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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
16 hout diabetes and who had a liver biopsy (29 NAFLD-NO and 15 NAFLD-Ob) and 20 CTs without obesity, by
18 timised the IGNIS kit to quantify APO-F as a NAFLD biomarker in serum using a single LC-MS acquisitio
20 and meta-analysis, we identified five adult NAFLD cohort studies reporting fibrosis stage-specific m
22 both cardiovascular and liver outcomes among NAFLD patients with moderate or lesser degrees of alcoho
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
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
35 ed the association between periodontitis and NAFLD within strata of serum CRP and separately within s
37 ppear to affect both insulin sensitivity and NAFLD/NASH pathogenesis at multiple levels, and these ap
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
44 alcoholic fatty liver disease and cirrhosis (NAFLD-cirrhosis) is unknown and needs to be systematical
46 50-65-year fulfilled the inclusion criteria (NAFLD with impaired fasting glucose or impaired glucose
48 e found that mildly hypothyroid mice develop NAFLD without down-regulation of hepatic TH signaling or
50 mutant of LRH-1 (LRH-1 K289R mice) developed NAFLD and early signs of nonalcoholic steatohepatitis (N
52 patients with NAFLD are caused by different NAFLD subtypes with specific serum metabolomic profiles,
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
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
62 to define nonalcoholic fatty liver disease (NAFLD) by proton magnetic resonance spectroscopy ((1) H-
65 therapy, non-alcoholic fatty liver disease (NAFLD) could soon emerge as the most common liver diseas
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).
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 (
78 ND & AIMS: Nonalcoholic fatty liver disease (NAFLD) is a consequence of defects in diverse metabolic
81 ND & AIMS: Nonalcoholic fatty liver disease (NAFLD) is associated with increased risk of hepatic, car
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
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
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
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
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
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
139 disease activity and severity of fibrosis in NAFLD and are potentially valuable tools for noninvasive
142 oxycholate ratio was significantly higher in NAFLD without (P = 0.005) and with (P = 0.02) diabetes.
149 hics known to impact fibrosis progression in NAFLD and the inclusion of patients with simple steatosi
155 t the pathogenesis of hypothyroidism-induced NAFLD is both intra- and extrahepatic; they also reveal
157 obese patients, nonobese patients had lower NAFLD activity score (3.3 +/- 1.3 vs. 3.8 +/- 1.2; P = 0
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.
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
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
174 nto clinical protocols for the assessment of NAFLD in children will require prospective evaluation.
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
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
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
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
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
208 covariate-adjusted prevalence odds ratio of NAFLD comparing participants with >/=30% of sites with P
210 cate that adiposity augments genetic risk of NAFLD at multiple loci that confer susceptibility to hep
212 ere also highly elevated in liver samples of NAFLD patients and correlated with disease severity.
214 y and genotype promoted the full spectrum of NAFLD, from steatosis to hepatic inflammation to cirrhos
217 hepatitis, we identified 2 major subtypes of NAFLD and markers that differentiate steatosis from NASH
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
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
232 The impact on study validity of recruiting NAFLD subjects as controls was estimated as likely, prob
236 We demonstrate that NR prevents and reverts NAFLD by inducing a sirtuin (SIRT)1- and SIRT3-dependent
242 a showed, for the first time in humans, that NAFLD patients show a marked eNOS dysfunction, which may
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
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
253 of these aberrations might determine whether NAFLD progresses to nonalcoholic steatohepatitis (NASH).
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
262 ower family SES at birth was associated with NAFLD in male offspring independent of adolescent obesit
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),
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
274 population-based sample of individuals with NAFLD in midlife, prospectively assessed alcohol use is
276 ir/emtricitabine or abacavir/lamivudine with NAFLD were randomized 1:1 to switch from EFV to RAL (400
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
282 ion after bariatric surgery in patients with NAFLD or steatohepatitis (NASH) may impair liver functio
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,
297 measured the AA profile of 44 subjects with NAFLD without diabetes and who had a liver biopsy (29 NA
299 not correlate with uACR in subjects without NAFLD (n = 212, p = 0.94), but correlated positively in
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