ライフサイエンスコーパス: steatosis

1 epatic injury despite an increase in hepatic steatosis.

2 .1% vs 19.4%; P = .02) than patients with no steatosis.

3 standard for diagnosing and grading hepatic steatosis.

4 ids and mediating susceptibility for hepatic steatosis.

5 culating lipid levels that prevented hepatic steatosis.

6 acy of 87% (kappa = 0.81) for the grading of steatosis.

7 th histologic NASH, and MRI-PDFF to estimate steatosis.

8 mmation and fibrosis without affecting liver steatosis.

9 muscle function and frailty, and myocardial steatosis.

10 ynthesis lead to LD accumulation and hepatic steatosis.

11 ptor alpha phosphorylation, thereby reducing steatosis.

12 velop obesity, insulin resistance, and liver steatosis.

13 ders from insulin resistance (IR) to hepatic steatosis.

14 raft survival compared to DCD donors with no steatosis.

15 is associated with hyperglycemia and hepatic steatosis.

16 ce gained the least weight and had the least steatosis.

17 temic dyslipidemia, and reduction of hepatic steatosis.

18 tary mouse model of obesity-mediated hepatic steatosis.

19 cts against diet-induced obesity and hepatic steatosis.

20 tter define the natural history of allograft steatosis.

21 f mice that received saline and SO developed steatosis.

22 sis, cholestasis, and cirrhosis with hepatic steatosis.

23 ers such as hypertriglyceridemia and hepatic steatosis.

24 ped, or reversed development of fibrosis and steatosis.

25 factors lead to a high likelihood of hepatic steatosis.

26 he risk in a clinical cohort without hepatic steatosis.

27 variants, INSR) causes hyperglycemia without steatosis.

28 ven treat the metabolic syndrome and hepatic steatosis.

29 nondrinkers with low genetic risk of hepatic steatosis.

30 tes intrahepatic storage of fat and risk for steatosis.

31 ral therapy-treated PWH exhibited myocardial steatosis.

32 levels when fed a diet that induces hepatic steatosis.

33 Thirty percent had FLD (20% steatosis, 10% steatohepatitis).

34 ed light into the pathogenesis of periportal steatosis, a hallmark of human pediatric non-alcoholic f

35 ssified using NAFLD activity score (NAS) and steatosis, activity and fibrosis (SAF) score.

36 is an independent risk factor of liver graft steatosis after liver transplantation that is additive t

37 Steatohepatitis or steatosis alone (versus none) were associated with highe

38 e used a mouse model of simple, diet-induced steatosis and assessed the impact of exercise on metabol

39 We aimed to characterize myocardial steatosis and associated potential risk factors among a

40 ients with steatosis, the relationship among steatosis and atherosclerosis, specific atherosclerotic

41 , including significant improvements in both steatosis and ballooning.

42 Steatosis and circulating lipids were unaffected but mil

43 ical NASH compared with patients with simple steatosis and correlated with hepatic CD34 immunoreactiv

44 Livers from Pi*Z-overexpressing mice had steatosis and down-regulation of genes involved in lipid

45 er risk for cirrhosis compared to those with steatosis and elevated ALT and not different from the ri

46 er stiffness measurement (LSMs) in assessing steatosis and fibrosis in patients with suspected nonalc

47 magnetic-resonance sensor for grading liver steatosis and fibrosis using diffusion-weighted multicom

48 86% (kappa = 0.78) in the ex vivo grading of steatosis and fibrosis, respectively.

49 lity of distinctive disease traits including steatosis and fibrosis.

50 ism and HDL oxidation and also induced liver steatosis and fibrosis.

51 k prevented miR-540 expression, and arrested steatosis and fibrosis.

52 s (HIV) or antiretroviral therapy on hepatic steatosis and fibrosis.

53 including neutral and polar lipids, grade of steatosis and fibrosis.

54 chronic glucagon treatment-reversing hepatic steatosis and glucose intolerance-were abrogated in Insp

55 ignificantly improved liver enzymes, hepatic steatosis and hepatic fibrosis.

56 ts administration triggers undesirable liver steatosis and hypertriglyceridemia due to increased fatt

57 on appears to be linked to both fibrosis and steatosis and increased in carriers of the TM6SF2 rs5854

58 Here, we show that hepatic steatosis and inflammation display diurnal rhythmicity i

59 moattractant protein (CCR2) prevented excess steatosis and inflammation in aging livers but did not r

60 sought to determine SHP's role in regulating steatosis and inflammation in NASH.

61 t gained less weight, developed less hepatic steatosis and inflammation, and had a lower mean serum l

62 stage, hepatic Shp plays an opposing role in steatosis and inflammation.

63 nduces lipodystrophy and its impact on liver steatosis and injury are not fully elucidated.

64 nerve/BAT/liver axis that counteracts liver steatosis and injury.

65 the liver and reversed diet-induced hepatic steatosis and insulin resistance.

66 in D ligands ameliorates liver inflammation, steatosis and insulin resistance.

67 Juvenile livers exhibited steatosis and iron accumulation following asparaginase e

68 ents, which are both associated with hepatic steatosis and its progressive form, nonalcoholic steatoh

69 tokine and chemokine release, macrovesicular steatosis and liver damage were attenuated.

70 ha activation is relatively weak exacerbated steatosis and liver injury.

71 s for population-based assessment of hepatic steatosis and nonalcoholic fatty liver disease, with obj

72 liver disease, as well as animal models with steatosis and nonalcoholic steatohepatitis (NASH), and (

73 en low serum NREP levels and the presence of steatosis and nonalcoholic steatohepatitis highlight the

74 ble quantitative US models to detect hepatic steatosis and quantify hepatic fat.

75 table, shares genetic correlation with liver steatosis and shares environmental correlation with live

76 te that, along with HFD, TCS induces hepatic steatosis and steatohepatitis jointly regulated by the t

77 ences observed in patients, with more severe steatosis and steatohepatitis, more proinflammatory/prof

78 etween liver sympathetic outflow and hepatic steatosis and suggest that manipulation of the liver sym

79 ulating metabolites, liver function, hepatic steatosis and the gut microbiome.

80 (S)-MRI-1867 reduced hepatic steatosis and the rate of hepatic VLDL secretion, upregu

81 FLD was defined as >=5% steatosis and/or steatohepatitis.

82 volume, intensity) for treatment of hepatic steatosis, and 4) evidence for a sustained protection ag

83 ocrine disruption, oxidative stress, hepatic steatosis, and adverse drug interactions.

84 HFD causes steatosis, and both SAP and 1866 reduced it.

85 yneuraminic acid inhibit weight gain, reduce steatosis, and decrease adipose tissue and liver inflamm

86 iorated obesity, insulin resistance, hepatic steatosis, and hyperlipidemia without changes in food in

87 ciated with inflammatory signaling pathways, steatosis, and increased collagen deposition.

88 tabolic diseases, including obesity, hepatic steatosis, and insulin resistance.

89 ne responses and protects from inflammation, steatosis, and obesity.

90 atory cells in adipose and liver tissue, and steatosis; and these effects were exacerbated on an HFD.

91 fraction quantification when other causes of steatosis are excluded.

92 luated whether the frequency and severity of steatosis are greater in the setting of HIV infection.

93 ion more accurately and thereby detect liver steatosis as a sign of liver damage earlier as well as t

94 has been shown to cause fatty liver disease (steatosis), as well as increased adiposity in many speci

95 MRI proton density fat fraction for hepatic steatosis assessment in nonalcoholic fatty liver disease

96 ive and therapeutic strategies against liver steatosis associated with metabolic dysfunction.

97 Taken together, our results show that the steatosis associated with PNPLA3(148M) is caused by accu

98 o TBT led to increased adiposity and hepatic steatosis at 14 and 20 weeks of age and increased liver

99 in situ determination of the grade of liver steatosis at the operation room as a fast, quantitative

100 Overall, 254 recipients developed allograft steatosis (at 10 years: 77.6% NASH recipients, 44.7% Non

101 Steatohepatitis was based on presence of steatosis, ballooning and perisinusoidal fibrosis.

102 improved fibrosis for both studies included steatosis, ballooning, Mallory-Denk bodies, and portal,

103 However, the assessment of liver steatosis before transplantation is typically based on a

104 There was no difference in hepatic steatosis between groups.

105 pared the prevalence and severity of hepatic steatosis between HIV-infected (HIV+) and uninfected per

106 The fatty liver index (FLI), a noninvasive steatosis biomarker, has recently drawn attention for it

107 urage the more systematic use of noninvasive steatosis biomarkers to help identify coinfected patient

108 ic ablation of hepatic p38a increases simple steatosis but ameliorates oxidative stress-driven NASH,

109 mice experienced exacerbated alcohol-induced steatosis, but neither adipocyte-specific mTOR nor adipo

110 Shp (Hep-/-) mice developed reduced steatosis, but surprisingly increased hepatic inflammati

111 pite LD mice have increased liver injury and steatosis by alcohol exposure, the number of CD45(+) cel

112 neration protein deficiency promotes hepatic steatosis by inducing oxidative stress and microRNA-540

113 Pancreatic steatosis can be considered a marker of metabolic syndro

114 but 43.3% (806 of 1861) of patients changed steatosis category between first and last scans.

115 t (Acox1-LKO) protected mice against hepatic steatosis caused by starvation or HFD due to induction o

116 Our results suggest that hepatic steatosis causes resistance to the effect of glucagon on

117 etabolic pathways putatively driving hepatic steatosis compared with changes induced by exercise; 2)

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

119 Hepatocyte-specific Fbp1 deletion results in steatosis, concomitant with activation and senescence of

120 n or lacking elastase were protected against steatosis correlating with lower JNK activation, reduced

121 14%-28%), and 1% (112 of 11 669) had severe steatosis (CT fat fraction >28%).

122 5%-14%), 8.8% (1025 of 11 669) had moderate steatosis (CT fat fraction of 14%-28%), and 1% (112 of 1

123 action <5%), 42.4% (4948 of 11 669) had mild steatosis (CT fat fraction of 5%-14%), 8.8% (1025 of 11

124 Surprisingly, Shp deletion after steatosis development exacerbated hepatic inflammation a

125 in recipient), with up to 20% macrovesicular steatosis, does not compromise graft function and outcom

126 tively; this was lower than in patients with steatosis/elevated ALT (cirrhosis: 3.85; 95% CI: 3.50-4.

127 Patients with steatosis/elevated ALT had a higher risk of developing c

128 ith hepatic steatosis/normal ALT, those with steatosis/elevated ALT were younger and more likely to b

129 h steatosis/normal ALT, 15,419 patients with steatosis/elevated ALT, and 9,267 patients with no steat

130 tosis/normal alanine aminotransferase (ALT), steatosis/elevated ALT, and no steatosis/normal ALT.

131 tant factors contributing to alcohol-induced steatosis, ER stress, apoptosis, and liver injury in bot

132 in harmful AR metabolites, toxic aldehydes, steatosis, ER stress, apoptosis, and liver injury.

133 The primary outcome was change in hepatic steatosis estimated by magnetic resonance imaging proton

134 content (a continuous marker for myocardial steatosis extent).

135 r study comprised 8,345 persons with hepatic steatosis (fatty liver index >60) who participated in he

136 iles in a group of mouse models with hepatic steatosis, fibrosis, inflammation, and, consequently, tu

137 can reduce the severity of NASH by reducing steatosis, fibrosis, oxidative stress, and inflammation.

138 (8) How relevant is donor steatosis for LT in NASH patients?

139 The mean decrease in hepatic steatosis from baseline to week 8 was significantly grea

140 abolite associations with ultrasound-defined steatosis, gene variants linked to liver fat (in GCKR, P

141 tosis grade, and between pancreatic PDFF and steatosis grade and hepatic PDFF.

142 409 genotypes, and nongenetic factors on the steatosis grade assessed 6-30 months after transplantati

143 gree of association between hepatic PDFF and steatosis grade, and between pancreatic PDFF and steatos

144 Pancreatic PDFF correlated with hepatic steatosis grades (R(S)=0.573, p<0.001) and hepatic PDFF

145 Hepatic PDFF measurements correlated with steatosis grades (R(S)=0.875, p<0.001).

146 Recipient high-BMI and a high-steatosis graft are both significant independent and equ

147 ted and compared between 4 cohorts: (1) high-steatosis graft in high-BMI recipient; (2) low-steatosis

148 eatosis graft in high-BMI recipient; (2) low-steatosis graft in high-BMI recipient; (3) high-steatosi

149 s graft in normal-BMI recipient; and (4) low-steatosis graft in normal-BMI recipient.

150 atosis graft in high-BMI recipient; (3) high-steatosis graft in normal-BMI recipient; and (4) low-ste

151 increase in mortality associated with a high-steatosis graft into a normal-BMI recipient is similar i

152 I recipient is similar in magnitude to a low-steatosis graft placed into a high-BMI recipient.

153 A high-steatosis graft was defined as donor graft macrosteatosi

154 A high-steatosis graft was the strongest independent predictor

155 High-steatosis grafts transplanted into obese recipients have

156 n between the mild macrosteatosis and the no steatosis groups except for the rate of EAD (56.8% vs 45

157 chemia time and large droplet macrovesicular steatosis (>=20%) were identified as independent risk fa

158 The STAM mice developed steatosis, hepatocyte ballooning, and inflammation, whic

159 sphate-activated kinase (AMPK) and mitigates steatosis; however, its impact on ischemia-reperfusion i

160 uced body weight gain, inflammation, hepatic steatosis, hyperglycemia, glucose intolerance, and insul

161 and reduced HFD-induced liver macrovesicular steatosis, hypertrophy, inflammation, and collagen conte

162 hanced CT for establishing the prevalence of steatosis in a large screening cohort.

163 The estimation of steatosis in a liver graft is mandatory prior to liver t

164 protection against fructose-induced hepatic steatosis in association with a bloom in Akkermansia and

165 nd markers of liver fibrosis but not hepatic steatosis in DKO mice.

166 of (low-density lipoprotein) cholesterol and steatosis in hepatocytes.

167 nsumption, obesity, hyperglycemia, and liver steatosis in HFD-treated male mice.

168 important factor in pathogenesis of hepatic steatosis in HH.

169 inhibited obesity, hyperglycemia, and liver steatosis in high-fat diet (HFD)-treated male mice.

170 ns mitigating insulin resistance and hepatic steatosis in high-fat-sucrose diet (HFS) induced obese m

171 tic de novo lipogenesis (DNL) contributes to steatosis in individuals with NAFLD.

172 eased fat mass and dyslipidemia, and hepatic steatosis in mice lacking C/EBP homologous protein (CHOP

173 eatic fat deposition correlates with hepatic steatosis in patients with chronic NALD, but not in thos

174 ic markers of hepatic inflammation, LSM, and steatosis in persons with NAFLD.

175 ure was associated with higher prevalence of steatosis in PWH.

176 ) feeding, induced periportal macrovesicular steatosis in Sirt5KO mice.

177 S, resulting in lipid peroxidation (LPO) and steatosis in the absence of iron overload.

178 inhibited obesity, hyperglycemia, and liver steatosis in the HFD-treated mice.

179 rged as possible risk factors for myocardial steatosis in this group.

180 and fibrosis and partially protected against steatosis in WD-fed animals, but it did not protect agai

181 al remission rate (achieving grade 0 hepatic steatosis) in HP-diet and beta-cryptoxanthin group (82.6

182 ty liver index (FLI), a biomarker of hepatic steatosis, in a population-based cross-sectional nationa

183 in the pathogenesis and development of liver steatosis including the progression to nonalcoholic stea

184 1 (LAP1) caused defective VLDL secretion and steatosis, including intranuclear lipid accumulation.

185 ver, exercise can effectively reduce hepatic steatosis independent of changes in body mass.

186 evidence for a sustained protection against steatosis induced by exercise.

187 neously developed liver disease with hepatic steatosis, inflammation, and degeneration.

188 Adipocytokines differentially modulate steatosis, inflammation, and fibrosis and are broadly pr

189 prevented the progression of NASH, including steatosis, inflammation, and fibrosis in a Western diet-

190 nd macrophage (MO) activation contributes to steatosis, inflammation, and fibrosis in alcoholic liver

191 g activation, leading to the dissociation of steatosis, inflammation, and fibrosis in NASH developmen

192 er disease worldwide and is characterized by steatosis, inflammation, and fibrosis.

193 liver disease (NAFLD) characterized by liver steatosis, inflammation, and hepatocellular damage.

194 of NAFLD in long-term HFD-fed mice including steatosis, inflammation, fibrosis, and HCC.

195 the impact of AMPK activity state on hepatic steatosis, inflammation, liver injury, and fibrosis duri

196 1 profoundly augmented alcohol-induced liver steatosis, injury, inflammation and fibrosis in male and

197 dietary iron supplementation did not prevent steatosis; instead, dietary iron restriction and antioxi

198 In this study, we found that hepatic steatosis is associated with robust hepatic sympathetic

199 Allograft steatosis is common but not associated with survival or

200 Moderate-to-severe hepatic steatosis is less common in PWH compared with demographi

201 Hepatic steatosis is linked to increased risk for insulin resist

202 Hepatic steatosis is prevalent in Western countries, but few stu

203 ther and what degree of graft macrovesicular steatosis is safe for both recipient and donor is debata

204 Hepatic steatosis is strongly associated with cardiovascular dis

205 Steatosis is the hepatic manifestation of the metabolic

206 d provided significant reductions in hepatic steatosis, liver biochemistry, and serum bile acids in p

207 In the absence of fibrosis or steatosis, liver stiffness and fat fraction did not show

208 Saroglitazar improved steatosis, lobular inflammation, hepatocellular ballooni

209 A 4-week-exercising program reversed steatosis, lowered insulin levels, and improved glucose

210 %-60%), mild macrosteatosis (5%-30%), and no steatosis (<5%).

211 the prevalence of moderate-to-severe hepatic steatosis (M-HS) in PWH with human immunodeficiency viru

212 Only macrovesicular steatosis (MaS) significantly impacted PP levels and slo

213 this knowledge, we hypothesized that hepatic steatosis might impair glucagon's action on hepatic amin

214 tations, using grafts with (Group A; 10%-20% steatosis, n = 92) and without (Group B; <10%, n = 531)

215 patients with biopsy-proven NAFLD, 25 simple steatosis (nonalcoholic fatty liver) and 25 nonalcoholic

216 ed patients into three groups: patients with steatosis/normal alanine aminotransferase (ALT), steatos

217 e risk of cirrhosis and HCC in patients with steatosis/normal ALT and those without steatosis was not

218 We identified 3,522 patients with steatosis/normal ALT, 15,419 patients with steatosis/ele

219 In patients with steatosis/normal ALT, the incidence rates of cirrhosis a

220 Compared to patients with hepatic steatosis/normal ALT, those with steatosis/elevated ALT

221 sis/elevated ALT, and 9,267 patients with no steatosis/normal ALT.

222 ferase (ALT), steatosis/elevated ALT, and no steatosis/normal ALT.

223 CI: 2.34-4.86; P < 0.01) than patients with steatosis/normal ALT; they also had a higher risk of HCC

224 eration 36 h post surgery, and the transient steatosis observed in wild type mice was virtually absen

225 High-fat diet (HFD)-induced inflammation and steatosis of adipose tissue and liver are associated wit

226 t factors that amplified the impact of donor steatosis on mortality and graft loss using interaction

227 s adiposity, insulin resistance, and hepatic steatosis on the complex integration of insulin secretio

228 B; <10%, n = 531) significant macrovesicular steatosis, on pre- or intraoperative biopsy.

229 id the confounding effect of obesity-related steatosis, only 70 individuals who had controlled attenu

230 macrophages were higher in NASH than simple steatosis or controls and correlated with serum LPS.

231 ge (P<10(-16)); we found no association with steatosis or probe type.

232 ore specifying microbial metabolism, hepatic steatosis, oxidative stress, nitric oxide modulation, an

233 ction obtained from MRI-PDFF correlated with steatosis (P < 0.05 for all).

234 lantation, was associated with lower risk of steatosis (P = 0.003).

235 C(12) oxidation is sufficient to induce the steatosis phenotype.

236 Other changes in the liver included hepatic steatosis, portal fibrosis, lymphocytic infiltrates and

237 was used to evaluate differences in time to steatosis post-LT, patient survival, and cardiovascular

238 Genetic factors and steatosis predispose to hepatocellular carcinoma (HCC) i

239 Myocardial steatosis predisposes to diastolic dysfunction, a heart

240 At present, how simple steatosis progresses to NASH remains obscure and effecti

241 To compare pancreatic and hepatic steatosis quantified by proton density fat fraction (PDF

242 0.001) and between pancreatic PDFF and liver steatosis (R(S)=0.608, p<0.001); however, in the subgrou

243 rformed selective liver biopsy, commonly for steatosis, raised transaminases and 1 or more features o

244 Steatosis regresses by 4 wk upon reappearance of ALR-exp

245 HFHF rats had mild, moderate, and severe steatosis, respectively, at 5, 10, and 15 weeks.

246 e results of this study suggest that hepatic steatosis results in hyperammonemia, which is associated

247 iction on regulating intrahepatic lipids and steatosis risk; 3) the effects of exercise training (mod

248 odontitis group presented an increase in the steatosis score (P < 0.05) for the histopathologic evalu

249 d identified factors associated with greater steatosis severity within both groups.

250 p < 0.001), correlating with lesser hepatic steatosis severity, compared to uninfected participants.

251 triol reduced liver inflammation and hepatic steatosis, significantly improving insulin sensitivity.

252 developed a full spectrum of liver diseases (steatosis, steatohepatitis, cirrhosis, and hepatocellula

253 atocytes protects against the development of steatosis, suggesting that JNK inhibition represents a p

254 normal ALR-H-HET mice gained more weight and steatosis than WT mice when challenged metabolically wit

255 ersistent environmental contaminant, induces steatosis that can progress to steatohepatitis with fibr

256 any features of metabolic syndrome and liver steatosis that developed in mice fed a high-fat diet, wi

257 atic triglyceride accumulation (i.e. hepatic steatosis), the incidence of NAFLD is increasing - in li

258 Hepatic steatosis, the excess storage of intrahepatic lipids, is

259 subclinical atherosclerosis in patients with steatosis, the relationship among steatosis and atherosc

260 d resulted in progression of hepatomegaly to steatosis, then hepatic injury phenotype.

261 a resulted in insulin resistance and hepatic steatosis through activation of LXR.

262 evelopment of insulin resistance and hepatic steatosis through inhibition of the transcription factor

263 NAFLD can range in severity from steatosis to fibrotic steatohepatitis and is a major cau

264 cterized by a clinical spectrum ranging from steatosis to hepatocellular carcinoma.

265 activity permits the transition from simple steatosis to hepatocellular death; thus, activation migh

266 pplement to prevent the progression of liver steatosis to inflammation and fibrosis in NASH.

267 s a spectrum of diseases ranging from simple steatosis to more severe forms of liver injury including

268 how this occurs during the progression from steatosis to NASH remains obscure.

269 ole of Shp specifically in the transition of steatosis to NASH, mice were fed the HFCF diet for 4 wee

270 on-alcoholic fatty liver disease ranges from steatosis to non-alcoholic steatohepatitis (NASH), poten

271 s a spectrum of diseases ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), cirrho

272 compasses a range of conditions, from simple steatosis to nonalcoholic steatohepatitis.

273 liver delineates the transition from hepatic steatosis to steatohepatitis (SH).

274 thin context of TCDD-elicited progression of steatosis to steatohepatitis with fibrosis.

275 overexpression of Cxcl1 and/or IL-8 promoted steatosis-to-NASH progression in HFD-fed mice by inducin

276 ression of Cxcl1 in the liver alone promotes steatosis-to-NASH progression in HFD-fed mice by inducin

277 erexpression of CXCL1 is sufficient to drive steatosis-to-NASH progression in HFD-fed mice through ne

278 tributes to both gluconeogenesis and hepatic steatosis.TRIAL REGISTRATIONClinicalTrials.gov NCT017785

279 The severity of liver steatosis varied between sexes and individual strains an

280 Moderate-to-severe hepatic steatosis was assessed by unenhanced computed tomography

281 ents had at least 2-site atherosclerosis and steatosis was associated with at least 2-site atheroscle

282 Steatosis was associated with carotid IMT and CAC, but n

283 Hepatic steatosis was defined by noncontrast computed tomography

284 Liver steatosis was determined via transient elastography-base

285 e, established high fat diet-induced hepatic steatosis was effectively reduced with pharmacological o

286 The degree of steatosis was evaluated from liver biopsy specimens.

287 Steatosis was evaluated in liver biopsies from 268 adult

288 Importantly, the reduction in steatosis was not accompanied by increased inflammation

289 Allograft steatosis was not associated with post-LT survival (P =

290 with steatosis/normal ALT and those without steatosis was not significantly different.

291 Steatosis was present in 33% of persons with HIV and onl

292 Hepatic steatosis was significantly more frequent in HH.

293 cipient phenotypes that would tolerate donor steatosis well, and are therefore best suited to receive

294 levels of liver enzymes and grade of hepatic steatosis were assessed at baseline and study endpoint a

295 injury (alanine aminotransferase [ALT]) and steatosis were prevented by CVC whether administered as

296 f NASH, ballooning and inflammation, but not steatosis, were independently associated with clinical o

297 D), also developed periportal macrovesicular steatosis when fed coconut oil, confirming that defectiv

298 , we found that CAP identified patients with steatosis with an AUROC of 0.87 (95% confidence interval

299 In human liver samples, the sensor graded steatosis with an overall accuracy of 93% (kappa = 0.88)

300 Patients with hepatic steatosis with persistently normal ALT are at lower risk