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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
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.

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