ArticlePDF Available

Abstract and Figures

AIM: To review all of epidemiological aspects of non-alcoholic fatty liver disease (NAFLD) and also prevent this disease is examined. METHODS: We conducted a systematic review according to the PRISMA guidelines. All searches for writing this review is based on the papers was found in PubMed (MEDLINE), Cochrane database and Scopus in August and September 2014 for topic of NAFLD in Asia and the way of prevention of this disease, with no language limitations. All relevant articles were accessed in full text and all relevant materials was evaluated and reviewed. RESULTS: NAFLD is the most common liver disorder in worldwide, with an estimated with 20%-30% prevalence in Western countries and 2%-4% worldwide. The prevalence of NAFLD in Asia, depending on location (urban vs rural), gender, ethnicity, and age is variable between 15%-20%. According to the many studies in the world, the relationship between NAFLD, obesity, diabetes mellitus, and metabolic syndrome (MS) is quiet obvious. Prevalence of NAFLD in Asian countries seems to be lower than the Western countries but, it has increased recently due to the rise of obesity, type 2 diabetes and MS in this region. One of the main reasons for the increase in obesity, diabetes and MS in Asia is a lifestyle change and industrialization. Today, NAFLD is recognized as a major chronic liver disease in Asia. Therefore, prevention of this disease in Asian countries is very important and the best strategy for prevention and control of NAFLD is lifestyle modifications. Lifestyle modification programs are typically designed to change bad eating habits and increase physical activity that is associated with clinically significant improvements in obesity, type 2 diabetes and MS. CONCLUSION: Prevention of NAFLD is very important in Asian countries particularly in Arab countries because of high prevalence of obesity, diabetes and MS.
Content may be subject to copyright.
Sara Ashtari, Mohamad Amin Pourhoseingholi, Mohamad Reza Zali
Sara Ashtari, Mohamad Amin Pourhoseingholi, Mohamad
Reza Zali, Gastroenterology and Liver Disease Research Center,
Research Institute for Gastroenterology and Liver Diseases, Shahid
Beheshti University of Medical Science, Tehran 1985717413, Iran
Author contributions: Pourhoseingholi MA and Zali MR
designed the research; Ashtari S performed the research and
writes the paper.
Supported by Gastroenterology and Liver Disease Research
Center, Research Institute for Gastroenterology and Liver Diseases,
Shahid Beheshti University of Medical Science.
Conflict-of-interest statement: The authors have not declared
any conflicts-of-interest.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article which was
selected by an in-house editor and fully peer-reviewed by external
reviewers. It is distributed in accordance with the Creative
Commons Attribution Non Commercial (CC BY-NC 4.0) license,
which permits others to distribute, remix, adapt, build upon this
work non-commercially, and license their derivative works on
different terms, provided the original work is properly cited and
the use is non-commercial. See: http://creativecommons.org/
licenses/by-nc/4.0/
Correspondence to: Sara Ashtari, MSc, Gastroenterology
and Liver Disease Research Center, Research Institute for Gastro-
enterology and Liver Diseases, Shahid Beheshti University
of Medical Science, Tabnak St, Yaman Ave, Velenjak, Tehran
1985717413, Iran. sara_ashtari@yahoo.com
Telephone: +98-21-22432515
Fax: +98-21-22432517
Received: October 11, 2014
Peer-review started: October 13, 2014
First decision: October 28, 2014
Revised: December 3, 2014
Accepted: May 5, 2015
Article in press: May 6, 2015
Published online: July 8, 2015
Abstract
AIM: To review all of epidemiological aspects of non-
alcoholic fatty liver disease (NAFLD) and also prevent
this disease is examined.
METHODS: W e co ndu cted a syst ema tic rev iew
according to the PRISMA guidelines. All searches for
writing this review is based on the papers was found
in PubMed (MEDLINE), Cochrane database and Scopus
in August and September 2014 for topic of NAFLD in
Asia and the way of prevention of this disease, with no
language limitations. All relevant articles were accessed
in full text and all relevant materials was evaluated and
reviewed.
RESULTS: NAFLD is the most common liver disorder in
worldwide, with an estimated with 20%-30% prevalence
in Western countries and 2%-4% worldwide. The
prevalence of NAFLD in Asia, depending on location
(urban
vs
rural), gender, ethnicity, and age is variable
between 15%-20%. According to the many studies in
the world, the relationship between NAFLD, obesity,
diabetes mellitus, and metabolic syndrome (MS) is
quiet obvious. Prevalence of NAFLD in Asian countries
seems to be lower than the Western countries but, it
has increased recently due to the rise of obesity, type 2
diabetes and MS in this region. One of the main reasons
for the increase in obesity, diabetes and MS in Asia is
a lifestyle change and industrialization. Today, NAFLD
is recognized as a major chronic liver disease in Asia.
Therefore, prevention of this disease in Asian countries
is very important and the best strategy for prevention
and control of NAFLD is lifestyle modifications. Lifestyle
modification programs are typically designed to change
bad eating habits and increase physical activity that is
associated with clinically significant improvements in
obesity, type 2 diabetes and MS.
CONCLUSION: Prevention of NAFLD is very important
SYSTEMATIC REVIEWS
Submit a Manuscript: http://www.wjgnet.com/esps/
Help Desk: http://www.wjgnet.com/esps/helpdesk.aspx
DOI: 10.4254/wjh.v7.i13.1788
1788 July 8, 2015
|
Volume 7
|
Issue 13
|
WJH
|
www.wjgnet.com
World J Hepatol 2015 July 8; 7(13): 1788-1796
ISSN 1948-5182 (online)
© 2015 Baishideng Publishing Group Inc. All rights reserved.
Non-alcohol fatty liver disease in Asia: Prevention and
planning
in Asian countries particularly in Arab countries because
of high prevalence of obesity, diabetes and MS.
Key words: Non-alcoholic fatty liver disease; Metabolic
risk factors; Asian countries; Prevention
© The Author(s) 2015. Published by Baishideng Publishing
Group Inc. All rights reserved.
Core tip: Today non-alcoholic fatty liver disease (NAFLD)
is one of the main concerns of the medical world. NAFLD
is identified as a main risk factor for chronic liver disease
across the world. NAFLD is clearly linked with obesity,
type 2 diabetes and metabolic syndrome (MS). The
prevalence of NAFLD is lower in Asian countries than
Western countries but, it has increased dramatically in
recent years because of increasing rate of obesity, type
2 diabetes and MS in this region. The high prevalence of
obesity with diabetes, and MS would increase the risk of
NAFLD in recent years. So, prevention of these factors is
the key strategy to reduce the incidence of NAFLD.
Ashtari S, Pourhoseingholi MA, Zali MR. Non-alcohol fatty
liver disease in Asia: Prevention and planning. World J Hepatol
2015; 7(13): 1788-1796 Available from: URL: http://www.
wjgnet.com/1948-5182/full/v7/i13/1788.htm DOI: http://dx.doi.
org/10.4254/wjh.v7.i13.1788
INTRODUCTION
Nowadays, non-alcoholic fatty liver disease (NAFLD) is a
major health concern worldwide which is characterized
by abnormal fat accumulation in liver cells[1,2]. The
development process of NAFLD can be started from
simple steatosis (NAFLD) to non-alcoholic steatohepatitis
(NASH) and nally leads to cirrhosis and hepatocellular
carcinoma in absence excessive alcohol intake[3,4].
NAFLD is one of the main cause of chronic liver disease
in industrializes countries[5,6]. According to the American
Association for the Study of Liver Disease Guidelines[7],
liver biopsy is the gold standard for the diagnosis of
NAFLD, nevertheless ultrasonography is more commonly
used particularly in developing countries, because of
increased health risks and high expenditures associated
with liver biopsies[2]. So, the prevalence of NAFLD varies
according to the method used to diagnosis and study
population[7-9]. In generally, the prevalence of NAFLD
ranges is from 6.3% to 33% worldwide, and prevalence
of NASH is from 3% to 5% in general population[7,10].
Despite the low prevalence of NAFLD in Asian countries
(12%-24%)[11], than in Western countries (> 20%)[12], it
is identied as a main risk factor for chronic liver disorder
in all over world[13]. In Asian countries, the prevalence of
NAFLD varies in different countries, and is related to the
age, gender, locality and ethnicity[11]. NAFLD prevalence
increases with age[6], and also men (40-49 years) tend
to get NAFLD earlier than women (over 50 years)[11,14].
According to the other studies especially in South-East
region of Asia[15-18], more men than women had NAFLD.
For diagnosis of NASH, liver biopsy is required and it’s
costly especially in low-income countries so the establish
the prevalence of NASH is difficult. More than 30% of
obese patients may have NASH and 12%-25% have
brosis[2,19,20]. In predictors and diagnosis of NASH and
brosis, diabetes and insulin resistance are the two main
factors than body mass index (BMI)[21,22].
MATERIALS AND METHODS
We conducted a systematic review according to the
PRISMA guidelines. All searches for writing this review is
based on the papers was found in PubMed (MEDLINE),
Cochrane database and Scopus in August and September
2014 for topic of NAFLD in Asia and the way of prevention
of this disease, with no language limitations. All relevant
articles were accessed in full text and all relevant
materials was evaluated and reviewed. We extracted data
on epidemiology of NAFLD, Burden and prevalence of
NAFLD, risk factors characteristics association NAFLD, and
prevention of NAFLD. We analyzed the data and reported
the results in the tables and text.
RESULTS
Based on systematic reviews, defines NAFLD as a
compound disorder delineated by a set of metabolic
syndrome (MS) risk factors, usually related to obesity,
diabetes, hypertension and dyslipidemia[3,11,23,24]. Insulin
resistance is the main factor in NAFLD pathogenesis,
because of association between NAFLD and MS[11].
The presence of obesity and type 2 diabetes mellitus
(T2DM) significantly increases the risk of NAFLD[11].
Available data from previous studies indicate that the
prevalence of NAFLD likely increases 65%-70%[2,25-27]
in T2DM populations and greater than 75% and 90%
in obese people[28,29] and morbidly obese patients[30,31],
respectively. In addition, NAFLD can be increase the
risk of cardiovascular events in obese and diabetic
people[2,32].
Obesity
Obesity has doubled worldwide since 1980. In Asia also,
based on several national health surveys[33-36] prevalence
of overweight and obese subjects has increased in the
past few decades, but it varies between countries[37] [Table
1: Provides the 2010 World Health Organization (WHO);
Global status report on non-communicable disease
statistics for overweigh and obesity prevalence in Asian
countries, Data adjusted for 2008 for comparability].
The prevalence of obesity in eastern Asia (e.g., China,
Japan, South Korea and Taiwan), Southern Asia (e.g.,
Bangladesh, India, Pakistan and Sri Lanka), and South-
Eastern Asia (e.g., Malaysia, Philippines, Singapore,
Thailand and Vietnam) is quite low compared with
developed countries such as the United States[38-40]. The
1789 July 8, 2015
|
Volume 7
|
Issue 13
|
WJH
|
www.wjgnet.com
Ashtari S
et al
. NAFLD in Asia
highest rate of obesity in these regions of Asia are in
Malaysia and Thailand, where 14% and 8.8% of adults
are reported to be obese, respectively[41]. The lowest
obesity rates in these regions are in the less developed
parts of Asia: 1.1% in Bangladesh, 1.7% in Vietnam and
1.9% in India[36,41]. In contrast to these regions of Asia,
in West Asian countries (Middle East countries; e.g., Iran,
Iraq, Bahrain, Egypt, Kuwait, Saudi Arabia, Oman and
Qatar) prevalence of obesity is very high and almost is
equal with the Western developed countries. So that in
countries such as Kuwait (42%), Saudi Arabia (33.3%),
Qatar (33.2%) and Egypt (33.1%), the prevalence of
obesity is higher than United States (33%)[41]. Except in
Japan, Rates of obesity among women are twice that of
men in all Asian countries.
NAFLD prevalence is much higher estimates in
obese people[42]. Population-based survey from Iran
reported that obesity and MS are the most predictive
factors of NAFLD[43]. In addition, in the other Population-
based study conducted China, the relationship between
NAFLD and obesity have been reported so that, among
661 patients with fatty liver, 611 (92%) patients were
obese[44]. The high prevalence of obesity in the West of
Asia also increases the risk of NAFLD[11].
Diabetes mellitus
Diabetes mellitus is present as one of the biggest
public health problems of the recent century[45]. The
International diabetes federation (IDF)[46] estimated the
global burden diabetes was 382 million (comparative
prevalence: 8.3%) in 2013 and it would be likely more
than double to 592 million (comparative prevalence:
8.8%) by 2035. Approximately 175 million people
worldwide living with diabetes are unaware of their
disease[46]. According to the 6th edition of the Diabetes
Atlas in 2013[46], Saudi Arabia (24%), Kuwait (23.1%)
and Qatar (2.9%) are among the world’s top ten
countries with the highest prevalence of diabetes in
20-79 years population are in the Middle-East countries.
And also from the ten countries with the highest
number of diabetic people (20-79 years), ve countries
are located in Asia that which includes; China, India,
Indonesia, Egypt and Japan. T2DM consist 85% to 95%
in high-income countries and even higher percentage
in low and middle income countries[47]. It is one of the
major health problems in the world, and also is known
as an important risk factor for NAFLD[48,49]. T2DM
prevalence is increasing in the world[50] and also in Asian
countries the prevalence rate of it has increased during
the past three decades[51]. Increasing the T2DM in Asian
countries for the following reasons is different from the
countries because of the short time spread, and that can
be seen in a younger age group and people with much
lower BMI[37]. Many ethnic studies on Asian population
pointed out, that they have more abdominal obesity
and visceral fat (3%-5%) than other ethnic groups[52-54].
Improper accumulation of fat in abdominal and visceral
adiposity can cause to increase hepatic insulin resistance
and T2DM, which can cause an abnormal accumulation
of fat in the liver[55,56]. This rapidly-growing prevalence of
T2DM among the Asian countries is related to the rapid
economic developments, aging, urbanization, changes
in nutrition, and increases in sedentary lifestyles, and
also increases with increasing prevalence of obesity and
1790 July 8, 2015
|
Volume 7
|
Issue 13
|
WJH
|
www.wjgnet.com
Country Overweight1Obesity2
Males Females Total Males Females Total
Kuwait 78.4 79.5 78.8 37.5 49.8 42.0
Saudi Arabia 69.1 68.8 69.0 28.6 39.1 33.3
Qatar 73.1 70.2 72.3 31.3 38.1 33.2
Egypt 60.4 75.3 67.9 21.4 44.5 33.1
Bahrain 70.9 70.3 70.6 29.5 38.0 32.9
UAE 71.3 71.2 71.3 30.0 39.0 32.7
Turkey 59.7 64.1 61.9 21.7 34.0 27.8
Lebanon 66.1 57.9 61.8 25.8 29.0 27.4
Iraq 59.5 65.1 62.3 20.6 33.4 27.0
Oman 56.9 54.2 55.8 18.9 23.8 20.9
Iran 46.0 56.8 51.4 12.4 26.5 19.4
Malaysia 42.1 46.3 44.2 10.4 17.6 14.0
Thailand 26.5 37.4 32.2 5.0 12.2 8.8
South Korea 34.3 29.2 31.8 7.2 8.3 7.7
Singapore 33.9 26.4 30.2 7.0 7.1 7.1
Philippines 24.6 28.4 26.5 4.6 8.0 6.3
China 25.5 25.4 25.4 4.7 6.7 5.7
Pakistan 19.1 27.1 23.0 3.3 7.8 5.5
Japan 30.1 19.2 24.4 5.8 4.4 5.0
India 9.9 12.2 11.0 1.3 2.4 1.9
Vietnam 9.5 10.9 10.2 1.2 2.1 1.7
Bangladesh 7.4 7.8 7.6 0.9 1.3 1.1
Table 1 Prevalence of overweight and obesity in Asian countries, estimates for 2008 (%)
1Overweight: The percentage of the population aged 20 or older having a body mass index (BMI) 25
kg/m2; 2Obesity: The percentage of the population aged 20 or older having a BMI 30 kg/m2. Adapted
from World Health Organization, non-communicable diseases report[41]. UAE: United Arab Emirates.
Ashtari S
et al
. NAFLD in Asia
1791 July 8, 2015
|
Volume 7
|
Issue 13
|
WJH
|
www.wjgnet.com
kg/m2), hypertriglyceridemia ( 150 mg/dL) or high
density lipoprotein cholesterol (HDL-C) values (< 35 in
males and < 40 in females) and microalbuminuria ( 20
μg/min)[65-67]. On the other hand, in 2001, the National
Cholesterol Education Program Adult Treatment Panel
(NCEP-ATP ) published a new set of criteria of MS
that included waist circumference as define obesity
( 102 cm in males and 88 cm in females), arterial
hypertension ( 130/85 mmHg), fasting glucose(
110 mg/dL) and blood lipids as HDL-C values (< 40
mg/dL in males and < 50 mg/dL in females) and
hypertriglyceridemia ( 150 mg/dL)[68]. The NCEP-ATP
denitions differed from WHO and European Group for
the study of Insulin Resistance denitions in that insulin
resistance is not necessary for diagnostic. In 2005, the
IDF published other criteria to define the MS which
proposed abdominal obesity as the essential components
of the diagnosis of MS, abdominal obesity (Europe men:
94 cm, Europe women 80 cm and for Asian men:
90 cm, Asian women 80 cm), arterial hypertension
( 130/85 mmHg), fasting glycaemia ( 100 mg/dL),
HDL-C values (< 40 mg/dL in males and < 50 mg/dL in
females) and hypertriglyceridemia ( 150 mg/dL)[69-72].
The American Heart Association/National Heart Lung
and Blood Institute (AHA/NHLBI) published a new set of
criteria of MS that abdominal obesity is not required as
a risk factor. The denition provided by the AHA/NHLBI
of abdominal obesity with IDF guidelines was quite
different[70,73]. So, in recent years AHA/NHLBI and IDF
offered a new denition of criteria that two side agreed
that abdominal obesity is 1 of 5 criteria for identifying
MS[57,58].
Middle East region, particularly Arab speaking
countries have some of the highest rate of diabetes in
the world[59]. The prevalence of T2DM has increased
dramatically in this region over the last three decades
because of industrial development. Most of countries
in the Middle East such as Kuwait, Saudi Arabia, Qatar,
Bahrain and the United Arab Emirates are the worlds
leaders in term of T2DM prevalence[60]. In both developed
and developing countries diabetes is the main cause of
NAFLD, and also the prevalence of NAFLD is higher in
people with diabetes than in non-diabetic[61] (Table 2:
Provides the 2013 IDF statistics for diabetes prevalence
in Asian countries).
MS
MS is known as a collection of interrelated abnormalities
that increase the risk of T2DM and NAFLD[62]. According
to the available data, experimental and epidemiological
studies describe the NAFLD as the hepatic manifestation
of MS[63,64]. Today prevalence of MS is increasing and
the main risk factors associated with MS are abdominal
obesity, hypertension, dyslipdemia, insulin resistance
and glycemia intolerance[24]. Different criteria have
been introduced in recent years to detect MS. The
first criteria definition of MS was published in 1998
by WHO, according to this definition impaired glucose
tolerance, and impaired fasting glucose, T2DM or insulin
resistance are known as essential components of the
MS, along with at least two of the following parameters:
hypertension (> 140/90 mmHg), obesity (BMI = 30
Table 2 Prevalence of diabetes in Asian countries, estimates for 2013
Country Adult population
(20-79) in 1000s
Diabetes cases
(20-79) in 1000s
Diabetes national
prevalence (%)
1Diabetes comparative
prevalence (%)
Diabetes related
deaths (20-79)
Saudi Arabia 18056.84 3650.89 20.22 23.87 22113
Kuwait 2293.74 407.53 17.77 23.09 1122
Qatar 1796.42 282.53 15.73 22.87 651
Bahrain 974.96 168.66 17.30 21.84 706
UAE 7443.81 745.94 10.02 18.98 1385
Egypt 48276.39 7510.60 15.56 16.80 86478
Lebanon 3295.49 478.96 14.53 14.99 6637
Oman 2493.25 199.78 8.01 14.24 1214
Malaysia 18919.44 1913.24 10.11 10.85 24049
Singapore 4058.27 498.19 12.28 10.42 4134
Iran 52145.45 4395.93 8.43 9.94 38002
Iraq 16473.21 1226.22 7.44 9.50 17643
India 760429.73 65076.36 8.56 9.09 1065053
China 1023050.42 98407.38 9.62 9.02 1271003
Yemen 11568.55 708.12 6.12 8.45 9892
Taiwan 17605.38 1721.06 9.78 8.30 -
Afghanistan 12619.61 794.70 6.30 8.27 18864
Pakistan 99369.82 6712.70 6.76 7.90 87354
South Korea 37365.67 3323.90 8.90 7.48 30836
Philippines 54210.53 3256.21 6.01 6.86 54535
Bangladesh 92271.61 5089.04 5.52 6.31 102139
Vietnam 61387.55 3299.11 5.37 5.81 54953
Thailand 49049.75 3150.67 6.42 5.67 66943
Japan 95304.38 7203.78 7.56 5.12 64680
1All comparisons between countries should be done using the comparative prevalence, which is adjusted to the world population.
Adapted from International Diabetes Institute[46]. UAE: United Arab Emirates.
Ashtari S
et al
. NAFLD in Asia
1792 July 8, 2015
|
Volume 7
|
Issue 13
|
WJH
|
www.wjgnet.com
but is not essential for diagnosis[74] (Table 3: Provides the
criteria for clinical diagnosis of the MS).
Prevalence of MS varies and depends on the criteria
used in different denitions[75,76]. And it is increasing in
different region like Asia[77] and developing countries[78],
it has been reported 12.8% to 41.1% in different part
of the world[79]. Prevalence of MS depends on criteria
used is different for example the IDF guidelines with
a lower abdominal obesity cut-off (90 cm for men, 80
cm for women) identify a greater prevalence of MS
than the NCEP-ATP [80-83]. In 2007, the prevalence of
MS in the Iran was reported by IDF and ATP criteria
32.1% and 33.2% respectively[84]. According to 2005
version of IDF criteria, China[67], Taiwan[85,86], Hong
Kong[87], and Thailand[88] had prevalence rates ranging
between 10%-15% (in 2008). On the other hand, rates
for Koreans[89], approximately one quarter, were higher
than the Chinese and Thais. India[90] had significantly
high prevalence rates compared to the rest of Asia.
Unfortunately, no many studies have been done in the
eld of MS in Arab countries[81]. Because of increasing
prevalence of obesity and diabetes in Middle-East
countries particularly in Arab countries, increased risk of
MS is high[91,92].
The major reason for the higher rate using in
the new definition is because of focus on abdominal
obesity, which is the most common component in Arab
countries[81]. The increased prevalence of MS was shown
in both genders, whereas the increased prevalence is
higher in women in Arab populations[91,93]. And also the
other components of the MS, diabetes is more common
among the Arab population than other regions of the
world and is estimated to have increased rapidly in the
region[81,91]. Approximately 50% of patients with T2DM
also suffer from MS, whereas the risk of NAFLD in these
patients is higher more than the other persons[94].
DISCUSSION
Due to the increasing rate of NAFLD, prevention of
this is one of the most important issues of the world.
Prevention methods of NAFLD that is limited to the
prevention of risk factors, because the pathogenesis of
this disease is unknown. So prevention of the risk factors
of NAFLD such as obesity, insulin resistance, T2DM and
MS is the key strategy to reduce the incidence rate of
NAFLD in the world[95]. Today, due to drastic changes in
lifestyle and desire to in sedentary lifestyle, because of
rapid economic and social changes in many countries,
including Asian countries, prevalence of obesity, T2DM
and MS are on the rise, which are important risk factors
for NAFLD.
Hence, the key management of NAFLD is lifestyle
modifications. Lifestyle modification programs are
typically designed to change bad eating habits and
increase physical activity that is associated with clinically
significant improvements in obesity, T2DM and MS.
Many studies indicate that lifestyle modication, including
a reduction in intake of saturated fat and refined car-
bohydrates and sweetened beverages, may reduce
aminotransferases and improve hepatic steatosis[96-99].
Earlier studies suggested that reduction of body weight
by 10% can normalize liver test, but recent studies have
shown that loss of at least 3%-5% of body weight can
achieve improvement in hepatic steatosis[100,101]. Control
and reduce the incidence of insulin resistance and MS is
another important aspect of prevention and management
of NAFLD[7,14]. Early detection, appropriate treatment,
and also care programs with essential training can be
an effective step in control and reduce the incidence of
MS, insulin resistance and also cardiovascular disease
and diabetes. Not only Lifestyle changes, weight loss and
regular physical activity are essential rst steps for the
prevention and treated patients with NAFLD, but also the
prevention of metabolic risk factors, such as diabetes,
dyslipidemia, hypertension is also very important[4].
However, in addition to lifestyle changes for the treatment
of patients with NAFLD, are there specic pharmacologic
therapies such as insulin sensitizers (metformin and
thiazolidinediones)[102-105], weight loss drugs (orlistat and
sibutramine)[106], antioxidants (vitamin E)[107], and have
also considered bariatric surgery for morbidly obese
patients[4,108].
ACKNOWLEDGMENTS
This project was completely supported and funded
by Gastroenterology and Liver Diseases Research
Table 3 American Heart Association/National Heart, Lung
and Blood Institute metabolic syndrome diagnostic criteria
Measure Categorical cut points
Elevated waist circumference1Population and country specic
denition
Elevated triglycerides 150 mg/dL (1.7 mmol/L) or drug
treatment for high triglycerides (i.e.,
brates or nicotinic acid)
Low HDL-C2< 40 mg/dL (1.0 mmol/L) in males
< 50 mg/dL (1.3 mmol/L) in females
Or drug treatment for low HDL-C (i.e.,
brates or nicotinic acid)
Elevated blood pressure Systolic 130 mmHg
Diastolic 85 mmHg
Or drug treatment for hypertension
Elevated fasting glucose 100 mg/dL
Or drug treatment for elevated glucose
1Waist circumference for abdominal obesity by different organization for
each population or country specic: (1) Asian (WHO) 90 cm men or
80 cm women; (2) Japanese (Japanese obesity society) 85 cm men or
90 cm women; (3) China (Cooperative Task Force) 85 cm men or 80
cm women; (4) Mediterranean and Middle East (Arab) population (IDF)
94 cm men or 80 cm women; (5) United States (AHA/NHLBI) 102 cm
men or 88 cm women; (6) South and Central American (WHO) 90 cm
men or 80 cm women; (7) European (European Cardiovascular Societies)
102 cm men or 88 cm women; and (8) Sub-Saharan African (IDF) 94
cm men or 80 cm women; 2High density lipoprotein cholesterol indicates
high-density lipoprotein cholesterol. Adapted from Alberti et al[74]. AHA/
NHLBI: American Heart Association/National Heart, Lung and Blood
Institute; WHO: World Health Organization; IDF: International diabetes
federation.
Ashtari S
et al
. NAFLD in Asia
1793 July 8, 2015
|
Volume 7
|
Issue 13
|
WJH
|
www.wjgnet.com
Center, Research Institute for Gastroenterology and
Liver Diseases, Shahid Beheshti University of Medical
Sciences.
COMMENTS
Background
Non-alcoholic fatty liver disease (NAFLD) is a major health concern worldwide
which is characterized by abnormal fat accumulation in liver cells. Today,
NAFLD is identied as a main cause of chronic liver disease in Asia. Due to the
increasing rate of NAFLD, prevention of this is one of the most important issues
of the world. Prevention methods of NAFLD that is limited to the prevention of
risk factors, because the pathogenesis of this disease is unknown.
Research frontiers
The objective of this study was to review systematically all of aspects of NAFLD
in Asia, provides updated epidemiological data on NAFLD and its etiology and
also this study has examined the current and future possibilities of prevention of
this disease in Asian countries.
Innovations and breakthroughs
Based on systematic reviews, NAFLD is tightly linked with obesity, type 2
diabetes mellitus (T2DM) and the presence of metabolic syndrome (MS).
Because of increasing prevalence of obesity, T2DM and MS in Asian countries
particularly in Arab countries, increased risk of NAFLD is high in this region. So,
by increasing the prevalence and incidence of NAFLD in this region prevention
of this disease is very important.
Applications
Prevention of NAFLD should be considered in the Asian countries, because it is
increasingly recognized as a major chronic liver disease in these regions.
Terminology
NAFLD is characterized by abnormal fat accumulation in liver cells. The
development process of NAFLD can be started from simple steatosis (NAFLD)
to non-alcoholic steatohepatitis and nally leads to cirrhosis and hepatocellular
carcinoma, in absence excessive alcohol intake.
Peer-review
This is a well-written and comprehensive review of the epidemiology of
nonalcoholic fatty liver disease in Asia.
REFERENCES
1 Bellentani S, Scaglioni F, Marino M, Bedogni G. Epidemiology of
non-alcoholic fatty liver disease. Dig Dis 2010; 28: 155-161 [PMID:
20460905 DOI: 10.1159/000282080]
2 Conlon BA, Beasley JM, Aebersold K, Jhangiani SS, Wylie-Rosett
J. Nutritional management of insulin resistance in nonalcoholic
fatty liver disease (NAFLD). Nutrients 2013; 5: 4093-4114 [PMID:
24152749 DOI: 10.3390/nu5104093]
3 Farrell GC, Larter CZ. Nonalcoholic fatty liver disease: from
steatosis to cirrhosis. Hepatology 2006; 43: S99-S112 [PMID:
16447287 DOI: 10.1002/hep.20973]
4 Fruci B, Giuliano S, Mazza A, Malaguarnera R, Belfiore A.
Nonalcoholic Fatty liver: a possible new target for type 2 diabetes
prevention and treatment. Int J Mol Sci 2013; 14: 22933-22966
[PMID: 24264040 DOI: 10.3390/ijms141122933]
5 Suzuki A, Angulo P, Lymp J, St Sauver J, Muto A, Okada T, Lindor
K. Chronological development of elevated aminotransferases in
a nonalcoholic population. Hepatology 2005; 41: 64-71 [PMID:
15690483 DOI: 10.1002/hep.20543]
6 Hassan K, Bhalla V, El Regal ME, A-Kader HH. Nonalcoholic
fatty liver disease: a comprehensive review of a growing epidemic.
World J Gastroenterol 2014; 20: 12082-12101 [PMID: 25232245
DOI: 10.3748/wjg.v20.i34.12082]
7 Chalasani N, Younossi Z, Lavine JE, Diehl AM, Brunt EM, Cusi
K, Charlton M, Sanyal AJ. The diagnosis and management of non-
alcoholic fatty liver disease: practice Guideline by the American
Association for the Study of Liver Diseases, American College
of Gastroenterology, and the American Gastroenterological
Association. Hepatology 2012; 55: 2005-2023 [PMID: 22488764
DOI: 10.1002/hep.25762]
8 Lee JY, Kim KM, Lee SG, Yu E, Lim YS, Lee HC, Chung YH,
Lee YS, Suh DJ. Prevalence and risk factors of non-alcoholic fatty
liver disease in potential living liver donors in Korea: a review of
589 consecutive liver biopsies in a single center. J Hepatol 2007;
47: 239-244 [PMID: 17400323 DOI: 10.1016/j.jhep.2007.02.007]
9 Williams CD, Stengel J, Asike MI, Torres DM, Shaw J, Contreras
M, Landt CL, Harrison SA. Prevalence of nonalcoholic fatty liver
disease and nonalcoholic steatohepatitis among a largely middle-
aged population utilizing ultrasound and liver biopsy: a prospective
study. Gastroenterology 2011; 140: 124-131 [PMID: 20858492
DOI: 10.1053/j.gastro.2010.09.038]
10 Vernon G, Baranova A, Younossi ZM. Systematic review: the
epidemiology and natural history of non-alcoholic fatty liver
disease and non-alcoholic steatohepatitis in adults. Aliment
Pharmacol Ther 2011; 34: 274-285 [PMID: 21623852 DOI:
10.1111/j.1365-2036.2011.04724.x]
11 Fan JG, Saibara T, Chitturi S, Kim BI, Sung JJ, Chutaputti A.
What are the risk factors and settings for non-alcoholic fatty liver
disease in Asia-Pacific? J Gastroenterol Hepatol 2007; 22: 794-800
[PMID: 17498218 DOI: 10.1111/j.1440-1746.2007.04952.x]
12 Kneeman JM, Misdraji J, Corey KE. Secondary causes of
nonalcoholic fatty liver disease. Therap Adv Gastroenterol 2012; 5:
199-207 [PMID: 22570680 DOI: 10.1177/1756283x11430859]
13 Wong VW. Nonalcoholic fatty liver disease in Asia: a story
of growth. J Gastroenterol Hepatol 2013; 28: 18-23 [PMID:
23094755 DOI: 10.1111/jgh.12011]
14 Chitturi S, Farrell GC, Hashimoto E, Saibara T, Lau GK, Sollano
JD. Non-alcoholic fatty liver disease in the Asia-Pacific region:
definitions and overview of proposed guidelines. J Gastroenterol
Hepatol 2007; 22: 778-787 [PMID: 17565630 DOI: 10.1111/
j.1440-1746.2007.05001.x]
15 Park SH, Jeon WK, Kim SH, Kim HJ, Park DI, Cho YK, Sung IK,
Sohn CI, Keum DK, Kim BI. Prevalence and risk factors of non-
alcoholic fatty liver disease among Korean adults. J Gastroenterol
Hepatol 2006; 21: 138-143 [PMID: 16706825 DOI: 10.1111/
j.1440-1746.2005.04086.x]
16 Shen L, Fan JG, Shao Y, Zeng MD, Wang JR, Luo GH, Li
JQ, Chen SY. Prevalence of nonalcoholic fatty liver among
administrative officers in Shanghai: an epidemiological survey.
World J Gastroenterol 2003; 9: 1106-1110 [PMID: 12717867]
17 Chen QK, Chen HY, Huang KH, Zhong YQ, Han JA, Zhu ZH,
Zhou XD. Clinical features and risk factors of patients with fatty
liver in Guangzhou area. World J Gastroenterol 2004; 10: 899-902
[PMID: 15040041]
18 Chen CH, Huang MH, Yang JC, Nien CK, Yang CC, Yeh YH,
Yueh SK. Prevalence and risk factors of nonalcoholic fatty liver
disease in an adult population of taiwan: metabolic significance
of nonalcoholic fatty liver disease in nonobese adults. J Clin
Gastroenterol 2006; 40: 745-752 [PMID: 16940890]
19 Wong VW, Wong GL, Choi PC, Chan AW, Li MK, Chan HY,
Chim AM, Yu J, Sung JJ, Chan HL. Disease progression of non-
alcoholic fatty liver disease: a prospective study with paired liver
biopsies at 3 years. Gut 2010; 59: 969-974 [PMID: 20581244 DOI:
10.1136/gut.2009.205088]
20 Sylvester JE, Greenberg P, Selch MT, Thomas BJ, Amstutz H. The
use of postoperative irradiation for the prevention of heterotopic
bone formation after total hip replacement. Int J Radiat Oncol
Biol Phys 1988; 14: 471-476 [PMID: 3343154 DOI: 10.5009/
gnl.2012.6.2.149]
21 Huang HL, Lin WY, Lee LT, Wang HH, Lee WJ, Huang KC.
Metabolic syndrome is related to nonalcoholic steatohepatitis in
severely obese subjects. Obes Surg 2007; 17: 1457-1463 [PMID:
18219772]
22 Kang H, Greenson JK, Omo JT, Chao C, Peterman D, Anderson
L, Foess-Wood L, Sherbondy MA, Conjeevaram HS. Metabolic
syndrome is associated with greater histologic severity, higher
carbohydrate, and lower fat diet in patients with NAFLD. Am J
Gast roenterol 2006; 101: 2247-2253 [PMID: 17032189 DOI:
10.1111/j.1572-0241.2006.00719.x]
23 Williams R. Global challenges in liver disease. Hepatology 2006;
44: 521-526 [PMID: 16941687 DOI: 10.1002/hep.21347]
COMMENTS
Ashtari S
et al
. NAFLD in Asia
1794 July 8, 2015
|
Volume 7
|
Issue 13
|
WJH
|
www.wjgnet.com
24 Souza MR, Diniz Mde F, Medeiros-Filho JE, Araújo MS.
Metabolic syndrome and risk factors for non-alcoholic fatty liver
disease. Arq Gastroenterol 2012; 49: 89-96 [PMID: 22481692]
25 Targher G, Byrne CD. Clinical Review: Nonalcoholic fatty liver
disease: a novel cardiometabolic risk factor for type 2 diabetes
and its complications. J Clin Endocrinol Metab 2013; 98: 483-495
[PMID: 23293330 DOI: 10.1210/jc.2012-3093]
26 Targher G, Bertolini L, Padovani R, Rodella S, Tessari R, Zenari
L, Day C, Arcaro G. Prevalence of nonalcoholic fatty liver disease
and its association with cardiovascular disease among type 2
diabetic patients. Diabetes Care 2007; 30: 1212-1218 [PMID:
17277038 DOI: 10.2337/dc06-2247]
27 Leite NC, Salles GF, Araujo AL, Villela-Nogueira CA, Cardoso
CR. Prevalence and associated factors of non-alcoholic fatty liver
disease in patients with type-2 diabetes mellitus. Liver Int 2009; 29:
113-119 [PMID: 18384521 DOI: 10.1111/j.1478-3231.2008.01718.
x]
28 Bellentani S, Saccoccio G, Masutti F, Crocè LS, Brandi G, Sasso F,
Cristanini G, Tiribelli C. Prevalence of and risk factors for hepatic
steatosis in Northern Italy. Ann Intern Med 2000; 132: 112-117
[PMID: 10644271]
29 Luyckx FH, Desaive C, Thiry A, Dewé W, Scheen AJ, Gielen JE,
Lefèbvre PJ. Liver abnormalities in severely obese subjects: effect
of drastic weight loss after gastroplasty. Int J Obes Relat Metab
Disord 1998; 22: 222-226 [PMID: 9539189]
30 Dixon JB, Bhathal PS, O’Brien PE. Nonalcoholic fatty liver
disease: predictors of nonalcoholic steatohepatitis and liver fibrosis
in the severely obese. Gastroenterology 2001; 121: 91-100 [PMID:
11438497]
31 García-Monzón C, Martín-Pérez E, Iacono OL, Fernández-
Bermejo M, Majano PL, Apolinario A, Larrañaga E, Moreno-
Otero R. Characterization of pathogenic and prognostic factors
of nonalcoholic steatohepatitis associated with obesity. J Hepatol
2000; 33: 716-724 [PMID: 11097478]
32 Targher G, Day CP, Bonora E. Risk of cardiovascular disease in
patients with nonalcoholic fatty liver disease. N Engl J Med 2010;
363: 1341-1350 [PMID: 20879883 DOI: 10.1056/NEJMra0912063]
33 Hajian-Tilaki KO, Heidari B. Prevalence of obesity, central
obesity and the associated factors in urban population aged 20-70
years, in the north of Iran: a population-based study and regression
approach. Obes Rev 2007; 8: 3-10 [PMID: 17212790 DOI:
10.1111/j.1467-789X.2006.00235.x]
34 Haddad J, Juif JG, Speeg-Schatz C, Messer J. [Unilateral
cerebellar atrophy in 2 newborn infants. Value of MRI]. Arch Fr
Pediatr 1992; 49: 47-49 [PMID: 1550451 DOI: 10.1136/bmj.333.7
564.362]
35 Sidik SM, Rampal L. The prevalence and factors associated with
obesity among adult women in Selangor, Malaysia. Asia Pac Fam
Med 2009; 8: 2 [PMID: 19358728 DOI: 10.1186/1447-056x-8-2]
36 Prentice AM. The emerging epidemic of obesity in developing
countries. Int J Epidemiol 2006; 35: 93-99 [PMID: 16326822 DOI:
10.1093/ije/dyi272]
37 Yoon KH, Lee JH, Kim JW, Cho JH, Choi YH, Ko SH, Zimmet
P, Son HY. Epidemic obesity and type 2 diabetes in Asia.
Lancet 2006; 368: 1681-1688 [PMID: 17098087 DOI: 10.1016/
S0140-6736(06)69703-1]
38 Deurenberg-Yap M, Chew SK, Lin VF, Tan BY, van Staveren
WA, Deurenberg P. Relationships between indices of obesity and
its co-morbidities in multi-ethnic Singap ore. Int J Obes Relat
Metab Disord 2001; 25: 1554-1562 [PMID: 11673781 DOI:
10.1038/sj.ijo.0801739]
39 Kim DM, Ahn CW, Nam SY. Prevalence of obesity in Korea. Obes
Rev 2005; 6: 117-121 [PMID: 15836462 DOI: 10.1111/j.1467-
789X.2005.00173.x]
40 Aekplakorn W, Chaiyapong Y, Neal B, Chariyalertsak S,
Kunanusont C, Phoolcharoen W, Suriyawongpaisal P. Prevalence
and determinants of overweight and obesity in Thai adults: results
of the Second National Health Examination Survey. J Med Assoc
Thai 2004; 87: 685-693 [PMID: 15279350]
41 Wor ld He al th Or ga ni za ti on . Noncommunicable diseases
report, chapter 1: mortality, morbidity and risk factors. 2011.
Available fro m: URL: http://www.who.i nt/ nmh/public ations/
ncd_report_full_en.pdf
42 Wong RJ, Ahmed A. Obesity and non-alcoholic fatty liver disease:
Disparate associations among Asian populations. World J Hepatol
2014; 6: 263-273 [PMID: 24868320 DOI: 10.4254/wjh.v6.i5.263]
43 Sohrabpour A, Rezvan H, Amini-Kafiabad S, Dayhim M, Merat S,
Pourshams A. Prevalence of Nonalcoholic Steatohepatitis in Iran:
A Population based Study. Middle East J Dig Dis 2010; 2: 14-19
[PMID: 25197507]
44 Fan JG, Zhu J, Li XJ, Chen L, Li L, Dai F, Li F, Chen SY.
Prevalence of and risk factors for fatty liver in a general population
of Shanghai, China. J Hepatol 2005; 43 : 508-514 [PMID:
16006003 DOI: 10.1016/j.jhep.2005.02.042]
45 Gadsby R. Epidemiology of diabetes. Adv Drug Deliv Rev 2002;
54: 1165-1172 [PMID: 12393299]
46 Bruc e DG, Davis WA, Davis TM. Glycemic control in older
subjects with type 2 diabetes mellitus in the Fremantle Diabetes
Study. J Am Geriatr Soc 2000; 48: 1449-1453 [PMID: 11083322]
47 International Diabetes Federation. IDF Diabetes Atlas. 4th ed.
Brussels Belgium: International Diabetes Federation, 2009
48 Passa P. Diabetes trends in Europe. Diabetes Metab Res Rev 2002;
18 Suppl 3: S3-S8 [PMID: 12324978 DOI: 10.1002/dmrr.276]
49 Hussain A, Vaaler S, Sayeed MA, Mahtab H, Ali SM, Khan
AK. Type 2 diabetes and impaired fasting blood glucose in rural
Bangladesh: a population-based study. Eur J Public Health 2007;
17: 291-296 [PMID: 17008328 DOI: 10.1093/eurpub/ckl235]
50 Lusignan S, Sismanidis C, Carey IM, DeWilde S, Richards N,
Cook DG. Trends in the prevalence and management of diagnosed
type 2 diabetes 1994-2001 in England and Wales. BMC Fam Pract
2005; 6: 13 [PMID: 15784133 DOI: 10.1186/1471-2296-6-13]
51 Kim SM, Lee JS, Lee J, Na JK, Han JH, Yoon DK, Baik SH,
Choi DS, Choi KM. Prevalence of diabetes and impaired fasting
glucose in Korea: Korean National Health and Nutrition Survey
2001. Diabetes Care 2006; 29: 226-231 [PMID: 16443864 DOI:
10.2337/diacare.29.02.06.dc05-0481]
52 Ma RC, Chan JC. Type 2 diabetes in East Asians: similarities and
differences with populations in Europe and the United States. Ann
N Y Acad Sci 2013; 1281: 64-91 [PMID: 23551121 DOI: 10.1111/
nyas.12098]
53 Lear SA, Humphries KH, Kohli S, Chockalingam A, Frohlich
JJ, Birmingham CL. Visceral adipose tissue accumulation differs
according to ethnic background: results of the Multicultural
Community Health Assessment Trial (M-CHAT). Am J Clin Nutr
2007; 86: 353-359 [PMID: 17684205]
54 Deurenberg P, Deurenberg-Yap M, Guricci S. Asians are different
from Caucasians and from each other in their body mass index/
body fat per cent relationship. Obes Rev 2002; 3: 141-146 [PMID:
12164465]
55 Wong VW. Gestational diabetes mellitus in five ethnic groups: a
comparison of their clinical characteristics. Diabet Med 2012; 29:
366-371 [PMID: 21913963 DOI: 10.1111/j.1464-5491.2011.03439.
x]
56 Taylor R. Pathogenesis of type 2 diabetes: tracing the reverse route
from cure to cause. Diabetologia 2008; 51: 1781-1789 [PMID:
18726585 DOI: 10.1007/s00125-008-1116-7]
57 Al-Moosa S, Allin S, Jemiai N, Al-Lawati J, Mossialos E. Diabetes
and urbanization in the Omani population: an analysis of national
survey data. Popul Health Metr 2006; 4: 5 [PMID: 16635266 DOI:
10.1186/1478-7954-4-5]
58 Shetty P, Schmidhuber J. Introductory lecture the epidemiology
and determinants of obesity in developed and developing countries.
Int J Vitam Nutr Res 2006; 76: 157-162 [PMID: 17243077 DOI:
10.1024/0300-9831.76.4.157]
59 Alhyas L, McKay A, Balasanthiran A, Majeed A. Prevalences
of overweight, obesity, hyperglycaemia, hypertension and
dyslipidaemia in the Gulf: systematic review. JRSM Short Rep
2011; 2: 55 [PMID: 21847437 DOI: 10.1258/shorts.2011.011019]
60 Badran M, Laher I. Type II Diabetes Mellitus in Arabic-Speaking
Countries. Int J Endocrinol 2012; 2012: 902873 [PMID: 22851968
Ashtari S
et al
. NAFLD in Asia
1795 July 8, 2015
|
Volume 7
|
Issue 13
|
WJH
|
www.wjgnet.com
DOI: 10.1155/2012/902873]
61 Vikram NK, Tandon N, Misra A, Srivastava MC, Pandey RM,
Mithal A, Sharma S, Ajmani A, Madhu SV, Batra CM, Gupta N.
Correlates of Type 2 diabetes mellitus in children, adolescents and
young adults in north India: a multisite collaborative case-control
study. Diabet Med 2006; 23: 293-298 [PMID: 16492213 DOI:
10.1111/j.1464-5491.2005.01782.x]
62 Kassi E, Pervanidou P, Kaltsas G, Chrousos G. Metabolic
syndrome: definitions and controversies. BMC Med 2011; 9: 48
[PMID: 21542944 DOI: 10.1186/1741-7015-9-48]
63 Marchesini G, Brizi M, Bianchi G, Tomassetti S, Bugianesi
E, Lenzi M, McCullough AJ, Natale S, Forlani G, Melchionda
N. Nonalcoholic fatty liver disease: a feature of the metabolic
syndrome. Diabetes 2001; 50: 1844-1850 [PMID: 11473047 DOI:
10.2337/diabetes.50.8.1844]
64 Marchesini G, Marzocchi R, Agostini F, Bugianesi E. Nonalcoholic
fatty liver disea se and the meta bolic syndr ome. Curr Opin
Lipidol 2005; 16: 421-427 [PMID: 15990591 DOI: 10.1097/01.
mol.0000174153.53683.f2]
65 Alberti KG, Zimmet PZ. Definition, diagnosis and classification
of diabetes mellitus and its complications. Part 1: diagnosis and
classification of diabetes mellitus provisional report of a WHO
consultation. Diabet Med 1998; 15: 539-553 [PMID: 9686693]
66 Balkau B, Charles MA. Comment on the provisional report
from the WHO consultation. European Group for the Study of
Insulin Resistance (EGIR) Diabet Med 1999; 16: 442-443 [PMID:
10342346]
67 Gu D, Reynolds K, Wu X, Chen J, Duan X, Reynolds RF, Whelton
PK, He J. Prevalence of the metabolic syndrome and overweight
among adults in China. Lancet 2005; 365: 1398-1405 [PMID:
15836888 DOI: 10.1016/s0140-6736(05)66375-1]
68 Expert Panel on Detection, Evaluation, and Treatment of
High Blood Cholesterol in Adults. Executive Summary of The
Third Report of The National Cholesterol Education Program
(NCEP) Expert Panel on Detection, Evaluation, And Treatment
of High Blood Cholesterol In Adults (Adult Treatment Panel III).
JAMA 2001; 285: 2486-2497 [PMID: 11368702 DOI: 10.1001/
jama.285.19.2486]
69 Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH,
Franklin BA, Gordon DJ, Krauss RM, Savage PJ, Smith SC,
Spertus JA, Costa F. Diagnosis and management of the metabolic
syndrome: an American Heart Association/National Heart, Lung,
and Blood Institute Scientific Statement. Circulation 2005; 112:
2735-2752 [PMID: 16157765 DOI: 10.1161/circulationaha.105.16
9404]
70 Alberti KG, Zimmet P, Shaw J. Metabolic syndrome--a
new world-wide definition. A Consensus Statement from the
International Diabetes Federation. Diabet Med 2006; 23: 469-480
[PMID: 16681555 DOI: 10.1111/j.1464-5491.2006.01858.x]
71 Khunti K, Taub N, Webb D, Srinivasan B, Stockman J, Griffin
SJ, Simmons RK, Davies MJ. Validity of self-assessed waist
circumference in a multi-ethnic UK population. Diabet Med 2012;
29: 404-409 [PMID: 21988535 DOI: 10.1111/j.1464-5491.2011.03
478.x]
72 Hernández Mijares A, Riera Fortuny C, Martínez Triguero ML,
Morillas Ariño C, Cubells Cascales P, Morales Suárez-Varela
M. [Metabolic syndrome in patients with coronary heart disease.
Results of using different diagnostic criteria]. Rev Esp Cardiol
2004; 57: 889-893 [PMID: 15373996 DOI: 10.1016/S1885-5857(0
6)60655-5]
73 Clinical Guidelines on the Identification, Evaluation, and
Treatment of Overweight and Obesity in Adults--The Evidence
Report. National Institutes of Health. Obes Res 1998; 6 Suppl 2:
51S-209S [PMID: 9813653]
74 Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman
JI, Donato KA, Fruchart JC, James WP, Loria CM, Smith SC.
Harmonizing the metabolic syndrome: a joint interim statement of
the International Diabetes Federation Task Force on Epidemiology
and Prevention; National Heart, Lung, and Blood Institute;
American Heart Association; World Heart Federation; International
Atherosclerosis Society; and International Association for the
Study of Obesity. Circulation 2009; 120: 1640-1645 [PMID:
19805654 DOI: 10.1161/circulationaha.109.192644]
75 Cornier MA, Dabelea D, Hernandez TL, Lindstrom RC, Steig
AJ, Stob NR, Van Pelt RE, Wang H, Eckel RH. The metabolic
syndrome. Endocr Rev 2008; 29: 777-822 [PMID: 18971485 DOI:
10.1210/er.2008-0024]
76 Barbagallo M, Dominguez LJ, Galioto A, Ferlisi A, Cani C,
Malfa L, Pineo A, Busardo’ A, Paolisso G. Role of magnesium in
insulin action, diabetes and cardio-metabolic syndrome X. Mol
Aspects Med 2003; 24: 39-52 [PMID: 12537988 DOI: 10.1016/
S0098-2997(02)00090-0]
77 Pan WH, Yeh WT, Weng LC. Epidemiology of metabolic
syndrome in Asia. Asia Pac J Clin Nutr 2008; 17 Suppl 1: 37-42
[PMID: 18296297]
78 Lameira D, Lejeune S, Mourad JJ. [Metabolic syndrome:
epidemiology and its risks]. Ann Dermatol Venereol 2008; 135
Suppl 4: S249-S253 [PMID: 18466792 DOI: 10.1016/s0151-
9638(08)70543-x]
79 Ramachandran A, Snehalatha C, Satyavani K, Sivasankari S,
Vijay V. Metabolic syndrome in urban Asian Indian adults--a
population study using modified ATP III criteria. Diabetes Res
Clin Pract 2003; 60: 199-204 [PMID: 12757982 DOI: 10.1016/
S0168-8227(03)00060-3]
80 Athyros VG, Ganotakis ES, Tziomalos K, Papageorgiou AA,
Anagnostis P, Griva T, Kargiotis K, Mitsiou EK, Karagiannis A,
Mikhailidis DP. Comparison of four definitions of the metabolic
syndrome in a Greek (Mediterranean) population. Curr Med Res
Opin 2010; 26: 713-719 [PMID: 20078335 DOI: 10.1185/0300799
1003590597]
81 Harzallah F, Alberti H, Ben Khalifa F. The metabolic syndrome in
an Arab population: a first look at the new International Diabetes
Federation criteria. Diabet Med 2006; 2 3: 441-444 [PMID:
16620275 DOI: 10.1111/j.1464-5491.2006.01866.x]
82 Sharifi F, Mousavinasab SN, Saeini M, Dinmohammadi M.
Prevalence of metabolic syndrome in an adult urban population of
the west of Iran. Exp Diabetes Res 2009; 2009: 136501 [PMID:
19893638 DOI: 10.1155/2009/136501]
83 Ma WY, Li HY, Hung CS, Lin MS, Chiu FC, Lin CH, Shih SR,
Chuang LM, Wei JN. Metabolic syndrome defined by IDF and
AHA/NHLBI correlates better to carotid intima-media thickness
than that def ined by NCEP ATP II I and WHO. Diabetes Res
Clin Pract 2009; 85: 335-341 [PMID: 19608293 DOI: 10.1016/
j.diabres.2009.06.020]
84 Zabetian A, Hadaegh F, Azizi F. Prevalence of metabolic
syndrome in Iranian adult population, concordance between the
IDF with the ATPIII and the WHO definitions. Diabetes Res
Clin Pract 2007; 77: 251-257 [PMID: 17234299 DOI: 10.1016/
j.diabres.2006.12.001]
85 Chen HJ, Pan WH. Probable blind spot in the International
Diabetes Federation definition of metabolic syndrome. Obesity
(Silver Spring) 2007; 15: 1096-1100 [PMID: 17495185 DOI:
10.1038/oby.2007.633]
86 Chuang SY, Chen CH, Chou P. Prevalence of metabolic syndrome
in a large health check-up population in Taiwan. J Chin Med Assoc
2004; 67: 611-620 [PMID: 15779484]
87 Ko GT, Cockram CS, Chow CC, Yeung V, Chan WB, So WY,
Chan NN, Chan JC. High prevalence of metabolic syndrome in
Hong Kong Chinese--comparison of three diagnostic criteria.
Diabetes Res Clin Pract 2005; 69: 160-168 [PMID: 16005365
DOI: 10.1016/j.diabres.2004.11.015]
88 Lohsoonthorn V, Dhanamun B, Williams MA. Prevalence of
metabolic syndrome and its relationship to white blood cell
count in a population of Thai men and women receiving routine
health examinations. Am J Hypertens 2006; 19: 339-345 [PMID:
16580566 DOI: 10.1016/j.amjhyper.2005.10.008]
89 Kim HM, Kim DJ, Jung IH, Park C, Park J. Prevalence of
the metabolic syndrome among Korean adults using the new
International Diabetes Federation definition and the new
abdominal obesity criteria for the Korean people. Diabetes Res
Ashtari S
et al
. NAFLD in Asia
1796 July 8, 2015
|
Volume 7
|
Issue 13
|
WJH
|
www.wjgnet.com
Clin Pract 2007; 77: 99-106 [PMID: 17118477 DOI: 10.1016/j.
diabres.2006.10.009]
90 Gupta R, Deedwania PC, Gupta A, Rastogi S, Panwar RB,
Kothari K. Prevalence of metabolic syndrome in an Indian urban
population. Int J Cardiol 2004; 97: 257-261 [PMID: 15458693
DOI: 10.1016/j.ijcard.2003.11.003]
91 Al-Lawati JA, Mohammed AJ, Al-Hinai HQ, Jousilahti P. Pre-
valence of the metabolic syndrome among Omani adults. Diabetes
Care 2003; 26: 1781-1785 [PMID: 12766109 DOI: 10.2337/diacare.
26.6.1781]
92 Abdul-Rahim HF, Husseini A, Bjertness E, Giacaman R,
Gordon NH, Jervell J. The metabolic syndrome in the West Bank
population: an urban-rural comparison. Diabetes Care 2001; 24:
275-279 [PMID: 11213878 DOI: 10.2337/diacare.24.2.275]
93 Jaber LA, Brown MB, Hammad A, Zhu Q, Herman WH. The
prevalence of the metabolic syndrome among arab americans.
Diabetes Care 2004; 27: 234-238 [PMID: 14693995 DOI: 10.2337/
diacare.27.1.234]
94 Ghamar Chehreh ME, Vahedi M, Pourhoseingholi MA, Ashtari
S, Khedmat H, Amin M, Zali MR, Alavian SM. Estimation of
diagnosis and treatment costs of non-alcoholic Fatty liver disease:
a two-year observation. Hepat Mon 2013; 13: e7382 [PMID:
23914227 DOI: 10.5812/hepatmon.7382]
95 Zelber-Sagi S, Lotan R, Shlomai A, Webb M, Harrari G, Buch A,
Nitzan Kaluski D, Halpern Z, Oren R. Predictors for incidence and
remission of NAFLD in the general population during a seven-
year prospective follow-up. J Hepatol 2012; 56: 1145-1151 [PMID:
22245895 DOI: 10.1016/j.jhep.2011.12.011]
96 Sreenivasa Baba C, Alexander G, Kalyani B, Pandey R, Rastogi
S, Pandey A, Choudhuri G. Effect of exercise and dietary
modification on serum aminotransferase levels in patients with
nonalcoholic steatohepatitis. J Gastroenterol Hepatol 2006; 21:
191-198 [PMID: 16706832 DOI: 10.1111/j.1440-1746.2005.04233.
x]
97 Larson-Meyer DE, Heilbronn LK, Redman LM, Newcomer BR,
Frisard MI, Anton S, Smith SR, Alfonso A, Ravussin E. Effect of
calorie restriction with or without exercise on insulin sensitivity,
beta-cell function, fat cell size, and ectopic lipid in overweight
subjects. Diabetes Care 2006; 29: 1337-1344 [PMID: 16732018
DOI: 10.2337/dc05-2565]
98 Kantartzis K, Thamer C, Peter A, Machann J, Schick F, Schraml
C, Königsrainer A, Königsrainer I, Kröber S, Niess A, Fritsche
A, Häring HU, Stefan N. High cardiorespiratory fitness is an
independent predictor of the reduction in liver fat during a lifestyle
intervention in non-alcoholic fatty liver disease. Gut 2009; 58:
1281-1288 [PMID: 19074179 DOI: 10.1136/gut.2008.151977]
99 Kirk E, Reeds DN, Finck BN, Mayurranjan SM, Patterson BW,
Klein S. Dietary fat and carbohydrates differentially alter insulin
sensitivity during caloric restriction. Gastroenterology 2009; 136:
1552-1560 [PMID: 19208352 DOI: 10.1053/j.gastro.2009.01.048]
100 Petersen KF, Dufour S, Befroy D, Lehrke M, Hendler RE,
Shulman GI. Reversal of nonalcoholic hepatic steatosis, hepatic
insulin resistance, and hyperglycemia by moderate weight reduction
in patients with type 2 diabetes. Diabetes 2005; 54: 603-608 [PMID:
15734833 DOI: 10.2337/diabetes.54.3.603]
101 Clark JM. Weight loss as a treatment for nonalcoholic fatty liver
disease. J Clin Gastroenterol 2006; 40 Suppl 1: S39-S43 [PMID:
16540766 DOI: 10.1097/01.mcg.0000168641.31321.fa]
102 Uygun A, Kadayifci A, Isik AT, Ozgurtas T, Deveci S, Tuzun A,
Yesilova Z, Gulsen M, Dagalp K. Metformin in the treatment of
patients with non-alcoholic steatohepatitis. Aliment Pharmacol
Ther 2004; 19: 537-544 [PMID: 14987322]
103 Nair S, Diehl AM, Wiseman M, Farr GH, Perrillo RP. Metformin
in the treatment of non-alcoholic steatohepatitis: a pilot open label
trial. Aliment Pharmacol Ther 2004; 20: 23-28 [PMID: 15225167
DOI: 10.1111/j.1365-2036.2004.02025.x]
104 Ratziu V, Giral P, Jacqueminet S, Charlotte F, Hartemann-Heurtier A,
Serfaty L, Podevin P, Lacorte JM, Bernhardt C, Bruckert E, Grimaldi
A, Poynard T. Rosiglitazone for nonalcoholic steatohepatitis:
one-year results of the randomized placebo-controlled Fatty
Liver Improvement with Rosiglitazone Therapy (FLIRT) Trial.
Gastroenterology 2008; 135: 100-110 [PMID: 18503774 DOI:
10.1053/j.gastro.2008.03.078]
105 Omer Z, Cetinkalp S, Akyildiz M, Yilmaz F, Batur Y, Yilmaz C,
Akarca U. Efficacy of insulin-sensitizing agents in nonalcoholic
fatty liver disease. Eur J Gastroenterol Hepatol 2010; 22: 18-23
[PMID: 19667999 DOI: 10.1097/MEG.0b013e32832e2baf]
106 Zelber-Sagi S, Kessler A, Brazowsky E, Webb M, Lurie Y, Santo
M, Leshno M, Blendis L, Halpern Z, Oren R. A double-blind
randomized placebo-controlled trial of orlistat for the treatment of
nonalcoholic fatty liver disease. Clin Gastroenterol Hepatol 2006;
4: 639-644 [PMID: 16630771 DOI: 10.1016/j.cgh.2006.02.004]
107 Sanyal AJ, Chalasani N, Kowdley KV, McCullough A, Diehl AM,
Bass NM, Neuschwander-Tetri BA, Lavine JE, Tonascia J, Unalp
A, Van Natta M, Clark J, Brunt EM, Kleiner DE, Hoofnagle JH,
Robuck PR. Pioglitazone, vitamin E, or placebo for nonalcoholic
steatohepatitis. N Engl J Med 2010; 362: 1675-1685 [PMID:
20427778 DOI: 10.1056/NEJMoa0907929]
108 Mathurin P, Hollebecque A, Arnalsteen L, Buob D, Leteurtre E,
Caiazzo R, Pigeyre M, Verkindt H, Dharancy S, Louvet A, Romon
M, Pattou F. Prospective study of the long-term effects of bariatric
surgery on liver injury in patients without advanced disease.
Gastroenterology 2009; 137: 532-540 [PMID: 19409898 DOI:
10.1053/j.gastro.2009.04.052]
P- Reviewer: Rajeshwari K, Tziomalos K S- Editor: Tian YL
L- Editor: A E- Editor: Liu SQ
Ashtari S
et al
. NAFLD in Asia
© 2015 Baishideng Publishing Group Inc. All rights reserved.
Published by Baishideng Publishing Group Inc
8226 Regency Drive, Pleasanton, CA 94588, USA
Telephone: +1-925-223-8242
Fax: +1-925-223-8243
E-mail: bpgofce@wjgnet.com
Help Desk: http://www.wjgnet.com/esps/helpdesk.aspx
http://www.wjgnet.com
... Nonalcoholic fatty liver disease (NAFLD) is a metabolic stress-related liver disease defined as the hepatic accumulation of lipids, mainly triglyceride, in the absence of substantial alcohol consumption (<20 g/day) or other secondary causes [1,2]. An important characteristic of nonalcoholic steatosis is the accumulation of triglyceride (TG) and total cholesterol (TC) in hepatocytes. ...
Article
Full-text available
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in most parts of the world. Although there is no first-line drug approved for the treatment of NAFLD, polyene phosphatidylcholine (PPC) is used by clinicians to treat NAFLD patients. This study aimed to evaluate the efficacy of PPC on a mice model of NAFLD, and to study the PPC’s mechanism of action. The mice were fed a choline-deficient, L-amino acid-defined (CDAA) diet to induce NAFLD and were subsequently treated with PPC. The treatment effects were evaluated by the liver index, histopathological examination, and routine blood chemistry analyses. Lipidomics and metabolomics analyses of 54 samples were carried out using ultraperformance liquid chromatography (UPLC) coupled to a mass spectrometer to select for changes in metabolites associated with CDAA diet-induced NAFLD and the effects of PPC treatment. The intestinal flora of mice were extracted for gene sequencing to find differences before and after the induction of NAFLD and PPC treatment. PPC significantly improved the CDAA diet-induced NAFLD condition in mice. A total of 19 metabolites including 5 polar metabolites and 14 lipids showed marked changes. In addition, significant differences in the abundance of Lactobacillus were associated with NAFLD. We inferred that the protective therapeutic effect of PPC on the liver was related to the supplement of phosphatidylcholine, lysophosphatidylcholine, and sphingomyelin (PC, LPC, and SM, resectively) and acylcarnitine metabolism. This study developed a methodology for exploring the pathogenesis of NAFLD and can be extended to other therapeutic agents for treating NAFLD.
... The total Prevalence of NAFLD based on a Meta-analytic study from 22 countries, has been reported as 25.24 % (4). In Asia, the number of patients with NAFLD is gradually increasing (5) due to lifestyle changes (high-fat diet, low physical activity, central obesity, and type 2 diabetes mellitus), which is comparable to Western countries (6). ...
Article
Full-text available
Background/objectives There are limited data on the association between dairy products consumption and nonalcoholic fatty liver disease (NAFLD). This study was conducted to evaluate the association between total intake of different dairy products and fatty liver index (FLI), a marker of subclinical fatty liver. Methods A total of 7,540 adults were included in this population-based cohort study. Dairy products consumption was evaluated by a validated interview questionnaire for food intake frequency. The FLI was calculated using the standard formula. Liver enzyme levels, lipid profiles, glycemic profiles and demographic characteristics were recorded for all participants. Univariate and multiple logistic regression models were used to respectively assess the mean percentage difference of mean FLI and odds ratios (ORs) for subclinical NAFLD across quantiles of dairy consumption. Results The mean age of all participants was 48.81 ± 9.631 years. FLI measurements for men and women were 26.71 ± 23.39 and 39.99 ± 26.64 respectively, which was significantly higher in women ( P < 0.05). Multiple logistic regression analysis demonstrated that the amount of milk consumption was an independent preventive predictor of FLI (OR = 0.96; 95% CI: 0.94–0.99), conversely, it did not predict higher levels of liver enzymes. In term of cheese intake, participants in the third tertile of cheese intake had significantly lower FLI than lower tertiles ( P = 0.01). However, there wasn't any significant association between cheese intake and the odds of FLI in the multivariate model ( P > 0.05). We didn't find any significant association between yogurt consumption and NAFLD indicators ( P > 0.05). Conclusion Higher milk consumption was inversely associated with FLI. However, there wasn't any significant association between other types of dairy products and NAFLD indicators.
... The global prevalence of NAFLD has increased from 15% in 2005 to 25% in 2010, and it keeps increasing steadily [4] . More noticeable growth in NAFLD prevalence has been observed in Asia and Pacific countries, which might be correlated with the increasing rate of obesity, type 2 diabetes, and metabolic syndromes in this region [4,5] . ...
Article
Full-text available
Genetic factors are involved in the development, progression, and severity of NAFLD. Polymorphisms in genes regulating liver functions may increase liver susceptibility to NAFLD. Therefore, we conducted this literature study to present recent findings on NAFLD-associated polymorphisms from published articles in PubMed from 2016 to 2021. From 69 selected research articles, 20 genes and 34 SNPs were reported to be associated with NAFLD. These mutated genes affect NAFLD by promoting liver steatosis (PNPLA3, MBOAT7, TM2SF6, PTPRD, FNDC5, IL-1B, PPARGC1A, UCP2, TCF7L2, SAMM50, IL-6, AGTR1, and NNMT), inflammation (PNPLA3, TNF-α, AGTR1, IL-17A, IL-1B, PTPRD, and GATAD2A), and fibrosis (IL-1B, PNPLA3, MBOAT7, TCF7L2, GATAD2A, IL-6, NNMT, UCP, AGTR1, and TM2SF6). The identification of these genetic factors helps to better understand the pathogenesis pathways of NAFLD.
... Opisthorchiasis is caused by a food-borne trematode, Opisthorchis viverrini , which is endemic in the Lower Mekong Subregion including Thailand, Lao PDR, Cambodia, Myanmar, and sumption [10] and is a common liver disorder in developed countries (20-30%) and northeastern Thailand [11] . The incidence of NAFLD tends to be higher in people who typically consume a high fat diet or have chronic stress and reduced physical activity [12] . CKD occurs worldwide and is characterized by abnormalities in renal structure and/or function [13] . ...
Article
A combination of Opisthorchis viverrini infection and high fat/high fructose diets (HFa/HFr) intake is likely to enhance fatty-liver and kidney pathologies. Here we investigated the combined effects of chronic O. viverrini infection and HFa/HFr intake on liver and kidney pathologies, metabolism and gut microbiome in hamsters. Animals were infected with O. viverrini and fed with either standard chow (OV group) or HFa/HFr diet (OH group) and non-infected hamsters fed with either standard chow (NC) or HFa/HFr diet (HF) for 8 months. The OH group exhibited dyslipidemia and the highest severity of fatty liver. Tubular damage, inflammatory-cell infiltration and tubular fibrosis were most prominently observed in this group, supported by increased expression of KIM-1, HMGB-1 and MCP-1. Urinary ¹H NMR metabolic profiles revealed that tauro-β-muricholic acid level was increased in the OV and OH groups whereas metabolites involved in the TCA cycle and gut microbiota-related metabolites (phenylacetylglycine, trimethylamine and trimethylamine-N-oxide) were lower in OV, HF and OH groups compared to the NC group. Gut microbial profiles in the OH group were also different from other groups. In conclusion, O. viverrini infection and HFa/HFr diet induced disturbance of metabolites and gut microbiota associated with concurrent liver and kidney pathologies in hamsters.
... The prevalence of nonalcoholic fatty liver disease (NAFLD), which ranges from simple steatosis to its progressive form nonalcoholic steatohepatitis (NASH) and further fibrosis, cirrhosis, has been rising in the last decades (Gruneau et al., 2021), with 20-30% incidence rate in Western countries and 15-20% in Asia (Ashtari et al., 2015). Among obese patients, the prevalence of NAFLD/NASH even rises to as high as 80% (Younossi et al., 2019). ...
Article
Full-text available
Aim To investigate the treating effect of Yiqi-Bushen-Tiaozhi (YBT) recipe on nonalcoholic steatohepatitis (NASH) mice, determine whether the outcome was associated with gut microbiota, and clarify the regulating mechanism. Methods NASH mice were induced by high-fat and high-fructose diets (HFFD). In the fifth week, mice in the YBT group were orally administrated YBT (22.12g·kg ⁻¹ ·d ⁻¹ ) daily for 12 weeks. Fresh stool of mice was collected at the 16 th week for fecal 16S rDNA analysis. Hepatic pathology and biochemical indicators were used to reflect the improvement of YBT on hepatic inflammation and lipid metabolism in NASH mice. Quantitative real-time PCR (qRT-PCR) was used to verify the results of PICRUSt analysis. Results Results of the pathological and biochemical index showed that YBT could improve NASH mice. Compared with improving inflammation and hepatocyte damage, YBT may be more focused on enhancing metabolic disorders in mice, such as increasing HDL-c level. The diversity and richness of the gut microbiota of NASH mice induced by HFFD are significantly different from the normal control (NC) group. After YBT treatment, the diversity and richness of the mice microbiota will be increased to similar NC mice. Intestinimonas, Acetatifactor, Alistipes, Intestinimonas, Acetatifactor , and Alistipes have the most significant changes in the class level. PICRUSt analysis was performed to predict genomic functions based on the 16S rDNA results and reference sequencing. The efficacy of YBT in the treatment of NASH can be achieved by regulating the diversity and richness of gut microbiota. PICRUSt analysis results showed that the most relevant function of the microbiota construction variations is α- Linolenic acid (ALA) metabolism. Results of qRT-PCR showed significant differences between groups in the expression of Fatty acid desaturase 1 (FADS1), Fatty acid desaturase 2 (FADS2), Acyl-CoA Oxidase 1 (ACOX1), and Acyl-CoA Oxidase 2 (ACOX2) related to ALA metabolism. The expression of the above genes will be inhibited in the liver and small intestine of the HFFD group mice, and the expression can be restored after YBT treatment. Conclusion YBT could treat NASH mice by improving the diversity and richness of gut microbiota and further the improvement of ALA metabolism.
... NAFLD is now considered a burning health problem and its prevalence is increasing worldwide in epidemic proportions and is estimated to be 25% [3]. This rise in prevalence is because of the western diet, lack of exercise, a high-fat diet, and industrialization [1,4]. Based on clinical and epidemiological data, NAFLD is associated with both liver-related morbidity and mortality and increased risk of cardiovascular complications like coronary heart disease, cardiac structure and function abnormalities, aortic valve sclerosis, and arrhythmias [5]. ...
Article
Full-text available
This study aimed to assess the efficacy of Nigella Sativa supplementation in regulating various metabolic parameters in non-alcoholic fatty liver diseases (NAFLD) patients by doing a meta-analysis. Electronic databases including PubMed, Cochrane Library, Science Direct, Google Scholar, and manual search were conducted for gathering all relevant randomized controlled trials of Nigella sativa in patients with NAFLD till Dec 2019. Four randomized controlled trials (RCTs) were included in the meta-analysis. Our random effect meta-analysis estimated results showed that N.sativa intervention significantly decreased alanine transaminase (ALT; SMD: 2.09, 95% CI [0.57, 3.61]; p=0.007; I²=96%), aspartate aminotransferase (AST; SMD:1.85, 95% CI[0.50, 3.19]; p=0.007; I²=95%), low density lipoproteins (LDL-C; SMD: 0.55; 95% CI [0.06, 1.03]; p=0.03; I² =63), triglycerides (TG; SMD: 0.37, 95% CI[-0.10, 0.64]; p=0.008; I²=0%) and improved high density lipoproteins levels (HDL-C; SMD: 0.82; 95% CI[-1.52, 0.12]; p=0.02; I²=80%). Although, N.sativa did not significantly reduced the body mass index (BMI; SMD:0.16, 95% CI[-0.08, 0.40]; p=0.18; I² =2%). This systematic review and meta-analysis evidence supports that N.sativa supplementation was beneficial for the treatment of NAFLD without causing adverse effects. Further high-quality clinical studies are needed to confirm these results.
... This cross-sectional study was conducted on 228 patients with severe obesity undergoing bariatric surgery in the Obesity Center of Mother and Child Hospital in Shiraz between June 2020 and June 2021. We calculated the sample size using the prevalence of NAFLD in Asian countries (12-24%) [9] with a power of 80%. The primary outcome of the study was the prevalence of NAFLD, and the secondary outcome was the investigation of the clinical and biochemical risk factors of NAFLD among morbidly obese patients. ...
Article
Full-text available
Background and aims: Nonalcoholic fatty liver disease (NAFLD) is common in severely obese individuals undergoing bariatric surgery. Assessing the prevalence and severity of NAFLD seems crucial since it may affect the prevention or development of more severe forms of fatty liver. Methods: This cross-sectional study was conducted on 228 severely obese individuals undergoing bariatric surgery. Abdominal ultrasonography was done, and clinical and biochemical factors (liver enzymes, lipid profile, and fasting blood sugar (FBS)) were assessed. Results: The mean body mass index (BMI) was 43.45 ± 5.92 kg/m2. The prevalence of NAFLD was 49.12% (mild steatosis: 37.5%, moderate steatosis: 36.6%, and severe steatosis: 25.8%). The main risk factors of NAFLD were weight (p = 0.002), BMI (p = 0.003), alanine aminotransferase (ALT) (p < 0.001), aspartate aminotransferase (AST) (p < 0.001), serum triglycerides (TGs) (p = 0.004), and FBS (p = 0.039). The results revealed a statistically significant decrease in the mean level of high-density lipoprotein cholesterol (HDL-C) (p = 0.044). However, no significant association was found between the severity of liver steatosis and the presence of comorbidities such as hypertension, diabetes, hypothyroidism, and dyslipidemia. Conclusions: More severe NAFLD was associated with increased weight and BMI. Elevated ALT, AST, TG, and FBS levels and decreased HDL-C levels were also the risk factors of NAFLD and its progress to more severe conditions.
Article
Methods for detecting life-threatening diseases like cardiac arrest and arrhythmias are urgently required that are affordable and selective. The creation of nanocomposite based on graphene oxide, zinc oxide, polypyrrole, and polyaniline is one embodiment of the current disclosure. The nanocomposite of the present invention has highly enhanced the detection sensitivity of cholesterol and bilirubin. The dispersion of components in 1 (M) sulphuric acid is used to generate nanocomposite using the direct mixing technique. Glassy carbon electrodes are employed as the substrate material in the fabrication of nanocomposite-based biosensors. The sensor has demonstrated sensitivity of 0.92 μA μM⁻¹ cm⁻² and 0.2 μA μM⁻¹ cm⁻² for the detection of cholesterol and bilirubin, respectively. The innovative technology has enhanced lower detection limits, lower quantification limits, and good selectivity, among other things. In comparison to existing reports, the developed sensor has demonstrated greater sensitivity for the detection of cholesterol and bilirubin. As a result, the composite platform is ideal for the creation of high-sensitivity biosensors for a wide range of biomarkers.
Article
Full-text available
Objective: To determine and compare serum ferritin levels in non-alcoholic fatty liver disease (NAFLD) patients of our ethnicity. Study Design: Cross sectional comparative study. Place and Duration of Study: The study was conducted at Methodology: A total number of 43 non-alcoholic fatty liver disease patients diagnosed after ultrasonography were included in the study. An equal number of age, gender and body mass index (BMI) matched healthy controls were selected by non-probability purposive sampling. Fasting serum ferritin levels, body mass index and waist circumference were measured in both the cases and controls. Data were entered and analyzed on SPSS 21. For quantitative data median IQR was calculated. Mann Whitney U-test was used for group comparison. To find an association, Spearman"s Ranked correlation was applied. A p-value of ≤0.05 was taken as significant. Results: The non-alcoholic fatty liver disease cases had significantly higher serum ferritin (p<0.001) compared to the controls and a significant correlation between ferritin with body mass index and waist circumference in the non-alcoholic fatty liver disease subjects was recorded (p=0.04 and p=0.03 respectively). Conclusion: The non-alcoholic fatty liver disease patients have higher levels of serum ferritin as compared to the healthy controls in our ethnicity but within normal range.
Article
Full-text available
BACKGROUND Non-alcoholic fatty liver disease/steatohepatitis (NAFLD/NASH) is the most common form of chronic liver disease worldwide and is no longer considered a benign disease. Its prevalence has not been determined in a large-scale population-based study in Iran. METHODS A total of 6583 individuals aged 18 to 65 were randomly selected from three geographically distinct provinces in Iran. Blood samples were obtained from each subject and a questionnaire was completed exploring data including self-admitted regular alcohol use. Serums were tested for anti-HCV antibody (anti-HCV), hepatitis B surface antigen and anti-hepatitis B core antibody. Positive samples for anti-HCV antibody were re-tested and those positive in a repeat ELISA were confirmed by a recombinant immunoblot assay (RIBA) test. Serums were also tested for ALT levels. Subjects with elevated ALT defined as serum ALT ≥40 IU/L with no history of alcohol consumption and negative HBV and HCV infection were considered as "presumed NASH". RESULTS In this study 5589 subjects were analyzed. Two hundred and forty two individuals (4.3%) were diagnosed with elevated ALT levels. Among individuals with elevated ALT, 15 (6.2%) were diagnosed with either hepatitis B or hepatitis C. The overall weighted prevalence of presumed NASH was 2.9%. According to multivariate analysis, male sex, urban lifestyle, and being overweight or obese were significantly associated with "presumed NASH". CONCLUSION Obesity and metabolic syndrome, the most predictive factors of fatty liver disease, are increasing in Iran, therefore the prevalence of NAFLD/NASH and related complications are expected to increase in the future. This population based study gives a crude estimate of the prevalence of NASH around the country. Studies with more accurate surrogates of NASH need to be done. The disparity among different provinces merits special consideration.
Article
Background: Different criteria have been proposed for the diagnosis of the metabolic syndrome (MES). In April 2005, the International Diabetes Federation (IDF) has formulated a new worldwide definition of the metabolic syndrome in a global consensus statement built on earlier WHO, the ATPIII definitions. The aim of this study was to estimate the prevalence of this syndrome using the IDF definition among Iranian adults and to compare it with the prevalence estimated using the two other definitions. Methods: The prevalence of the MES was determined according to the three different definitions in 10368 men and women aged≥20 years participated in the cross-sectional phase of the Tehran Lipid and Glucose Study (TLGS). To assess the degree of agreement between different MES definitions, the k test was used. Results: The prevalence of MES (95% confidence interval) was 32.1% (31.2-33.0) by the IDF definition, 33.2% (32.3-34.1) by the ATPIII and 18.4% (17.6-19.2) according to the WHO definition. The sensitivity, specificity and concordance of the IDF definition for detecting MES were 91%, 89% for the ATPIII definitions and 73%, 77% for the WHO definition, respectively. The k statistics for the agreement of the IDF definition was 66.3±0.01 with the ATPIII and 39.5±0 with the WHO definition. Conclusion: In the Iranian population, the IDF definition for MES has a good concordance with the ATP III definition and a low concordance with the WHO definition.
Article
Background: Although hepatic steatosis is seen with increasing frequency in clinical practice, its prevalence and risk factors are unknown. Objective: To investigate the prevalence of and risk factors for hepatic steatosis, such as alcohol consumption and obesity. Design: Cross-sectional, observational study. Setting: Participants in the Dionysos Study. Patients: 257 participants assigned to one of four categories (67 controls, 66 obese persons, 69 heavy drinkers, and 55 obese heavy drinkers). Measurements: Ethanol intake, assessed by a validated questionnaire and expressed as daily (g/d) and lifetime (kg) consumption, and body mass, expressed as body mass index. Biochemical tests of liver and metabolic function and hepatic ultrasonography were done. Results: The prevalence of steatosis was increased in heavy drinkers (46.4% [95% Cl, 34% to 59%]) and obese persons (75.8% [CI, 63% to 85%]) compared with controls (16.4% [Cl, 8% to 25%]). Steatosis was found in 94.5% (Cl, 85% to 99%) of obese heavy drinkers. Compared with controls, the risk for steatosis was higher by 2.8-fold (Cl, 1.4-fold to 7.1-fold) in heavy drinkers, 4.6-fold (Cl, 2.5-fold to 11.0-fold) in obese persons, and 5.8-fold (Cl, 3.2-fold to 12.3-fold) in persons who were obese and drank heavily. In heavy drinkers, obesity increased the risk for steatosis by twofold (Cl, 1.5-fold to 3.0-fold) (P < 0.001), but heavy drinking was associated with only a 1.3-fold (Cl, 1.02-fold to 1.6-fold) increase in risk in obese persons (P = 0.0053). Elevated alanine aminotransferase and triglyceride levels are the most reliable markers of steatosis. Conclusions: Steatosis is frequently encountered in healthy persons and is almost always present in obese persons who drink more than 60 g of alcohol per day. Steatosis is more strongly associated with obesity than with heavy drinking, suggesting a greater role of overweight than alcohol consumption in accumulation of fat in the liver.
Article
Background/Aims: The aim of the study was to evaluate the prevalence and risk factors of biopsy-proven non-alcoholic fatty liver disease (NAFLD) in potential living liver donors and to evaluate the efficacy of imaging techniques for the detection of steatosis in donors. Methods: We reviewed the results of liver biopsy, ultrasonography (USG) and computed tomography (CT) and biochemical data performed in 589 consecutive potential liver donors as a pretransplantation work up from July 2004 to September 2005 at Asan Medical Centre. Results: Of 589 participants, 408 (69.3%) were men, with a mean age of 31.1 ± 9.5 years. NAFLD (≥5% steatosis in biopsy) was diagnosed in 303 (51.4%); >30% steatosis in 61 (10.4%) and non-alcoholic steatohepatitis in 13 (2.2%). The independent risk factors for >30% steatosis were age over 30 (OR = 2.223; p = 0.014), obesity (OR = 5.320; p < 0.001) and hypertriglyceridemia (OR = 2.253; p = 0.019) by multivariate analysis. The sensitivity of USG and CT for detecting >30% steatosis was 92.3% and 64.1%, and positive predictive value was only 34.5% and 45.1%, respectively. Conclusions: NAFLD was highly prevalent in potential living liver donors. The independent risk factors for significant steatosis were older age, obesity and hypertriglyceridemia. USG and CT had limitations in detecting significant steatosis in liver donors.
Article
Nonalcoholic fatty liver disease (NAFLD) is quickly becoming one of the most prominent causes of liver disease worldwide. The increasing incidence of NAFLD is tied to the obesity epidemic and the subsequent metabolic derangements brought along with it. Current efforts to elucidate the mechanism and causes of the disease have answered some questions, but much remains unknown about NAFLD. The aim of this article is to discuss the current knowledge regarding the pathogenesis of the disease, as well as the current and future diagnostic, preventative, and therapeutic options available to clinicians for the management of NAFLD.
Article
About 97 million adults in the United States are overweight or obese. Obesity and overweight substantially increase the risk of morbidity from hypertension; dyslipidemia; type 2 diabetes; coronary heart disease; stroke; gallbladder disease; osteoarthritis; sleep apnea and respiratory problems; and endometrial, breast, prostate, and colon cancers. Higher body weights are also associated with increases in all-cause mortality. The aim of this guideline is to provide useful advice on how to achieve weight reduction and maintenance of a lower body weight. It is also important to note that prevention of further weight gain can be a goal for some patients. Obesity is a chronic disease, and both the patient and the practitioner need to understand that successful treatment requires a life-long effort. Assessment of Weight and Body Fat Two measures important for assessing overweight and total body fat content are; determining body mass index (BMI) and measuring waist circumference. 1. Body Mass Index: The BMI, which describes relative weight for height, is significantly correlated with total body fat content. The BMI should be used to assess overweight and obesity and to monitor changes in body weight. Measurements of body weight alone can be used to determine efficacy of weight loss therapy. BMI is calculated as weight (kg)/height squared (m 2). To estimate BMI using pounds and inches, use: [weight (pounds)/height (inches) 2 ] x 703. Weight classifications by BMI, selected for use in this report, are shown in the table below. • Pregnant women who, on the basis of their pre-pregnant weight, would be classified as obese may encounter certain obstetrical risks. However, the inappropriateness of weight reduction during pregnancy is well recognized (Thomas, 1995). Hence, this guideline specifically excludes pregnant women. Source (adapted from): Preventing and Managing the Global Epidemic of Obesity. Report of the World Health Organization Consultation of Obesity. WHO, Geneva, June 1997.
Article
Obesity is a global epidemic contributing to an increasing prevalence of obesity-related systemic disorders, including nonalcoholic fatty liver disease. The rising prevalence of nonalcoholic steatohepatitis (NASH) will in the near future lead to end-stage liver disease in a large cohort of patients with NASH-related cirrhosis and NASH is predicted to be a leading indication for liver transplantation in the coming decade. However, the prevalence of obesity and the progression of hepatic histological damage associated with NASH exhibit significant ethnic disparities. Despite a significantly lower body mass index and lower rates of obesity compared to other ethnic groups, Asians continue to demonstrate a significant prevalence of hypertension, diabetes, metabolic syndrome and NASH. Ethnic disparities in central adiposity and visceral fat distribution have been hypothesized to contribute to these ethnic disparities. The current review focuses on the epidemiology of obesity and NASH among Asian populations.