ライフサイエンスコーパス: hepatic

1 X-box binding protein 1 (XBP1) disrupts the hepatic 12-hour clock and promotes spontaneous non-alcoh

2 This was associated with hepatic accumulation of G6P, glycogen, and lipids, where

3 otein kinase B-dependent manner, to regulate hepatic acetyl-CoA and cholesterol synthesis.

4 However, the route from dietary fructose to hepatic acetyl-CoA and lipids remains unknown.

5 Hepatic Acox1 deficiency markedly lowered total cytosoli

6 utcomes included 1-year survival, cardiac or hepatic allograft rejection, and infection.

7 o acids also play an important role and that hepatic amino acid metabolism and glucagon are linked in

8 steatosis might impair glucagon's action on hepatic amino acid metabolism and lead to hyperaminoacid

9 associated with a significant activation of hepatic AMP-activated protein kinase (AMPK), peroxisome

10 er in vitro activity than ivermectin against hepatic and blood stage infections, respectively.

11 s and healthy control participants underwent hepatic and cardiac MRI.

12 significantly reduced triptolide-associated hepatic and cardiac toxicities.

13 ell as alcohol abuse can also influence both hepatic and cardiovascular outcomes.

14 NF-kB, reduced the hepatic and circulating FGF21 levels and altered the non

15 Objective AEs were defined as hepatic and objective muscular AEs.

16 ammatory parameters were normal, as were his hepatic and renal function.

17 ration of fenofibrate decreased the elevated hepatic and renal triglyceride and hepatic glycogen leve

18 ractions and whole-body insulin sensitivity, hepatic and visceral fat, and SCD-1 levels.

19 core of 2 or less and adequate haematologic, hepatic, and renal function.

20 ces PPARgamma hepatic expression and induces hepatic antioxidant activity.

21 ous glucose administration or restoration of hepatic AnxA6 expression rescued AnxA6(-/-) mice surviva

22 Of physiologic significance, deletion of hepatic ApoJ or muscle LRP2 causes insulin resistance an

23 formed using NMP via double perfusion of the hepatic artery and portal vein.

24 d that administration of PRRT via the proper hepatic artery did not reproduce the increase in hepatic

25 Surgery (hepatic artery ligation n = 26; resection n = 13; emboli

26 An increased rate of graft failure due to hepatic artery thrombosis <=14 days from initial LT was

27 dules delivered by an infusion pump into the hepatic artery were mathematically investigated.

28 demonstrate that the dendritic nature of the hepatic artery, portal vein and hepatic vein can be pred

29 igenetically links nutrient deprivation with hepatic autophagy and lipid degradation in mammals.

30 Taken together, these data show that hepatic autophagy impairment in GSD-Ia is mediated by do

31 ent mice at both pre-tumor and tumor stages, hepatic autophagy impairment was attributed to downregul

32 e disease type-Ia (GSD-Ia) leads to impaired hepatic autophagy, a recycling process important for cel

33 h S63845 displayed a significant decrease in hepatic B lymphocytes compared to untreated mice as asse

34 whether gastric BA changes were regulated by hepatic BA synthesis, C57BL/6J mice were intervened with

35 vened with GW4064/resin to decrease/increase hepatic BA synthesis.

36 t of low lipoproteins, may result in reduced hepatic bacterial clearance in the juvenile host with se

37 outcomes in the adult host through increased hepatic bacterial clearance.

38 th reduced hepatic lipogenesis and increased hepatic beta-oxidation at organ programming peak in earl

39 protects from high fat diet (HFD)-dependent hepatic cancer.

40 n leads to chronic inflammation and promotes hepatic carcinogenesis.

41 PC with hallmarks of cell proliferation and hepatic carcinogenesis.

42 However, there is no reliable model of hepatic cardiomyopathy in mice.

43 f inflammatory mediators in the pathology of hepatic cardiomyopathy.

44 Although hepatic CC1 deficiency augmented cold stress-triggered A

45 ids, elevated transaminase levels, increased hepatic CD8+ and F4/80+ cells, overexpression of hepatic

46 ing glucose homeostasis was deciphered using hepatic cell line system, which found up-regulation of g

47 at fluoxazolevir inhibits fusion of HCV with hepatic cells by binding HCV envelope protein 1 to preve

48 (MAPK) signaling pathways in intestinal and hepatic cells, respectively, and thereby regulates diver

49 istinct signaling pathways in intestinal and hepatic cells.

50 ated gut-liver signaling axis that regulates hepatic cholesterol and bile acid homeostasis.

51 Conversely, hepatic LGR4 knockdown increased hepatic cholesterol synthesis and decreased the phosphor

52 ee (3%) patients (abnormal hepatic function, hepatic cirrhosis, and pneumonitis).

53 s in serum insulin concentrations (-53%) and hepatic citrate synthase flux (-38%), respectively.

54 Prospective predictions of human hepatic clearance for anionic/zwitterionic compounds, wh

55 Vitamin K activates both hepatic coagulation factors and extrahepatic endothelial

56 e risk of acute rejection without increasing hepatic complications in HCV+ KT recipients.

57 sustained virological response (SVR) develop hepatic complications.

58 ory liver for this pathogenic process in the hepatic conditional beta-catenin knockout mouse model.

59 ration was seen in all patients, and chronic hepatic congestion in 8 patients.

60 ibuting to loss of function and, thereby, to hepatic copper toxicosis in Wilson disease.

61 The superfamily of hepatic cytochrome P450 (CYP) enzymes is responsible for

62 abolic consequences of directly lowering the hepatic cytosolic NADH/NAD(+) ratio in mice.

63 Hepatic de novo lipogenesis (DNL) contributes to steatos

64 78% versus 49%, P < 0.01) and lower rates of hepatic decompensation (37% versus 62%, P = 0.04) than c

65 ted with a significant reduction in incident hepatic decompensation (6.5% vs. 11.6%, adjusted odds ra

66 FLIS was independently predictive of a first hepatic decompensation (adjusted hazard ratio, 3.7; 95%

67 Conclusion: PREsTo accurately predicts hepatic decompensation (HD) in PSC and exceeds the perfo

68 The risk of clinical relapse and hepatic decompensation after cessation of NA was explore

69 isease who are at increased risk for a first hepatic decompensation and for mortality.

70 nt had a viral rebound during follow-up with hepatic decompensation and was placed on TDF therapy.

71 clinical relapse occurred in 10 (19.6 %) and hepatic decompensation in 2 (3.9%).

72 t develop advanced liver disease: cirrhosis, hepatic decompensation, or hepatocellular carcinoma.

73 vents (i.e., hepatocellular carcinoma [HCC], hepatic decompensation, or liver-related death/transplan

74 fibrosis stage and a presence or history of hepatic decompensation: nonadvanced CLD, compensated adv

75 ith developing clinical outcomes were: prior hepatic decompensations (3.42 [1.28-9.12]), pretreatment

76 al: 1.1, 12.6; P = .04), but not for further hepatic decompensations in patients with DACLD (adjusted

77 , alterations in visceral adipose tissue and hepatic development, and persistent diet-responsive tran

78 Hepatic DNL was measured before and after an oral fructo

79 Hepatic ductular reactions, pericellular fibrosis, and b

80 Significant hepatic dysfunction with clinical jaundice is rare in KD

81 Patients may develop hepatic encephalopathy (HE), pulmonary hypertension (PaH

82 ents with cirrhosis (62% with ascites and/or hepatic encephalopathy [HE]) who were within 7 days of b

83 ciated with some complications, particularly hepatic encephalopathy and infections.

84 ts (ASA) class >=3, and 72% had a history of hepatic encephalopathy, ascites, varices, hepatorenal sy

85 g, progressive telomere dysfunction impaired hepatic endoderm formation.

86 Hepatic endoplasmic reticulum (ER) stress, whether trigg

87 izing the importance of AMPK for maintaining hepatic energy charge.

88 S and cellular TG accumulation, and to alter hepatic energy metabolism to support complete oxidation

89 thionine may serve unique functions to alter hepatic energy metabolism.

90 f an immune-based mechanism for the observed hepatic enzyme elevations.

91 C-reactive protein level were elevated, and hepatic enzymes were normal in the laboratory findings.

92 Hepatic epithelioid hemangioendothelioma (HEHE) is a rar

93 ctions of VDR in macrophages are critical in hepatic ER stress resolution in mice.

94 ng ER stress-induced inflammation to promote hepatic ER stress resolution.

95 farnesoid X receptor (FXR) reduces PPARgamma hepatic expression and induces hepatic antioxidant activ

96 betes, hyperinsulinemia maintains heightened hepatic expression of cyclin D1, suggesting a plausible

97 non-alcoholic fatty liver disease patients, hepatic expression of JMJD3, ATG7, LC3, and ULK1 is subs

98 Alcohol-fed mice demonstrated increased hepatic expression of the cGAS-IRF3 pathway.

99 of the adipokine adiponectin and subsequent hepatic expression of the hormone FGF21.

100 The presumably protective HFD-induced hepatic expression of the metabolic regulator fibroblast

101 fibrosis as measured by collagen deposition, hepatic expressions of collagen-1a, alpha-smooth muscle

102 (1%) patients in the durvalumab group (acute hepatic failure and hepatitis), two (1%) patients in the

103 and one (<1%) patient in the placebo group (hepatic failure).

104 She progressed to haemodynamic and hepatic failure, with clinical features of acute-on-chro

105 and positively correlated with visceral and hepatic fat and SCD-1 activity in both groups.

106 se in body fat and an increase in soleus and hepatic fat content (p < 0.05).

107 The hepatic fat fraction was 4.9% and the pancreatic fat fra

108 Pancreatic fat fraction and hepatic fat fraction were positively associated (OR=69.4

109 Hepatic fat was measured by proton magnetic resonance sp

110 BAM15 decreases hepatic fat, decreases inflammatory lipids, and has stro

111 th, decreased white adipose tissue (WAT) and hepatic fat, improved glucose and insulin tolerance and

112 Hepatic fat, insulin sensitivity index, and SCD-1 were s

113 els to detect hepatic steatosis and quantify hepatic fat.

114 l lipopolysaccharide (LPS) are implicated in hepatic fibrogenesis.

115 wever, anti-BAFF treatment did not attenuate hepatic fibrosis as measured by collagen deposition, hep

116 Ghr treatment reduced ductular reaction and hepatic fibrosis in Mdr2KO mice, regulating cholangiocyt

117 ell population, macrophage accumulation, and hepatic fibrosis in the Mdr2(-/-) model of cholestasis.

118 ent during and after DAA therapy can improve hepatic fibrosis remains unclear.

119 the first family, the proband presents with hepatic fibrosis, retinitis pigmentosa, and postaxial po

120 mproved liver enzymes, hepatic steatosis and hepatic fibrosis.

121 adder, displacement of the transverse colon, hepatic flexure and duodenum.

122 yndromes) and 66% were located distal to the hepatic flexure.

123 ge, data supported by in vitro studies where hepatic flush from CC1-deficient livers enhanced macroph

124 Loss of hepatic fructose-1, 6-bisphosphate aldolase B (Aldob) le

125 obesity and investigated the alterations of hepatic function and underlying mechanisms.

126 and its derivatives on gastrointestinal and hepatic function in health and disease.

127 regulation of beta-cell, skeletal muscle and hepatic function may represent a new therapeutic target

128 ated deaths in three (3%) patients (abnormal hepatic function, hepatic cirrhosis, and pneumonitis).

129 In the current study, we explore the hepatic functions of GPRC6A by conditionally deleting Gp

130 able small interfering RNA (siRNA) targeting hepatic FXIII-B could safely decrease FXIII-A.

131 Importantly, restoration of hepatic G6Pase-alpha expression in G6pc-/- mice corrects

132 endent deacetylase, is pivotal in regulating hepatic gene expression and has emerged as a key therape

133 Appropriate control of hepatic gluconeogenesis is essential for the organismal

134 e signal for mediating hyperglycemia through hepatic gluconeogenesis, which is necessary for anticipa

135 on, mitochondrial dysfunctions, and enhanced hepatic gluconeogenesis.

136 Under metabolic stress, alanine is the main hepatic gluconeogenic substrate, and its availability is

137 reatic clamp with somatostatin and evaluated hepatic glucose and amino acid metabolism when glucagon

138 glucokinase expression resulting in reduced hepatic glucose production and increased hepatic glycoge

139 rglycemia through significant suppression of hepatic glucose production.

140 gerated sympathoadrenal activity and reduced hepatic glutamate dehydrogenase enzymatic activity.

141 We performed quantitative in situ hepatic glutathione redox mapping in zebrafish larvae ca

142 ced hepatic glucose production and increased hepatic glycogen accumulation.

143 elevated hepatic and renal triglyceride and hepatic glycogen levels found in control G6pc -/- mice.

144 glucagon, which is known to rapidly deplete hepatic glycogen.

145 MM affected only hepatic GSH, with lower values in fish fed the OM diets.

146 We targeted hepatic H2HR in Mdr2(-/-) mice using vivo-morpholino.

147 contrast to the reduction of InsP3R1 levels, hepatic HAX-1 deficiency increases bile salt exporter pr

148 iculum-mitochondria calcium homeostasis with hepatic HAX-1 inactivation suggest that this may be a po

149 rotease that plays a key role in suppressing hepatic hepcidin expression.

150 phils contribute to the maintenance of daily hepatic homeostasis through the regulation of the NE/JNK

151 al Caco-2 cells, but increased expression in hepatic Huh7 cells.

152 ratio, 1.7; 95% CI: 1.04, 2.7; P = .03) and hepatic hydrothorax (odds ratio, 2.2; 95% CI: 1.1, 4.2;

153 y6e knockout mice was accompanied by loss of hepatic immune cells, higher splenic viral burden and re

154 ltransferase 1 (PRMT1) is a key regulator of hepatic immune responses.

155 ur findings inform organ transplantation and hepatic immunotherapy, revealing remarkably long-lived p

156 Moreover, hepatic in vitro rates scaled to whole body biotransform

157 or a mechanism by which PPARalpha attenuates hepatic inflammasome activation in response to metabolic

158 educed steatosis, but surprisingly increased hepatic inflammation and fibrosis after being fed a high

159 ocytes determine susceptibility to perinatal hepatic inflammation in late gestation fetuses and neona

160 ght, blood biochemical parameters as well as hepatic inflammation response were investigated.

161 temic insulin resistance, hyperglycemia, and hepatic inflammation, highlighting the physiological cos

162 CB(2) -R activation markedly improved hepatic inflammation, impaired microcirculation, and fib

163 ll population promotes macrophage-associated hepatic inflammation.

164 reasing gluconeogenesis, and upregulated the hepatic inflammatory responses.

165 isease severity, and appears to reflect true hepatic injury.

166 stigated the contributions of these cells to hepatic injury.

167 ions, including plant sterols, interact with hepatic innate immune activation promoted by products of

168 f a 3% decrease in body weight and decreased hepatic insulin resistance (-58%) despite an increase in

169 This leads to increased hepatic insulin sensitivity with increased phosphorylati

170 The primary outcome was the change in hepatic insulin sensitivity, assessed by infusion of ins

171 mation, thereby improving adipose tissue and hepatic insulin sensitivity.

172 intestinal inflammation and apoptosis after hepatic IR in intestinal TLR9 deficient mice.

173 cids butyrate and propionate protect against hepatic IR injury and intestinal apoptosis/inflammation

174 of butyrate or propionate protected against hepatic IR injury in intestinal TLR9 deficient mice.

175 Suggesting a potential therapy for hepatic IR, exogenous administration of butyrate or prop

176 hich phlebotomy promotes the mobilization of hepatic iron stores are not well understood.

177 ine whether/how CEACAM1 signaling may affect hepatic ischemia-reperfusion injury (IRI) and OLT outcom

178 We found that hepatic JNK deficiency alters cholesterol metabolism and

179 Extrapulmonary manifestations included hepatic, kidney, splenic, and bone marrow involvement, a

180 We found hepatic LCN2 expression and serum LCN2 level markedly in

181 Hepatic LDLr plays a critical role in the flow of macrop

182 abnormal in 6 of them, and a newly detected hepatic lesion was present by US in 4.

183 Conversely, hepatic LGR4 knockdown increased hepatic cholesterol syn

184 Our findings demonstrate that p16 represses hepatic lipid catabolism during fasting and may thus par

185 with metabolic consequences such as impaired hepatic lipid metabolism and development of nonalcoholic

186 k and proposed to be a dominant regulator of hepatic lipid metabolism.

187 several genes involved in the regulation of hepatic lipid metabolism.

188 fed control bacteria and had alterations in hepatic lipids, including oxylipins.

189 r-1 alpha (PGC1alpha) signaling with reduced hepatic lipogenesis and increased hepatic beta-oxidation

190 In conclusion, FGF15/19 represses hepatic lipogenesis by activating SHP and DNMT3A physiol

191 chicken hepatocytes, and that orexin induced hepatic lipogenesis via activation of ERK1/2 signaling p

192 VDR expression is induced in hepatic macrophages by ER stress, and VDR plays a dual r

193 Hepatic macrophages express the highest level of vitamin

194 s are involved in ALD progression, including hepatic macrophages.

195 omozygotes (n = 1596), there were 3 incident hepatic malignancies and 60 deaths, but the associations

196 ut the associations between homozygosity and hepatic malignancy (HR, 2.1 [95% CI, 0.7-6.5]; P = .22)

197 ificantly increased risk of incident primary hepatic malignancy and death compared with men without p

198 r liver transplantation (LT) or severe extra-hepatic manifestations.

199 sitive primary tumor, >=4 CRLM, and positive hepatic margin.

200 ic analyses, we observed striking changes in hepatic metabolic profiles in Atp7b (-/-) mice, includin

201 emains unclear whether protective effects on hepatic metabolism are already seen in the offspring ear

202 nocarcinoma on the lobar distribution of its hepatic metastases based on the streamline hypothesis.

203 ation failed to demonstrate higher uptake by hepatic metastases than patients who received intravenou

204 C) patients with inoperable, chemorefractory hepatic metastases.

205 olorectal tumour, and the side and number of hepatic metastases.

206 Hepatic miR-802 levels are increased in FXR-knockout (KO

207 bers in vitro, and decreased ketogenesis and hepatic mitochondrial activity in vivo Finally, gene exp

208 ity and NAFLD has the potential to aggravate hepatic mitochondrial dysfunction.

209 al of NAFLD by KD: That is, markedly altered hepatic mitochondrial fluxes and redox state to promote

210 lore the underlying mechanism, we quantified hepatic mitochondrial fluxes and their regulators in hum

211 otic steatohepatitis and is a major cause of hepatic morbidity.

212 eatment leads to HIF-2alpha stabilization in hepatic MPhis and that HIF-2alpha subsequently reprogram

213 and that HIF-2alpha subsequently reprograms hepatic MPhis to produce the hepatoprotective cytokine I

214 tic CD8+ and F4/80+ cells, overexpression of hepatic mRNA associated with inflammatory signaling path

215 es than males, perhaps because inhibition of hepatic mTORC2 (mTOR Complex 2) specifically reduces the

216 identifying a sex hormone-dependent role for hepatic mTORC2 in female longevity, our results demonstr

217 otes midlife survival of female mice lacking hepatic mTORC2, significantly increasing the survival of

218 a) production which then enhances reparative hepatic neutrophil recruitment.

219 ore likely to show progressive disease, with hepatic nuclear factor 1alpha-inactivated hepatocellular

220 e, we identified that aging alters Sirtuin-1-hepatic nuclear factor 4alpha circuit in hepatocytes to

221 e-dependent effects of TCDD were examined on hepatic OCM in mice.

222 We developed a hepatic organoid platform with human cells that can be u

223 a high-throughput format and induced to form hepatic organoids; development of functional bile canali

224 Hepatic overexpression of Cxcl1 and/or IL-8 promoted ste

225 total respiratory exchange rates and higher hepatic oxidative capacity.

226 ductular reactive (DR) cells extend into the hepatic parenchyma and promote inflammation and fibrosis

227 ined significant between pancreatic PDFF and hepatic PDFF (R(S)=0.632, p<0.001) and between pancreati

228 y for solitary metastases, with percutaneous hepatic perfusion with melphalan or with tebentafusp.

229 with liver fibrosis after BDL had increased hepatic PFKFB3; injection of 3PO immediately after the s

230 ntly expressed in the liver, its function in hepatic physiology remains unknown.

231 presenting with a predominantly cholestatic hepatic picture.

232 creates a microenvironment for the growth of hepatic progenitor cells (HPCs) at the periportal area a

233 When hepatic recurrences after ALPPS was amenable to surgical

234 A to transarterial chemoembolization (TACE), hepatic resection (HR) and chemotherapy (CTX).

235 total of 151 patients who underwent a major hepatic resection were randomized (mean age = 62.8 years

236 oholic cirrhosis or normal liver tissue from hepatic resection.

237 Hepatic resections are associated with a significant acu

238 hibit several differences in feeding-induced hepatic responses in gene expression, especially in lipo

239 icate that: (a) PID affects inflammatory and hepatic serum biochemical parameters, and (b) following

240 Hepatic SIRT1 overexpression corrects defective autophag

241 poprotein metabolism and to characterize key hepatic species-related, physiological differences.

242 icochemical properties (pK(a) and log D) and hepatic stability of several AOXD derivatives were exper

243 Our study comprised 8,345 persons with hepatic steatosis (fatty liver index >60) who participat

244 side A significantly improved liver enzymes, hepatic steatosis and hepatic fibrosis.

245 ltivariable quantitative US models to detect hepatic steatosis and quantify hepatic fat.

246 to circulating metabolites, liver function, hepatic steatosis and the gut microbiome.

247 ty and metabolic pathways putatively driving hepatic steatosis compared with changes induced by exerc

248 xhibited reduced body weight, adiposity, and hepatic steatosis compared with WT controls.

249 asis of this knowledge, we hypothesized that hepatic steatosis might impair glucagon's action on hepa

250 To compare pancreatic and hepatic steatosis quantified by proton density fat fract

251 Patients with hepatic steatosis with persistently normal ALT are at lo

252 Clinical remission rate (achieving grade 0 hepatic steatosis) in HP-diet and beta-cryptoxanthin gro

253 alities, volume, intensity) for treatment of hepatic steatosis, and 4) evidence for a sustained prote

254 126 ameliorated obesity, insulin resistance, hepatic steatosis, and hyperlipidemia without changes in

255 e spontaneously developed liver disease with hepatic steatosis, inflammation, and degeneration.

256 Other changes in the liver included hepatic steatosis, portal fibrosis, lymphocytic infiltra

257 Hepatic steatosis, the excess storage of intrahepatic li

258 t from the risk in a clinical cohort without hepatic steatosis.

259 le risk factors lead to a high likelihood of hepatic steatosis.

260 ent or even treat the metabolic syndrome and hepatic steatosis.

261 in lean nondrinkers with low genetic risk of hepatic steatosis.

262 ce (IR) is associated with hyperglycemia and hepatic steatosis.

263 FFA contributes to both gluconeogenesis and hepatic steatosis.TRIAL REGISTRATIONClinicalTrials.gov N

264 Compared to patients with hepatic steatosis/normal ALT, those with steatosis/eleva

265 Co-cultures of human hepatoma and hepatic stellate (HSCs) cells were exposed to free fatty

266 We investigated mechanisms of hepatic stellate cell (HSC) activation, which contribute

267 rs and consequences of hepatocyte-macrophage-hepatic stellate cell (HSC) crosstalk.

268 Finally, LPI promoted the initiation of hepatic stellate cell activation by stimulating GPR55 an

269 Hepatic stellate cells (HSC) are the major cellular cont

270 oncomitant with activation and senescence of hepatic stellate cells (HSCs), exhibiting a senescence-a

271 to activate cultured fibroblasts and primary hepatic stellate cells (myofibroblast precursors in the

272 Hepatic stellate cells are key players in the progressio

273 nthesis; and as ammonia is known to activate hepatic stellate cells, we hypothesized that ammonia may

274 pha SMA) revealed a significant reduction in hepatic stellate cells.

275 strating that platelet CLEC-2 influences the hepatic sterile inflammatory response and that this can

276 stress and inflammation is regulated during hepatic stress response.

277 Hepatic SULT1E1 mRNA levels are constitutively up-regula

278 s biphasic and required further IVIG for non-hepatic symptoms.

279 small interfering RNA, was shown to inhibit hepatic synthesis of PCSK9 in adults with heterozygous f

280 Hepatic TG production and intestinal TG absorption were

281 sed at a higher level compared to Prmt1v1 in hepatic tissue and cells.

282 very of therapeutic oligonucleotide to extra-hepatic tissues continues to be a challenging endeavor a

283 The hepatic transcriptional response in mice on high-fat die

284 Hepatic transcriptome analysis identified alterations in

285 nt with either of two BMP inhibitors reduced hepatic triglyceride content in diabetic (db/db) mice.

286 In fact, VSG corrected hepatic triglyceride dysregulation in CD36KO mice, and c

287 espite high lipolysis, INSR subjects had low hepatic triglycerides (0.5% [interquartile range 0.1%-0.

288 s exhibited increased body and liver weight, hepatic triglycerides, and inflammatory gene expression

289 argets for inhibiting HSC activation and the hepatic tumor microenvironment.

290 tic artery did not reproduce the increase in hepatic tumor uptake that was previously reported.

291 ly, this report elucidates the mechanisms of hepatic uptake of androgen glucuronides.

292 can be reinforcing, revealing a role for the hepatic vagus nerve in transforming sugar sensing by the

293 othelial RAS-MAPK1 signaling pathway rescued hepatic vascular cavernoma formation in endothelial KRAS

294 These results uncover a major cause of hepatic vascular cavernomas and provide a road map for t

295 this was accompanied by complete absence of hepatic vascular endothelial growth factor (VEGF)-stroma

296 (estimated blood loss, duration of surgery, hepatic vascular occlusion (rate or duration), portal ve

297 xpression of multiple Notch1 target genes in hepatic vasculature, suggesting constitutive functional

298 ature of the hepatic artery, portal vein and hepatic vein can be predicted, together with their geome

299 The SHAPE gradient between the portal and hepatic veins was in good overall agreement with the HVP

300 We show that hepatic XBP1 predominantly regulates the 12-hour rhythmi