ライフサイエンスコーパス: lipogenesis

1 in-stimulated lipid synthesis in adipocytes (lipogenesis).

2 d genes encoding enzymes involved in de novo lipogenesis.

3 , reduced hepatic cholesterol, and decreased lipogenesis.

4 including free fatty acid uptake and de novo lipogenesis.

5 mans, and increases rates of hepatic de novo lipogenesis.

6 down-regulation to prevent excessive de novo lipogenesis.

7 A as well as other genes involved in de novo lipogenesis.

8 ssential for HCMV growth and virally induced lipogenesis.

9 p-regulated beta-oxidation at the expense of lipogenesis.

10 ive to C in females, indicative of increased lipogenesis.

11 r triglycerides, along with impaired hepatic lipogenesis.

12 creased ChREBP and markers of adipose tissue lipogenesis.

13 lular hexose-phosphate sensor and inducer of lipogenesis.

14 ced SREBP-1 processing, and promoted de novo lipogenesis.

15 of ERK2, induction of FASN, and promotion of lipogenesis.

16 so regulates interplay between autophagy and lipogenesis.

17 f IL-6 on citrate uptake and reduced hepatic lipogenesis.

18 glucose production is predicted to increase lipogenesis.

19 , and ER stress from the negative effects on lipogenesis.

20 duction, yet successfully stimulates de novo lipogenesis.

21 patic synthesis of triglycerides and de novo lipogenesis.

22 egatively regulates hepatic Akt activity and lipogenesis.

23 y correlated with the suppression of de novo lipogenesis.

24 P-1c activation and inhibits hepatic de novo lipogenesis.

25 e antimicrobial metabolite itaconate and for lipogenesis.

26 e shown inhibit SREBP activation and de novo lipogenesis.

27 at promotes cholesterol removal and inhibits lipogenesis.

28 lic pathway that generates intermediates for lipogenesis.

29 amate) are important indicators of adipocyte lipogenesis.

30 2 positively regulates mSREBP1 stability and lipogenesis.

31 ed uptake, along with an increase in de novo lipogenesis.

32 ogy through the regulation of glycolysis and lipogenesis.

33 tein activity, which leads to an increase in lipogenesis.

34 Cancer cells feature increased de novo lipogenesis.

35 f elongation and desaturation in relation to lipogenesis.

36 have a role in transcriptional repression of lipogenesis.

37 del, presumably by enhancing hepatic de novo lipogenesis.

38 hat C/EBPalpha is required for the increased lipogenesis.

39 dentified Slug as an epigenetic regulator of lipogenesis.

40 microorganism-derived acetate contribute to lipogenesis.

41 tone modifiers, directing specificity toward lipogenesis.

42 liver cells, including carbon metabolism and lipogenesis.

43 genic diet paralleled lower rates of de novo lipogenesis.

44 nes and alters the diurnal rhythm of de novo lipogenesis.

45 mice is unable to suppress fructose-induced lipogenesis.

46 ch are maintained by FASN1-dependent de novo lipogenesis.

47 n response to perturbations in lipolysis and lipogenesis.

48 s that impair endocrine control of adipocyte lipogenesis.

49 oric ingestion and were coupled to increased lipogenesis.

50 viral effects of LXRalpha are independent of lipogenesis.

51 inked to storage of fatty acids from de novo lipogenesis, a process increased in NAFLD.

52 ion by >=35%, and exhibited impaired fasting lipogenesis activity and a shift in soluble epoxide hydr

53 Second, we highlight the role of mTOR in lipogenesis, adipogenesis, beta-oxidation of lipids, and

54 umulation of lipotoxins that promote hepatic lipogenesis, adipose tissue lipolysis, and impaired beta

55 of hepatic mitochondrial oxidative flux and lipogenesis aids in the healthy embryonic-to-neonatal tr

56 ides (48-50 carbons) associated with de novo lipogenesis, alongside increases in circulating levels o

57 PPARgamma promotes metabolic adaptations of lipogenesis and aerobic glycolysis under the control of

58 and SREBP-2 target genes involved in de novo lipogenesis and cholesterol biosynthetic pathways in liv

59 It promotes lipogenesis and cholesterol efflux, but suppresses endop

60 he liver of treated mice by inducing de novo lipogenesis and decreasing beta-oxidation.

61 GLUT4 in adipocytes (AG4OX) have elevated AT lipogenesis and enhanced glucose tolerance despite being

62 ulate substrate utilization, contributing to lipogenesis and fat mass accumulation during positive en

63 nd transcription factors involved in de novo lipogenesis and fat storage.

64 c genes and the products involved in in situ lipogenesis and fatty acid beta-oxidation were analyzed.

65 anges in expression of genes associated with lipogenesis and fatty acid oxidation.

66 that a metabolic transition that suppresses lipogenesis and favors energy production is an essential

67 ng independent of changes in hepatic de novo lipogenesis and food intake.

68 finity and exhibits agonist activity in both lipogenesis and glucose uptake assays.

69 and gluconeogenesis in the fasted state and lipogenesis and glycolysis in the fed state.

70 R and Ras/MAPK cascades as well as increased lipogenesis and glycolysis.

71 t, in prostate cancer (PCa) cells, augmented lipogenesis and growth are due to increased DGAT1 expres

72 a dysregulation of liver enzymes related to lipogenesis and higher mRNA expression of Fitm1.

73 iver, resulting in increased hepatic de novo lipogenesis and hyperlipidemia.

74 sts MNK2 plays a role in adipogenesis and/or lipogenesis and in macrophage biology.

75 a (PGC1alpha) signaling with reduced hepatic lipogenesis and increased hepatic beta-oxidation at orga

76 ) from CDK4-deficient mice exhibits impaired lipogenesis and increased lipolysis.

77 regulation of PLIN2 protein, GW9662 elevated lipogenesis and increased triglyceride levels.

78 However, it is unclear how de novo lipogenesis and its metabolic consequences affect autoph

79 allowed for more accurate measurement in the lipogenesis and LD dimensions, and can break the optical

80 anscription of pivotal genes responsible for lipogenesis and lipid droplet formation in the liver and

81 bolite and enzyme levels indicating elevated lipogenesis and lipid oxidation.

82 n but also results in dysfunctional elevated lipogenesis and lipolysis activities in mouse WAT as wel

83 y acid (FA) cycling in WAT through impacting lipogenesis and lipolysis.

84 s may stem from the concomitant increases in lipogenesis and LPL activity.

85 ZBTB20 is an essential regulator of hepatic lipogenesis and may be a therapeutic target for the trea

86 of TNF-alpha and JAK/STAT pathway on de novo lipogenesis and PCSK9 expression in HepG2 cells.

87 HFD-induced hepatic steatosis by inhibiting lipogenesis and PPARgamma-mediated lipid storage.

88 signaling pathway to inhibit hepatic de novo lipogenesis and prevent the onset of hepatic steatosis a

89 In summary, our data demonstrate that both lipogenesis and proliferation of BAs contribute to postn

90 wed that Leptin deficiency (ob/ob) increased lipogenesis and prolonged survival of Trex1(-/-) mice wi

91 nhanced expression of proteins implicated in lipogenesis and promoted triglyceride accumulation.

92 pletion of Slug, or Lsd1 inhibition, reduced lipogenesis and protected against obesity-associated NAF

93 establish an unexpected relationship between lipogenesis and protein synthesis in mitotic cell divisi

94 and lower Cyp7a1 mRNA, would lead to greater lipogenesis and reduced cholesterol catabolism into bile

95 n MS imaging (DESI-MSI), specific changes in lipogenesis and specific lipids are identified.

96 expression levels of key enzymes involved in lipogenesis and that this upregulation is caused by incr

97 ctivity of PCK1 in the activation of SREBPs, lipogenesis and the development of HCC.

98 stone modifiers can lead to dysregulation of lipogenesis and thus hepatosteatosis leading to insulin

99 Differential regulation of lipogenesis and triglyceride clearance are 2 possible me

100 -PKCzeta axis that activates hepatic de novo lipogenesis and triglyceride synthesis, resulting in lip

101 reatment induced the rate of hepatic de novo lipogenesis and triglyceride synthesis.

102 ical function of mTORC2 in the regulation of lipogenesis and warrant further study in this direction.

103 (13)C palmitate (a marker of hepatic de novo lipogenesis), and lactate concentrations were monitored

104 e dinucleotide phosphate (NADPH) production, lipogenesis, and colorectal cancers in which ME1 transcr

105 rial citrate synthesis to facilitate de novo lipogenesis, and genetic ablation of ACO2 reduced total

106 pid metabolism [including cardiolipin (CL)], lipogenesis, and gluconeogenesis.

107 ed mTORC1 and mTORC2 to drive glycolysis and lipogenesis, and glucose transporter 1-mediated glucose

108 of fatty acid synthase resulting in de novo lipogenesis, and increased nuclear factor kappa B-mediat

109 nscripts of key pathways of gluconeogenesis, lipogenesis, and inflammatory cytokines were reduced in

110 maturation of ribosomes, may have a role in lipogenesis, and is implicated in several diseases.

111 mentation on serum triglycerides, markers of lipogenesis, and lipoprotein lipase (LPL) activity in ad

112 insulinotropic peptide, glucose intolerance, lipogenesis, and metabolic inflexibility.

113 Here, we show that KRAS activates lipogenesis, and this activation results in distinct pro

114 helial cells is sufficient to induce de novo lipogenesis, and this occurs through the convergent acti

115 tiple mechanisms, and alterations in de novo lipogenesis appear to contribute.

116 High rates of hepatic lipid oxidation and lipogenesis are also central features of non-alcoholic f

117 chondrial tricarboxylic acid (TCA) cycle and lipogenesis are central features of embryonic-to-neonata

118 hepatic glycogen storage and hepatic de novo lipogenesis are linked is an attractive prospect.

119 Finally, we identify de novo lipogenesis as a common transcriptional signature of E8

120 lipid metabolism by inhibiting liver de novo lipogenesis as a downstream player of the p63 network.

121 is, and autophagy and propose Acc1-dependent lipogenesis as a fundamental metabolic path downstream o

122 gy of lipids, especially focusing on de novo lipogenesis as a process that gives rise to key messenge

123 l CoA desaturase 1 (SCD1) is a key enzyme in lipogenesis as it catalyzes the synthesis of monounsatur

124 ed mice, glucose was directed toward hepatic lipogenesis as judged by the activity, protein levels, a

125 LERKO mice, resulting from increased hepatic lipogenesis as reflected by increased mRNA levels of fat

126 Acetyl-CoA is the substrate for de novo lipogenesis as well as for histone acetylation.

127 Diabetes is characterized by increased lipogenesis as well as increased endoplasmic reticulum (

128 ghlight altered glyceroplipid metabolism and lipogenesis, as key metabolic phenotypes of mutant PIK3C

129 A core of 23 lipogenesis associated genes was identified and their ex

130 ion of genes involved in gluconeogenesis and lipogenesis, attenuated ER stress response and ER stress

131 imaging revealed a substantial difference in lipogenesis between the fluconazole-susceptible and -res

132 tty acid synthase-a key enzyme that mediates lipogenesis-blunted the effects of Agrp neuron activatio

133 wn reduced downstream glycolysis and de novo lipogenesis but also strongly suppressed hepatic VLDL li

134 decreased cell-autonomous insulin-stimulated lipogenesis but did not alter lipolysis or glucose uptak

135 iated with increased glucose consumption and lipogenesis, but how these pathways are interlinked is u

136 In conclusion, FGF15/19 represses hepatic lipogenesis by activating SHP and DNMT3A physiologically

137 cellular lipids is through enhancing de novo lipogenesis by activating the sterol regulatory element-

138 ented in its mature form (mSREBP1), enhances lipogenesis by increasing transcription of several of it

139 sis, whereas loss of hepatic CES2 stimulates lipogenesis by inducing endoplasmic reticulum stress.

140 d by insulin signaling, and that it promotes lipogenesis by recruiting the histone demethylase Lsd1 t

141 ketone bodies together can therefore inhibit lipogenesis by restricting localization of ChREBP to the

142 bits hepatic glucose production and promotes lipogenesis by suppressing FOXO1-dependent activation of

143 vation by diverse stimuli, thereby promoting lipogenesis, cholesterol synthesis, and protein choleste

144 nally, the pericentral expression of de novo lipogenesis contributed to pericentral steatosis when ad

145 Furthermore, increased lipogenesis correlated with elevated mTORC2 activity and

146 unaffected but mild effects on regulators of lipogenesis could not be excluded, as indicated by small

147 piration and lipolysis and increased de novo lipogenesis, culminating in reduced energy expenditure,

148 levels arise from increased hepatic de novo lipogenesis, decreased hepatic free fatty acid oxidation

149 l, and resulted in increased hepatic de novo lipogenesis, decreased intrahepatic fatty acid oxidation

150 ing: antitumor effects through inhibition of lipogenesis; decreased expression of invasion associated

151 omparison with isotopically measured de novo lipogenesis (DNL(Meas)).

152 (ACC) ACC1 and ACC2, reduces hepatic de novo lipogenesis (DNL) and favorably affects steatosis, infla

153 vational studies often infer hepatic de novo lipogenesis (DNL) by measuring circulating fatty acid (F

154 Hepatic de novo lipogenesis (DNL) contributes to steatosis in individual

155 Hepatic de novo lipogenesis (DNL) converts carbohydrates into triglyceri

156 differentiated by 1) relatively high de novo lipogenesis (DNL) FAs and low n-6 (omega-6) FAs, 2) high

157 s a key transcriptional regulator of de novo lipogenesis (DNL) in response to carbohydrates and in he

158 rum glucose levels, which stimulates de novo lipogenesis (DNL) in the liver.

159 k at 4 degrees C), genes controlling de novo lipogenesis (DNL) including Srebp1, the master transcrip

160 Elevated hepatic de novo lipogenesis (DNL) is a key distinguishing characteristic

161 De novo lipogenesis (DNL) is the primary metabolic pathway synth

162 Adipose tissue de novo lipogenesis (DNL) positively influences insulin sensitiv

163 horylation of AMPK; (3) up-regulated de novo lipogenesis (DNL) related proteins expression (ACC, SCD1

164 Metabolic labeling of de novo lipogenesis (DNL) using (2)H(2)O revealed that 5-PAHSA p

165 Just 7 days after aLivGHRkd, hepatic de novo lipogenesis (DNL) was increased in male and female chow-

166 epatic defects: 1.6-fold accelerated de novo lipogenesis (DNL), 45% slower fatty acid ss-oxidation, a

167 -05175157 led to robust reduction of de novo lipogenesis (DNL), albeit with concomitant reductions in

168 version of fructose to fat in liver (de novo lipogenesis [DNL]) may be a modifiable pathogenetic path

169 to power oxidative phosphorylation and fuel lipogenesis, enabling tumour progression through metabol

170 ctivated the Arntl-Sirt1 axis, and inhibited lipogenesis, ER stress, and inflammation, providing prel

171 ive activation of the TOR-pathway target and lipogenesis factor Sterol regulatory element binding pro

172 ytes to altered metabolic pathways including lipogenesis, fatty acid desaturation, and generation of

173 and downstream signaling pathways regulating lipogenesis, fatty acid oxidation, and glucose homeostas

174 Cancer cells increase lipogenesis for their proliferation and the activation o

175 control of processes that indirectly support lipogenesis, for instance, by supplying reducing power i

176 ACSS2-KO human fibroblasts both HCMV-induced lipogenesis from glucose and viral growth were sharply r

177 olic acetyl-CoA pathways partially decoupled lipogenesis from nitrogen starvation and unleashed the l

178 ssociated with transcriptional activation of lipogenesis, FXR-RXR, PPAR-alpha mediated lipid oxidatio

179 A lipogenesis gene module associated with weight loss was

180 lysis, KRAS is shown to be associated with a lipogenesis gene signature and specific induction of fat

181 at2 deficiency reduced expression of de novo lipogenesis genes and lowered liver TGs by ~70%.

182 expression, and downregulated lipolysis and lipogenesis genes in epididymal WAT.

183 f the critical fatty acid uptake and de novo lipogenesis genes Pparg, Mogat1, Cd36, Acaab1, Fabp2, an

184 (VLDL)-associated apolipoproteins in de novo lipogenesis, glucose metabolism, complement activation,

185 Unexpectedly, mice lacking hepatic lipogenesis have a twofold increase in tumour incidence

186 leads to increases in lipid uptake, de novo lipogenesis, hyperinsulinemia, and hyperglycemia accompa

187 ue-types: cell-division, biomass and energy, lipogenesis, immune-interaction and invasion and tissue-

188 ates of adipose tissue lipolysis and de novo lipogenesis, impaired mitochondrial fatty acid beta-oxid

189 tment or SHP overexpression in mice inhibits lipogenesis in a DNA methyltransferase-3a (DNMT3A)-depen

190 er show that loss of hepatic CES2 stimulates lipogenesis in a sterol regulatory element-binding prote

191 not only adipocyte differentiation but also lipogenesis in adipocytes in vitro.

192 ion, presumably to prevent excessive de novo lipogenesis in adipose tissue.

193 c-Met mice, we determined the requirement of lipogenesis in AKT/c-Met driven hepatocarcinogenesis usi

194 , without significant differences in de novo lipogenesis in both abdominal and gluteal depots, compar

195 nthase was suppressed, along with suppressed lipogenesis in cells exposed to INK128.

196 Blocking lipogenesis in cultured liver cancer cells is sufficient

197 creasing fatty acid oxidation and decreasing lipogenesis in G6pc-/- mice.

198 atty acid oxidation and by decreased de novo lipogenesis in high fat-fed mice.

199 g insulin resistance, glucose metabolism and lipogenesis in juvenile fish fed with graded levels of d

200 Furthermore, lipogenesis in LBs is significantly regulated by coral h

201 ntestine, lipoprotein secretion, and de novo lipogenesis in liver.

202 Herein, we inhibit hepatic lipogenesis in mice by liver-specific knockout of acetyl

203 romotes a gene expression program of de novo lipogenesis in non-small cell lung cancer (NSCLC).

204 bcutaneous adipose tissue (SAT) adipogenesis/lipogenesis in obese adolescents with altered abdominal

205 ruvate transport and reduced insulin-induced lipogenesis in organoids that expressed FXRalpha2 but no

206 Fructose intake triggers de novo lipogenesis in the liver(4-6), in which carbon precursor

207 ed FGF21 expression, together with decreased lipogenesis in the liver.

208 s ergosterol biosynthesis, only affected the lipogenesis in the susceptible strain.

209 y; however, it is not known whether blocking lipogenesis in vivo can prevent liver tumorigenesis.

210 Consequently, JMJD1C promotes lipogenesis in vivo to increase hepatic and plasma trigl

211 lasmic citrate influx, and augmented hepatic lipogenesis in vivo.

212 id-pupae that promotes glucose oxidation and lipogenesis in young adults.

213 two-pronged mechanism that regulates hepatic lipogenesis, in which fructolysis within hepatocytes pro

214 diates of the pentose phosphate pathway, and lipogenesis, including primarily phospholipids, sphingol

215 BW and improved liver function by decreased lipogenesis, increased fatty acid oxidation and improved

216 c triglyceride export and decreasing de novo lipogenesis independently of caloric intake.

217 Overexpression of FLRL2 resolved steatosis, lipogenesis, inflammation, and endoplasmic reticulum (ER

218 n of genes involved in fatty acid synthesis, lipogenesis, inflammation, and packaging of triglyceride

219 AGE-mediated autophagy is not influenced by lipogenesis inhibitors, suggesting that the turnover of

220 ctions contribute to SREBP-regulated de novo lipogenesis involved in non-alcoholic fatty liver diseas

221 Hepatic de novo lipogenesis is a major contributor to nonalcoholic fatty

222 Although AGE-mediated lipogenesis is affected by autophagy inhibitors, AGE-med

223 Hepatic de novo lipogenesis is also upregulated by the inability to synt

224 This study shows that lipogenesis is dispensable for liver tumorigenesis in mi

225 The metabolic pathway of de novo lipogenesis is frequently upregulated in human liver tum

226 Hepatic lipogenesis is normally tightly regulated but is aberran

227 ism in the liver, but its role in regulating lipogenesis is not well understood.

228 This study advances our understanding of how lipogenesis is regulated downstream of insulin signaling

229 Lipogenesis is significantly affected by pretreatment of

230 ), a key regulator of glycolysis and de novo lipogenesis, is increased in GSD 1a.

231 significant metabolic alterations related to lipogenesis, ketogenesis, and inflammation in db/db mice

232 for these lipogenic enzymes to drive de novo lipogenesis leading to ELA, a detrimental event toward r

233 f energy expenditure) without any effects on lipogenesis, lipolysis or lipid uptake and transport.

234 y signaling and considers CLA's linkage with lipogenesis, lipolysis, thermogenesis, and browning of w

235 sent study demonstrates that despite reduced lipogenesis, liver specific SCD1 deficiency activates th

236 n who progress to T2D and suggest endogenous lipogenesis may be a driving force for future diabetes o

237 mmatory stimuli and that the upregulation of lipogenesis may contribute to the resolution of inflamma

238 SEC mice had decreased lipogenesis mediated by hepatic cholesterol responsive e

239 th increased activation of genes involved in lipogenesis mediated by SREBP1c and decreased expression

240 rther expansion of the BAT was mainly due to lipogenesis-mediated BAs volume increase.

241 d that increased adipose tissue capacity for lipogenesis might help protect MNO people from weight ga

242 n in brown adipose tissue and suppression of lipogenesis, mitochondrial biogenesis and thermogenesis.

243 ys, including substrate delivery for de novo lipogenesis; mitochondrial energy use; lipid droplet ass

244 importantly, the induction of TCA cycle and lipogenesis occurred together with the downregulation of

245 be inaccurate in measuring the instantaneous lipogenesis of the living cells.

246 ese data support a novel role, distinct from lipogenesis, of SREBP1 on mitochondrial function in muta

247 stance is prevented during increased hepatic lipogenesis only if adipose tissue lipid storage capacit

248 iochemical pathways such as gluconeogenesis, lipogenesis, or the metabolic response to oxidative stre

249 sis (Warburg effect), fatty acid metabolism (lipogenesis, oxidation, lipolysis, esterification) and f

250 These INSTIs induced adipogenesis, lipogenesis, oxidative stress, fibrosis, and insulin res

251 ated the relationship between alterations in lipogenesis pathway and gemcitabine resistance by utiliz

252 Moreover, western blot analysis showed that lipogenesis pathway enzymes in the liver of db/db mice w

253 trate lyase (ACLY), an enzyme in the de novo lipogenesis pathway, as a novel LMW-E-interacting protei

254 ene SCO2, fatty acid uptake (CAV1, CD36) and lipogenesis (PPARA, PPARD, MLXIPL) genes were enriched i

255 ult primarily from increased hepatic de novo lipogenesis (PRIM) or secondarily from adipose tissue li

256 ic metabolism of fructose leading to de novo lipogenesis, production of uric acid, and accumulation o

257 SREBP2) and the transcription of downstream lipogenesis-related genes, proliferation of tumour cells

258 ellular lipidome is highly regulated through lipogenesis, rendering diverse double-bond positional is

259 De novo lipogenesis requires fatty acid synthase, and recent stu

260 The inflammation-dependent increase in lipogenesis requires the induction of the liver X recept

261 lucose production yet continues to stimulate lipogenesis, resulting in hyperglycemia, hyperlipidemia,

262 ivity (ADIPOQ, GLUT4, PPARG2, and SIRT1) and lipogenesis (SREBP1c, ACC, LPL, and FASN).

263 but also to biological processes during oil lipogenesis (styrene).

264 evels of key enzymes involved in the de novo lipogenesis, such as fatty-acid synthase, stearoyl-CoA d

265 precipitation targets would further increase lipogenesis, supporting hepatosteatosis while lowering g

266 or complex containing NCoR1 and HDAC3 to its lipogenesis targets in hepatocytes.

267 explained in part by an increase in de novo lipogenesis that results from increased sterol element b

268 Dysregulation of lipogenesis therefore has the potential to increase lipi

269 lts reveal that tribbles-1 regulates hepatic lipogenesis through posttranscriptional regulation of C/

270 d that BBR could reverse ER stress-activated lipogenesis through the ATF6/SREBP-1c pathway in vitro.

271 eroxisomes and promoted flux through de novo lipogenesis to concomitantly drive high levels of fatty-

272 HCV 3'UTR, activating IKK-alpha and cellular lipogenesis to facilitate viral assembly.

273 ic flux and downstream pathways like de novo lipogenesis to glucose availability in many cell types i

274 glycerophospholipid chains, linking de novo lipogenesis to the phospholipidome.

275 epatocyte diverted more acetyl-CoA away from lipogenesis toward ketogenesis and TCA cycle, a milieu w

276 eports, hepatic REVERBalpha does not repress lipogenesis under basal conditions.

277 cts (volatile organic compounds) and de novo lipogenesis (using deuterium incorporation) will also be

278 hepatocytes, and that orexin induced hepatic lipogenesis via activation of ERK1/2 signaling pathway.

279 Fructose increases hepatic de novo lipogenesis via numerous mechanisms: by altering transcr

280 Lipogenesis was assessed with the lipogenic index and co

281 Their role in lipogenesis was confirmed by a knockdown experiment.

282 tty acid synthase expression associated with lipogenesis was decreased in G6pc-/- mice treated with b

283 The expression of proteins responsible for lipogenesis was down regulated.

284 However, de novo lipogenesis was higher and fatty acid oxidation was lowe

285 cultured primary hepatocytes, we found that lipogenesis was increased by 40% in LGSKO cells compared

286 Conversely, lipolysis was decreased and lipogenesis was increased in mice expressing a mutant hy

287 -fold increase in TB14 rats, whereas de novo lipogenesis was markedly lower in the incorporation of g

288 Unexpectedly, lipogenesis was not significantly altered in cells subje

289 alternate treatment in period 2; and hepatic lipogenesis was stimulated with oral fructose administra

290 To better understand how fructose induces lipogenesis, we compared the effects of fructose and glu

291 ct actions of GH on lipid uptake and de novo lipogenesis, whereas its actions on extrahepatic tissues

292 increases fatty acid oxidation and inhibits lipogenesis, whereas loss of hepatic CES2 stimulates lip

293 acyltransferase I (DGAT1) is a key enzyme in lipogenesis which is increased in metabolically active c

294 ydrate consumption increases hepatic de novo lipogenesis, which has been linked to the development of

295 implicates them in pathways such as de novo lipogenesis, which is presumably upregulated in the cont

296 burg effect) and become dependent on de novo lipogenesis, which sustains rapid proliferation and resi

297 he intermediary metabolic pathway of de novo lipogenesis, which synthesizes lipids from simple precur

298 tein 1c (SREBP-1c) is a central regulator of lipogenesis whose activity is controlled by proteolytic

299 steatosis upon induction of hepatic de novo lipogenesis with fructose feeding.

300 anisms regulating mitochondrial function and lipogenesis, with potential implications towards treatme