ライフサイエンスコーパス: liver steatosis

1 ied interim analysis of safety and efficacy (liver steatosis).

2 e deposition of fat (triacylglycerol) in the liver (steatosis).

3 racterized by the accumulation of fat in the liver (steatosis).

4 significant disease outcomes, such as fatty liver (steatosis).

5 insulin sensitivity, plasma lipid levels and liver steatosis.

6 plays a protective role in alcohol-mediated liver steatosis.

7 iated with obesity, such as dyslipidemia and liver steatosis.

8 Forty patients had liver steatosis.

9 increased adiposity, insulin resistance, and liver steatosis.

10 inflammation and fibrosis without affecting liver steatosis.

11 in the management of obesity, diabetes, and liver steatosis.

12 w target for therapies aimed at nonalcoholic liver steatosis.

13 s an in vivo regulator of SIRT1 activity and liver steatosis.

14 atty acid beta-oxidation plays a key role in liver steatosis.

15 itochondrial beta-oxidation, contributing to liver steatosis.

16 the formation of triacylglycerols leading to liver steatosis.

17 2b1 develop obesity, insulin resistance, and liver steatosis.

18 ap between MASLD and ALD, and rare causes of liver steatosis.

19 to both biopsy and MRI in the assessment of liver steatosis.

20 er disease in multiple etiologies, including liver steatosis.

21 ed in overweight subjects and those with and liver steatosis.

22 axis disrupts lipid homeostasis, leading to liver steatosis.

23 patocyte co-culture (MPCC) was used to model liver steatosis.

24 ) diet-induced blood glucose intolerance and liver steatosis.

25 roperties that can control hyperglycemia and liver steatosis.

26 al for manipulating GP130 signaling in human liver steatosis.

27 strategy for the intervention of obesity and liver steatosis.

28 148M with ABHD5 on LD is required to promote liver steatosis.

29 sulin sensitivity, and decreased HFD-induced liver steatosis.

30 hronic liver diseases or secondary causes of liver steatosis.

31 -944.81), respectively, for the diagnosis of liver steatosis.

32 al validation of quantitative biomarkers for liver steatosis.

33 on increased the number of detected cases of liver steatosis.

34 rol (HFHC) diet-induced hyperinsulinemia and liver steatosis.

35 pan and were prone to spontaneous tumors and liver steatosis.

36 pontaneous tumors, chronic inflammation, and liver steatosis.

37 duced hypothalamic inflammation, and reduced liver steatosis.

38 glucose intolerance, insulin resistance, and liver steatosis.

39 ion promotes adipose fat storage and reduces liver steatosis.

40 sociated obesity, adipocyte hypertrophy, and liver steatosis.

41 e for screening patients with a suspicion of liver steatosis.

42 rexpression of kappaOR in this area promoted liver steatosis.

43 triglyceride metabolism and protects against liver steatosis.

44 educed melanin concentrating hormone-induced liver steatosis.

45 d acylcarnitine profile and the reduction of liver steatosis.

46 sis, hyperinsulinemia, and early symptoms of liver steatosis.

47 is under both physiological and pathological liver steatosis.

48 s well as in the pathogenesis of obesity and liver steatosis.

49 g and as a contributor to obesity-associated liver steatosis.

50 al hepatectomy (PH) in mice with and without liver steatosis.

51 eased flux from PE to PC, but do not develop liver steatosis.

52 HBDL4 are sensitive to ER stress and develop liver steatosis, a phenotype associated with unresolved

53 zation showed that the diabetic rats develop liver steatosis, abdominal fat accumulation, nephropathy

54 5(-/-) mice were protected from diet-induced liver steatosis accompanied by decreased protein levels

55 e to high-fat diet (HFD)-induced obesity and liver steatosis, accompanied by improved insulin sensiti

56 n cholesterol synthesis underpins persistent liver steatosis after weaning off PN.

57 ood indicator to assess the relation between liver steatosis and a cardiometabolic disorders in clini

58 ay be used as biomarkers for the presence of liver steatosis and appear to be superior to BMI.

59 imals exhibit facial alopecia, have moderate liver steatosis and are slightly smaller than heterozygo

60 ompanied by the side effects of weight gain, liver steatosis and bone loss associated with current in

61 tative therapeutic targets in the context of liver steatosis and cancer.

62 gon-like peptide 1 receptor agonists reduces liver steatosis and cardiometabolic risk (CMR).

63 reater mTORC1 activation to HF, resulting in liver steatosis and cell death.

64 gest that a leaky gut barrier is linked with liver steatosis and could be a new target for future ste

65 n contrast, knockdown of hepatic CES2 causes liver steatosis and damage in chow- or Western diet-fed

66 ) mice trade reduced adiposity for increased liver steatosis and develop aggravated systemic insulin

67 o diet-induced obesity, type 2 diabetes, and liver steatosis and experienced decreased food intake an

68 ynoid ratio (A:G ratio) to the prevalence of liver steatosis and fibrosis in males and females.

69 -sided magnetic-resonance sensor for grading liver steatosis and fibrosis using diffusion-weighted mu

70 Liver steatosis and fibrosis were measured using transie

71 ene effects between PRO-C3 concentration and liver steatosis and fibrosis, and the association betwee

72 h clinical and laboratory data, histological liver steatosis and fibrosis, and with components of the

73 levels of alanine aminotransferase (ALT) and liver steatosis and fibrosis, compared with mice given i

74 we found CAP and LSM by FibroScan to assess liver steatosis and fibrosis, respectively, with AUROC v

75 elastography to assess body composition and liver steatosis and fibrosis, respectively.

76 etabolism and HDL oxidation and also induced liver steatosis and fibrosis.

77 MRIs were used to assess liver steatosis and fibrosis.

78 romoted fatty acid oxidation and ameliorated liver steatosis and glucose intolerance in diet-induced

79 d fatty acid beta-oxidation; and ameliorated liver steatosis and glucose intolerance.

80 ive effects on weight loss, fat composition, liver steatosis and glucose tolerance; however, in the l

81 ond, B cell-specific Chop deletion prevented liver steatosis and hepatomegaly in aged HFD-fed mice wi

82 treated Tiparp(-/-) mice exhibited increased liver steatosis and hepatotoxicity.

83 agonists administration triggers undesirable liver steatosis and hypertriglyceridemia due to increase

84 ver-specific knockdown of TRAP80 ameliorated liver steatosis and hypertriglyceridemia induced by LXR

85 w-density lipoprotein secretion and promotes liver steatosis and hypolipidemia in an HNF4alpha-depend

86 *Z-overexpressing mice, we found evidence of liver steatosis and impaired lipid secretion.

87 ver semaglutide is its low-dose reduction of liver steatosis and improvement of liver health in nonal

88 t Zbtb20 ablation protects from diet-induced liver steatosis and improves hepatic insulin resistance.

89 vin A dramatically mitigated MASLD, reducing liver steatosis and inflammation as well as systemic fat

90 The potency of I3A in alleviating liver steatosis and inflammation clearly demonstrates it

91 Liver steatosis and inflammation were assessed.

92 ficient mice were protected from HFD-induced liver steatosis and inflammation, despite the developmen

93 these mice, GFT505 also prevented WD-induced liver steatosis and inflammation, indicating a contribut

94 ohol induces lipodystrophy and its impact on liver steatosis and injury are not fully elucidated.

95 istently reduced in multiple mouse models of liver steatosis and injury as well as in liver biopsies

96 eration of BHMT is associated with alcoholic liver steatosis and injury.

97 xpression of H19 exacerbated ethanol-induced liver steatosis and injury.

98 thetic nerve/BAT/liver axis that counteracts liver steatosis and injury.

99 agy by rapamycin attenuates EtOH-LPS-induced liver steatosis and injury.

100 n db/db or HFD-fed mice markedly ameliorates liver steatosis and insulin resistance.

101 c male mice improve their glucose tolerance, liver steatosis and insulin sensitivity after treatment

102 Sevelamer treatment significantly reduced liver steatosis and lobular inflammation.

103 on of B7.1/B7.2 deteriorates obesity-related liver steatosis and metabolic dysregulation, likely a re

104 ly mitigates their hyperphagia, obesity, and liver steatosis and normalizes deficits in glucose homeo

105 Ethanol feeding significantly increased liver steatosis and oxidative damage, compared with wild

106 In these mice, as observed in humans, liver steatosis and oxidative stress promoted NASH devel

107 SHD865 treatment also corrected liver steatosis and plasma hyperlipidemia to normal leve

108 Given the association between liver steatosis and poor response to immune checkpoint t

109 and irrespective of the diet, they developed liver steatosis and progressive insulin resistance.

110 This was accompanied by reduced liver steatosis and reduced hepatic expression of marker

111 acute knockdown of PNPLA3 exhibit aggravated liver steatosis and reduced plasma VLDL-triglyceride lev

112 n-alcoholic fatty liver disease, we examined liver steatosis and related clinical and molecular trait

113 taneous inactivation of Hif-1beta suppressed liver steatosis and rescued the mice from death.

114 s heritable, shares genetic correlation with liver steatosis and shares environmental correlation wit

115 Liver steatosis and significant liver fibrosis (>= F2) w

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

117 ation in individuals with varying degrees of liver steatosis and to assess the correlation of each ma

118 se in serum alanine aminotransferase levels, liver steatosis and triglyceride levels suggesting liver

119 Alcohol-induced liver steatosis and triglyceride were attenuated in alco

120 d with control diet developed hyperglycemia, liver steatosis, and adipocyte hypertrophy, conditions d

121 uding metabolic syndrome, diabetes, obesity, liver steatosis, and Alzheimer disease.

122 st diet-induce obesity, glucose intolerance, liver steatosis, and atherogenesis.

123 resistant to high-fat diet-induced obesity, liver steatosis, and diabetes.

124 proved glucose intolerance, fasting glucose, liver steatosis, and fibrosis in rodents.

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

126 nce, hyperinsulinemia, hypertriglyceridemia, liver steatosis, and hepatocellular injury.

127 hagia, improved glucose utilization, reduced liver steatosis, and improvement of disease-associated b

128 , were protected against atherosclerosis and liver steatosis, and lived longer.

129 Myosteatosis, obesity, liver steatosis, and myopenia were associated with incre

130 tion, is associated with insulin resistance, liver steatosis, and type 2 diabetes, the metabolic impa

131 e epidemics of metabolic diseases, including liver steatosis, are associated with an increased freque

132 tenuation more accurately and thereby detect liver steatosis as a sign of liver damage earlier as wel

133 ely available and could be valuable asset in liver steatosis assessment outside liver biopsy.

134 and abdominal ultrasound with fibroscan for liver steatosis assessment were performed.

135 reventive and therapeutic strategies against liver steatosis associated with metabolic dysfunction.

136 in high levels in green leafy vegetables, on liver steatosis associated with metabolic syndrome.

137 aining beverages in infancy may help prevent liver steatosis at school age.

138 or the in situ determination of the grade of liver steatosis at the operation room as a fast, quantit

139 syndrome and increased with the severity of liver steatosis at ultrasound.

140 Conclusion To stage liver steatosis, attenuation coefficient accuracy varied

141 However, the assessment of liver steatosis before transplantation is typically base

142 on was found with the histological degree of liver steatosis (beta, 0.15; standard error: 0.06; P = 0

143 ere resistant to high-fat diet (HFD)-induced liver steatosis, both of which were reproduced by liver-

144 associated with liver function tests or with liver steatosis by magnetic resonance spectroscopy.

145 meostatic model assessment index (HOMA), and liver steatosis by sonography and the fatty liver index

146 The biliary SCT/SCTR/miR-125b axis promotes liver steatosis by up-regulating lipid biosynthesis gene

147 Background The extent of liver steatosis can be assessed using US attenuation coe

148 SIRT1-mediated activation of FGF21 prevents liver steatosis caused by fasting.

149 the adeno-associated virus vector attenuated liver steatosis caused by the CDAHFD in wild-type C57BL/

150 with higher serum alanine aminotransferase, liver steatosis, cirrhosis, triglycerides and obesity; a

151 ent for potential therapeutic attenuation of liver steatosis, combinatorial targeting of a second pat

152 low in ob/ob mice and alcohol-fed mice with liver steatosis, compared with controls.

153 Histopathologic liver steatosis correlated well with liver SI loss on op

154 TGH deficiency did not further increase liver steatosis despite lowering plasma lipids, mainly d

155 gest that hepatocellular HMGB1 protects from liver steatosis development.

156 uding interchangeability between systems for liver steatosis diagnosis and follow-up imaging.

157 Liver steatosis did not significantly change over time.

158 n and whether obese patients with or without liver steatosis differ in this function.

159 Parallel to this was a striking reduction in liver steatosis due to significantly reduced TG accumula

160 pecific deletion of Il11ra1 protects against liver steatosis, fibrosis and inflammation while reducin

161 14% (P < 0.001), and a marked improvement in liver steatosis (from 88% to 8%), inflammation (from 23%

162 IRT1 and for the development of experimental liver steatosis, genetic deletion of Dbc1 in mice led to

163 sity and obesity-related disorders including liver steatosis, glucose intolerance, or elevated serum

164 Body weight, body fat and lean mass, liver steatosis, glucose tolerance and pancreatic beta c

165 e 9 (PCSK9) levels correlate positively with liver steatosis grade.

166 ibrosis (stages F1, F2, and F3) and baseline liver steatosis >=10%.

167 eased serum ALT, hepatic triglycerides (TG), liver steatosis, hepatocyte ballooning, lobular inflamma

168 In liver steatosis (i.e. fatty liver), hepatocytes accumula

169 sectional comparison of the detectability of liver steatosis in a study group of 108 patients analyse

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

171 lipid and cholesterol levels and attenuated liver steatosis in diet-induced and genetically obese mi

172 effect of GSH deficiency on alcohol-induced liver steatosis in Gclm knockout (KO) mice that constitu

173 ood consumption, obesity, hyperglycemia, and liver steatosis in HFD-treated male mice.

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

175 is superior to CAP in detecting and grading liver steatosis in human NAFLD.

176 on MCH neurons is protective against DIO and liver steatosis in male and female mice.

177 diet increased body fat content and induced liver steatosis in males and females regardless of genot

178 Compound 38 blocked alcohol-induced liver steatosis in mice and has good ADME properties for

179 PI3K p110-alpha, and not p110-beta, promotes liver steatosis in mice fed an HFD.

180 ood glucose levels, blood lipid disorder and liver steatosis in mice with high-fat diet (HFD)-induced

181 ing-based model is a novel tool for studying liver steatosis in mouse models on paraffin sections and

182 Liver steatosis in patients with chronic infection of he

183 ble NOX2-derived peptide and the severity of liver steatosis in subjects with non-alcoholic fatty liv

184 g of hepatic Fsp27 abolishes fasting-induced liver steatosis in the absence of changes in plasma lipi

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

186 cence in the pathogenesis and development of liver steatosis including the progression to nonalcoholi

187 indicate that the reduced adiposity, reduced liver steatosis, increased energy expenditure, and incre

188 supplemented (MCS) diet feeding evidenced by liver steatosis, increased triglycerides, inflammatory c

189 from the observation that BCMO1 mice develop liver steatosis independent of the vitamin A content of

190 was performed using a dietary mouse model of liver steatosis, induced by a high fat diet (HFD).

191 aminotransferases, histological analysis of liver steatosis, inflammation (galectin-3) and fibrosis

192 pressing C3ar1, has no significant effect on liver steatosis, inflammation or fibrosis in a dietary M

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

194 uired for the development of alcohol-induced liver steatosis, inflammation, and injury.

195 rum of high-fat diet-induced NAFLD including liver steatosis, inflammation, fibrosis, and hepatocellu

196 gnificantly contribute to the development of liver steatosis, inflammation, fibrosis, cirrhosis, and

197 g exacerbated the HFD-induced NASH such that liver steatosis, inflammation, fibrosis, oxidative stres

198 is a heterogeneous disorder characterized by liver steatosis; inflammation and fibrosis are features

199 of Ucp1 profoundly augmented alcohol-induced liver steatosis, injury, inflammation and fibrosis in ma

200 It also promotes the development of liver steatosis, insulin resistance, hyperglycemia, and

201 Liver steatosis is a common health problem associated wi

202 Severe liver steatosis is a known risk factor for increased isc

203 Liver steatosis is an increasing health issue with few t

204 Donor liver steatosis is frequently encountered and often asso

205 indicator of increased fibrosis in diseased liver; steatosis may influence some perfusion parameters

206 Moreover, empagliflozin ameliorates liver steatosis more effectively them pioglitazone.

207 aracteristic curve (AUCs) for the staging of liver steatosis (MRI PDFF: >=5.5% for grade >=S1 and >=1

208 to clarify the association between obesity, liver steatosis, myopenia, and myosteatosis and the risk

209 for age, sex, smoking status, myosteatosis, liver steatosis, myopenia, type 2 diabetes, obesity, vis

210 its role in the progression of nonalcoholic liver steatosis (NAFL) to NASH has not been elucidated.

211 ver, this trend did not translate into worse liver steatosis, necroinflammation or fibrosis.

212 y composition was defined by the presence of liver steatosis, obesity, muscle fatty infiltration (myo

213 In the liver, steatosis often proceeds cancer formation; howeve

214 is, and new factors possibly contributing to liver steatosis or fibrosis under ER stress (e.g., major

215 VSL#3 failed to prevent MCD-induced liver steatosis or inflammation.

216 e and lipid metabolism, insulin sensitivity, liver steatosis, or adipose inflammation.

217 the technical state of the art for three key liver steatosis pulse-echo quantitative US biomarkers: a

218 32, p<0.001) and between pancreatic PDFF and liver steatosis (R(S)=0.608, p<0.001); however, in the s

219 We showed that alcohol-induced liver steatosis rapidly resolved after alcohol cessation

220 n genetically obese mice indeed results from liver steatosis rather than the disruption of leptin sig

221 vide potential new mechanistic insights into liver steatosis reduction, inflammation and serum trigly

222 FD throughout life in males resulted in less liver steatosis relative to mice with shorter duration o

223 tic p63, a transcription factor that induces liver steatosis, revealed MAVS as a target downstream of

224 need for quantitative imaging biomarkers of liver steatosis, review the current state of various ima

225 Alcoholic liver steatosis/steatohepatitis can progress to liver fi

226 d metabolism, and reduces body adiposity and liver steatosis, suggesting an alternative target for tr

227 e >2-fold higher in patients with persistent liver steatosis than in those without steatosis or contr

228 tion coefficient detected more patients with liver steatosis than qualitative assessment based on B-m

229 ificant improvement of glucose tolerance and liver steatosis than the restrictive procedure.

230 nted many features of metabolic syndrome and liver steatosis that developed in mice fed a high-fat di

231 ohepatitis (MASH) is the progressive form of liver steatosis, the most common liver disease, and subs

232 s obtained in Padi4KO mice on metabolism and liver steatosis, thereby uncovering a druggable role for

233 Alcohol consumption induces liver steatosis; therefore, this study investigated the

234 fat diet-induced NAFLD with progression from liver steatosis to histological features compatible with

235 ive supplement to prevent the progression of liver steatosis to inflammation and fibrosis in NASH.

236 WND presentations vary from liver steatosis to inflammation, fibrosis, and liver fai

237 bility in obese individuals with and without liver steatosis undergoing a weight-reduction program to

238 al role in reducing the risk of diabetes and liver steatosis, unveiling a vital muscle-brain communic

239 nt study was to evaluate: 1) the presence of liver steatosis using Fatty Liver Index (FLI), Hepatic S

240 The severity of liver steatosis varied between sexes and individual stra

241 plicate a novel mechanism protecting against liver steatosis via an oxidative stress adaptive respons

242 Liver steatosis was assessed by magnetic resonance imagi

243 Liver steatosis was detected in 86%, 84% and 80% of peop

244 Liver steatosis was detected in approximately half of th

245 Liver steatosis was determined via transient elastograph

246 However, mild liver steatosis was observed, although no changes in liv

247 values for HSI and TyG index when detecting liver steatosis were 0.76 and 0.629, respectively.

248 ension, diabetes mellitus, dyslipidemia, and liver steatosis) were also similar between the groups.

249 ): 43.7 +/- 5.2; 78% with moderate or severe liver steatosis] were included in the follow-up interven

250 exhibited reduced body weight, fat mass, and liver steatosis when fed with a high fat diet (HFD).

251 orrelate with increasing adiposity and fatty liver (steatosis), while with weight loss VA levels and

252 pecific Hmgb1 deficiency display exacerbated liver steatosis, while Hmgb1-overexpressing mice exhibit

253 atients in the high probability category for liver steatosis, while the FIB-4 (1.94 +/- 0.81) and NFS

254 resistant to diet-induced hyperinsulinemia, liver steatosis, white adipose tissue (WAT) inflammation

255 -induced whitening of BAT, cold intolerance, liver steatosis, white adipose tissue inflammation, and

256 A cutoff value of CAP of 249 dB/m rules in liver steatosis with a very high specificity.

257 n), these factors could increase the risk of liver steatosis with necroinflammatory lesions and fibro

258 tal cholesterol in conjunction with improved liver steatosis, with greater reductions (p < 0.05) comp