ライフサイエンスコーパス: NAFLD

1 NAFLD and nonalcoholic steatohepatitis (NASH) in AYAs of

2 NAFLD is associated not only with lipid enrichment, but

3 NAFLD is associated to Insulin Resistance (IR).

4 NAFLD is associated with significantly altered circulati

5 NAFLD is common among patients with HIV, and might be mo

6 NAFLD is common and often overlooked in volunteers for c

7 NAFLD was assessed clinically and quantified by MRI prot

8 NAFLD was defined as liver attenuation <51 Hounsfield Un

9 NAFLD was diagnosed in 15.2% of adolescents at age 17 ye

10 NAFLD was diagnosed on established ultrasound criteria f

11 NAFLD was induced by impaired suppression of adipose tis

12 NAFLD was significantly associated with being breast fed

13 o NAFLD patients with no fibrosis (stage 0), NAFLD patients with fibrosis were at an increased risk f

14 d who had a liver biopsy (29 NAFLD-NO and 15 NAFLD-Ob) and 20 CTs without obesity, by gas chromatogra

15 ts; based on this signature, we identified 2 NAFLD subtypes.

16 hout diabetes and who had a liver biopsy (29 NAFLD-NO and 15 NAFLD-Ob) and 20 CTs without obesity, by

17 Included were 1,495 NAFLD patients with 17,452 patient years of follow-up.

18 timised the IGNIS kit to quantify APO-F as a NAFLD biomarker in serum using a single LC-MS acquisitio

19 APO-F decreased across NAFLD stages.

20 and meta-analysis, we identified five adult NAFLD cohort studies reporting fibrosis stage-specific m

21 n protects severely hypothyroid mice against NAFLD.

22 both cardiovascular and liver outcomes among NAFLD patients with moderate or lesser degrees of alcoho

23 ic marker of liver apoptosis both in ALD and NAFLD.

24 genesis of alcoholic liver disease (ALD) and NAFLD, although studies of ALD have focused on pathologi

25 rental pregnancy-related characteristics and NAFLD in 1,170 adolescent offspring aged 17 years partic

26 tudy of individuals with type 2 diabetes and NAFLD at a tertiary medical center in Germany from June

27 BCAAs, in patients with type 2 diabetes and NAFLD.

28 h, we were able to differentiate healthy and NAFLD liver in mouse and human tissue samples, finding s

29 risk-stratification of patients with HIV and NAFLD are becoming increasingly important for accurately

30 with probing pocket depth (PD) >/=4 mm, and NAFLD status was determined using liver ultrasound asses

31 to non-alcoholic steatohepatitis (NASH) and NAFLD-related fibrosis or cirrhosis in these patients th

32 pically resistant to HFD-induced obesity and NAFLD, develop full disease characteristics at thermoneu

33 observed mainly in subjects with obesity and NAFLD, likely as a consequence of increased IR and prote

34 d the relationship between periodontitis and NAFLD ( Pinteraction = 0.01).

35 ed the association between periodontitis and NAFLD within strata of serum CRP and separately within s

36 fy the association between periodontitis and NAFLD.

37 ppear to affect both insulin sensitivity and NAFLD/NASH pathogenesis at multiple levels, and these ap

38 rovement of obesity-related diseases such as NAFLD.

39 osis in patients undergoing biopsy to assess NAFLD.

40 nt clinical and diagnostic methods assessing NAFLD diagnosis, progression, and outcomes; compare the

41 to determine a potential association between NAFLD and CCA, stratifying by its subtypes; intrahepatic

42 Dietary fat content probably influences both NAFLD and insulin resistance; however, the immediate eff

43 In some cases, NAFLD is also accompanied by insulin resistance, resulti

44 alcoholic fatty liver disease and cirrhosis (NAFLD-cirrhosis) is unknown and needs to be systematical

45 Consecutive NAFLD patients who underwent liver biopsy were prospecti

46 50-65-year fulfilled the inclusion criteria (NAFLD with impaired fasting glucose or impaired glucose

47 and discriminating approach for determining NAFLD presence and severity in clinical samples.

48 e found that mildly hypothyroid mice develop NAFLD without down-regulation of hepatic TH signaling or

49 nonobese Americans and Asians still develop NAFLD.

50 mutant of LRH-1 (LRH-1 K289R mice) developed NAFLD and early signs of nonalcoholic steatohepatitis (N

51 openia is a novel risk factor for developing NAFLD.

52 patients with NAFLD are caused by different NAFLD subtypes with specific serum metabolomic profiles,

53 1-butanol, and 2-butanone could discriminate NAFLD patients from CTRLs.

54 alcoholic and alcoholic fatty liver disease (NAFLD and AFLD, respectively) are major health problems,

55 ients with nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) is still unsett

56 including nonalcoholic fatty liver disease (NAFLD) and diabetes, and has received great attention as

57 ributor to nonalcoholic fatty liver disease (NAFLD) and insulin resistance, but the mechanisms that i

58 Nonalcoholic fatty liver disease (NAFLD) and resulting nonalcoholic steatohepatitis (NASH)

59 stages of nonalcoholic fatty liver disease (NAFLD) are characterized by the accumulation of fat in t

60 jects with nonalcoholic fatty liver disease (NAFLD) as controls can compromise study validity and sub

61 nction in non alcoholic fatty liver disease (NAFLD) by altering inflammatory signalling in RSF.

62 to define nonalcoholic fatty liver disease (NAFLD) by proton magnetic resonance spectroscopy ((1) H-

63 Nonalcoholic fatty liver disease (NAFLD) can progress from simple steatosis (i.e., nonalco

64 Nonalcoholic fatty liver disease (NAFLD) contributes to premature death along with obesity

65 therapy, non-alcoholic fatty liver disease (NAFLD) could soon emerge as the most common liver diseas

66 Nonalcoholic fatty liver disease (NAFLD) has become highly prevalent, now considered the m

67 Non-alcoholic fatty liver disease (NAFLD) has been recently identified as a risk factor of

68 ntitis and nonalcoholic fatty liver disease (NAFLD) has been reported by experimental animal and epid

69 ents with non-alcoholic fatty liver disease (NAFLD) in a randomized clinical trial (NCT01806506).

70 Nonalcoholic fatty liver disease (NAFLD) in non-obese patients remains a clinical conditio

71 CT-defined nonalcoholic fatty liver disease (NAFLD) in the offspring cohort of the Framingham Heart S

72 pectrum of nonalcoholic fatty liver disease (NAFLD) includes fatty liver (NAFL) and steatohepatitis (

73 idence of non-alcoholic fatty liver disease (NAFLD) increases with age.

74 Nonalcoholic fatty liver disease (NAFLD) is a burgeoning health problem worldwide and an i

75 Non-alcoholic fatty liver disease (NAFLD) is a common metabolic disorder in obese individua

76 Nonalcoholic fatty liver disease (NAFLD) is a common problem across the world.

77 Nonalcoholic fatty liver disease (NAFLD) is a complex chronic liver disorder.

78 ND & AIMS: Nonalcoholic fatty liver disease (NAFLD) is a consequence of defects in diverse metabolic

79 Nonalcoholic fatty liver disease (NAFLD) is a significant health burden in adolescents and

80 dence that nonalcoholic fatty liver disease (NAFLD) is affected by gut microbiota.

81 ND & AIMS: Nonalcoholic fatty liver disease (NAFLD) is associated with increased risk of hepatic, car

82 Nonalcoholic fatty liver disease (NAFLD) is characterized by excess accumulation of fat in

83 Although nonalcoholic fatty liver disease (NAFLD) is closely linked to obesity, around 10%-20% of n

84 ients with nonalcoholic fatty liver disease (NAFLD) is common, yet the effects on cardiovascular and

85 lopment of nonalcoholic fatty liver disease (NAFLD) is not well understood.

86 Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease

87 Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder and is

88 Nonalcoholic fatty liver disease (NAFLD) is the most prevalent liver disease worldwide.

89 Nonalcoholic fatty liver disease (NAFLD) is widespread in adults and children.

90 ression of nonalcoholic fatty liver disease (NAFLD) over time is lacking.

91 ients with nonalcoholic fatty liver disease (NAFLD) receiving EFV plus 2 nucleoside analogues.

92 Non-alcoholic fatty liver disease (NAFLD) represents a spectrum of conditions that include

93 Nonalcoholic fatty liver disease (NAFLD) represents an emerging cause of hepatocellular ca

94 Nonalcoholic fatty liver disease (NAFLD) represents the hepatic manifestation of metabolic

95 Nonalcoholic fatty liver disease (NAFLD) was the most common cause of CLD in all ethnic gr

96 Nonalcoholic fatty liver disease (NAFLD), a common prelude to cirrhosis and hepatocellular

97 ated with non-alcoholic fatty liver disease (NAFLD), but the mechanisms involved in the development o

98 variant of nonalcoholic fatty liver disease (NAFLD), is becoming an increasingly common indication fo

99 gnosed as non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), hereditary

100 valence of nonalcoholic fatty liver disease (NAFLD), therapeutic options and noninvasive markers of d

101 ression of nonalcoholic fatty liver disease (NAFLD).

102 ents with non-alcoholic fatty liver disease (NAFLD).

103 ients with nonalcoholic fatty liver disease (NAFLD).

104 atures of non-alcoholic fatty liver disease (NAFLD).

105 rtality in nonalcoholic fatty liver disease (NAFLD).

106 ed risk of nonalcoholic fatty liver disease (NAFLD).

107 of having nonalcoholic fatty liver disease (NAFLD).

108 ovement of nonalcoholic fatty liver disease (NAFLD).

109 arker for non-alcoholic fatty liver disease (NAFLD).

110 iated with nonalcoholic fatty liver disease (NAFLD).

111 ibrosis in nonalcoholic fatty liver disease (NAFLD).

112 iated with nonalcoholic fatty liver disease (NAFLD).

113 lopment of nonalcoholic fatty liver disease (NAFLD).

114 ients with nonalcoholic fatty liver disease (NAFLD).

115 outcome in nonalcoholic fatty liver disease (NAFLD).

116 creased in nonalcoholic fatty liver disease (NAFLD); however, if this is due to increased muscular pr

117 linked to nonalcoholic fatty liver disease (NAFLD); however, the sugar-associated effects that lead

118 atitis B; nonalcoholic fatty liver diseases (NAFLD); and alcoholic liver disease, are a leading cause

119 protection from thermoneutral-housing-driven NAFLD amplification.

120 vides a sex-independent model of exacerbated NAFLD in mice and represents a novel approach for interr

121 sis (using the histologic scoring system for NAFLD from the Nonalcoholic Steatohepatitis Clinical Res

122 A Markov model was used to forecast NAFLD disease progression.

123 Fifty-four NAFLD patients were consecutively enrolled.

124 ol-induced non-obese NAFLD are distinct from NAFLD occurring as a consequence of metabolic syndrome.

125 demonstrated a reduced function induced from NAFLD platelets as compared with controls (p < 0.001), a

126 Forty two (8.4%) had NAFLD.

127 rs evaluated 55 patients suspected of having NAFLD (40 men, 15 women).

128 itis C virus (HCV), hepatitis B virus (HBV), NAFLD, and alcoholic liver diseases; (2) performance of

129 vel was independently associated with higher NAFLD activity score (adjusted odds ratio [OR], 1.644; P

130 derstood; in particular, it is not known how NAFLD and its early progression affects the distribution

131 tecting and grading liver steatosis in human NAFLD.

132 beneficial than moderate activity to improve NAFLD/nonalcoholic steatohepatitis.

133 across the spectrum of IHTG accumulation in NAFLD (r = -0.38; P < 0.001).

134 usion MPO-Gd showed elevated MPO activity in NAFLD mouse models and human liver biopsy samples.

135 ne concentrations are known to be altered in NAFLD.

136 NT, may represent an alternative approach in NAFLD and obesity treatment.

137 Projected changes in NAFLD-related cirrhosis, advanced liver disease, and liv

138 Compared to CTRLs, in NAFLD patients Actinobacteria were significantly increas

139 disease activity and severity of fibrosis in NAFLD and are potentially valuable tools for noninvasive

140 Hepatic collagen FSR in NAFLD increased with advancing disease stage (e.g., high

141 his study is to investigate eNOS function in NAFLD patients.

142 oxycholate ratio was significantly higher in NAFLD without (P = 0.005) and with (P = 0.02) diabetes.

143 d valine, but not leucine, were increased in NAFLD-NO subjects compared to CTs.

144 ether prediction of liver fibrosis by LSM in NAFLD patients is affected by CAP values.

145 of all-cause and liver-related mortality in NAFLD.

146 y account for the impaired LR that occurs in NAFLD.

147 Most AAs were increased only in NAFLD-Ob subjects.

148 factors mostly affecting LSM performance in NAFLD.

149 hics known to impact fibrosis progression in NAFLD and the inclusion of patients with simple steatosi

150 26 were up-regulated and 2 down-regulated in NAFLD patients.

151 dation of benefit of moderate alcohol use in NAFLD cannot be made.

152 chanistic studies of moderate alcohol use in NAFLD exist.

153 edly exacerbated high-fat diet (HFD)-induced NAFLD pathogenesis.

154 Hypothyroidism-induced NAFLD has generally been attributed to reduced TH signal

155 t the pathogenesis of hypothyroidism-induced NAFLD is both intra- and extrahepatic; they also reveal

156 In Italian NAFLD patients, the rs641738 T allele was associated wit

157 obese patients, nonobese patients had lower NAFLD activity score (3.3 +/- 1.3 vs. 3.8 +/- 1.2; P = 0

158 An age-, sex-, and fibrosis-stage matched NAFLD cohort (n = 30) was used for comparison.

159 ces of M30/65 were found between the matched NAFLD and ALD cohort.

160 gical changes in female rat liver that mimic NAFLD with testosterone-treated rats showing impaired BC

161 mass index [BMI] > 25 kg/m(2) ), healthy non-NAFLD controls (normal ALT and BMI), or indeterminate.

162 Nonobese NAFLD patients tend to have less-severe disease and may

163 ff of 25 kg/m(2) was used to define nonobese NAFLD.

164 e severity and clinical outcomes of nonobese NAFLD patients.

165 paired in the hepatocytes from AFLD, but not NAFLD, animals.

166 sms underlying cholesterol-induced non-obese NAFLD are distinct from NAFLD occurring as a consequence

167 to steatosis and hepatitis in this non-obese NAFLD model were driven by a combination of effects dire

168 all the characteristic features of non-obese NAFLD, we aimed to advance mechanistic understanding of

169 y and hepatic cholesterol in human non-obese NAFLD/NASH patients.

170 y (NAFLD-NO) compared to those with obesity (NAFLD-Ob) display altered plasma AAs compared to control

171 d a) if subjects with NAFLD without obesity (NAFLD-NO) compared to those with obesity (NAFLD-Ob) disp

172 In 2015, approximately 20% of NAFLD cases were classified as NASH, increasing to 27% b

173 to be elucidated how BBR improves aspects of NAFLD.

174 nto clinical protocols for the assessment of NAFLD in children will require prospective evaluation.

175 Increased awareness of NAFLD prevalence and stricter ALT cutoffs may ameliorate

176 he mechanisms involved in the development of NAFLD in PCOS are not well known.

177 ylation of LRH-1 promotes the development of NAFLD under lipogenic conditions through regulation of O

178 ssion of PGC1A contributes to development of NAFLD using mouse models, primary hepatocytes, and human

179 y a role in the heterogeneous development of NAFLD.

180 naling that may contribute to development of NAFLD.REGISTRATION.

181 hosen a priori as possible discriminators of NAFLD were measured in participants enrolled in the Nona

182 alcium signaling, we examined the effects of NAFLD on expression of the type II inositol 1,4,5-trisph

183 and may help slow the advancing epidemic of NAFLD in the next generation.

184 ndomly ascertained to be without evidence of NAFLD and 69 of their first-degree relatives.

185 Strategies to slow the growth of NAFLD cases and therapeutic options are necessary to mit

186 Incidence of NAFLD was based on historical and projected changes in a

187 national surveillance data for incidence of NAFLD-related HCC.

188 Indices of NAFLD, including hepatic ceramide levels, oxidative stre

189 The magnitude of NAFLD on CCA risk is greater for iCCA than eCCA subtype,

190 Several mechanisms of NAFLD pathogenesis are postulated to explain the disease

191 rain of C57BL/6 J:129S1/SvImJ mice) model of NAFLD that closely mimics most aspects of human disease.

192 7 cells, in liver tissue from a rat model of NAFLD, and in liver biopsy specimens of patients with si

193 r of hepatic lipid accumulation in models of NAFLD.

194 can be applied to understand other models of NAFLD.

195 ures of genetic and dietary animal models of NAFLD; and highlight pharmacological approaches for dise

196 egies are currently based on modification of NAFLD risk factors, many new drugs are now in clinical t

197 The occurrence of NAFLD parallels high rates of obesity and metabolic synd

198 ly associated with higher prevalence odds of NAFLD, and this relationship was modified by serum CRP l

199 ar mechanisms underlying the pathogenesis of NAFLD has been hampered by a lack of animal models that

200 oved understanding of the pathophysiology of NAFLD and technologic advances have led to algorithms th

201 on, our data suggest that in the presence of NAFLD elevated fetuin-A levels may impair renal function

202 We aimed to determine the prevalence of NAFLD and its associations in Sri Lankan adolescents liv

203 Given the rising prevalence of NAFLD in the general population, we sought to identify i

204 Prevalence of NAFLD was high in Sri Lankan adolescents, and was associ

205 s for increasing awareness and prevention of NAFLD in AYAs are greatly needed.

206 The molecular progression of NAFLD involves a metabolic perturbation which triggers s

207 protect obese offspring from progression of NAFLD.

208 covariate-adjusted prevalence odds ratio of NAFLD comparing participants with >/=30% of sites with P

209 y be considered in first-degree relatives of NAFLD-cirrhosis patients.

210 cate that adiposity augments genetic risk of NAFLD at multiple loci that confer susceptibility to hep

211 provide insights into the origins of risk of NAFLD in offspring.

212 ere also highly elevated in liver samples of NAFLD patients and correlated with disease severity.

213 zed they might be related to the severity of NAFLD.

214 y and genotype promoted the full spectrum of NAFLD, from steatosis to hepatic inflammation to cirrhos

215 microRNA upregulated in a broad spectrum of NAFLD.

216 ts with simple steatosis for each subtype of NAFLD.

217 hepatitis, we identified 2 major subtypes of NAFLD and markers that differentiate steatosis from NASH

218 nction and promotes pathological symptoms of NAFLD.

219 a new therapeutic approach for treatment of NAFLD and other obesity-related diseases.

220 Overall NAFLD patients had increased levels of Bradyrhizobium, A

221 Overall NAFLD prevalence among the adult population (aged >/=15

222 Overall, NAFLD was associated with an increased risk for CCA, wit

223 investigated its modifications in pediatric NAFLD patients using targeted metagenomics and metabolom

224 esity and DM along with an aging population, NAFLD-related liver disease and mortality will increase

225 Subjects were classified as presumed NAFLD (pNF; alanine aminotransferase [ALT] level >/= 20

226 Prevalent NAFLD cases are forecasted to increase 21%, from 83.1 mi

227 OAT7/TMC4 variant predisposes to progressive NAFLD, but the impact on hepatic carcinogenesis is unkno

228 tabolomes of 535 patients with biopsy-proven NAFLD (353 with simple steatosis and 182 with NASH) and

229 erized cohort of patients with biopsy-proven NAFLD, this study demonstrates that hepatic scar in NASH

230 and severity in patients with biopsy-proven NAFLD.

231 Among 307 recruited NAFLD patients, 72 (23.5%) were nonobese.

232 The impact on study validity of recruiting NAFLD subjects as controls was estimated as likely, prob

233 Recurrent NAFLD is common post-LT occurring in nearly 88% of all p

234 ients with liver biopsy, 88.2% had recurrent NAFLD, whereas 41.2% had recurrent NASH.

235 had a TE and were defined to have recurrent NAFLD.

236 We demonstrate that NR prevents and reverts NAFLD by inducing a sirtuin (SIRT)1- and SIRT3-dependent

237 t bolus resulted in the induction of several NAFLD-associated genes.

238 ure prospective studies aimed at stratifying NAFLD-HCC risk.

239 When classified by subtypes, NAFLD was associated with both iCCA and eCCA, with ORs o

240 Twenty-one patients with suspected NAFLD ingested heavy water ((2) H2 O, 50-mL aliquots) tw

241 Our findings demonstrate that NAFLD occurs when TH levels are mildly reduced, but, par

242 a showed, for the first time in humans, that NAFLD patients show a marked eNOS dysfunction, which may

243 This meta-analysis suggests that NAFLD may potentially increase the risk of CCA developme

244 at 33.5% in 2030, and the median age of the NAFLD population will increase from 50 to 55 years durin

245 e data on the relationships of bile acids to NAFLD and the potential for therapeutically targeting bi

246 Compared to NAFLD patients with no fibrosis (stage 0), NAFLD patient

247 Up-regulation of DNL also contributes to NAFLD.

248 Early-life contributors to NAFLD show considerable sexual dimorphism.

249 to primary BA ratio inversely correlated to NAFLD activity score.

250 ently developed hepatic pathology similar to NAFLD and nonalcoholic steatohepatitis (NASH) without ch

251 When combining data from an independent UK NAFLD cohort, in the overall cohort of non-cirrhotic pat

252 Whether NAFLD is a risk factor for cholangiocarcinoma (CCA) rema

253 of these aberrations might determine whether NAFLD progresses to nonalcoholic steatohepatitis (NASH).

254 Adolescents with NAFLD also had a higher amount of total body fat (p < 0.

255 rangements was higher among adolescents with NAFLD than those without (85.8 vs 26.3 in controls, p <

256 ssion, factors independently associated with NAFLD after adjusting for obesity in adolescent females

257 0.02) remained significantly associated with NAFLD after multivariate modeling adjusted for adolescen

258 e analysis, maternal factors associated with NAFLD in female offspring were younger maternal age (P =

259 gestational weight gain were associated with NAFLD in female offspring, whereas lower family SES at b

260 dy mass index (BMI) were not associated with NAFLD in female offspring.

261 own that eNOS dysfunction is associated with NAFLD in humans.

262 ower family SES at birth was associated with NAFLD in male offspring independent of adolescent obesit

263 estational weight gain, were associated with NAFLD in male offspring.

264 metabolic changes typically associated with NAFLD, such as hypertriglyceridemia and low high-density

265 s, the rs641738 T allele was associated with NAFLD-HCC (OR 1.65, 1.08-2.55; n = 765), particularly in

266 and MBOAT7 risk variants was associated with NAFLD-HCC independently of clinical factors (p < 0.001),

267 encoding Gly482Ser) has been associated with NAFLD.

268 statistically significant associations with NAFLD histology were evaluated in multivariable models a

269 erative liver biopsies were categorized with NAFLD Activity Score (NAS) and liver function tests were

270 2 diabetes and prediabetes in children with NAFLD and assess type 2 diabetes and prediabetes as risk

271 rosis and advanced fibrosis in children with NAFLD and to assess agreement between manual and novel a

272 of two-dimensional (2D) MRE in children with NAFLD.

273 estimate hepatic stiffness in children with NAFLD.

274 population-based sample of individuals with NAFLD in midlife, prospectively assessed alcohol use is

275 Up to one third of individuals with NAFLD will develop nonalcoholic steatohepatitis (NASH),

276 ir/emtricitabine or abacavir/lamivudine with NAFLD were randomized 1:1 to switch from EFV to RAL (400

277 Of the 570 participants with NAFLD (mean age, 50 years; 54% black; 46% female), 332 (

278 noninvasive stratification of patients with NAFLD and identification of targets for therapeutic inte

279 alysis of serum metabolomes of patients with NAFLD and MAT1A-KO mice with steatohepatitis, we identif

280 he diverse defects observed in patients with NAFLD are caused by different NAFLD subtypes with specif

281 A higher proportion of patients with NAFLD die from cardiovascular disorders than patients wi

282 ion after bariatric surgery in patients with NAFLD or steatohepatitis (NASH) may impair liver functio

283 In patients with NAFLD, CAP values should always be taken into account in

284 In rodent models and patients with NAFLD, hepatic expression of peroxisome proliferator-act

285 ing all grades of steatosis in patients with NAFLD.

286 is associated with CVD risk in patients with NAFLD.

287 not reduce the risk of CVD in patients with NAFLD.

288 ovascular and liver disease in patients with NAFLD.

289 e-intake alone in pre-diabetic patients with NAFLD.

290 r benefits would be observed in persons with NAFLD remains largely unstudied.

291 of a prospective cohort of 26 probands with NAFLD-cirrhosis and 39 first-degree relatives.

292 that first-degree relatives of probands with NAFLD-cirrhosis have a 12 times higher risk of advanced

293 s in first-degree relatives of probands with NAFLD-cirrhosis was significantly higher than that in th

294 the first-degree relatives of probands with NAFLD-cirrhosis were odds ratio 14.9 (95% CI, 1.8-126.0,

295 s in first-degree relatives of probands with NAFLD-cirrhosis.

296 , but correlated positively in subjects with NAFLD (n = 105, p = 0.0005).

297 measured the AA profile of 44 subjects with NAFLD without diabetes and who had a liver biopsy (29 NA

298 Thus, we evaluated a) if subjects with NAFLD without obesity (NAFLD-NO) compared to those with

299 not correlate with uACR in subjects without NAFLD (n = 212, p = 0.94), but correlated positively in

300 cutaneous fat (p < 0.001) than those without NAFLD.