Pubmed FattyLiver Set

PMID- 35710982
OWN - NLM
STAT- MEDLINE
DCOM- 20220929
LR - 20221101
IS - 1759-5053 (Electronic)
IS - 1759-5045 (Linking)
VI - 19
IP - 10
DP - 2022 Oct
TI - Metabolic (dysfunction)-associated fatty liver disease in individuals of
normal
weight.
PG - 638-651
LID - 10.1038/s41575-022-00635-5 [doi]
AB - Metabolic (dysfunction)-associated fatty liver disease (MAFLD) affects up to
a
third of the global population; its burden has grown in parallel with rising
rates of type 2 diabetes mellitus and obesity. MAFLD increases the risk of
end-stage liver disease, hepatocellular carcinoma, death and liver
transplantation and has extrahepatic consequences, including cardiometabolic
disease and cancers. Although typically associated with obesity, there is
accumulating evidence that not all people with overweight or obesity develop
fatty liver disease. On the other hand, a considerable proportion of patients
with MAFLD are of normal weight, indicating the importance of metabolic
health in
the pathogenesis of the disease regardless of body mass index. The clinical
profile, natural history and pathophysiology of patients with so-called lean
MAFLD are not well characterized. In this Review, we provide epidemiological
data
on this group of patients and consider overall metabolic health and metabolic
adaptation as a framework to best explain the pathogenesis of MAFLD and its
heterogeneity in individuals of normal weight and in those who are above
normal
weight. This framework provides a conceptual schema for interrogating the
MAFLD
phenotype in individuals of normal weight that can translate to novel
approaches
for diagnosis and patient care.
CI - © 2022. Springer Nature Limited.
FAU - Eslam, Mohammed
AU - Eslam M
AUID- ORCID: 0000-0002-4315-4144
AD - Storr Liver Centre, Westmead Institute for Medical Research, Westmead
Hospital
and University of Sydney, Sydney, New South Wales, Australia.
[email protected].
FAU - El-Serag, Hashem B
AU - El-Serag HB
AUID- ORCID: 0000-0001-5964-7579
AD - Department of Medicine, Baylor College of Medicine, Houston, TX, USA.
FAU - Francque, Sven
AU - Francque S
AUID- ORCID: 0000-0002-7527-4714
AD - Department of Gastroenterology and Hepatology, Antwerp University Hospital,
Antwerp, Belgium.
AD - Laboratory of Experimental Medicine and Paediatrics (LEMP), Faculty of
Medicine
and Health Sciences, University of Antwerp, Antwerp, Belgium.
FAU - Sarin, Shiv K
AU - Sarin SK
AUID- ORCID: 0000-0002-0544-5610
AD - Department of Hepatology, Institute of Liver and Biliary Sciences, New Delhi,
India.
FAU - Wei, Lai
AU - Wei L
AD - Hepatopancreatobiliary Center, Beijing Tsinghua Changgung Hospital, Tsinghua
University, Beijing, China.
FAU - Bugianesi, Elisabetta
AU - Bugianesi E
AD - Department of Medical Sciences, Division of Gastroenterology and Hepatology,
A.O.
Città della Salute e della Scienza di Torino, University of Turin, Turin,
Italy.
FAU - George, Jacob
AU - George J
AUID- ORCID: 0000-0002-8421-5476
AD - Storr Liver Centre, Westmead Institute for Medical Research, Westmead
Hospital
and University of Sydney, Sydney, New South Wales, Australia.
[email protected].
LA - eng
GR - P30 DK056338/DK/NIDDK NIH HHS/United States
PT - Journal Article
PT - Research Support, N.I.H., Extramural
PT - Research Support, Non-U.S. Gov't
PT - Review
DEP - 20220616
PL - England
TA - Nat Rev Gastroenterol Hepatol
JT - Nature reviews. Gastroenterology & hepatology
JID - 101500079
SB - IM
MH - *Carcinoma, Hepatocellular/pathology
MH - *Diabetes Mellitus, Type 2/complications/etiology
MH - Humans
MH - *Liver Neoplasms
MH - *Non-alcoholic Fatty Liver Disease/complications
MH - Obesity/complications
EDAT- 2022/06/18 06:00
MHDA- 2022/09/30 06:00
CRDT- 2022/06/17 00:24
PHST- 2022/05/13 00:00 [accepted]
PHST- 2022/06/18 06:00 [pubmed]
PHST- 2022/09/30 06:00 [medline]
PHST- 2022/06/17 00:24 [entrez]
AID - 10.1038/s41575-022-00635-5 [pii]
AID - 10.1038/s41575-022-00635-5 [doi]
PST - ppublish
SO - Nat Rev Gastroenterol Hepatol. 2022 Oct;19(10):638-651. doi:
10.1038/s41575-022-00635-5. Epub 2022 Jun 16.
PMID- 28642059
OWN - NLM
STAT- MEDLINE
DCOM- 20180605
LR - 20220410
IS - 0168-8278 (Linking)
VI - 67
IP - 4
DP - 2017 Oct
TI - New trends on obesity and NAFLD in Asia.
PG - 862-873
LID - S0168-8278(17)32073-1 [pii]
LID - 10.1016/j.jhep.2017.06.003 [doi]
AB - Traditionally, obesity and its related diseases have been considered a
problem in
Western countries. However, in the past two decades, urbanisation in many
Asian
countries has led to a sedentary lifestyle and overnutrition, setting the
stage
for the epidemic of obesity. This article reviews the epidemiological trend
of
obesity in Asia, with special emphasis on the emerging condition of non-
alcoholic
fatty liver disease (NAFLD). Currently, the population prevalence of NAFLD in
Asia is around 25%, like many Western countries. While hepatocellular
carcinoma
and end-stage liver disease secondary to NAFLD remain uncommon, a rising
trend
has emerged. Around 8-19% of Asians with body mass indexes less than
25kg/m(2)
are also found to have NAFLD, a condition often described as "lean" or
"non-obese" NAFLD. Although this condition is generally less severe than that
in
more obese patients, steatohepatitis and fibrotic disease are well
recognized.
Central adiposity, insulin resistance and weight gain are major risk factors,
and
genetic predisposition, such as the PNPLA3 polymorphism appears to be more
important in the development of NAFLD in the non-obese population. Lifestyle
modification remains the cornerstone of management for obesity and NAFLD, but
few
patients can achieve adequate weight reduction and even fewer can maintain
the
weight in the long run. While pharmacological agents have entered phase III
development for steatohepatitis, Asian patients are under-represented in most
drug trials. Future studies should define the optimal management of obesity
and
NAFLD in Asia.
CI - Copyright © 2017 European Association for the Study of the Liver. Published
by
Elsevier B.V. All rights reserved.
FAU - Fan, Jian-Gao
AU - Fan JG
AD - Center for Fatty Liver, Department of Gastroenterology, Xin Hua Hospital
Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai,
China.
Electronic address: [email protected].
FAU - Kim, Seung-Up
AU - Kim SU
AD - Department of Internal Medicine, Institute of Gastroenterology, Yonsei
University
College of Medicine, Seoul, South Korea.
FAU - Wong, Vincent Wai-Sun
AU - Wong VW
AD - Department of Medicine and Therapeutics, The Chinese University of Hong Kong,
Hong Kong, China; State Key Laboratory of Digestive Disease, The Chinese
University of Hong Kong, Hong Kong, China. Electronic address:
[email protected].
LA - eng
PT - Review
DEP - 20170619
PL - Netherlands
TA - J Hepatol
JT - Journal of hepatology
JID - 8503886
RN - 0 (Membrane Proteins)
RN - EC 3.1.1.3 (Lipase)
RN - EC 3.1.1.3 (adiponutrin, human)
SB - IM
MH - Asia/epidemiology
MH - Body Mass Index
MH - Diet
MH - Genetic Predisposition to Disease
MH - Hepatitis B, Chronic/complications
MH - Humans
MH - Incidence
MH - Lipase/genetics
MH - Membrane Proteins/genetics
MH - Metabolic Syndrome/complications
MH - Non-alcoholic Fatty Liver Disease/*epidemiology/etiology/therapy
MH - Obesity/complications/*epidemiology/therapy
MH - Prevalence
MH - Risk Factors
MH - Sarcopenia/complications
MH - Sedentary Behavior
OTO - NOTNLM
OT - Body mass index
OT - China
OT - Fatty liver
OT - Korea
OT - Non-alcoholic steatohepatitis
OT - Waist circumference
EDAT- 2017/06/24 06:00
MHDA- 2018/06/06 06:00
CRDT- 2017/06/24 06:00
PHST- 2017/03/24 00:00 [received]
PHST- 2017/05/31 00:00 [revised]
PHST- 2017/06/07 00:00 [accepted]
PHST- 2017/06/24 06:00 [pubmed]
PHST- 2018/06/06 06:00 [medline]
PHST- 2017/06/24 06:00 [entrez]
AID - S0168-8278(17)32073-1 [pii]
AID - 10.1016/j.jhep.2017.06.003 [doi]
PST - ppublish
SO - J Hepatol. 2017 Oct;67(4):862-873. doi: 10.1016/j.jhep.2017.06.003. Epub 2017
Jun
19.
PMID- 35842345
OWN - NLM
STAT- MEDLINE
DCOM- 20220824
LR - 20230325
IS - 0016-5085 (Print)
IS - 0016-5085 (Linking)
VI - 163
IP - 3
DP - 2022 Sep
TI - AGA Clinical Practice Update: Diagnosis and Management of Nonalcoholic Fatty
Liver Disease in Lean Individuals: Expert Review.
PG - 764-774.e1
LID - S0016-5085(22)00628-X [pii]
LID - 10.1053/j.gastro.2022.06.023 [doi]
AB - DESCRIPTION: Nonalcoholic fatty liver disease (NAFLD) is well recognized as a
leading etiology for chronic liver disease, affecting >25% of the US and
global
populations. Up to 1 in 4 individuals with NAFLD have nonalcoholic
steatohepatitis, which is associated with significant morbidity and mortality
due
to complications of liver cirrhosis, hepatic decompensation, and
hepatocellular
carcinoma. Although NAFLD is observed predominantly in persons with obesity
and/or type 2 diabetes mellitus, an estimated 7%-20% of individuals with
NAFLD
have lean body habitus. Limited guidance is available to clinicians on
appropriate clinical evaluation in lean individuals with NAFLD, such as for
inherited/genetic disorders, lipodystrophy, drug-induced NAFLD, and
inflammatory
disorders. Emerging data now provide more robust evidence to define the
epidemiology, natural history, prognosis, and mortality of lean individuals
with
NAFLD. Multiple studies have found that NAFLD among lean individuals is
associated with increased cardiovascular, liver, and all-cause mortality
relative
to those without NAFLD. This American Gastroenterological Association
Clinical
Practice Update provides Best Practice Advice to assist clinicians in
evidence-based approaches to the diagnosis, staging, and management of NAFLD
in
lean individuals. METHODS: This expert review was commissioned and approved
by
the American Gastroenterological Association (AGA) Institute Clinical
Practice
Updates Committee and the AGA Governing Board to provide timely guidance on a
topic of high clinical importance to the AGA membership and underwent
internal
peer review by the Clinical Practice Updates Committee and external peer
review
through standard procedures of Gastroenterology. Best Practice Advice
Statements
BEST PRACTICE ADVICE 1: Lean NAFLD should be diagnosed in individuals with
NAFLD
and body mass index <25 kg/m(2) (non-Asian race) or body mass index <23
kg/m(2)
(Asian race). BEST PRACTICE ADVICE 2: Lean individuals with NAFLD should be
evaluated routinely for comorbid conditions, such as type 2 diabetes
mellitus,
dyslipidemia, and hypertension. BEST PRACTICE ADVICE 3: Lean individuals with
NAFLD should be risk stratified for hepatic fibrosis to identify those with
advanced fibrosis or cirrhosis. BEST PRACTICE ADVICE 4: Lean individuals in
the
general population should not undergo routine screening for NAFLD; however,
screening should be considered for individuals older than 40 years with type
2
diabetes mellitus. BEST PRACTICE ADVICE 5: NAFLD should be considered in lean
individuals with metabolic diseases (such as type 2 diabetes mellitus,
dyslipidemia, and hypertension), elevated liver biochemical tests, or
incidentally noted hepatic steatosis. BEST PRACTICE ADVICE 6: Clinicians
should
query patients routinely regarding alcohol consumption patterns in all
patients
with lean NAFLD. BEST PRACTICE ADVICE 7: In patients with lean NAFLD, other
causes of liver disease should be ruled out, including other causes of fatty
liver, such as HIV, lipodystrophy, lysosomal acid lipase deficiency, familial
hypobetalipoproteinemia, and medication-induced hepatic steatosis
(methotrexate,
amiodarone, tamoxifen, and steroids). BEST PRACTICE ADVICE 8: Current
evidence is
inadequate to support routine testing for genetic variants in patients with
lean
NAFLD. BEST PRACTICE ADVICE 9: Liver biopsy, as the reference standard,
should be
considered if there is uncertainty regarding contributing causes of liver
injury
and/or the stage of liver fibrosis. BEST PRACTICE ADVICE 10: Serum indices
(NAFLD
fibrosis score and Fibrosis-4 score) and imaging techniques (transient
elastography and magnetic resonance elastography) may be used as alternatives
to
liver biopsy for fibrosis staging and patient follow-up. These tests can be
performed at the time of diagnosis and repeated at intervals of 6 months to 2
years, depending on fibrosis stage and the patient's response to
intervention.
BEST PRACTICE ADVICE 11: If noninvasive tests (eg, Fibrosis-4 and NAFLD
fibrosis
score) are indeterminate, a second noninvasive test (eg, transient
elastography
or magnetic resonance elastography) should be performed to confirm the stage
and
prognosis of NAFLD. BEST PRACTICE ADVICE 12: In lean patients with NAFLD,
lifestyle intervention, including exercise, diet modification, and avoidance
of
fructose- and sugar-sweetened drinks, to target a modest weight loss of 3%-5%
is
suggested. BEST PRACTICE ADVICE 13: Administration of vitamin E may be
considered
in lean persons with biopsy-confirmed nonalcoholic steatohepatitis, but
without
type 2 diabetes mellitus or cirrhosis. Oral pioglitazone 30 mg daily may be
considered in lean persons with biopsy-confirmed nonalcoholic steatohepatitis
without cirrhosis. BEST PRACTICE ADVICE 14: The therapeutic role of glucagon-
like
peptide-1 agonists and sodium-glucose cotransporter-2 inhibitors in the
management of lean NAFLD is not fully defined and requires further
investigation.
BEST PRACTICE ADVICE 15: Hepatocellular carcinoma surveillance with abdominal
ultrasound with or without serum α-fetoprotein twice per year is suggested in
patients with lean NAFLD and clinical markers compatible with liver
cirrhosis.
CI - Copyright © 2022 AGA Institute. Published by Elsevier Inc. All rights
reserved.
FAU - Long, Michelle T
AU - Long MT
AD - Section of Gastroenterology, Boston Medical Center, Boston University School
of
Medicine, Boston, Massachusetts. Electronic address: [email protected].
FAU - Noureddin, Mazen
AU - Noureddin M
AD - Fatty Liver Program, Karsh Division of Gastroenterology and Hepatology,
Cedars
Sinai Medical Center, Los Angeles, California.
FAU - Lim, Joseph K
AU - Lim JK
AD - Section of Digestive Diseases and Yale Liver Center, Yale University School
of
Medicine, New Haven, Connecticut.
LA - eng
GR - K23 DK113252/DK/NIDDK NIH HHS/United States
GR - UL1 TR001430/TR/NCATS NIH HHS/United States
GR - UL1 TR001863/TR/NCATS NIH HHS/United States
PT - Practice Guideline
PT - Research Support, N.I.H., Extramural
DEP - 20220714
PL - United States
TA - Gastroenterology
JT - Gastroenterology
JID - 0374630
SB - IM
CIN - Gastroenterology. 2023 Mar;164(3):502-503. PMID: 35961379
MH - Humans
MH - *Non-alcoholic Fatty Liver Disease/diagnosis/therapy
MH - *Thinness/epidemiology
PMC - PMC9398982
MID - NIHMS1815846
COIS- Conflicts of Interest: MTL is on the advisory board for Novo Nordisk and
receives
research grant support from Echosens Corporation and Gilead Sciences. MN has
been
on the advisory board/consultant for 89BIO, Altimmune, Gilead, cohBar,
Cytodyn,
Intercept, Pfizer, Novo Nordisk, Blade, EchoSens, Fractyl, Madrgial,
NorthSea,
Prespecturm, Terns, Siemens and Roche diagnostic; MN has received research
support from Allergan, BMS, Gilead, Galmed, Galectin, Genfit, Conatus,
Enanta,
Madrigal, Novartis, Pfizer, Shire, Viking and Zydus; MN is a shareholder or
has
stocks in Anaetos, Chrownwell, Ciema, Rivus Pharma and Viking. JKL has
received
research contracts (to Yale University) from Allergan, Celgene, Genfit,
Gilead,
Intercept, Pfizer, and Viking.
EDAT- 2022/07/17 06:00
MHDA- 2022/08/25 06:00
PMCR- 2023/09/01
CRDT- 2022/07/16 22:03
PHST- 2022/05/16 00:00 [received]
PHST- 2022/05/31 00:00 [revised]
PHST- 2022/06/02 00:00 [accepted]
PHST- 2023/09/01 00:00 [pmc-release]
PHST- 2022/07/17 06:00 [pubmed]
PHST- 2022/08/25 06:00 [medline]
PHST- 2022/07/16 22:03 [entrez]
AID - S0016-5085(22)00628-X [pii]
AID - 10.1053/j.gastro.2022.06.023 [doi]
PST - ppublish
SO - Gastroenterology. 2022 Sep;163(3):764-774.e1. doi:
10.1053/j.gastro.2022.06.023.
Epub 2022 Jul 14.
PMID- 33217052
OWN - NLM
STAT- MEDLINE
DCOM- 20211101
LR - 20211101
IS - 0815-9319 (Linking)
VI - 36
IP - 6
DP - 2021 Jun
TI - A review of non-alcoholic fatty liver disease in non-obese and lean
individuals.
PG - 1497-1507
LID - 10.1111/jgh.15353 [doi]
AB - Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of
hepatic disorders. It represents a wide range of chronic liver diseases in
patients with no history of significant alcohol consumption, starting with
simple
steatosis and progressing towards non-alcoholic steatohepatitis, cirrhosis,
and
ultimately hepatocellular carcinoma. NAFLD is usually associated with type 2
diabetes mellitus, dyslipidemia, metabolic syndrome, and obesity. This
disease
has mostly been studied in obese individuals; however, it has been widely
reported and studied among the lean/non-obese population in recent years. The
pathogenesis of NAFLD in non-obese patients is associated with various
genetic
predispositions, particularly a patatin-like phospholipase domain-containing
protein 3 G allele polymorphism, which results in the accumulation of
triglyceride in the liver and resistance to insulin. Additionally, dietary
factors such as high fructose consumption seem to play a substantial role in
the
pathology of non-obese NAFLD. Although there is not enough evidence on the
treatment of NAFLD in non-obese patients, the standard approach is to advise
altering one's lifestyle in order to diminish visceral adiposity. Dietary
modification, weight loss, and increased physical activity are highly
recommended. We aimed to review and summarize the existing information on the
prevalence, pathogenesis, genetic predispositions, diagnosis, and treatment
of
NAFLD in non-obese patients according to the latest literature.
CI - © 2020 Journal of Gastroenterology and Hepatology Foundation and John Wiley &
Sons Australia, Ltd.
FAU - Ahadi, Mitra
AU - Ahadi M
AD - Department of Gastroenterology and Hepatology, Mashhad University of Medical
Sciences, Mashhad, Iran.
FAU - Molooghi, Kasra
AU - Molooghi K
AUID- ORCID: 0000-0002-0761-7092
AD - School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
FAU - Masoudifar, Negin
AU - Masoudifar N
AUID- ORCID: 0000-0002-7258-2981
AD - School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
FAU - Namdar, Ali Beheshti
AU - Namdar AB
FAU - Vossoughinia, Hassan
AU - Vossoughinia H
FAU - Farzanehfar, Mohammadreza
AU - Farzanehfar M
LA - eng
PT - Review
DEP - 20201215
PL - Australia
TA - J Gastroenterol Hepatol
JT - Journal of gastroenterology and hepatology
JID - 8607909
RN - 0 (Membrane Proteins)
RN - 0 (Triglycerides)
RN - EC 3.1.1.3 (Lipase)
RN - EC 3.1.1.3 (adiponutrin, human)
SB - IM
MH - Adiposity
MH - Alleles
MH - Diet, Healthy
MH - Exercise
MH - Female
MH - Healthy Lifestyle
MH - Humans
MH - Insulin Resistance
MH - Intra-Abdominal Fat
MH - Lipase/genetics
MH - Liver/metabolism
MH - Male
MH - Membrane Proteins/genetics
MH - Non-alcoholic Fatty Liver Disease/epidemiology/*etiology/genetics/prevention
&
control
MH - Polymorphism, Genetic
MH - Prevalence
MH - *Thinness
MH - Triglycerides/metabolism
OTO - NOTNLM
OT - body mass index
OT - fatty liver
OT - lean
OT - non-alcoholic fatty liver disease
OT - obesity
EDAT- 2020/11/21 06:00
MHDA- 2021/11/03 06:00
CRDT- 2020/11/20 17:17
PHST- 2020/10/26 00:00 [revised]
PHST- 2020/06/07 00:00 [received]
PHST- 2020/11/10 00:00 [accepted]
PHST- 2020/11/21 06:00 [pubmed]
PHST- 2021/11/03 06:00 [medline]
PHST- 2020/11/20 17:17 [entrez]
AID - 10.1111/jgh.15353 [doi]
PST - ppublish
SO - J Gastroenterol Hepatol. 2021 Jun;36(6):1497-1507. doi: 10.1111/jgh.15353.
Epub
2020 Dec 15.
PMID- 30454647
OWN - NLM
STAT- MEDLINE
DCOM- 20190827
LR - 20211006
IS - 0092-8674 (Print)
IS - 0092-8674 (Linking)
VI - 175
IP - 5
DP - 2018 Nov 15
TI - Obesity Drives STAT-1-Dependent NASH and STAT-3-Dependent HCC.
PG - 1289-1306.e20
LID - S0092-8674(18)31304-7 [pii]
LID - 10.1016/j.cell.2018.09.053 [doi]
AB - Obesity is a major driver of cancer, especially hepatocellular carcinoma
(HCC).
The prevailing view is that non-alcoholic steatohepatitis (NASH) and fibrosis
or
cirrhosis are required for HCC in obesity. Here, we report that NASH and
fibrosis
and HCC in obesity can be dissociated. We show that the oxidative hepatic
environment in obesity inactivates the STAT-1 and STAT-3 phosphatase T cell
protein tyrosine phosphatase (TCPTP) and increases STAT-1 and STAT-3
signaling.
TCPTP deletion in hepatocytes promoted T cell recruitment and ensuing NASH
and
fibrosis as well as HCC in obese C57BL/6 mice that normally do not develop
NASH
and fibrosis or HCC. Attenuating the enhanced STAT-1 signaling prevented
T cell
recruitment and NASH and fibrosis but did not prevent HCC. By contrast,
correcting STAT-3 signaling prevented HCC without affecting NASH and
fibrosis.
TCPTP-deletion in hepatocytes also markedly accelerated HCC in mice treated
with
a chemical carcinogen that promotes HCC without NASH and fibrosis. Our
studies
reveal how obesity-associated hepatic oxidative stress can independently
contribute to the pathogenesis of NASH, fibrosis, and HCC.
CI - Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.
FAU - Grohmann, Marcus
AU - Grohmann M
AD - Monash Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800,
Australia; Department of Biochemistry and Molecular Biology, Monash
University,
Clayton, VIC 3800, Australia.
FAU - Wiede, Florian
AU - Wiede F
Australia; Peter MacCallum Cancer Centre, Melbourne, VIC 3000, Australia;
Department of Biochemistry and Molecular Biology, Monash University, Clayton,
VIC
3800, Australia.
FAU - Dodd, Garron T
AU - Dodd GT
University,
FAU - Gurzov, Esteban N
AU - Gurzov EN
Australia.
FAU - Ooi, Geraldine J
AU - Ooi GJ
AD - Monash University Department of Surgery, Alfred Hospital, Melbourne, VIC
3004,
Australia.
FAU - Butt, Tariq
AU - Butt T
University,
FAU - Rasmiena, Aliki A
AU - Rasmiena AA
AD - Peter MacCallum Cancer Centre, Melbourne, VIC 3000, Australia.
FAU - Kaur, Supreet
AU - Kaur S
University,
FAU - Gulati, Twishi
AU - Gulati T
FAU - Goh, Pei K
AU - Goh PK
Australia; Peter MacCallum Cancer Centre, Melbourne, VIC 3000, Australia;
Department of Biochemistry and Molecular Biology, Monash University, Clayton,
VIC
3800, Australia.
FAU - Treloar, Aislinn E
AU - Treloar AE
FAU - Archer, Stuart
AU - Archer S
Australia; Monash Bioinformations Platform, Monash University, Clayton, VIC
3800,
Australia.
FAU - Brown, Wendy A
AU - Brown WA
AD - Monash University Department of Surgery, Alfred Hospital, Melbourne, VIC
3004,
Australia.
FAU - Muller, Mathias
AU - Muller M
AD - Institute of Animal Breeding and Genetics, University of Veterinary Medicine
Vienna, Vienna, Austria.
FAU - Watt, Matthew J
AU - Watt MJ
Australia.
FAU - Ohara, Osamu
AU - Ohara O
AD - RIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa 230-0045,
Japan; Kazusa DNA Research Institute Kisarazu, Chiba 292-0818, Japan.
FAU - McLean, Catriona A
AU - McLean CA
AD - Anatomical Pathology, Alfred Hospital, Prahran, VIC 3004, Australia.
FAU - Tiganis, Tony
AU - Tiganis T
Australia; Peter MacCallum Cancer Centre, Melbourne, VIC 3000, Australia.
LA - eng
GR - 12-1172/AICR_/Worldwide Cancer Research/United Kingdom
DEP - 20181025
PL - United States
TA - Cell
JT - Cell
JID - 0413066
RN - 0 (STAT1 Transcription Factor)
RN - 0 (STAT3 Transcription Factor)
RN - EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 2)
SB - IM
CIN - Nat Rev Endocrinol. 2018 Dec;15(1):2. PMID: 30425341
CIN - Nat Rev Gastroenterol Hepatol. 2018 Dec;15(12):718. PMID: 30429585
CIN - Nat Rev Cancer. 2019 Jan;19(1):5. PMID: 30451985
CIN - Cell Metab. 2019 Jan 8;29(1):3-4. PMID: 30625307
CIN - Hepatobiliary Surg Nutr. 2019 Aug;8(4):395-397. PMID: 31489312
CIN - Hepatobiliary Surg Nutr. 2019 Aug;8(4):407-410. PMID: 31489316
CIN - Hepatobiliary Surg Nutr. 2020 Feb;9(1):73-76. PMID: 32140483
CIN - Hepatobiliary Surg Nutr. 2020 Feb;9(1):106-108. PMID: 32140493
MH - Animals
MH - CD8-Positive T-Lymphocytes/immunology/metabolism
MH - Carcinoma, Hepatocellular/metabolism/*pathology
MH - Diet, High-Fat
MH - Disease Models, Animal
MH - Hepatocytes/metabolism
MH - Humans
MH - Liver/metabolism/pathology
MH - Liver Cirrhosis/metabolism/pathology
MH - Liver Neoplasms/metabolism/*pathology
MH - Mice
MH - Mice, Inbred C57BL
MH - Mice, Knockout
MH - Non-alcoholic Fatty Liver Disease/metabolism/*pathology
MH - Obesity/metabolism/*pathology
MH - Oxidative Stress
MH - Protein Tyrosine Phosphatase, Non-Receptor Type
2/deficiency/genetics/metabolism
MH - STAT1 Transcription Factor/*metabolism
MH - STAT3 Transcription Factor/*metabolism
MH - Signal Transduction
PMC - PMC6242467
OTO - NOTNLM
OT - PTPN2
OT - STAT-1
OT - STAT-3
OT - T cells
OT - fibrosis
OT - hepatocellular carcinoma
OT - non-alcoholic steatohepatitis
OT - nonalcoholic fatty liver disease
OT - obesity
OT - oxidative stress
OT - protein tyrosine phosphatase
EDAT- 2018/11/21 06:00
MHDA- 2019/08/28 06:00
CRDT- 2018/11/21 06:00
PHST- 2018/07/05 00:00 [received]
PHST- 2018/08/20 00:00 [revised]
PHST- 2018/09/26 00:00 [accepted]
PHST- 2018/11/21 06:00 [entrez]
PHST- 2018/11/21 06:00 [pubmed]
PHST- 2019/08/28 06:00 [medline]
AID - S0092-8674(18)31304-7 [pii]
AID - 10.1016/j.cell.2018.09.053 [doi]
PST - ppublish
SO - Cell. 2018 Nov 15;175(5):1289-1306.e20. doi: 10.1016/j.cell.2018.09.053. Epub
2018 Oct 25.
PMID- 28759385
OWN - NLM
STAT- MEDLINE
DCOM- 20170919
LR - 20220409
IS - 1470-2045 (Linking)
VI - 18
IP - 8
DP - 2017 Aug
TI - Physical activity, sedentary behaviour, diet, and cancer: an update and
emerging
new evidence.
PG - e457-e471
LID - S1470-2045(17)30411-4 [pii]
LID - 10.1016/S1470-2045(17)30411-4 [doi]
AB - The lifestyle factors of physical activity, sedentary behaviour, and diet are
increasingly being studied for their associations with cancer. Physical
activity
is inversely associated with and sedentary behaviour is positively (and
independently) associated with an increased risk of more than ten types of
cancer, including colorectal cancer (and advanced adenomas), endometrial
cancers,
and breast cancer. The most consistent dietary risk factor for premalignant
and
invasive breast cancer is alcohol, whether consumed during early or late
adult
life, even at low levels. Epidemiological studies show that the inclusion of
wholegrain, fibre, fruits, and vegetables within diets are associated with
reduced cancer risk, with diet during early life (age <8 years) having the
strongest apparent association with cancer incidence. However, randomised
controlled trials of diet-related factors have not yet shown any conclusive
associations between diet and cancer incidence. Obesity is a key contributory
factor associated with cancer risk and mortality, including in dose-response
associations in endometrial and post-menopausal breast cancer, and in degree
and
duration of fatty liver disease-related hepatocellular carcinoma. Obesity
produces an inflammatory state, characterised by macrophages clustered around
enlarged hypertrophied, dead, and dying adipocytes, forming crown-like
structures. Increased concentrations of aromatase and interleukin 6 in
inflamed
breast tissue and an increased number of macrophages, compared with healthy
tissue, are also observed in women with normal body mass index, suggesting a
metabolic obesity state. Emerging randomised controlled trials of physical
activity and dietary factors and mechanistic studies of immunity,
inflammation,
extracellular matrix mechanics, epigenetic or transcriptional regulation,
protein
translation, circadian disruption, and interactions of the multibiome with
lifestyle factors will be crucial to advance this field.
CI - Copyright © 2017 Elsevier Ltd. All rights reserved.
FAU - Kerr, Jacqueline
AU - Kerr J
AD - Moores Cancer Center, University of California, La Jolla, San Diego, CA, USA;
Department of Family Medicine and Public Health, University of California, La
Jolla, San Diego, CA, USA.
FAU - Anderson, Cheryl
AU - Anderson C
Department of Family Medicine and Public Health, University of California, La
Jolla, San Diego, CA, USA.
FAU - Lippman, Scott M
AU - Lippman SM
Department of Medicine, University of California, La Jolla, San Diego, CA,
USA.
LA - eng
PT - Review
DEP - 20170726
PL - England
TA - Lancet Oncol
JT - The Lancet. Oncology
JID - 100957246
SB - IM
CIN - Lancet Oncol. 2017 Nov;18(11):e631. PMID: 29208385
MH - Breast Neoplasms/epidemiology
MH - Colorectal Neoplasms/epidemiology
MH - *Diet
MH - *Exercise
MH - Female
MH - Health Behavior
MH - Humans
MH - Incidence
MH - Liver Neoplasms/epidemiology
MH - Male
MH - Neoplasms/*epidemiology/mortality
MH - Obesity/*epidemiology
MH - Pancreatic Neoplasms/epidemiology
MH - Prostatic Neoplasms/epidemiology
MH - Risk Factors
MH - *Sedentary Behavior
EDAT- 2017/08/02 06:00
MHDA- 2017/09/20 06:00
CRDT- 2017/08/01 06:00
PHST- 2016/12/21 00:00 [received]
PHST- 2017/04/21 00:00 [revised]
PHST- 2017/04/27 00:00 [accepted]
PHST- 2017/08/01 06:00 [entrez]
PHST- 2017/08/02 06:00 [pubmed]
PHST- 2017/09/20 06:00 [medline]
AID - S1470-2045(17)30411-4 [pii]
AID - 10.1016/S1470-2045(17)30411-4 [doi]
PST - ppublish
SO - Lancet Oncol. 2017 Aug;18(8):e457-e471. doi: 10.1016/S1470-2045(17)30411-4.
Epub
2017 Jul 26.
PMID- 36062393
OWN - NLM
STAT- MEDLINE
DCOM- 20230321
LR - 20230328
IS - 0270-9139 (Linking)
VI - 77
IP - 4
DP - 2023 Apr 1
TI - Geographical similarity and differences in the burden and genetic
predisposition
of NAFLD.
PG - 1404-1427
LID - 10.1002/hep.32774 [doi]
AB - NAFLD has become a major public health problem for more than 2 decades with a
growing prevalence in parallel with the epidemic of obesity and type 2
diabetes
(T2D). The disease burden of NAFLD differs across geographical regions and
ethnicities. Variations in prevalence of metabolic diseases, extent of
urban-rural divide, dietary habits, lifestyles, and the prevalence of NAFLD
risk
and protective alleles can contribute to such differences. The rise in NAFLD
has
led to a remarkable increase in the number of cases of cirrhosis,
hepatocellular
carcinoma, hepatic decompensation, and liver-related mortality related to
NAFLD.
Moreover, NAFLD is associated with multiple extrahepatic manifestations. Most
of
them are risk factors for the progression of liver fibrosis and thus worsen
the
prognosis of NAFLD. All these comorbidities and complications affect the
quality
of life in subjects with NAFLD. Given the huge and growing size of the
population
with NAFLD, it is expected that patients, healthcare systems, and the economy
will suffer from the ongoing burden related to NAFLD. In this review, we
examine
the disease burden of NAFLD across geographical areas and ethnicities,
together
with the distribution of some well-known genetic variants for NAFLD. We also
describe some special populations including patients with T2D, lean patients,
the
pediatric population, and patients with concomitant liver diseases. We
discuss
extrahepatic outcomes, patient-reported outcomes, and economic burden related
to
NAFLD.
CI - Copyright © 2023 American Association for the Study of Liver Diseases.
FAU - Yip, Terry Cheuk-Fung
AU - Yip TC
AUID- ORCID: 0000-0002-1819-2464
AD - Medical Data Analytics Center, Department of Medicine and Therapeutics , The
Chinese University of Hong Kong , Hong Kong.
AD - State Key Laboratory of Digestive Disease , The Chinese University of Hong
Kong ,
Hong Kong.
FAU - Vilar-Gomez, Eduardo
AU - Vilar-Gomez E
AUID- ORCID: 0000-0003-1435-4013
AD - Division of Gastroenterology and Hepatology, Department of Medicine , Indiana
University School of Medicine , Indianapolis , Indiana , USA.
FAU - Petta, Salvatore
AU - Petta S
AUID- ORCID: 0000-0002-0822-9673
AD - Section of Gastroenterology and Hepatology, Dipartimento Di Promozione Della
Salute, Materno Infantile, Medicina Interna e Specialistica Di Eccellenza
(PROMISE) , University of Palermo , Palermo , Italy.
FAU - Yilmaz, Yusuf
AU - Yilmaz Y
AD - Department of Gastroenterology, School of Medicine , Recep Tayyip Erdogan
University , Rize , Turkey.
AD - Liver Research Unit , Institute of Gastroenterology , Marmara University ,
Istanbul , Turkey.
FAU - Wong, Grace Lai-Hung
AU - Wong GL
AUID- ORCID: 0000-0002-2863-9389
Kong ,
Hong Kong.
FAU - Adams, Leon A
AU - Adams LA
AUID- ORCID: 0000-0002-3968-7909
AD - Department of Hepatology , Sir Charles Gairdner Hospital , Perth , Australia.
AD - Medical School , University of Western Australia , Perth , Australia.
FAU - de Lédinghen, Victor
AU - de Lédinghen V
AD - Hepatology Unit , Hôpital Haut Lévêque, Bordeaux University Hospital ,
Bordeaux ,
France.
AD - INSERM U1312 , Bordeaux University , Bordeaux , France.
FAU - Sookoian, Silvia
AU - Sookoian S
AUID- ORCID: 0000-0001-5929-5470
AD - School of Medicine, Institute of Medical Research A Lanari , University of
Buenos
Aires , Ciudad Autónoma de Buenos Aires , Argentina.
AD - Department of Clinical and Molecular Hepatology, Institute of Medical
Research
(IDIM) , National Scientific and Technical Research Council (CONICET),
University
of Buenos Aires , Ciudad Autónoma de Buenos Aires , Argentina.
FAU - Wong, Vincent Wai-Sun
AU - Wong VW
AUID- ORCID: 0000-0003-2215-9410
Kong ,
Hong Kong.
LA - eng
PT - Review
DEP - 20221011
PL - United States
TA - Hepatology
JT - Hepatology (Baltimore, Md.)
JID - 8302946
SB - IM
MH - Child
MH - Humans
MH - *Non-alcoholic Fatty Liver Disease/epidemiology/genetics/complications
MH - *Diabetes Mellitus, Type 2/epidemiology/genetics/complications
MH - Quality of Life
MH - Disease Progression
MH - Liver Cirrhosis/epidemiology/genetics/complications
MH - Prevalence
MH - *Liver Neoplasms/epidemiology
EDAT- 2022/09/06 06:00
MHDA- 2023/03/22 06:00
CRDT- 2022/09/05 04:32
PHST- 2022/05/15 00:00 [received]
PHST- 2022/09/01 00:00 [accepted]
PHST- 2022/09/06 06:00 [pubmed]
PHST- 2023/03/22 06:00 [medline]
PHST- 2022/09/05 04:32 [entrez]
AID - 01515467-202304000-00031 [pii]
AID - 10.1002/hep.32774 [doi]
PST - ppublish
SO - Hepatology. 2023 Apr 1;77(4):1404-1427. doi: 10.1002/hep.32774. Epub 2022 Oct
11.
PMID- 33580453
OWN - NLM
STAT- MEDLINE
DCOM- 20211027
LR - 20211027
IS - 1936-0533 (Linking)
VI - 15
IP - 2
DP - 2021 Apr
TI - The epidemiology of NAFLD and lean NAFLD in Japan: a meta-analysis with
individual and forecasting analysis, 1995-2040.
PG - 366-379
LID - 10.1007/s12072-021-10143-4 [doi]
AB - BACKGROUND: NAFLD is increasing in Asia including Japan, despite its lower
obesity rate than the West. However, NAFLD can occur in lean people, but data
are
limited. We aimed to investigate the epidemiology of NAFLD in Japan with a
focus
on lean NAFLD. METHODS: We searched PubMed, Cochrane Library, EMBASE, Web of
Science, and the Japan Medical Abstracts Society (inception to 5/15/2019) and
included 73 eligible full-text original research studies (n = 258,531). We
used
random-effects model for pooled estimates, Bayesian modeling for trend and
forecasting, contacted authors for individual patient data and analyzed
14,887
(7752 NAFLD; 7135 non-NAFLD-8 studies) patients. RESULTS: The overall NAFLD
prevalence was 25.5%, higher in males (p < 0.001), varied by regions (p <
0.001),
and increased over time (p = 0.015), but not by per-person income or gross
prefectural productivity, which increased by 0.64% per year (1983-2012) and
is
forecasted to reach 39.3% in 2030 and 44.8% in 2040. The incidence of NAFLD,
HCC,
and overall mortality were 23.5, 7.6 and 5.9 per 1000 person-years,
respectively.
Individual patient-level data showed a lean NAFLD prevalence of 20.7% among
the
NAFLD population, with lean NAFLD persons being older and with a higher all-
cause
mortality rate (8.3 vs. 5.6 per 1000 person-years for non-lean NAFLD, p =
0.02).
Older age, male sex, diabetes, and FIB-4 were independent predictors of
mortality, but not lean NAFLD. CONCLUSION: NAFLD prevalence has increased in
Japan and may affect half of the population by 2040. Lean NAFLD individuals
makeup 20% of the NAFLD population, were older, and had higher mortality.
FAU - Ito, Takanori
AU - Ito T
AD - Department of Gastroenterology and Hepatology, Nagoya University Graduate
School
of Medicine, Nagoya, Japan.
FAU - Ishigami, Masatoshi
AU - Ishigami M
School
FAU - Zou, Biyao
AU - Zou B
AD - Division of Gastroenterology and Hepatology, Department of Medicine, Stanford
University Medical Center, 780 Welch Road, CJ250K, Palo Alto, CA, 94304, USA.
FAU - Tanaka, Taku
AU - Tanaka T
School
FAU - Takahashi, Hirokazu
AU - Takahashi H
AD - Liver Center, Saga University Hospital, Saga, Japan.
AD - Division of Metabolism and Endocrinology, Faculty of Medicine, Saga
University,
Saga, Japan.
FAU - Kurosaki, Masayuki
AU - Kurosaki M
AD - Department of Gastroenterology and Hepatology, Musashino Red Cross Hospital,
Tokyo, Japan.
FAU - Maeda, Mayumi
AU - Maeda M
FAU - Thin, Khin Naing
AU - Thin KN
AD - Yangon Specialty Hospital, Yangon, Myanmar.
FAU - Tanaka, Kenichi
AU - Tanaka K
University,
Saga, Japan.
FAU - Takahashi, Yuka
AU - Takahashi Y
AD - Department of Gastroenterology and Hepatology, Musashino Red Cross Hospital,
Tokyo, Japan.
FAU - Itoh, Yoshito
AU - Itoh Y
AD - Department of Molecular Gastroenterology and Hepatology, Kyoto Prefectural
University of Medicine, Kyoto, Japan.
FAU - Oniki, Kentaro
AU - Oniki K
AD - Division of Pharmacology and Therapeutics, Graduate School of Pharmaceutical
Sciences, Kumamoto University, Kumamoto, Japan.
FAU - Seko, Yuya
AU - Seko Y
AD - Department of Molecular Gastroenterology and Hepatology, Kyoto Prefectural
University of Medicine, Kyoto, Japan.
FAU - Saruwatari, Junji
AU - Saruwatari J
AD - Division of Pharmacology and Therapeutics, Graduate School of Pharmaceutical
Sciences, Kumamoto University, Kumamoto, Japan.
FAU - Kawanaka, Miwa
AU - Kawanaka M
AD - Department of General Internal Medicine 2, Kawasaki Medical School General
Medical Center, Okayama, Japan.
FAU - Atsukawa, Masanori
AU - Atsukawa M
AD - Division of Gastroenterology and Hepatology, Nippon Medical School, Tokyo,
Japan.
FAU - Hyogo, Hideyuki
AU - Hyogo H
AD - Department of Gastroenterology and Hepatology, JA Hiroshima General Hospital,
Hiroshima, Japan.
FAU - Ono, Masafumi
AU - Ono M
AD - Department of Internal Medicine, Tokyo Women's Medical University Medical
Center
East, Tokyo, Japan.
FAU - Ogawa, Eiichi
AU - Ogawa E
AD - Department of General Internal Medicine, Kyushu University Hospital, Fukuoka,
Japan.
FAU - Barnett, Scott D
AU - Barnett SD
FAU - Stave, Christopher D
AU - Stave CD
AD - Lane Medical Library, Stanford University School of Medicine, Palo Alto, CA,
USA.
FAU - Cheung, Ramsey C
AU - Cheung RC
AD - Palo Alto Veterans Affairs Healthcare System, Palo Alto, CA, USA.
FAU - Fujishiro, Mitsuhiro
AU - Fujishiro M
School
FAU - Eguchi, Yuichiro
AU - Eguchi Y
AD - Liver Center, Saga University Hospital, Saga, Japan.
University,
Saga, Japan.
FAU - Toyoda, Hidenori
AU - Toyoda H
AD - Department of Gastroenterology and Hepatology, Ogaki Municipal Hospital,
Ogaki,
Japan.
FAU - Nguyen, Mindie H
AU - Nguyen MH
AUID- ORCID: 0000-0002-6275-4989
[email protected].
LA - eng
PT - Meta-Analysis
DEP - 20210212
PL - United States
TA - Hepatol Int
JT - Hepatology international
JID - 101304009
SB - IM
MH - Aged
MH - Bayes Theorem
MH - Carcinoma, Hepatocellular
MH - Female
MH - Humans
MH - Japan/epidemiology
MH - Liver Neoplasms
MH - Male
MH - *Non-alcoholic Fatty Liver Disease/epidemiology
MH - Prevalence
OTO - NOTNLM
OT - Body Mass Index
OT - FIB-4 Index
OT - Fatty liver
OT - Fibrosis
OT - Hepatocellular carcinoma
OT - Japanese
OT - Metabolic syndrome
OT - Nonalcoholic steatohepatitis
OT - Prognosis
OT - Systematic review
EDAT- 2021/02/14 06:00
MHDA- 2021/10/28 06:00
CRDT- 2021/02/13 05:54
PHST- 2020/12/01 00:00 [received]
PHST- 2021/01/16 00:00 [accepted]
PHST- 2021/02/14 06:00 [pubmed]
PHST- 2021/10/28 06:00 [medline]
PHST- 2021/02/13 05:54 [entrez]
AID - 10.1007/s12072-021-10143-4 [pii]
AID - 10.1007/s12072-021-10143-4 [doi]
PST - ppublish
SO - Hepatol Int. 2021 Apr;15(2):366-379. doi: 10.1007/s12072-021-10143-4. Epub
2021
Feb 12.
PMID- 30292107
OWN - NLM
STAT- MEDLINE
DCOM- 20191128
LR - 20191128
IS - 0955-2863 (Linking)
VI - 62
DP - 2018 Dec
TI - Liraglutide modulates gut microbiota and reduces NAFLD in obese mice.
PG - 143-154
LID - S0955-2863(17)31133-6 [pii]
LID - 10.1016/j.jnutbio.2018.07.009 [doi]
AB - Metabolic disorders such as insulin resistance and diabetes are associated
with
obesity and nonalcoholic fatty liver disease (NAFLD). The aggressive form of
a
fatty liver disease may progress to cirrhosis and hepatocellular carcinoma.
Furthermore, recent studies demonstrated that there is a dysbiosis in the gut
microbiota associated with early stages of metabolic disease. Therefore, the
identification and repurposing of drugs already used to treat insulin
resistance
may be an excellent option for other disorders. We evaluated the effect of
liraglutide on obesity, NAFLD and gut microbiota modulation in two different
animal models of obesity: the ob/ob mice and the high-fat diet (HFD)-fed
mice.
Liraglutide treatment induced significant weight loss in both obesity models,
showed improvements in glycemic parameters and reduced inflammatory cell
infiltration in the cecum and the liver. In ob/ob mice, the liraglutide
treatment
was able to reduce the accumulation of liver fat by 78% and reversed
steatosis in
the HFD mice. The gut microbiota analysis showed that liraglutide changed the
overall composition as well as the relative abundance of weight-relevant
phylotypes such as a reduction of Proteobacteria and an increase of
Akkermansia
muciniphila in the treated HFD group. We show that liraglutide can lead to
weight
loss and gut microbiota modulations, and is associated with an improvement of
NAFLD. Furthermore, by generating a profile of the intestinal microbiota, we
compiled a list of potential bacterial targets that may modulate metabolism
and
induce a metabolic profile that is considered normal or clinically
controlled.
CI - Copyright © 2018 Elsevier Inc. All rights reserved.
FAU - Moreira, G V
AU - Moreira GV
AD - Institute Biomedical Sciences, University of Sao Paulo-Department of
Physiology
and Biophysical.
FAU - Azevedo, F F
AU - Azevedo FF
AD - State University of Campinas-School of Nursing.
FAU - Ribeiro, L M
AU - Ribeiro LM
Physiology
and Biophysical.
FAU - Santos, A
AU - Santos A
AD - Department of Internal Medicine, State University of Campinas.
FAU - Guadagnini, D
AU - Guadagnini D
FAU - Gama, P
AU - Gama P
AD - Institute Biomedical Sciences, University of Sao Paulo-Department of Cell and
Developmental Biology.
FAU - Liberti, E A
AU - Liberti EA
AD - Institute Biomedical Sciences, University of Sao Paulo-Department of Anatomy.
FAU - Saad, Mja
AU - Saad M
FAU - Carvalho, Cro
AU - Carvalho C
Physiology
and Biophysical. Electronic address: [email protected].
LA - eng
DEP - 20180811
PL - United States
TA - J Nutr Biochem
JT - The Journal of nutritional biochemistry
JID - 9010081
RN - 839I73S42A (Liraglutide)
SB - IM
MH - Adipose Tissue/drug effects
MH - Animals
MH - Cecum/drug effects/physiopathology
MH - Diet, High-Fat/adverse effects
MH - Gastrointestinal Microbiome/*drug effects/physiology
MH - Liraglutide/*pharmacology
MH - Male
MH - Mice, Inbred C57BL
MH - Mice, Obese
MH - Non-alcoholic Fatty Liver Disease/*drug therapy/microbiology
MH - Obesity/*complications/drug therapy/etiology
OTO - NOTNLM
OT - Analog of GLP-1
OT - Gut microbiota
OT - Liraglutide
OT - NAFLD
OT - Obesity
EDAT- 2018/10/07 06:00
MHDA- 2019/11/30 06:00
CRDT- 2018/10/07 06:00
PHST- 2017/12/27 00:00 [received]
PHST- 2018/05/19 00:00 [revised]
PHST- 2018/07/26 00:00 [accepted]
PHST- 2018/10/07 06:00 [pubmed]
PHST- 2019/11/30 06:00 [medline]
PHST- 2018/10/07 06:00 [entrez]
AID - S0955-2863(17)31133-6 [pii]
AID - 10.1016/j.jnutbio.2018.07.009 [doi]
PST - ppublish
SO - J Nutr Biochem. 2018 Dec;62:143-154. doi: 10.1016/j.jnutbio.2018.07.009. Epub
2018 Aug 11.
PMID- 35332111
OWN - NLM
STAT- PubMed-not-MEDLINE
LR - 20220414
IS - 2508-6235 (Print)
IS - 2508-6235 (Linking)
VI - 31
IP - 1
DP - 2022 Mar 30
TI - Recent Epidemiology and Risk Factors of Nonalcoholic Fatty Liver Disease.
PG - 17-27
LID - 10.7570/jomes22021 [doi]
AB - Because of the global obesity epidemic, the incidence and prevalence of
nonalcoholic fatty liver disease (NAFLD) have increased worldwide, including
among Koreans. Recently, the incidence rate of NAFLD in Korea was reported to
be
45.1 per 1,000 person-years, and the prevalence as approximately 30%
depending on
the diagnostic methods used. The incidence of advanced fibrosis and
hepatocellular carcinoma, as well as all-cause and liver-related mortality in
NAFLD patients has increased substantially, imposing considerable public
health
costs in Korea. Genetic, demographic, environmental, and clinical factors are
involved in the pathogenesis of NAFLD. Some genetic variants, such as
patatin-like phospholipase domain-containing 3 (PNPLA-3) and sorting and
assembly
machinery component 50 (SAMM-50), play a major role in the occurrence of
NAFLD.
The risk of NAFLD and fibrosis increases with advancing age and in men.
Nutritional factors, inadequate exercise, and sleep duration are also
associated
with increased risk of NAFLD. Obesity is a major risk factor for NAFLD;
however,
NAFLD in lean individuals has been noted in recent studies. Insulin
resistance,
type 2 diabetes, and metabolic syndrome and its components are closely
associated
with NAFLD development and liver fibrosis with various underlying mechanisms.
Sarcopenia likely shares a common pathophysiology with NAFLD. The rapidly
increasing incidence and prevalence of NAFLD and its complications, as well
as
the associated healthcare burden, warrant early assessment of NAFLD and its
risk
factors to prevent NAFLD-related complications in high risk groups.
FAU - Huh, Youn
AU - Huh Y
AD - Department of Family Medicine, Uijeongbu Eulji Medical Center, Eulji
University
School of Medicine, Uijeongbu, Korea.
FAU - Cho, Yoon Jeong
AU - Cho YJ
AUID- ORCID: 0000-0002-0960-5976
AD - Department of Family Medicine, Daegu Catholic University School of Medicine,
Daegu, Korea.
FAU - Nam, Ga Eun
AU - Nam GE
AUID- ORCID: 0000-0002-6739-9904
AD - Department of Family Medicine, Korea University Guro Hospital, Korea
University
College of Medicine, Seoul, Korea.
LA - eng
PT - Review
PL - Korea (South)
TA - J Obes Metab Syndr
JT - Journal of obesity & metabolic syndrome
JID - 101704724
PMC - PMC8987457
OTO - NOTNLM
OT - Epidemiology
OT - Incidence
OT - Nonalcoholic fatty liver disease
OT - Prevalence
OT - Risk factor
COIS- CONFLICTS OF INTEREST Ga Eun Nam has worked as an Associate Editor of the
journal
since 2020. However, she was not involved in peer reviewer selection,
evaluation,
or the decision process for this article. There are no other potential
conflicts
of interest relevant to this article to report.
EDAT- 2022/03/26 06:00
MHDA- 2022/03/26 06:01
CRDT- 2022/03/25 05:36
PHST- 2022/03/10 00:00 [received]
PHST- 2022/03/22 00:00 [revised]
PHST- 2022/03/23 00:00 [accepted]
PHST- 2022/03/26 06:00 [pubmed]
PHST- 2022/03/26 06:01 [medline]
PHST- 2022/03/25 05:36 [entrez]
AID - jomes22021 [pii]
AID - jomes-31-1-17 [pii]
AID - 10.7570/jomes22021 [doi]
PST - ppublish
SO - J Obes Metab Syndr. 2022 Mar 30;31(1):17-27. doi: 10.7570/jomes22021.

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