ライフサイエンスコーパス: steatosis

1 e lipid accumulation in hepatocytes (hepatic steatosis).

2 zed by the accumulation of fat in the liver (steatosis).

3 of adiponectin, but did not prevent hepatic steatosis.

4 rly fibrosis stages and across all stages of steatosis.

5 mide synthase 6 in mouse and human alcoholic steatosis.

6 rment of mitochondrial oxidation and hepatic steatosis.

7 idation in progression of NASH beyond simple steatosis.

8 us understand its role in the development of steatosis.

9 isorders, including dyslipidemia and hepatic steatosis.

10 R stress, preventing sustained apoptosis and steatosis.

11 PXR deficiency suppressed these changes and steatosis.

12 cells promotes hepatic fat accumulation and steatosis.

13 prevented adiposity, insulin resistance, and steatosis.

14 d analyzing liver biopsy specimens to detect steatosis.

15 th blood levels of liver enzymes and hepatic steatosis.

16 sulin resistance, hyperlipidemia and hepatic steatosis.

17 al hypoxia-inducible factor (HIF) in hepatic steatosis.

18 patients with NASH from patients with simple steatosis.

19 s also independently associated with hepatic steatosis.

20 ed obesity, adipocyte hypertrophy, and liver steatosis.

21 screening patients with a suspicion of liver steatosis.

22 sis that are thought to emanate from hepatic steatosis.

23 yzed to evaluate their relation with hepatic steatosis.

24 o feeding, exacerbating diet-induced hepatic steatosis.

25 mong alcohol drinkers and those with hepatic steatosis.

26 49) were higher in participants with hepatic steatosis.

27 ciated with the diffusion parameters than is steatosis.

28 were protected from diet-induced obesity and steatosis.

29 homeostasis and prevents obesity and hepatic steatosis.

30 c architecture in liver biopsies with simple steatosis.

31 s and prevents high-fat diet-induced hepatic steatosis.

32 The primary outcomes were fibrosis and steatosis.

33 hepatocellular ballooning and microvesicular steatosis.

34 hanced M1 macrophages and the development of steatosis.

35 A-IV gene expression in the setting of acute steatosis.

36 significant shared gene effects with hepatic steatosis.

37 ing for higher susceptibility to pericentral steatosis.

38 ipose tissue lipolysis, ameliorating hepatic steatosis.

39 taminophen hepatotoxicity or fasting-induced steatosis.

40 pidemia and atherosclerosis without inducing steatosis.

41 dult cnr2 mutants are susceptible to hepatic steatosis.

42 ted liver ultrasound examination for hepatic steatosis.

43 ose intolerance and high fat-induced hepatic steatosis.

44 ay be a novel therapeutic strategy to reduce steatosis.

45 genes and lowers glycemia without concurrent steatosis.

46 and quercetin (D+Q) reduces overall hepatic steatosis.

47 ing studies performed were positive only for steatosis.

48 l Red O staining were performed to determine steatosis.

49 decreased gluconeogenesis, and less hepatic steatosis.

50 stage of alcoholic liver disease, alcoholic steatosis.

51 ted in zone 3 hepatocytes in human alcoholic steatosis.

52 HIV patients develop hepatic steatosis.

53 ion and lipolysis, and thus promoted hepatic steatosis.

54 be used to improve noninvasive detection of steatosis.

55 mong alcohol drinkers and those with hepatic steatosis.

56 esity-induced hepatic insulin resistance and steatosis.

57 d by lobular inflammation (0.48; P < 0.001), steatosis (0.46; P < 0.001), but less with fibrosis (0.2

58 8 +/- 1.2; P = 0.019), mainly contributed by steatosis (1.7 +/- 0.8 vs. 2.0 +/- 0.8; P = 0.014) and p

59 ts of Gsta4(-/-) and Ppara(-/-) silencing on steatosis, 4-hydroxynonenal adduct formation, oxidative

60 re protected against fasting-induced hepatic steatosis (a model of enhanced exogenous FA delivery) ye

61 s of inhalation exposure to PM2.5 on hepatic steatosis, a precursor or manifestation of metabolic syn

62 was a significant increase in microvesicular steatosis accompanied by a marked reduction in NG2+ peri

63 steatosis were assessed with the METAVIR and steatosis, activity, and fibrosis (or SAF) scoring syste

64 d AdSod2 KO mice were protected from hepatic steatosis, adipose tissue inflammation, and glucose and

65 tion of patients without significant hepatic steatosis after 48 weeks was greater for those who switc

66 We hypothesize that steatosis alters the microenvironment to promote prolife

67 ns between ambient air pollution and hepatic steatosis among 2,513 participants from the Framingham (

68 virenz (EFV) to raltegravir (RAL) on hepatic steatosis among HIV-infected patients with nonalcoholic

69 ts with biopsy-proven NAFLD (353 with simple steatosis and 182 with NASH) and compared them with seru

70 et protein that is up-regulated in alcoholic steatosis and associated with hepatic accumulation of ce

71 achine used for LSM and associated with both steatosis and body mass index, the two factors mostly af

72 therapeutic targets in the context of liver steatosis and cancer.

73 ere found in WD-fed WT mice harboring simple steatosis and CD-fed FXR KO mice, in which the steatosis

74 nsity fat fraction (PDFF) in grading hepatic steatosis and change in hepatic steatosis in adults with

75 hat a leaky gut barrier is linked with liver steatosis and could be a new target for future steatosis

76 ates that cellular senescence drives hepatic steatosis and elimination of senescent cells may be a no

77 graphy (TE, Fibroscan(R)) have been used for steatosis and fibrosis assessment.

78 genous hepatic FA use modulates both hepatic steatosis and fibrosis in the setting of hepatic Mttp de

79 of alanine aminotransferase (ALT) and liver steatosis and fibrosis, compared with mice given injecti

80 c Mttp knockout mice (Mttp-LKO) exhibit both steatosis and fibrosis, which is exacerbated by a high-t

81 nsient elastography (TE) to evaluate hepatic steatosis and fibrosis.

82 d fatty acid oxidation and ameliorated liver steatosis and glucose intolerance in diet-induced obese

83 y acid beta-oxidation; and ameliorated liver steatosis and glucose intolerance.

84 revealed that systemic mechanisms leading to steatosis and hepatitis in this non-obese NAFLD model we

85 male WD-fed FXR KO mice had the most severe steatosis and highest hepatic and serum lipids as well a

86 lipolysis, glucocorticoid- initiated hepatic steatosis and hypertriglyceridemia were improved in AKO

87 20 ablation protects from diet-induced liver steatosis and improves hepatic insulin resistance.

88 and lipid homeostasis in mice with alcoholic steatosis and in ethanol-incubated human hepatoma VL17A

89 urther, liver shear stiffness decreased with steatosis and increased with inflammation and fibrosis a

90 the generally accepted cut-off of 5% fat for steatosis and indicate 20% as a threshold of more severe

91 t, bile acids, sex, and dysbiosis in hepatic steatosis and inflammation.

92 rapamycin attenuates EtOH-LPS-induced liver steatosis and injury.

93 On high-fat diet, JAK2L mice had hepatic steatosis and insulin resistance despite protection from

94 tected against high-fat diet-induced hepatic steatosis and insulin resistance.

95 b or HFD-fed mice markedly ameliorates liver steatosis and insulin resistance.

96 ractive target for the management of hepatic steatosis and insulin resistance.

97 (PNPLA3) is robustly associated with hepatic steatosis and its progression to steatohepatitis, fibros

98 Omega3FA reversed HFD-induced steatosis and markedly protected against I/R, improved L

99 to successfully differentiate between simple steatosis and more severe NASH, based on a set of short-

100 increased in liver biopsies of patients with steatosis and NASH compared to controls.

101 ed in a percentage fat-dependent increase in steatosis and necroinflammatory injury (P < 0.05).

102 rbances reflected peroxisomal proliferation, steatosis and necrosis.

103 sponse to fasting and feeding contributes to steatosis and nonalcoholic fatty liver and obesity.

104 ver biopsy specimens of patients with simple steatosis and nonalcoholic steatohepatitis (NASH).

105 LD and the inclusion of patients with simple steatosis and nonalcoholic steatohepatitis without fibro

106 if2a, in which high-fat-diet-induced hepatic steatosis and obesity were substantially lower as compar

107 isms by which hepatic GH resistance leads to steatosis and overall insulin resistance, independent of

108 changes were accompanied by reduced hepatic steatosis and oxidative stress in adipose tissue and bra

109 obesity or Western-style diet (WD) increases steatosis and oxidative stress in fetal liver and is ass

110 injury with significantly increased hepatic steatosis and serum AST level as well as hepatic cellula

111 Hepatic RetSat expression correlates with steatosis and serum triglycerides (TGs) in humans.

112 On chow, JAK2L mice had hepatic steatosis and severe whole-body and hepatic insulin resi

113 The association of lnc18q22.2 to liver steatosis and steatohepatitis was replicated in 44 indep

114 ects mice from high-fat diet-induced hepatic steatosis and that mutation of the SLC13A5 orthologues i

115 o fatty acid and lipid synthesis, leading to steatosis and tumor development.

116 onship between liver fibrosis, inflammation, steatosis, and alanine aminotransferase (ALT) levels and

117 metabolic disorders, such as obesity, liver steatosis, and for ageing.

118 esis inhibition on hepatic PLIN2 expression, steatosis, and glucose and lipid homeostasis in mice wit

119 mice transferred sensitivity to weight gain, steatosis, and hyperglycemia to wild type germ free mice

120 after cardiac death donors, livers with >30% steatosis, and livers split between 2 recipients.

121 ine aminotransferase concentrations; hepatic steatosis; and hepatic expression of IL-1alpha, -beta, -

122 emics of metabolic diseases, including liver steatosis, are associated with an increased frequency of

123 AL showed decreases in the degree of hepatic steatosis, as measured by CAP, compared with those conti

124 tivity, which acts to suppress apoptosis and steatosis associated with hepatic ER stress.

125 y effective in a preclinical murine model of steatosis-associated liver cancer.

126 Changes in hepatic steatosis at 48 weeks of follow-up over baseline levels

127 magnesium intake and alcohol use and hepatic steatosis at baseline were not significant (P > 0.05), i

128 ubjects with PDFF values of 5.0% or more had steatosis based on histopathology findings (100% specifi

129 negative result), 22 were determined to have steatosis based on histopathology findings (53% sensitiv

130 nhancing WAT lipolysis could produce ectopic steatosis because of an overflow of lipids from the WAT

131 (beta = -0.3, P = .02, R(2) = 0.33) than did steatosis (beta = -0.5, P < .001, R(2) = 0.33).

132 from individuals with NASH (n = 48), simple steatosis but no NASH (n = 11), and healthy controls (n

133 Omega3FA are known to reverse steatosis, but how these lipids affect key factors defin

134 rrent PDFF cut-off value (5%) used to define steatosis by magnetic resonance was derived from studies

135 -induced hepatic metabolic dysregulation and steatosis by restoring changes in hepatic mRNA or protei

136 tic model assessment index (HOMA), and liver steatosis by sonography and the fatty liver index (FLI).

137 lergies, type 1 and type 2 diabetes, hepatic steatosis, cardiovascular disease, and inflammatory bowe

138 Effective treatments are needed for hepatic steatosis characterized by accumulation of triglycerides

139 gher serum EtOH levels and developed hepatic steatosis characterized by micro- and macrovesicular lip

140 t variables of type (DCD vs DBD), donor age, steatosis, cold ischemic time, peak aspartate transamina

141 eability is increased in obese patients with steatosis compared with obese patients without.

142 Hdc(-/-) HFD mice had increased steatosis compared with WT HFD mice.

143 ped a multi-component classifier for hepatic steatosis comprised of phenotypic, genomic, and proteomi

144 pulse imaging or shear wave elastography) or steatosis (controlled attenuation parameter or magnetic

145 herwise fatal liver disease characterized by steatosis, death of hepatocytes, and ultrastructural abn

146 ess damages the liver, causing apoptosis and steatosis despite the activation of the unfolded protein

147 ome, but not other, individuals with hepatic steatosis develop NASH.

148 y, contributes to mitochondrial dysfunction, steatosis development, and insulin resistance under high

149 whether obese patients with or without liver steatosis differ in this function.

150 Zip14 KO mice show greater levels of hepatic steatosis due to higher expression of genes involved in

151 on contributes to the development of hepatic steatosis, dyslipidemia and hyperglycemia.

152 t metabolism have been implicated in hepatic steatosis, dyslipidemia, obesity, and insulin resistance

153 Besides metabolic pathologies, steatosis enhances hepatic sensitivity to ischemia reper

154 We compared steatosis estimates by PDFF vs histology.

155 Sat may represent a therapeutic approach for steatosis.Fatty liver is one of the major features of me

156 d mouse model of high fat diet (HFD)-induced steatosis followed by Omega3FA treatment and the subsequ

157 ited enhanced liver regeneration and reduced steatosis following partial hepatectomy.

158 patients with NASH from patients with simple steatosis for each subtype of NAFLD.

159 glucose intolerance, insulin resistance and steatosis formation in transgenic CCDC3 mice on high-fat

160 ypes of NAFLD and markers that differentiate steatosis from NASH in each subtype.

161 We identified 136 biopsies with simple steatosis from the Royal Free Hospital Archives with bot

162 nd ameliorates high-fat-diet-induced hepatic steatosis, glucose tolerance, and insulin resistance.

163 ol db/db mice developed similar body weight, steatosis, glycemia, and insulin levels after a glucose

164 seline of 7.4%+/-8.7%), 49% had no change in steatosis grade (mean increase in PDFF from baseline of

165 ine of 0.3%+/-6.3%), and 9% had an increased steatosis grade (mean increase in PDFF from baseline of

166 ic vs placebo, 42% of subjects had a reduced steatosis grade (mean reduction in PDFF from baseline of

167 At baseline, 34% of subjects had steatosis grade 0 or 1, 39% had steatosis grade 2, and 2

168 PDFF classified steatosis grade 0-1 vs 2-3 with an area under the ROC cu

169 subjects had steatosis grade 0 or 1, 39% had steatosis grade 2, and 27% had steatosis grade 3; corres

170 or 1, 39% had steatosis grade 2, and 27% had steatosis grade 3; corresponding mean PDFF values were 9

171 Histologic steatosis grade was scored in consensus by a pathology c

172 ease of 5.6% identified those with increased steatosis grade with 90% specificity and 57% sensitivity

173 on of 5.15% identified subjects with reduced steatosis grade with 90% specificity and 58% sensitivity

174 OC of 0.81 (95% CI, 0.71-0.91) and increased steatosis grade with an AUROC of 0.81 (95% CI, 0.63-0.99

175 PDFF change identified subjects with reduced steatosis grade with an AUROC of 0.81 (95% CI, 0.71-0.91

176 Results Steatosis grades at liver biopsy were distributed as fol

177 CAP and PDFF were compared between steatosis grades by using the Jonckheere-Terpstra test.

178 4 vs 0) and MRI-PDFF vs CAP for diagnosis of steatosis (grades 1-3 vs 0) with respect to findings fro

179 and CAP helped detect histologically proven steatosis (>/=S1), but PDFF showed better diagnostic acc

180 eatosis and CD-fed FXR KO mice, in which the steatosis had a potential to develop into liver cancer.

181 us tumors and liver abnormalities, including steatosis, hepatitis, and hepatocellular carcinoma.

182 capacity had no impact on WD-induced hepatic steatosis; however, rats bred for low aerobic capacity d

183 Hepatic steatosis (HS) is common in individuals with hepatitis C

184 In liver steatosis (i.e. fatty liver), hepatocytes accumulate man

185 ver disease (NAFLD) can progress from simple steatosis (i.e., nonalcoholic fatty liver [NAFL]) to non

186 parameter (CAP) in the diagnosis of hepatic steatosis in a series of overweight or obese children by

187 ding hepatic steatosis and change in hepatic steatosis in adults with nonalcoholic steatohepatitis (N

188 ceramide synthesis reduced PLIN2 and hepatic steatosis in alcohol-fed mice, but only de novo synthesi

189 ayed susceptibility to high fat diet-induced steatosis in association with reduced hepatic mitochondr

190 olesterol in the WD induced hepatomegaly and steatosis in both HCR and LCR rats, while producing grea

191 For the evaluation of liver steatosis in children CAP performs better than US, which

192 forced PHLPP2 expression ameliorates hepatic steatosis in diet-induced obese mice.

193 However, PM2.5 exposure relieved hepatic steatosis in high-fat diet-induced obese mice.

194 ugs with a lower potential to induce hepatic steatosis in human immunodeficiency virus (HIV) infectio

195 perior to CAP in detecting and grading liver steatosis in human NAFLD.

196 high-fat/high-sucrose diet produced greater steatosis in LCR and high capacity runner (HCR) rats.

197 tural compound that protects against hepatic steatosis in mice fed the high-fat diet, as a novel agon

198 onfers hepatoprotection against diet-induced steatosis in murine models and extends lifespan of Caeno

199 was associated with reduced risk of hepatic steatosis in participants (odds ratio, 0.69; 95% CI= 0.5

200 attenuation parameter (CAP) for diagnosis of steatosis in patients undergoing biopsy to assess NAFLD.

201 accurate than CAP in detecting all grades of steatosis in patients with NAFLD.

202 sed in noninvasive diagnosis of fibrosis and steatosis in patients with nonalcoholic fatty liver dise

203 Both diets induced severe hepatic steatosis in the LTKO mice as compared to WT controls.

204 h intake diets leading to the development of steatosis in the model, we identify key differences betw

205 nostic tests have been developed for hepatic steatosis in the setting of obesity.

206 dipose tissue lipolysis and improved hepatic steatosis in these mice.

207 We investigated hepatic steatosis in transgenic mice expressing the HIV-1 access

208 cally up-regulated in experimental alcoholic steatosis in vivo and in vitro and was up-regulated in z

209 :2 species with complete reversal of hepatic steatosis, increased hepatic injury, and worsened fibros

210 omes were compared with lean liver to assess steatosis-independent effects.

211 s (BMI), fatty liver index (FLI) and hepatic steatosis index (HSI) was analyzed using the imperfect g

212 bacteria and bile acids (BAs) contribute to steatosis induced by diet and farnesoid X receptor (FXR)

213 infiltrating macrophages as a key source for steatosis-induced Wnt expression.

214 pNaKtide reduced obesity as well as hepatic steatosis, inflammation and fibrosis.

215 gher at high frequencies for the presence of steatosis, inflammation grade, and fibrosis stage (low f

216 coholic liver disease (ALD) characterized by steatosis, inflammation, and eventually cirrhosis.

217 novo lipogenesis (DNL) and favorably affects steatosis, inflammation, and fibrosis in animal models o

218 Histologic features (steatosis, inflammation, and fibrosis) and modified nona

219 ies (low frequency: 0.08, 0.24, and 0.20 for steatosis, inflammation, and fibrosis, respectively; hig

220 -MIR122 before ethanol feeding had increased steatosis, inflammation, and serum levels of alanine ami

221 Gender differences in WD-induced steatosis, insulin sensitivity, and predicted microbiota

222 d fatty liver and insulin resistance.Hepatic steatosis is a common disease closely associated with me

223 Hepatocyte steatosis is a component of metabolic syndrome and insul

224 Hepatic steatosis is caused by metabolic imbalances that could b

225 ediated activation of ethanol (EtOH)-induced steatosis is unclear.

226 Nonalcoholic fatty liver disease (steatosis) is the most prevalent liver disease in the We

227 d with markers of liver function and hepatic steatosis, laying the groundwork for future diagnostic a

228 es in hepatic tissues such as microvesicular steatosis, likely caused by an increase in oxidative str

229 Steatosis limits the application of liver surgery, still

230 Consistent with the development of steatosis, lipogenic gene induction was significantly in

231 nd prevalence ratios for presence of hepatic steatosis (LPR </= 0.33) using generalized linear models

232 Hepatic steatosis may be benign or progress to hepatocyte injury

233 sis, insulin sensitivity, insulin secretion, steatosis, metabolic inflammation, pancreatic islet morp

234 egarded as the reference for differentiating steatosis (NAFL) from nonalcoholic steatohepatitis, for

235 out mice are leaner and resistant to hepatic steatosis, obesity and insulin resistance under a lipoge

236 nt an effective therapy for managing hepatic steatosis, obesity, and diabetes.

237 e highest area under the ROC curve (AUC) for steatosis of PNPLA3 rs738409 genotype, 8 proteins, or 19

238 In the liver, steatosis often proceeds cancer formation; however, the

239 characteristics curves to detect ballooning, steatosis, or steatohepatitis (SH) were slightly better

240 9 group, manifested by reduced inflammation, steatosis, oxidative stress, and apoptosis and increased

241 PDFF, but not CAP, enabled the grading of steatosis (P < .0001).

242 r severe steatosis than in those without any steatosis (P < 0.001).

243 say, a set of 19 clinical variables, and the steatosis predisposing PNPLA3 rs738409 single nucleotide

244 06, -0.001) and higher prevalence of hepatic steatosis (prevalence ratio = 1.16, 95% confidence inter

245 formation; however, the mechanisms by which steatosis promotes carcinogenesis is unknown.

246 tly correlated with NAFLD activity score and steatosis (R = 0.28 and 0.22, respectively), whereas SSI

247 Hepatic steatosis renders liver more vulnerable to ischemia/repe

248 invasive assessments of hepatic fibrosis and steatosis, respectively.

249 The biopsy was graded for fibrosis (F) and steatosis (S) stagings.

250 dy had a high prevalence of elevated hepatic steatosis scores.

251 fibrosis scores, and 54 (78.3%) had elevated steatosis scores.

252 ey BAs were associated with higher grades of steatosis (taurocholate), lobular (glycocholate) and por

253 s higher in patients with moderate or severe steatosis than in those without any steatosis (P < 0.001

254 revealed that asparaginase provoked hepatic steatosis that coincided with activation of another eIF2

255 Intriguingly, NR also ameliorated the steatosis that normally accompanies liver regeneration.

256 duced by infiltrating macrophages induced by steatosis that promotes growth of tumor progenitor cells

257 with logistic regression models to classify steatosis, that were then tested against a 133 sample bl

258 eatosis and could be a new target for future steatosis therapies.

259 -2alpha could be a viable target for hepatic steatosis therapy.

260 usion, a time point that results in isolated steatosis, there was no increase of blood EVs.

261 d composition and in fasting-induced hepatic steatosis through a novel mechanism involving activation

262 e loci that confer susceptibility to hepatic steatosis through diverse metabolic mechanisms.

263 donor cardiac disease, black ethnicity, and steatosis to be additional risk factors.

264 pe promoted the full spectrum of NAFLD, from steatosis to hepatic inflammation to cirrhosis.

265 c flux, was associated with progression from steatosis to NASH in liver biopsies.

266 a possible specific contribution of hepatic steatosis to subclinical vascular impairment.

267 This transient, regeneration-associated steatosis (TRAS) is required for liver recovery, but its

268 s, collagen content, inflammatory cytokines, steatosis, triglycerides, and NAFLD activity score were

269 in obese individuals with and without liver steatosis undergoing a weight-reduction program to test

270 ients and wild-type (WT) mice that developed steatosis upon feeding HFD.

271 nhanced exogenous FA delivery) yet developed steatosis upon induction of hepatic de novo lipogenesis

272 uracy of (1)H-MRS PDFF in the measurement of steatosis using histopathology analysis as the standard.

273 ine if chemical exposure can prime liver for steatosis via modulation of NRF2 and epigenetic mechanis

274 ristic curve to distinguish NASH from simple steatosis was 0.87 (95% confidence interval: 0.72, 1.00)

275 Optimal cutoff of CAP for detecting steatosis was 249 dB/m.

276 Hepatic steatosis was assessed at baseline and after 72 weeks of

277 Ultrasound (US) assessment of steatosis was carried out using ultrasound systems.

278 Steatosis was detected in 49 (87.5%) of the patients who

279 Steatosis was detected in 50/289 (17.3%) children by US

280 The liver graft with severe macrovesicular steatosis was donated from a 25-year-old man.

281 Steatosis was graded using the conventional histopatholo

282 ttp-LKO, i.e., double knockout mice) hepatic steatosis was greatly diminished and fibrosis prevented,

283 .5 exposure on high-fat diet-induced hepatic steatosis was mediated through PM2.5-induced hepatic aut

284 Steatosis was the only factor independently associated w

285 ostic accuracies of CAP and PDFF for grading steatosis were assessed with receiver operating characte

286 Fibrosis, inflammation, and steatosis were assessed with the METAVIR and steatosis,

287 7 +/- 5.2; 78% with moderate or severe liver steatosis] were included in the follow-up intervention s

288 eight gain, glucose intolerance, and hepatic steatosis when challenged with high-fat diet.

289 ely classifies grades and changes in hepatic steatosis when histologic analysis of biopsies is used a

290 In quiescent liver, PTEN causes pathological steatosis when lost, whereas its role in regenerating li

291 ated with inflammation, oxidative stress and steatosis, which deserves exploration in human trials.

292 t-off value to 3.0% identified patients with steatosis with 100% specificity and 79% sensitivity; a P

293 t-off value of 2.0% identified patients with steatosis with 94% specificity and 87% sensitivity.

294 toff value of CAP of 249 dB/m rules in liver steatosis with a very high specificity.

295 95% CI, 0.91-0.98), and grade 0-2 vs grade 3 steatosis with an AUROC of 0.96 (95% CI, 0.93-0.99).

296 MRI-PDFF detected any steatosis with an AUROC of 0.99 (95% CI, 0.98-1.00), whi

297 ionship of liver fibrosis, inflammation, and steatosis with the magnetic resonance (MR) viscoelastic

298 lucose intolerance, increased adiposity, and steatosis, with large lipid droplets in their hepatocyte

299 d chronic high-fat/high-sucrose diet-induced steatosis, without observed increases in liver inflammat

300 eride transfer protein (Mttp) causes hepatic steatosis, yet the risks for developing hepatic fibrosis