ライフサイエンスコーパス: fatty liver

1 ensuing hepatic lipid overload, resulting in fatty liver.

2 ased miR-802 levels, insulin resistance, and fatty liver.

3 These mice also developed fatty liver.

4 c tolerance and the regenerative capacity of fatty liver.

5 olic, ischemic, and regenerative deficits of fatty liver.

6 were provided written information regarding fatty liver and advised to make lifestyle changes.

7 rders of nutrition and metabolism, including fatty liver and diabetes, and appear to be influenced by

8 ere fed a high-fat diet (HFD), we found that fatty liver and dyslipidemia are prominent early signs o

9 bilities in the pathogenesis of nonalcoholic fatty liver and early nonalcoholic steatohepatitis at th

10 was associated with multiple risk factors of fatty liver and increased likelihood of fatty liver in a

11 od socioeconomic disadvantage with adulthood fatty liver and tested adulthood risk factors of fatty l

12 ven NAFLD, 25 simple steatosis (nonalcoholic fatty liver) and 25 nonalcoholic steatohepatitis (NASH),

13 e offspring of obese mice developed obesity, fatty liver, and insulin resistance, with adult female o

14 altered progression of diet-induced obesity, fatty liver, and insulin resistance.

15 ailure, but early risk factors for adulthood fatty liver are poorly understood.

16 y liver and tested adulthood risk factors of fatty liver as possible mediators of this link.

17 tes, usually accompanied by dyslipidemia and fatty liver, as seen in lipodystrophies.

18 Fatty liver associated with metabolic dysfunction is com

19 ecretion, providing a likely explanation for fatty liver-associated hyperglucagonemia.

20 , and mice fed a high-fat diet (HFD) develop fatty liver but are resistant to NASH development.

21 13% had borderline zone 3 NASH, and 21% had fatty liver but not NASH.

22 health-screening program and diagnosed with fatty liver by abdominal ultrasound.

23 IMP2 deficiency promotes modest diet-induced fatty liver by impairing fatty acid oxidation through in

24 Fatty liver causes premature death worldwide and require

25 reviously observed marked protection against fatty liver conferred by global IMP2 deficiency in mice

26 ecruits circulating macrophages and promotes fatty liver development, and ultimately contributes to i

27 diet-induced obesity, insulin resistance and fatty liver development.

28 edge, and metabolic (dysfunction) associated fatty liver disease "MAFLD" was suggested as a more appr

29 .5%), hepatitis C (13.4%), and non-alcoholic fatty liver disease (5.7%).

30 Those with concurrent nonalcoholic fatty liver disease (AOR 1.39; 95% CI, 1.05, 1.83), cirr

31 Hepatitis B (HBV) and fatty liver disease (FLD) are common etiologies of liver

32 Fatty liver disease (FLD) is a disorder in which accumul

33 Fatty liver disease (FLD) was defined as log LSI >=3.0.

34 stology, defined as decrease in nonalcoholic fatty liver disease (NAFLD) Activity Score >=2 points wi

35 t patients with definite NASH, non-alcoholic fatty liver disease (NAFLD) activity score of at least 4

36 Non-alcoholic fatty liver disease (NAFLD) affects 1 in 3 Americans and

37 Nonalcoholic fatty liver disease (NAFLD) affects a quarter of the adu

38 Non-alcoholic fatty liver disease (NAFLD) affects over 30% of adults i

39 The prevalence and outcomes of non-alcoholic fatty liver disease (NAFLD) among elderly have not been

40 energy metabolism is common in non-alcoholic fatty liver disease (NAFLD) and appears to also be assoc

41 xamined the association between nonalcoholic fatty liver disease (NAFLD) and bone mineral density (BM

42 Nonalcoholic fatty liver disease (NAFLD) and cardiovascular disease (

43 stigate the association between nonalcoholic fatty liver disease (NAFLD) and cerebral small vessel di

44 gehog (SHH) is associated with Non-alcoholic fatty liver disease (NAFLD) and development of Non-alcoh

45 ssociated with human and rodent nonalcoholic fatty liver disease (NAFLD) and hepatocellular carcinoma

46 In patients with nonalcoholic fatty liver disease (NAFLD) and in obese mice, occupancy

47 omponent in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) and insulin resistance.

48 is the inflammatory subtype of nonalcoholic fatty liver disease (NAFLD) and is associated with disea

49 HTG) is the hallmark feature of nonalcoholic fatty liver disease (NAFLD) and is decreased by weight l

50 The development of nonalcoholic fatty liver disease (NAFLD) and its progression to NASH

51 istinguishing characteristic of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepat

52 esistance), and the presence of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepat

53 The prevalence of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepat

54 4), and (c) obese subjects with nonalcoholic fatty liver disease (NAFLD) and prediabetes (obese-NAFLD

55 eity captured under the acronym nonalcoholic fatty liver disease (NAFLD) and provide suggestions on t

56 Abnormal glucose metabolism and nonalcoholic fatty liver disease (NAFLD) are common in patients with

57 echanisms of HCC development in nonalcoholic fatty liver disease (NAFLD) are incompletely understood.

58 obesity, type II diabetes and non-alcoholic fatty liver disease (NAFLD) are increasing and may joint

59 morphisms in the development of nonalcoholic fatty liver disease (NAFLD) are still poorly understood.

60 ocesses driving the severity of nonalcoholic fatty liver disease (NAFLD) as reflected in the transcri

61 ially in diabetes mellitus and non-alcoholic fatty liver disease (NAFLD) but studies examining the sh

62 itis (NASH) is a severe form of nonalcoholic fatty liver disease (NAFLD) characterized by liver steat

63 d the contribution of ChREBP to nonalcoholic fatty liver disease (NAFLD) development in a mouse model

64 Nonalcoholic fatty liver disease (NAFLD) encompasses a range of condi

65 ), Forns (n = 122,419), and the nonalcoholic fatty liver disease (NAFLD) fibrosis scores (NFS, n = 13

66 ata on dietary risk factors for nonalcoholic fatty liver disease (NAFLD) from population-based studie

67 Nonalcoholic fatty liver disease (NAFLD) has now become a common caus

68 Worldwide, nonalcoholic fatty liver disease (NAFLD) has reached epidemic proport

69 ral, physical activity (PA) and nonalcoholic fatty liver disease (NAFLD) have an inverse association.

70 eded to monitor key features of nonalcoholic fatty liver disease (NAFLD) in children that relate to i

71 A care pathway for nonalcoholic fatty liver disease (NAFLD) in Kaiser Permanente San Die

72 sk of disease for patients with nonalcoholic fatty liver disease (NAFLD) in the absence of elevated e

73 rbohydrate (HF/HC) diet-induced nonalcoholic fatty liver disease (NAFLD) in wild-type (WT), hepatocyt

74 itochondrial adaptation during non-alcoholic fatty liver disease (NAFLD) include remodeling of ketoge

75 The US prevalence of nonalcoholic fatty liver disease (NAFLD) is 30.6% and increasing.

76 Non-alcoholic fatty liver disease (NAFLD) is a complex chronic disease

77 Non-alcoholic fatty liver disease (NAFLD) is a frequent condition in o

78 Nonalcoholic fatty liver disease (NAFLD) is a global and growing heal

79 Nonalcoholic fatty liver disease (NAFLD) is a global public health co

80 Nonalcoholic fatty liver disease (NAFLD) is a leading cause of chroni

81 Non-alcoholic fatty liver disease (NAFLD) is a leading cause of chroni

82 Nonalcoholic fatty liver disease (NAFLD) is a leading etiology for ch

83 Non-alcoholic fatty liver disease (NAFLD) is a substantial cause of co

84 Non-alcoholic fatty liver disease (NAFLD) is an emerging disease, wher

85 Nonalcoholic fatty liver disease (NAFLD) is an increasing global publ

86 ving with HIV (PLWH), of which non-alcoholic fatty liver disease (NAFLD) is an increasingly recognise

87 Non-alcoholic fatty liver disease (NAFLD) is an obesity- and insulin r

88 In HIV-uninfected patients, nonalcoholic fatty liver disease (NAFLD) is associated with incident

89 Nonalcoholic fatty liver disease (NAFLD) is associated with obesity b

90 Nonalcoholic fatty liver disease (NAFLD) is becoming a major health i

91 Nonalcoholic fatty liver disease (NAFLD) is considered the next major

92 The burden of nonalcoholic fatty liver disease (NAFLD) is growing in people living

93 Non-alcoholic fatty liver disease (NAFLD) is highly prevalent and caus

94 Nonalcoholic fatty liver disease (NAFLD) is increasing in prevalence

95 The worldwide prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing rapidly.

96 The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing worldwide.

97 The prevalence of nonalcoholic fatty liver disease (NAFLD) is increasing worldwide.

98 f stress in the development of non-alcoholic fatty liver disease (NAFLD) is largely unexplored.

99 Nonalcoholic fatty liver disease (NAFLD) is now the most common liver

100 Non-alcoholic fatty liver disease (NAFLD) is often associated with obe

101 Nonalcoholic fatty liver disease (NAFLD) is on the verge of becoming

102 Nonalcoholic fatty liver disease (NAFLD) is the most common liver dis

103 Nonalcoholic fatty liver disease (NAFLD) is the most common pediatric

104 Non-alcoholic fatty liver disease (NAFLD) is the most prevalent chroni

105 sted at least 4 hours using the nonalcoholic fatty liver disease (NAFLD) liver fat score and NAFLD fi

106 ween serum vitamin D levels and nonalcoholic fatty liver disease (NAFLD) parameters, such as metaboli

107 A crucial component of nonalcoholic fatty liver disease (NAFLD) pathogenesis is lipid stress

108 In non-alcoholic fatty liver disease (NAFLD) patients and obese mice, occ

109 onsidered as a pivotal stage in nonalcoholic fatty liver disease (NAFLD) progression, given that it p

110 uidelines for the management of nonalcoholic fatty liver disease (NAFLD) recommend a healthy diet as

111 ed liver fibrosis secondary to non-alcoholic fatty liver disease (NAFLD) remains challenging.

112 ution to the pathophysiology of nonalcoholic fatty liver disease (NAFLD) remains unknown.

113 Nonalcoholic fatty liver disease (NAFLD) represents a burgeoning worl

114 Nonalcoholic fatty liver disease (NAFLD) represents a growing cause o

115 Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of dis

116 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD) to receive liraglutide, sita

117 NASH) is a progressive form of Non-alcoholic fatty liver disease (NAFLD), a chronic liver disease wit

118 (HBV), hepatitis C virus (HCV), nonalcoholic fatty liver disease (NAFLD), and alcohol-associated live

119 ciated with reduced severity of nonalcoholic fatty liver disease (NAFLD), based on histologic analysi

120 ccharides (LPS) is increased in nonalcoholic fatty liver disease (NAFLD), but its relationship with l

121 ritical for the progression of non-alcoholic fatty liver disease (NAFLD), but the underlying mechanis

122 chronic liver diseases, such as nonalcoholic fatty liver disease (NAFLD), etiological treatments are

123 In nonalcoholic fatty liver disease (NAFLD), fibrosis is the most import

124 ed in human liver samples with non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatit

125 sociate with increased risk of non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatit

126 development of type 2 diabetes, nonalcoholic fatty liver disease (NAFLD), or cardiovascular disease.

127 endous research advancements in nonalcoholic fatty liver disease (NAFLD), our understanding of sex di

128 ic diseases including obesity, non-alcoholic fatty liver disease (NAFLD), type 2 diabetes and cardiov

129 Nonalcoholic fatty liver disease (NAFLD), which has an unknown pathog

130 ty triggers the development of non-alcoholic fatty liver disease (NAFLD), which involves alterations

131 tal role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD), which is the third leading

132 l stages in the development of non-alcoholic fatty liver disease (NAFLD).

133 complications in patients with non-alcoholic fatty liver disease (NAFLD).

134 nesis is a major contributor to nonalcoholic fatty liver disease (NAFLD).

135 obiota has been associated with nonalcoholic fatty liver disease (NAFLD).

136 associated with the severity of nonalcoholic fatty liver disease (NAFLD).

137 ion against the development of non-alcoholic fatty liver disease (NAFLD).

138 a number of diseases, including nonalcoholic fatty liver disease (NAFLD).

139 fat fraction quantification in nonalcoholic fatty liver disease (NAFLD).

140 ned popularity in management of nonalcoholic fatty liver disease (NAFLD).

141 y, cardiovascular diseases, and nonalcoholic fatty liver disease (NAFLD).

142 ance of lipids is a hallmark of nonalcoholic fatty liver disease (NAFLD).

143 biomarker of liver fibrosis in nonalcoholic fatty liver disease (NAFLD).

144 e of mortality in patients with nonalcoholic fatty liver disease (NAFLD).

145 ociated with the development of nonalcoholic fatty liver disease (NAFLD).

146 the development and severity of nonalcoholic fatty liver disease (NAFLD).

147 which manifests in the liver as nonalcoholic fatty liver disease (NAFLD).

148 d metabolism and development of nonalcoholic fatty liver disease (NAFLD).

149 clock and promotes spontaneous non-alcoholic fatty liver disease (NAFLD).

150 abolic abnormalities including non-alcoholic fatty liver disease (NAFLD).

151 loit such information to assess nonalcoholic fatty liver disease (NAFLD).

152 tection of advanced fibrosis in nonalcoholic fatty liver disease (NAFLD).

153 -58 (CGI-58) mutations manifest nonalcoholic fatty liver disease (NAFLD).

154 t and/or beta-cryptoxanthin in non-alcoholic fatty liver disease (NAFLD).

155 ntal exposure to TBT has been shown to cause fatty liver disease (steatosis), as well as increased ad

156 sociated with susceptibility to nonalcoholic fatty liver disease [NAFLD]) is associated with decrease

157 coholic steatohepatitis (NASH) (nonalcoholic fatty liver disease activity score >= 4), fibrosis (F1-F

158 ia were biopsy-proven NASH with Nonalcoholic Fatty Liver Disease Activity Score >=4, stage 2 or 3 fib

159 of NASH and disease activity by nonalcoholic fatty liver disease activity score (NAS) using the three

160 2, NGM282 significantly reduced nonalcoholic fatty liver disease activity score (NAS; -1.9; 95% confi

161 ned as a 2-point improvement in nonalcoholic fatty liver disease activity score without worsening of

162 gnificant effect on fibrosis or nonalcoholic fatty liver disease activity score, and liver-related ou

163 Conclusion: High risk of fatty liver disease amplifies the ALT-lowering effect of

164 nd fibrosis in mouse models of non-alcoholic fatty liver disease and advanced fibrosis, as well as to

165 a are accurate for diagnosis of nonalcoholic fatty liver disease and hepatic fat fraction quantificat

166 In nonalcoholic fatty liver disease and in patients with type 2 diabetes

167 hepatic lipid metabolism cause nonalcoholic fatty liver disease and insulin resistance, and these pa

168 apidly increasing prevalence of nonalcoholic fatty liver disease and its aggressive form, nonalcoholi

169 In an effort to probe the pathophysiology of fatty liver disease and its progression, research over t

170 standing the pathophysiology of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis.

171 uct medical conditions, such as nonalcoholic fatty liver disease and nonspecific cirrhosis, to intrah

172 cular disease (CVD) may increase the risk of fatty liver disease and other metabolic disorders.

173 more prevalent in patients with nonalcoholic fatty liver disease and predicted major adverse cardiac

174 in metabolic disorders such as nonalcoholic fatty liver disease and steatohepatitis (NAFLD/NASH) and

175 associated polypeptide 1 (LAP1), resulted in fatty liver disease and steatohepatitis, likely from a s

176 ECS in metabolism, obesity, and nonalcoholic fatty liver disease and the anti-inflammatory effects of

177 r therapies that aim to reverse nonalcoholic fatty liver disease and type-2 diabetes.

178 ation across the full range and nonalcoholic fatty liver disease are associated with cardiometabolic

179 Chronic hepatitis B (CHB) and nonalcoholic fatty liver disease are increasingly observed together i

180 The effects of alcohol use in nonalcoholic fatty liver disease are unclear.

181 ammation in type 2 diabetes and nonalcoholic fatty liver disease by reestablishing a conventional pro

182 Left untreated, fatty liver disease can progress to more severe patholog

183 knockout mice and was accompanied by severe fatty liver disease compared with wild type littermates.

184 A GRS for fatty liver disease confers up to a 12-fold higher risk

185 Nonalcoholic fatty liver disease encompasses a spectrum of diseases r

186 pairment in PROs: ELF, >=10.43; Nonalcoholic Fatty Liver Disease Fibrosis Score, >=1.80; Fibrotest sc

187 ohepatitis (NASH), a subtype of nonalcoholic fatty liver disease has also augmented considerably bein

188 ty are common in cirrhosis and non-alcoholic fatty liver disease has become an important cause of cir

189 ta from the TONIC (Treatment of Nonalcoholic Fatty Liver Disease in Children) trial.

190 oholic liver disease (ALD), and nonalcoholic fatty liver disease in the United States.

191 thesized that a genetic risk score (GRS) for fatty liver disease influences the risk of cirrhosis and

192 Nonalcoholic fatty liver disease is a major risk factor for cardiomet

193 Nonalcoholic fatty liver disease is a rapidly rising problem in the 2

194 Even low alcohol intake in fatty liver disease is associated with increased risks f

195 Nonalcoholic fatty liver disease is closely associated with a constel

196 Monitoring the progression of non-alcoholic fatty liver disease is hindered by a lack of suitable no

197 Fatty liver disease is persistent.

198 Nonalcoholic fatty liver disease is the most prevalent liver disease

199 and streptozotocin-western diet nonalcoholic fatty liver disease mouse models, and in vitro on endoth

200 d increasing incidence of metabolic syndrome fatty liver disease now affects a large portion of the w

201 We investigated the impact of alcohol use in fatty liver disease on incident liver, cardiovascular, a

202 -choline-deficient diet causing nonalcoholic fatty liver disease or to Lieber DeCarli diet causing et

203 microbiota signatures; improve nonalcoholic fatty liver disease outcomes; and detail, when available

204 , and SERPINA1) and key pathways involved in fatty liver disease pathobiology.

205 Remarkably, in non-alcoholic fatty liver disease patients, hepatic expression of JMJD

206 Nonalcoholic fatty liver disease prevalences were 1.0%, 9.1%, and 25.

207 In 25% of patients, nonalcoholic fatty liver disease progresses to nonalcoholic steatohep

208 Non-alcoholic fatty liver disease ranges from steatosis to non-alcohol

209 sease or diabetes or with conditions such as fatty liver disease remains fragmented and is not linked

210 noncoding RNA FLRL2 alleviated nonalcoholic fatty liver disease through Arntl-Sirt1 pathway.

211 variants in the progression of non-alcoholic fatty liver disease to non-alcoholic steatohepatitis and

212 of non-alcoholic chronic liver failure from fatty liver disease to steatohepatitis are unavailable.

213 magnetic resonance imaging, and nonalcoholic fatty liver disease was defined as liver fat fraction >=

214 mal range (<5.0% liver fat) and nonalcoholic fatty liver disease were associated with higher blood pr

215 ncreasing rates of obesity and non-alcoholic fatty liver disease(2-4).

216 histologically-defined NAFLD (non-alcoholic fatty liver disease) activity score (NAS) >= 4 and Klein

217 hich is the progressive form of nonalcoholic fatty liver disease, a disorder underlying a strong lipi

218 bin, surgery category, emergency indication, fatty liver disease, American Society of Anesthesiologis

219 R acts as an exercise mimetic in settings of fatty liver disease, an important finding given the comp

220 acts diseases such as diabetes, nonalcoholic fatty liver disease, and anorexia-cachexia syndrome.

221 o cardiovascular disease, diabetes mellitus, fatty liver disease, and cancer.

222 diposity, such as hypertension, nonalcoholic fatty liver disease, and depression.

223 herapeutic target for diabetes, nonalcoholic fatty liver disease, and inflammatory bowel diseases (IB

224 patitis B virus, hepatitis C virus, alcohol, fatty liver disease, and other environmental factors, su

225 hological conditions, including nonalcoholic fatty liver disease, atherosclerosis, viral infections,

226 tions, alcoholic cirrhosis, and nonalcoholic fatty liver disease, genetic factors that contribute to

227 uctural changes associated with nonalcoholic fatty liver disease, such as decay of bile canaliculi ne

228 a diet-induced mouse model of non-alcoholic fatty liver disease, the sensor achieved overall accurac

229 ese findings may also apply to non-alcoholic fatty liver disease, which shares similar pathological a

230 ssment of hepatic steatosis and nonalcoholic fatty liver disease, with objective data that match well

231 ol intake, viral hepatitis and non-alcoholic fatty liver disease, with the clinical spectrum ranging

232 sion of alcohol-associated and non-alcoholic fatty liver disease-the most common chronic liver diseas

233 of metabolic syndrome, such as non-alcoholic fatty liver disease.

234 ociated with the development of nonalcoholic fatty liver disease.

235 hepatic steatosis assessment in nonalcoholic fatty liver disease.

236 genetic factor predisposing to nonalcoholic fatty liver disease.

237 y virus (PWH) may be at risk of nonalcoholic fatty liver disease.

238 ave only examined patients with nonalcoholic fatty liver disease.

239 nsulin resistance, obesity, and nonalcoholic fatty liver disease.

240 including type 2 diabetes and non-alcoholic fatty liver disease.

241 cations for the pathogenesis of nonalcoholic fatty liver disease.

242 ism in HH and susceptibility to nonalcoholic fatty liver disease.

243 cts that have implications for non-alcoholic fatty liver disease.

244 cardiac events independently of nonalcoholic fatty liver disease.

245 cts such as type 2 diabetes and nonalcoholic fatty liver disease.

246 , type 2 diabetes mellitus and non-alcoholic fatty liver disease.

247 e previously been implicated in nonalcoholic fatty liver disease.

248 ng treatment, and alcoholic and nonalcoholic fatty liver disease.

249 n and women, which is linked to nonalcoholic fatty liver disease.

250 ASH) is the progressive form of nonalcoholic fatty liver disease.

251 ty, alcohol consumption, and genetic risk of fatty liver disease.

252 a hallmark of human pediatric non-alcoholic fatty liver disease.

253 ing population with increasing prevalence of fatty liver disease.

254 se significant dyslipidemia and nonalcoholic fatty liver disease; the diet has an especially strong e

255 Non-alcoholic fatty-liver disease (NAFLD) is frequent in obese patient

256 The presence of cirrhosis in nonalcoholic-fatty-liver-disease (NAFLD) is the most important predic

257 Nonalcoholic fatty liver diseases (NAFLDs), especially nonalcoholic s

258 The heterogeneous pathogenesis of metabolic fatty liver diseases and inaccuracies in terminology and

259 Patients with fatty liver diseases present altered mitochondrial morph

260 tabolic diseases, which include nonalcoholic fatty liver diseases, through the gut-liver axis.

261 f pathogens and molecules that contribute to fatty liver diseases.

262 f 7%-10% to improve features of nonalcoholic fatty liver diseases.

263 t risk for diabetic kidney disease (DKD) and fatty liver, emphasizing the importance of insulin resis

264 e and extra-hepatic actions of Plin2 mediate fatty liver formation in WD-fed mice through distinct me

265 ypes, including a propensity for obesity and fatty livers, hyperinsulinemia and glucose response defe

266 s of fatty liver and increased likelihood of fatty liver in adulthood.

267 ated with the development of risk factors of fatty liver in adulthood.

268 A total of 18.9% of the participants had fatty liver in adulthood.

269 highly elevated in NASH patients but not in fatty livers in obese individuals or in high-fat diet (H

270 ng childhood socioeconomic disadvantage with fatty liver included waist circumference (proportion med

271 for age, sex, and childhood risk factors of fatty liver, including high body mass index, elevated in

272 The occurrence of FLI >= 60% indicating fatty liver increased from 2.4% in men with zero risk fa

273 prised 8,345 persons with hepatic steatosis (fatty liver index >60) who participated in health-examin

274 The fatty liver index (FLI) is a non-invasive surrogate mark

275 d joint effects of lifestyle risk factors on fatty liver index (FLI), a biomarker of hepatic steatosi

276 The fatty liver index (FLI), a noninvasive steatosis biomark

277 NAFLD was defined by United States Fatty Liver Index in the absence of other causes of live

278 P2) in mice causes resistance to obesity and fatty liver induced by a high-fat diet (HFD), whereas li

279 Fatty liver is a preventable cause of liver failure, but

280 lic inflammation-in part, emanating from the fatty liver-is the engine that drives cellular dysfuncti

281 ctors for recurrent and de novo nonalcoholic fatty liver (NAFLD) and nonalcoholic steatohepatitis (NA

282 Leptin is a vital biomarker of non-alcoholic fatty liver (NAFLD), and its evaluation of the concentra

283 platelets (HELLP) syndrome and half to acute fatty liver of pregnancy (AFLP), although, in some insta

284 ly, the presentation and management of acute fatty liver of pregnancy and intrahepatic cholestasis of

285 e children, whereas 18% of the children with fatty liver or borderline NASH developed definite NASH.

286 ales, but TBT did not lead to an increase in fatty liver or tumor development in female offspring.

287 = 0.02), diabetes (OR = 1.72, p = 0.01), and fatty liver (OR = 1.66, p = 0.01) in multivariable model

288 n presenting with NAFLD, secondary causes of fatty liver particularly inherited metabolic defects sho

289 In humans, only 20%-40% of patients with fatty liver progress to NASH, and mice fed a high-fat di

290 iling analysis revealed a potential role for fatty liver-related lncRNA 2 (FLRL2) in the pathogenesis

291 age was associated with an increased risk of fatty liver (risk ratio [95% confidence interval], 1.42

292 x, body mass index, alcohol consumption, and fatty liver status.

293 tabolic inflammation as a key process in the fatty liver that contributes to multiorgan morbidity.

294 eatment of NASH and the clinical practice in fatty liver transplantation, highlights its limitations

295 Mechanistically, weak p38alpha activation in fatty liver up-regulated the genes involved in fatty aci

296 Fatty liver was determined by ultrasound during the last

297 An ultrasound diagnosis of fatty liver was made based on standard criteria, and the

298 yte-specific deletion of p38a in HFD-induced fatty liver where p38alpha activation is relatively weak

299 Decrease in BMI predicted resolution of fatty liver with 42% of those in the top quartile of BMI

300 mice fed a high-fat diet (HFD) only develop fatty liver without significant neutrophil infiltration