ライフサイエンスコーパス: lipogenesis

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

2 down-regulation to prevent excessive de novo lipogenesis.

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

4 e antimicrobial metabolite itaconate and for lipogenesis.

5 e shown inhibit SREBP activation and de novo lipogenesis.

6 at promotes cholesterol removal and inhibits lipogenesis.

7 lic pathway that generates intermediates for lipogenesis.

8 amate) are important indicators of adipocyte lipogenesis.

9 2 positively regulates mSREBP1 stability and lipogenesis.

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

11 ogy through the regulation of glycolysis and lipogenesis.

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

13 Cancer cells feature increased de novo lipogenesis.

14 f elongation and desaturation in relation to lipogenesis.

15 del, presumably by enhancing hepatic de novo lipogenesis.

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

17 ing and fuel availability to SREBP-dependent lipogenesis.

18 tivated protein kinase that leads to reduced lipogenesis.

19 BaP exerts anticancer effects by disrupting lipogenesis.

20 e PPP plays a significant role during fungal lipogenesis.

21 ion of hepatic SREBP1C and decreased de novo lipogenesis.

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

23 t, lipogenic gene transcription, and de novo lipogenesis.

24 s, and increased hepatic gluconeogenesis and lipogenesis.

25 n factors are central regulators of cellular lipogenesis.

26 C1/SREBP1 pathway to shift energy storage to lipogenesis.

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

28 ipid metabolism, thereby inhibiting sebocyte lipogenesis.

29 ed in the regulation of HCMV-induced de novo lipogenesis.

30 r triglycerides, along with impaired hepatic lipogenesis.

31 atty acid (FFA) and triacylglycerol flux and lipogenesis.

32 cytes, demonstrating an inhibitory effect on lipogenesis.

33 increased fatty acid oxidation and decreased lipogenesis.

34 anges in fatty acid oxidation and/or de novo lipogenesis.

35 creased ChREBP and markers of adipose tissue lipogenesis.

36 lular hexose-phosphate sensor and inducer of lipogenesis.

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

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

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

40 so regulates interplay between autophagy and lipogenesis.

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

42 glucose production is predicted to increase lipogenesis.

43 ssential for HCMV growth and virally induced lipogenesis.

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

45 duction, yet successfully stimulates de novo lipogenesis.

46 patic synthesis of triglycerides and de novo lipogenesis.

47 egatively regulates hepatic Akt activity and lipogenesis.

48 y correlated with the suppression of de novo lipogenesis.

49 gy is evident), indicates early induction of lipogenesis/adipogenesis within dysferlin-deficient musc

50 r-activated receptor gamma (master switch of lipogenesis), adipose differentiation-related protein (m

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

52 liver health (ie, liver fat, hepatic de novo lipogenesis, alanine aminotransferase, AST, and gamma-gl

53 ased weight gain and adiposity, and enhanced lipogenesis and adipogenesis.

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

55 tenance of SREBP1 maturation and facilitates lipogenesis and availability of appropriate levels of fa

56 triglycerides by promoting adipogenesis and lipogenesis and by shutting down catabolic processes suc

57 ed two miRNAs, miR-185 and 342, that control lipogenesis and cholesterogenesis in prostate cancer cel

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 falpha, which are involved in thermogenesis, lipogenesis and chronic inflammation in the liver and ad

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

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

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

64 ledge of genetic factors relevant to de novo lipogenesis and fatty acid biology.

65 We used isotope analyses to compare de novo lipogenesis and fatty acid flux between subjects with NA

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

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

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

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

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

71 n factor that regulates genes in the de novo lipogenesis and glycolysis pathways.

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

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

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

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

76 cose transporter in adipocytes have elevated lipogenesis and increased glucose tolerance despite bein

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

78 Insulin regulates glycaemia, lipogenesis and increases mRNA translation.

79 ndrial beta-oxidation, inhibition of hepatic lipogenesis and inflammation, and sensitization of insul

80 t TRAP80 is a selective regulator of hepatic lipogenesis and is required for LXR-dependent SREBP-1c a

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

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

83 ocytes displayed decreased levels of de novo lipogenesis and lipogenic enzymes, supporting the notion

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

85 ccharides (GE) from P. sajor-caju stimulated lipogenesis and lipolysis but attenuated protein carbony

86 Because insulin promotes lipogenesis and liver fat accumulation, to explain the e

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

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

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

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

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

92 dietary sugar content, which drives de novo lipogenesis and promotes the hepatic accumulation of sat

93 Myelin-associated lipogenesis and protein gene regulation are strongly rel

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

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

96 itrate via retrograde TCA cycling, promoting lipogenesis and reprogramming of glutamine metabolism.

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

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

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

100 age, more immune infiltration, and increased lipogenesis and, as a result, displayed classical NASH s

101 Thus, knockdown of FoxO1 (decreased lipogenesis) and overexpression of FoxA2 (increased beta

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

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

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

105 rated fatty acids reduce insulin resistance, lipogenesis, and inflammation, which are features of non

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

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

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

109 etabolite levels associated with glycolysis, lipogenesis, and redox pathways, confirmed at the transc

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

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

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

113 The decreased lipogenesis appears to be a direct consequence of very l

114 Disturbances in hepatic lipogenesis are also associated with systemic metabolic

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

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

117 an essential role for ACC1-mediated de novo lipogenesis as a regulator of CD8(+) T cell expansion, a

118 alpha2M* induces a 2-3-fold increase in lipogenesis as determined by 6-[(14)C]glucose or 1-[(14)

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

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

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

122 lin-induced gene 1 (Insig1), an inhibitor of lipogenesis, as a novel target of miR-24.

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

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

125 high fat diet feeding, and the expression of lipogenesis-associated genes is decreased.

126 glucokinase during fasting, thus increasing lipogenesis at the expense of glucose production.

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

128 any changes in key genes involved in de novo lipogenesis, beta-oxidation, or lipolysis.

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

130 resultant increased signaling may facilitate lipogenesis, but are not the major drivers of the phenot

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

132 Tumors exhibit increased glucose uptake and lipogenesis, but the mechanisms controlling this are poo

133 For example, sugar feeding promotes lipogenesis by activating glycolytic and lipogenic genes

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

135 ica's native metabolism for superior de novo lipogenesis by coupling combinatorial multiplexing of li

136 inhibits the LXRalpha signaling and reduces lipogenesis by decreasing SREBP-1c expression in primary

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

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

139 It strongly suppressed lipogenesis by modulating the IGF-1R/phosphatidylinositi

140 gnificantly inhibited the Warburg effect and lipogenesis by reducing glycolytic and lipogenic gene ex

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 organism to create a strain with significant lipogenesis capability.

144 ression of mRNA for a gene involved in early lipogenesis, CCAAT/enhancer binding protein-delta, in 3-

145 d increased expression of genes that control lipogenesis, compared with fasted control mice.

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

147 Furthermore, increased lipogenesis correlated with elevated mTORC2 activity and

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 ort, we advance fundamental understanding of lipogenesis, demonstrate non-canonical environmental and

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

152 ental evidence suggests that hepatic de novo lipogenesis (DNL) affects insulin homeostasis via synthe

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

154 tose metabolism provides carbons for de novo lipogenesis (DNL) and stimulates enterocyte secretion of

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 in-dependent glucose utilization for de novo lipogenesis (DNL) in adipose tissue.

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

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

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

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

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

163 exposure, single-dose inhibition of de novo lipogenesis (DNL), and changes in indirect calorimetry c

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

165 ene Cd36 whereas that of genes implicated in lipogenesis, fatty acid oxidation, and VLDL secretion wa

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

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

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

169 ental and intracellular stimuli and uncouple lipogenesis from nitrogen starvation.

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

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

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

173 bacterial fermentation, and altered hepatic lipogenesis, gluconeogenesis, and glycogenolysis in an A

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

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

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

177 In contrast, lipogenesis, hypertriglyceridemia, and hepatic steatosis

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

179 cilitate the tight coupling of lipolysis and lipogenesis in activated brown fat.

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

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

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

183 served by a compensatory increase in de novo lipogenesis in Angptl3(-/-) mice.

184 tive mutant of AKT nearly normalized de novo lipogenesis in Bmal1(-/-) hepatocytes.

185 creased fatty acid oxidation while decreased lipogenesis in both liver and fat.

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

187 of MGAT2 with DGAT1 significantly increased lipogenesis in COS-7 cells, indicating the functional im

188 Blocking lipogenesis in cultured liver cancer cells is sufficient

189 ion of 5-HT synthesis leads to inhibition of lipogenesis in epididymal white adipose tissue (WAT), in

190 show diminished fructose uptake and de novo lipogenesis in fructose-challenged GLUT8-deficient hepat

191 p-regulates the contribution of glutamine to lipogenesis in hypoxia, but not in normoxia.

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

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

194 y homeostasis at least in part by regulating lipogenesis in liver and WAT, and hence, may constitute

195 in regulating glucose metabolism and de novo lipogenesis in metabolic tissues and cancer cells.

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

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

198 that ACLY mediates glucose-dependent de novo lipogenesis in response to LPS signaling and identify a

199 is metabolized, in part, to support de novo lipogenesis in response to LPS stimulation of splenic B

200 have been few studies of the role of de novo lipogenesis in the development of nonalcoholic fatty liv

201 sferred with FGF21 gene displayed suppressed lipogenesis in the liver and enhanced thermogenesis in b

202 stemic metabolic phenotypes, suggesting that lipogenesis in the liver communicates with peripheral ti

203 re, but is associated with increased de novo lipogenesis in the liver.

204 e role of BMAL1 in refeeding-induced de novo lipogenesis in the liver.

205 mma, a nuclear receptor that acts to promote lipogenesis in the liver.

206 ound to be the NADPH producers responding to lipogenesis in the oleaginous microbes.

207 In contrast, rates of glucose oxidation and lipogenesis in the presence of high glucose concentratio

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

209 etabolic changes support theories of de novo lipogenesis in tumor tissue and the role of stroma tissu

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

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

212 and carbon-source independent nature of this lipogenesis in Y. lipolytica highlight the potential of

213 induced increased glutamine utilization for lipogenesis, in part through reductive carboxylation, as

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

215 ays and genes associated with adipose tissue lipogenesis increased in MNO, but not MAO, subjects.

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

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

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

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

220 These results indicate that upregulation of lipogenesis is a pre-requisite for DCIS formation by end

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

222 rom the present study show that HCMV-induced lipogenesis is also controlled by the induction of ChREB

223 Increased adipose tissue lipogenesis is associated with enhanced insulin sensitiv

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

227 Lipogenesis is significantly affected by pretreatment of

228 Since FASN, a key enzyme required in lipogenesis, is important in KSHV latency, these finding

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

230 effects of Pleurotus sajor-caju mushroom on lipogenesis, lipolysis and oxidative stress in 3T3-L1 ce

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

232 -fed Ptpn6(H-KO) mice displayed 1) augmented lipogenesis, marked by increased expression of several h

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

234 hepatocytes and negatively regulates de novo lipogenesis mediated by LXR and SREBP1c in a cell-autono

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

236 These findings indicate that lipogenesis might be a therapeutic target for NAFLD.

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

238 ells reprogram metabolism to support de novo lipogenesis necessary for proliferation and expansion of

239 ation increases mitochondrial metabolism and lipogenesis, necessary for normal myelination.

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

241 d not suppress the contribution from de novo lipogenesis on fasting.

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

243 no impact on cellular triglyceride content, lipogenesis, or oxygen consumption, but lipolysis and br

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

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

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

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

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

249 otein 7 (FBXW7), and other components of the lipogenesis pathway.

250 of which indicated activation of the de novo lipogenesis pathway.

251 lysis and biosynthetic activities, including lipogenesis pathways.

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

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

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

255 egulates central metabolic functions such as lipogenesis, protein synthesis, gluconeogenesis, and bil

256 r glucose production and Srebp-1c regulating lipogenesis, provides a potential explanation.

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

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

259 ase (FASN), a key enzyme involved in de novo lipogenesis, results in robust death of ovarian cancer c

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

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

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

263 Low PUFA levels combined with elevated lipogenesis suggests a role for dietary PUFA supplementa

264 e, Nrf2 protects against NASH by suppressing lipogenesis, supporting mitochondrial function, increasi

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

266 is by coupling combinatorial multiplexing of lipogenesis targets with phenotypic induction.

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

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

269 3-bromopyruvate, is a powerful antagonist of lipogenesis through pyruvylation of CoA.

270 viously reported that HCMV infection induces lipogenesis through the activation of sterol regulatory

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

272 However, the contributions of de novo lipogenesis to acquisition and maintenance of CD8(+) T c

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

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

275 its mammalian target of rapamycin (mTOR) and lipogenesis--two crucial arms of cancer growth--AMPK als

276 anism that integrates glucose production and lipogenesis under the unifying control of FoxO.

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

278 Elevated blood glucose promotes lipogenesis via activating SREBP transcription factors.

279 ction of hepatic BMAL1 that promotes de novo lipogenesis via the insulin-mTORC2-AKT signaling during

280 entage of triacylglycerol palmitate, de novo lipogenesis was 2-fold higher in subjects with HighLF (2

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

282 e expression prior to and after the onset of lipogenesis was determined by transcriptomics using the

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

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

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

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

287 g revealed that after 2 h (study A), de novo lipogenesis was responsible for 80% of newly stored hepa

288 Fasting hepatic lipogenesis was significantly higher in HCV (2.80 +/- 0.

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 Glycolysis and lipogenesis were also highly coupled with the cancer phe

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

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

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

295 as NCOA2, drives glutamine-dependent de novo lipogenesis, which supports tumor cell survival and even

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 otective gene expression profile and induces lipogenesis without apparent signs of inflammation or fi