycolysis, gluconeogenesis, the tricarboxylic acid (TCA) cycle, and
270 in the levels of intermediates of glycolysis/gluconeogenesis, the tricarboxylic acid cycle, and monos
271 atic beta-cell function and enhanced hepatic gluconeogenesis, thereby resulting in hyperglycemia and
272 er demonstrated that E(2) suppresses hepatic gluconeogenesis through activation of estrogen receptor
273 that insulin-activated SREBP1c downregulates gluconeogenesis through CRY1-mediated FOXO1 degradation
274 ed GRalpha's function and attenuated hepatic gluconeogenesis through downregulation of phosphoenolpyr
275 nsulin-induced SREBP1c and decreases hepatic gluconeogenesis through FOXO1 degradation, at least, at
276  mediating the switch between glycolysis and gluconeogenesis through the conversion of glucose 1-phos
277 fication, the pentose phosphate pathway, and gluconeogenesis through the tricarboxylic acid cycle.
278 ased glycemia, and hampered glucagon-induced gluconeogenesis, thus preventing a proper and complete a
279  technique, and the relative contribution of gluconeogenesis to EGP was quantitated using deuterated
280   INSR subjects had a higher contribution of gluconeogenesis to HGP, approximately 77%, versus 52% to
281 cer cells may utilize at least some steps of gluconeogenesis to overcome the detrimental metabolic si
282 rboxylic acid (TCA) cycle and early steps of gluconeogenesis to promote glucose-independent cell prol
283 energetically demanding processes, including gluconeogenesis, translation, and lipid synthesis.
284 r several decades have offered insights into gluconeogenesis under euglycemic and diabetic conditions
285              Although Pck is associated with gluconeogenesis under standard growth conditions, the en
286  elucidate a mechanism by which GCs regulate gluconeogenesis utilizing the transcription factor Krupp
287  pyruvate and that their metabolism requires gluconeogenesis, valine metabolism, the Krebs cycle, the
288 rstand the mechanism by which E(2) regulates gluconeogenesis via an interaction with hepatic Foxo1.
289 bolism, enhancing glycolysis, and inhibiting gluconeogenesis via elevated translation of the transcri
290 rboxylase, which catalyzes the first step of gluconeogenesis, was also downregulated by hypoxia with
291 ity, FoxO1 phosphorylation, which diminishes gluconeogenesis, was impaired; in contrast, Akt-dependen
292 , the effects of GCG neuronal stimulation on gluconeogenesis were lost, while the food intake-lowerin
293 timulatory effects of PRMT1V2 in controlling gluconeogenesis were observed in human HepG2 cells.
294 ynthesis, ribosome biogenesis and glycolysis/gluconeogenesis were significantly associated with the c
295 ic acid cycle and by concurrently activating gluconeogenesis, which guarantee a continued biogenesis
296  for mediating hyperglycemia through hepatic gluconeogenesis, which is necessary for anticipating and
297  amino acids and a switch from glycolysis to gluconeogenesis while those of cells carrying the missen
298 es fasting glucose levels and blunts hepatic gluconeogenesis without affecting systemic glucose toler
299 sulin resistance due to unrestrained hepatic gluconeogenesis, without alterations in glucose-stimulat
300 the signaling pathways that regulate hepatic gluconeogenesis would allow better insight into the proc

 
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