ライフサイエンスコーパス: gluconeogenesis

1 iver glycogen and newly synthesized glucose (gluconeogenesis).

2 promoted both hepatic insulin resistance and gluconeogenesis.

3 al coactivator PGC-1alpha to control hepatic gluconeogenesis.

4 kinase (PEPCK) is well known for its role in gluconeogenesis.

5 rve a beneficial role in suppressing hepatic gluconeogenesis.

6 ntain glucose balance by stimulating hepatic gluconeogenesis.

7 enes in human liver cells, thereby enhancing gluconeogenesis.

8 the pathogenesis of diabetes by upregulating gluconeogenesis.

9 iminished substrate availability for hepatic gluconeogenesis.

10 regulator that promotes FOXO1-driven hepatic gluconeogenesis.

11 thway has now been characterized for hepatic gluconeogenesis.

12 stimulation of Pck1 expression and increased gluconeogenesis.

13 in which statin treatment suppresses hepatic gluconeogenesis.

14 d after GBP and bile acids are inhibitors of gluconeogenesis.

15 atty acid oxidation, glucose utilization, or gluconeogenesis.

16 sed the effects of dietary iron on circadian gluconeogenesis.

17 s, and loss of Wnt-3a-mediated repression of gluconeogenesis.

18 slation regulation, DNA damage response, and gluconeogenesis.

19 iption factors form a complex that regulates gluconeogenesis.

20 glucose production to an enhanced intestinal gluconeogenesis.

21 ediated hepatic inflammation, steatosis, and gluconeogenesis.

22 organs and provides necessary substrate for gluconeogenesis.

23 esults point to DBC1 as a novel regulator of gluconeogenesis.

24 ased liver mRNA for several genes related to gluconeogenesis.

25 glucose tolerance, insulin sensitivity, and gluconeogenesis.

26 etabolism through the suppression of hepatic gluconeogenesis.

27 dependent pathway contributes importantly to gluconeogenesis.

28 ic FBP1 complex, the rate-limiting enzyme in gluconeogenesis.

29 decreased rates of fatty acid oxidation and gluconeogenesis.

30 n plays a critical role in the modulation of gluconeogenesis.

31 aled that PEMT deficiency greatly attenuated gluconeogenesis.

32 d glycerol to glucose, and decreased hepatic gluconeogenesis.

33 lycolysis, oxidative phosphorylation, and/or gluconeogenesis.

34 e and malate, consistent with down-regulated gluconeogenesis.

35 aintain glucose balance by promoting hepatic gluconeogenesis.

36 se (G6PC), key regulatory enzymes of hepatic gluconeogenesis.

37 a wasting syndrome associated with decreased gluconeogenesis.

38 y upregulation of the glyoxylate pathway and gluconeogenesis.

39 tilization of pyruvate, the critical step in gluconeogenesis.

40 , may promote hyperglycemia through enhanced gluconeogenesis.

41 ed in mitochondrial fatty acid oxidation and gluconeogenesis.

42 activity may play an important role in cell gluconeogenesis.

43 y for mitochondrial respiration and reducing gluconeogenesis.

44 ze its transcriptional activities in hepatic gluconeogenesis.

45 affected many metabolic processes, including gluconeogenesis.

46 cetyl coenzyme A (acetyl-CoA) production and gluconeogenesis.

47 ases FOXO1 protein but also enhances hepatic gluconeogenesis.

48 -phosphatase (G6Pase) and suppressed hepatic gluconeogenesis.

49 of glucose and the large sugar phosphates is gluconeogenesis.

50 s ER stress, insulin resistance, and hepatic gluconeogenesis.

51 sulin resistance, hepatic triglycerides, and gluconeogenesis.

52 ts of hypoxia and iron deficiency on hepatic gluconeogenesis.

53 uvate and decreased pyruvate utilization for gluconeogenesis.

54 ted a repressive effect of TCF7L2 on hepatic gluconeogenesis, a recent study using liver-specific Tcf

55 zyme SULT2B1b in the liver inhibited hepatic gluconeogenesis and alleviated metabolic abnormalities b

56 In particular, gluconeogenesis and amino acid catabolism are affected b

57 GLPX and GPM2 is required for disruption of gluconeogenesis and attenuation of Mtb in a mouse model

58 ing FoxO1 and FoxA2, which play key roles in gluconeogenesis and beta-oxidation of fatty acid, respec

59 Liver-specific deletion of MKP-1 enhances gluconeogenesis and causes hepatic insulin resistance in

60 st-translational control of FoxO1, regulates gluconeogenesis and controls metabolic pathways via mito

61 F4A), a transcription factor associated with gluconeogenesis and diabetes, as a central regulatory hu

62 y elevate Sirt1 and Sirt6 levels, increasing gluconeogenesis and DNA repair from the oxidative damage

63 b-3p, and -92b-3p co-regulate the glycolysis/gluconeogenesis and focal adhesion in cancers of kidney,

64 CF7L2DN, but not wild-type TCF7L2, increased gluconeogenesis and gluconeogenic gene expression.

65 was no association with the contribution of gluconeogenesis and glycogenolysis to EGP.

66 an enzyme which catalyses the final step of gluconeogenesis and glycogenolysis.

67 ffect the localization of a mediator of both gluconeogenesis and glycolysis regulation, CRTC2, to the

68 ater hepatic glycogen synthesis and impaired gluconeogenesis and glycolysis related to low cytosolic

69 C]Phosphoenolpyruvate, a key branch point in gluconeogenesis and glycolysis, was monitored in functio

70 owed reduced expression of genes involved in gluconeogenesis and glycolysis.

71 r fructose-6-P, which likely influences both gluconeogenesis and glycolysis.

72 te pathway, substrate-level phosphorylation, gluconeogenesis and glycolysis.

73 ss of hepatic cyclin D1 results in increased gluconeogenesis and hyperglycaemia.

74 A axis activity, in promoting higher hepatic gluconeogenesis and hyperglycemia in poorly controlled d

75 energy expenditure, as well as inhibition of gluconeogenesis and increased rate of glucose disposal d

76 ific ablation of SIK2 alone has no effect on gluconeogenesis and insulin does not modulate SIK2 phosp

77 n metabolic disorders associated with active gluconeogenesis and insulin resistance (obesity, metabol

78 ving mice (a model of persistently activated gluconeogenesis and insulin resistance).

79 mia in disorders with persistently activated gluconeogenesis and insulin resistance.

80 derangement that is associated with greater gluconeogenesis and insulin resistance.

81 carbon flux through the glyoxylate shunt and gluconeogenesis and into synthesis of trehalose, a disac

82 mechanisms of transcriptional regulation of gluconeogenesis and into the roles of chromatin readers

83 In Aspergillus fumigatus, AcuM governs gluconeogenesis and iron acquisition in vitro and virule

84 taacuK DeltaacuM double mutants had impaired gluconeogenesis and iron acquisition, similar to the Del

85 sphatase (FBP1) is a rate-limiting enzyme in gluconeogenesis and is frequently lost in various types

86 kinase 1 (PEPCK1) is the critical enzyme for gluconeogenesis and is linked with type II diabetes.

87 n this study, we analysed starvation-induced gluconeogenesis and ketogenesis in mouse strains lacking

88 aling plays a key role in the maintenance of gluconeogenesis and lipid metabolism in males.

89 vels are also increased, resulting in higher gluconeogenesis and lipid synthesis.

90 the hepatic expression of genes involved in gluconeogenesis and lipogenesis, attenuated ER stress re

91 glucocorticoid excess, and increased hepatic gluconeogenesis and lipogenesis.

92 ulation of glucose homeostasis by modulating gluconeogenesis and may be a useful therapeutic target f

93 to the malate-aspartate shuttle, urea cycle, gluconeogenesis and myelin synthesis.

94 /cataplerotic pathways that are essential to gluconeogenesis and other biosynthetic activities.

95 y modulating expression of genes involved in gluconeogenesis and other liver fasting responses.

96 erate independent of glucose due to enhanced gluconeogenesis and oxidations of glutamine and branched

97 mportantly, we show that cyclin D1 represses gluconeogenesis and OxPhos in part via inhibition of per

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 e quantified liver-specific rates of hepatic gluconeogenesis and substrate oxidation in conjunction w

103 ied cytosolic isoform (PEPCK-C) potentiating gluconeogenesis and TCA flux.

104 also participates in the reverse reaction in gluconeogenesis and the Calvin-Benson cycle.

105 any transcription factors to influence liver gluconeogenesis and the development of specialized cells

106 fatty acids like acetic acid, which induces gluconeogenesis and thereby accounts for glucose intoler

107 ysis and amino acid release to sustain liver gluconeogenesis and tissue protein synthesis.

108 es away from the energy-consuming process of gluconeogenesis and toward the anabolic process of growt

109 PPARalpha near genes involved in glycolysis/gluconeogenesis and uncovered a role for this factor in

110 y rat hepatocytes with amino acids increased gluconeogenesis and ureagenesis and, despite nutrient ex

111 prediction accuracy in a simulation model of gluconeogenesis and using experimental MS/MS data in Bac

112 the opposing effects of atRA and insulin on gluconeogenesis, and also suggest an interaction between

113 ions such as lipogenesis, protein synthesis, gluconeogenesis, and bile acid (BA) homeostasis through

114 or-gamma and genes regulating thermogenesis, gluconeogenesis, and carnitine biosynthesis and transpor

115 unction, intermediate metabolism, glycolysis/gluconeogenesis, and citrate cycle.

116 so showed increased ketogenesis, accelerated gluconeogenesis, and decelerated glycogenolysis.

117 econdary to an inhibition of glycogenolysis, gluconeogenesis, and glucose-6-phosphatase flux.

118 rmentation, and altered hepatic lipogenesis, gluconeogenesis, and glycogenolysis in an AHR-dependent

119 systemic glucose tolerance, reduced hepatic gluconeogenesis, and increased insulin sensitivity.

120 inductions of hepatic fatty acid oxidation, gluconeogenesis, and ketogenesis.

121 eted metabolite profiling to the glycolysis, gluconeogenesis, and Krebs cycle (n = 48) and an explora

122 ed browning of the adipose tissue, decreased gluconeogenesis, and less hepatic steatosis.

123 ayed elevated gluconeogenic gene expression, gluconeogenesis, and loss of Wnt-3a-mediated repression

124 including the citrate acid cycle, glycolysis/gluconeogenesis, and metabolism of branched chain amino

125 rate the dependence of key metabolic fluxes, gluconeogenesis, and signaling on the cytosolic or mitoc

126 ssion, whereas mRNAs involved in glycolysis, gluconeogenesis, and T cell activation were unaffected.

127 hosphoenolpyruvate carboxykinase to initiate gluconeogenesis; and (v) (13)C-MFA together with RNA-seq

128 Glycogenolysis and gluconeogenesis are sensitive to nutritional state, and

129 the effects of various signaling pathways on gluconeogenesis are well established, the downstream sig

130 rance test), demonstrating defective hepatic gluconeogenesis as a cause for the T. cruzi-induced hypo

131 Collectively, our results implicate gluconeogenesis as the key mechanism behind organophosph

132 e had reduced expression of liver markers of gluconeogenesis associated with increased glucose tolera

133 DHA enters gluconeogenesis at the level of the trioses.

134 nt with the inhibitory role of bile acids on gluconeogenesis, bile diversions promote a blunting in h

135 role of TGF-beta1/Smad3 signaling in hepatic gluconeogenesis, both in normal physiology and in the pa

136 ta1/Smad3 signaling pathway promotes hepatic gluconeogenesis, both upon prolonged fasting and during

137 mass, and increased hepatic ureagenesis and gluconeogenesis but decreased glycolysis.

138 icarboxylic acid (TCA) cycle, glycolysis and gluconeogenesis by conversion of mitochondrial oxaloacet

139 We conclude that apoA-IV inhibits hepatic gluconeogenesis by decreasing Glc-6-Pase and PEPCK gene

140 ), and pyruvate phosphate dikinase (PPDK) in gluconeogenesis by generating the respective Leishmania

141 f glucose uptake by muscle and inhibition of gluconeogenesis by liver.

142 ease in hepatic NADH, which inhibits hepatic gluconeogenesis by reducing the conversion of lactate to

143 e, which is likely due to the suppression of gluconeogenesis by salidroside as the protein levels of

144 Mechanistically, CS and SULT2B1b inhibited gluconeogenesis by suppressing the expression of acetyl

145 CS and SULT2B1b inhibited gluconeogenesis by targeting the gluconeogenic factor he

146 te carboxykinase (PEPCK), a key regulator of gluconeogenesis, by consuming NAD(+) and decreasing Sirt

147 glucose-depleted conditions, suggesting that gluconeogenesis can feed the PPP to provide NADPH.

148 Pathways such as glycolysis/gluconeogenesis, citric acid cycle, amino acid metabolis

149 hepatic glycogenolysis but similar rates of gluconeogenesis compared to those on the mixed diet.

150 understanding of the role of mitochondria in gluconeogenesis control.Hepatic gluconeogenesis is tight

151 emical modification known to inhibit hepatic gluconeogenesis, could be potentially used for treatment

152 mediate concentrations, and impaired hepatic gluconeogenesis due to sequestration of free coenzyme A

153 h fat (LCHF) diet would have higher rates of gluconeogenesis during exercise compared to those who fo

154 in response to stress by increasing hepatic gluconeogenesis during fasting.

155 gy-deficiency in any tissue had no effect on gluconeogenesis during starvation.

156 sugar as well as metabolites associated with gluconeogenesis, entailing a critical nodal role of PEPC

157 ndent carboxylases catalyze key reactions in gluconeogenesis, fatty acid synthesis, and amino acid ca

158 ose, a relationship that can only arise from gluconeogenesis followed by passage of substrates throug

159 ructose conversion into blood (13)C glucose (gluconeogenesis from fructose), blood VLDL-(13)C palmita

160 cited by HFD feeding is linked with enhanced gluconeogenesis from glycerol and with alterations in BA

161 ase (G6pc) expression in liver and increased gluconeogenesis from glycerol.

162 of enhanced glycolysis, but it also enhances gluconeogenesis from lactate in the liver that contribut

163 oxaloacetate is an absolute requirement for gluconeogenesis from mitochondrial substrates.

164 nous glucose production, glycogenolysis, and gluconeogenesis from phosphoenolpyruvate.

165 caused mild hyperglycemia, increased hepatic gluconeogenesis from pyruvate, and augmented production

166 -(13)C3]glucose in equal proportions through gluconeogenesis from the level of trioses.

167 , which was associated with up-regulation of gluconeogenesis gene expression as well as decreased gly

168 ate that Tup11/12 repress transcription of a gluconeogenesis gene, fbp1(+), by three distinct mechani

169 cortisol led to stronger upregulation of the gluconeogenesis genes g6pca and pepck1.

170 The expression of gluconeogenesis genes was evaluated in both the liver an

171 Certain gluconeogenesis genes, such as FBP1 (encoding fructose-1

172 including amino acid metabolism, TCA cycle, gluconeogenesis, glutathione metabolism, pantothenate an

173 xidation, cellular redox and ATP production, gluconeogenesis, glycerolipid synthesis, and fatty acid

174 Using various stable isotopes, we found that gluconeogenesis, glycogen, and mannose salvaged from gly

175 activation of the cytoskeletal motility and gluconeogenesis/glycolysis pathways was most prominent i

176 occurs via hepatic glycogenolysis (GLY) and gluconeogenesis (GNG) and plays an important role in mai

177 egulating the balance between glycolysis and gluconeogenesis; however, in vivo regulation of PK flux

178 ional changes of biomarker genes involved in gluconeogenesis, immune response and circadian rhythm in

179 oscopy (MRS) to determine changes in hepatic gluconeogenesis in a high-fat diet (HFD)-induced mouse m

180 Also, DBC1 KO mice display higher gluconeogenesis in a normal and a high-fat diet.

181 We show that the higher rates of hepatic gluconeogenesis in all these models could be attributed

182 e, a single oral dose of shizukaol F reduced gluconeogenesis in C57BL/6 J mice.

183 Still, the role of gluconeogenesis in cancer is unknown.

184 ion of fructose-1,6-bisphosphatase (FBP1) in gluconeogenesis in conjunction with up-regulation of mos

185 a key deleterious role in increased hepatic gluconeogenesis in diabetes, but the mechanism whereby t

186 ed hepatic miR-22-3p expression and impaired gluconeogenesis in diabetic db/db mice via the regulatio

187 uantitate the contribution and regulation of gluconeogenesis in humans.

188 e propose a revision in the current model of gluconeogenesis in Leishmania, emphasizing the differenc

189 Glucagon receptor signaling and gluconeogenesis in Mgat5(-/-) cultured hepatocytes was i

190 nt in the control of cell fate in cancer and gluconeogenesis in models of type 2 diabetes.

191 Our work affirms a role for gluconeogenesis in Mtb virulence and reveals previously

192 c nutrients and needs the ability to perform gluconeogenesis in order to colonize mice precolonized w

193 expression on HepG2 cells is enough to blunt gluconeogenesis in parallel with an up-regulation of AMP

194 levels during fasting, and decreased hepatic gluconeogenesis in response to a pyruvate challenge.

195 oposed to inhibit anabolic processes such as gluconeogenesis in response to cellular energy stress.

196 r metabolic reprogramming from glycolysis to gluconeogenesis in Saccharomyces cerevisiae.

197 tive FBPase (GPM2, Rv3214) that can maintain gluconeogenesis in the absence of GLPX.

198 ted2) was recently shown to be essential for gluconeogenesis in the adult mouse.

199 role AMPD and uric acid in mediating hepatic gluconeogenesis in the diabetic state, via a mechanism i

200 pathways, including fatty acid oxidation and gluconeogenesis in the fasted state and lipogenesis and

201 d the expression levels of genes involved in gluconeogenesis in the liver and the kidney and signific

202 hat otherwise induce free radicals impacting gluconeogenesis in the liver.

203 nd cysteine normalized TCA intermediates and gluconeogenesis in the livers of ketogenesis-insufficien

204 ific Ddb1 deletion leads to impaired hepatic gluconeogenesis in the mouse liver but protects mice fro

205 rk with a higher degree of hypoxia and lower gluconeogenesis in the perivenous zone as compared to th

206 LIRKO mice, even though FGF21 did not reduce gluconeogenesis in these animals.

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 uvate carboxykinase 1 (a protein involved in gluconeogenesis) in livers of mice, increased levels of

212 es the production of sugar, a process called gluconeogenesis, in the liver.

213 to suppress expression of genes involved in gluconeogenesis, in the process improving glucose handli

214 ptake, although all genes for glycolysis and gluconeogenesis, including bifunctional unidirectional f

215 rate-limiting enzymes for glycogenolysis and gluconeogenesis, including liver glycogen phosphorylase

216 Hepatic gluconeogenesis increased by 70%, and net glycogenolysis

217 ch from lactate to glycerol as substrate for gluconeogenesis, indicating an intricate balance of exac

218 tic metabolism, response to hormone stimuli, gluconeogenesis, inflammatory responses, and protein tra

219 rated significant upregulation of glycolysis/gluconeogenesis intermediates (e.g., glucose/fructose, C

220 Gluconeogenesis is a complex metabolic process that invo

221 Hepatic gluconeogenesis is a concerted process that integrates t

222 Gluconeogenesis is a fundamental metabolic process that

223 Failure to inhibit hepatic gluconeogenesis is a major mechanism contributing to fas

224 However, enhanced gluconeogenesis is also a signature feature of type 2 di

225 Gluconeogenesis is an active pathway in Leishmania amast

226 most widely accepted technique to determine gluconeogenesis is by measuring the incorporation of deu

227 Gluconeogenesis is controlled at multiple levels by a va

228 Gluconeogenesis is critical to fuel the transition from

229 Hepatic gluconeogenesis is crucial to maintain normal blood gluc

230 Gluconeogenesis is essential for the conversion of fatty

231 Liver gluconeogenesis is essential to provide energy to glycol

232 patic glucose production, whereas intestinal gluconeogenesis is increased in the gut segments devoid

233 Increased gluconeogenesis is mediated by reduced TORC2 phosphoryla

234 ian liver, the switch between glycolysis and gluconeogenesis is regulated by the bifunctional 6-phosp

235 that under fasting conditions, when hepatic gluconeogenesis is stimulated, pyruvate recycling is rel

236 A rate-limiting step in gluconeogenesis is the conversion of fructose 1,6-bispho

237 ochondria in gluconeogenesis control.Hepatic gluconeogenesis is tightly regulated at transcriptional

238 carboxykinase 1 (AT4G37870), a key enzyme in gluconeogenesis, is enhanced upon MC9-dependent proteoly

239 ncluding metabolites involved in glycolysis, gluconeogenesis, lipid metabolism, citric acid cycle, an

240 Transcripts of key pathways of gluconeogenesis, lipogenesis, and inflammatory cytokines

241 es often target biochemical pathways such as gluconeogenesis, lipogenesis, or the metabolic response

242 Revealing that gluconeogenesis may be of nonenzymatic origin, our resul

243 brain metastasis and suggest that targeting gluconeogenesis may help eradicate this deadly feature i

244 the existing trunk pathway of glycolysis and gluconeogenesis may represent a maximal flux solution.

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 rol in the tricarboxylic acid cycle prior to gluconeogenesis or glyceroneogenesis.

249 d GK, PEPCK, and PPDK are key players in the gluconeogenesis pathway in Leishmania, although stage-sp

250 Proteins involved in the glycolysis/gluconeogenesis pathway were up-regulated at high pressu

251 rack the conversion of metabolites along the gluconeogenesis pathway, lung cancer cell lines were inc

252 ne expression related to both glycolysis and gluconeogenesis pathways.

253 include carbohydrate metabolism (glycolysis/gluconeogenesis, pentose phosphate pathway, pyruvate met

254 data suggest that RDN downregulated hepatic gluconeogenesis primarily by upregulating liver X recept

255 nduced WAT lipolysis also stimulates hepatic gluconeogenesis, promoting fasting and postprandial hype

256 a cycle), pyruvate carboxylase (anaplerosis, gluconeogenesis), propionyl-CoA carboxylase, and 3-methy

257 parallel, the central metabolism, including gluconeogenesis, protein biosynthesis, and purine/pyrimi

258 a the targeting of key regulators of hepatic gluconeogenesis, protein phosphatase 2A (PP2A), AMP-acti

259 Hepatic gluconeogenesis provides fuel during starvation, and is

260 ruvate depletion corresponded with increased gluconeogenesis (pyruvate consumption).

261 vate and its major determinants (glycolysis, gluconeogenesis, pyruvate dehydrogenase [PDH], and H2O2

262 Consistent with its predicted role, gluconeogenesis rates from hepatocytes lacking PEPCK-M a

263 ondrial (Pgc1a, Cox5b and Cox7a) and hepatic gluconeogenesis related genes (Pepck) in liver.

264 ition of IRS-1 mRNA levels and activation of gluconeogenesis-related gene expression.

265 ion of circulating fatty acids, amino acids, gluconeogenesis-related metabolites, and many other mole

266 echanism by which metformin inhibits hepatic gluconeogenesis remains unknown.

267 Gluconeogenesis results in the generation of glucose fro

268 2(-/-) livers allows unrestricted PA-induced gluconeogenesis significantly contributing to the develo

269 e metabolism and PGC-1alpha-mediated hepatic gluconeogenesis, suggesting that influencing methionine

270 Gluconeogenesis-supported NADPH supply may also be impor

271 rate-limiting enzymes in both glycolysis and gluconeogenesis, supporting the formation of multienzyme

272 hydroxyisobutyrylation, including glycolysis/gluconeogenesis, TCA cycle, starch biosynthesis, lipid m

273 ars to be involved in suppression of hepatic gluconeogenesis, the molecular mechanism is not thorough

274 atic beta-cell function and enhanced hepatic gluconeogenesis, thereby resulting in hyperglycemia and

275 that insulin-activated SREBP1c downregulates gluconeogenesis through CRY1-mediated FOXO1 degradation

276 ed GRalpha's function and attenuated hepatic gluconeogenesis through downregulation of phosphoenolpyr

277 nsulin-induced SREBP1c and decreases hepatic gluconeogenesis through FOXO1 degradation, at least, at

278 mediating the switch between glycolysis and gluconeogenesis through the conversion of glucose 1-phos

279 fication, the pentose phosphate pathway, and gluconeogenesis through the tricarboxylic acid cycle.

280 al rodents and in rodent models of increased gluconeogenesis to better understand the role of CRTC2 i

281 technique, and the relative contribution of gluconeogenesis to EGP was quantitated using deuterated

282 cer cells may utilize at least some steps of gluconeogenesis to overcome the detrimental metabolic si

283 rboxylic acid (TCA) cycle and early steps of gluconeogenesis to promote glucose-independent cell prol

284 energetically demanding processes, including gluconeogenesis, translation, and lipid synthesis.

285 ates and end products of both glycolysis and gluconeogenesis under both conditions, including [2,5-(1

286 Although Pck is associated with gluconeogenesis under standard growth conditions, the en

287 upregulation of enzymes involved in hepatic gluconeogenesis was a primary event leading to dysregula

288 The contribution of Car5B to ureagenesis and gluconeogenesis was evident only on a Car5A null backgro

289 rboxylase, which catalyzes the first step of gluconeogenesis, was also downregulated by hypoxia with

290 ity, FoxO1 phosphorylation, which diminishes gluconeogenesis, was impaired; in contrast, Akt-dependen

291 regulator of insulin-mediated suppression of gluconeogenesis, we provide genetic evidence that liver-

292 , the effects of GCG neuronal stimulation on gluconeogenesis were lost, while the food intake-lowerin

293 ynthesis, ribosome biogenesis and glycolysis/gluconeogenesis were significantly associated with the c

294 er plastids or mitochondria or to glycolysis/gluconeogenesis, which are localized to the cytosol, chl

295 ic acid cycle and by concurrently activating gluconeogenesis, which guarantee a continued biogenesis

296 CRTC2 is an important regulator of gluconeogenesis with tremendous impact in models of elev

297 on sites, increasing metabolites involved in gluconeogenesis, with stark increases in succinate, whic

298 es fasting glucose levels and blunts hepatic gluconeogenesis without affecting systemic glucose toler

299 etes because it specifically reduces hepatic gluconeogenesis without increasing insulin secretion, in

300 the signaling pathways that regulate hepatic gluconeogenesis would allow better insight into the proc