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74 Original article
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Aerobic exercises versus low-caloric diet for mild fatty
liverpatients with central obesityHany F.E.M. Elsisia, Fatma M.M.
Abdeen Sallamaa, Awny F. Rahmya,Mohammed A. Sweilamb
aPhysical Therapy of Cardiovascular/
Respiratory Disorder and Geriatrics, Cairo
University, Cairo, Egypt, bDepartment of
Clinical and Chemical Pathology, Tanta
University, Tanta, Egypt
Correspondence to Fatma Mohammed
Mohammed Abdeen Sallama, BS, Faculty of
Physical Therapy, Cairo University, Egypt, 2008
Gharbia, El-Santa, El Magles El Mahaly St;
Tel: 0404470526; fax: 01014101210;
e-mail: [email protected]
Received 22 December 2016Accepted 5 June 2017
Bulletin of Faculty of Physical Therapy2017, 22:74–82
© 2018 Bulletin of Faculty of Physical Therapy | Publishe
Background and aimsExercise and weight loss are the first-line
therapy for patients with mild fatty liverwith central obesity. We
aimed to (i) summarize a moderate aerobic exerciseprogram and
low-caloric diet program and (ii) to compare the effect of
moderateaerobic exercise program versus low-caloric diet program on
liver biochemistry.The purpose of this studywas to determine the
response of liver enzymes to aerobicexercise versus low-caloric
diet in mild fatty liver patients with central obesity.Patients and
methodsThe study was carried out on 40 patients with mild fatty
liver, central obesity, andelevated liver enzymes. Their ages
ranged between 30 and 45 years; the patientswere assigned to two
groups equal in number. Group 1 received a program ofmoderate
intensity aerobic exercise on electronic treadmill (60–70% of
maximumheart rate) for 50min three times a week for 8 weeks. Group
2 followed a program oflow-caloric diet for 8 weeks. Liver enzymes,
BMI, waist circumference, and fatcontent were measured for both
groups before and after program.ResultsThe results of this study
showed that there were no significant (P>0.05)
differencesbetween the findings of both groups. However, there were
significant (P
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In addition, hepatomegaly can be found on physicalexamination
[5].
A 4-week aerobic exercise program results in asignificant
reduction in visceral adipose tissue, thuspositively affecting the
levels of circulating free fattyacids and hepatic lipid
accumulation, but appearsto be too short a time frame to reduce
insulinresistance. Unfortunately, the disruption of inflam-matory
biomarkers has been not addressed byJohnson et al. [6]. Promrat et
al. [7] were able todemonstrate this, providing evidence that
patientsundergoing consistent abdominal adipose tissue losshave
improved lobular inflammation and also reducedinsulin resistance
[8].
Obese patients are advised to achieve a gradualand sustained
weight loss through proper nutritionand exercise. For patients with
nonalcoholicsteatohepatitis who are not overweight and notdiabetic,
a low-fat diet is often recommended. It isalso recommended that
people avoid drinking alcoholas it can cause and contribute to
fatty liver disease.Patients with fatty liver disease should see
their primaryhealthcare providers on a regular basis [9].
It was reported that short-term calorie restrictiondecreases
intrahepatic TG before significant weightloss. It is clear that
weight loss from reduced calorieintake is effective in reducing
intrahepatic TG.However, similar to the overfeeding studies, it is
notclear whether this benefit is due to weight loss orongoing
negative caloric balance [10].
It was hypothesized that there may be no significantdifference
between the effects of aerobic exercises andlow-caloric diet on
fatty liver patients with centralobesity.
Patients and methodsForty patients with mild fatty liver and
central obesitybetween 30 and 45 years of age were screened
andselected randomly to be enrolled into this 8-weekblinded
randomized comparative clinical trial. Theywere recruited from
outpatient clinics of internalmedicine of El Santa Hospital to
participate in thisstudy. This study was approved by the
EthicsCommittee for Scientific Research of the Faculty ofPhysical
Therapy, Cairo University No: P.T.REC/012/00818. Instructions and
details of the studywere explained for each patient. Patients
whoaccepted to participate in the study were asked tosign a consent
form Appendix 1.
Outcome measuresBoth groups underwent an identical battery
oftests: baseline (before training) and after 8 weeks
(aftertraining). Initially, data on the participants’
characteristicswere collected in the first session, including
alanineaminotransferase (ALT) and aspartate
aminotransferase(AST)using3 cmofblood for blood
analysis.Weightwasmeasured using a standard weight scale. Height
wasmeasured with the participant standing in an erectposition
against a vertical scale. BMI and fat contentweremeasured using the
Body Stat device (Bodystat Ltd.P.O. Box 50 Douglas isle of Man IM99
1DQ British,Isles). Waist circumference (WC) was measured
usingsimple tapemeasurement fromthe level ofumbilicus.Theprimary
outcome measures in this study were ALT andAST, and the
secondaryoutcomemeasureswereBMI, fatcontent, and WC.
Sample size calculationA preliminary power analysis [power (1α
error P)=0.85, α=0.01, effect size=0.5] determined a sample sizeof
40 for this study. This effect size was chosen becauseit yielded a
realistic sample size.
Procedures of the studyInitialmedical screeningwas performed for
every patientby thephysician, diagnosedasmild fatty
liverbymeansofabdominal ultrasound by the radiologist and
liverenzymes were measured in the laboratory.
Initially, 74 patients were selected from the outpatientclinic
of internal medicine of El-Santa Hospital fromMarch 2015 to June
2016 and identified as potentiallyeligible for the study as mild
fatty liver patients withcentral obesity. On blood analysis for
measuring liverenzymes for each patient, 34 patients were found to
beineligible according to inclusion and exclusion criteriaand
therefore excluded. Forty patients were found tobe eligible and
already participated in the study. All40 participants had completed
the 8 weeks’ programto the end. The study was conducted at Abed
PhysicalTherapy Center in El-Santa, Gharbia governorate,Egypt.
Eligibility criteria: all participants had mild fatty liverwith
liver enzymes above accepted cutoffs withcentral obesity, free from
any immunodeficiencydisorders or diseases that can affect the
treatmentprocess. Criteria of fatty liver: patients werediagnosed
with mild fatty liver using abdominalultrasound when more than
5–10% of liver cellswere filled with fat droplets with mild
elevatedliver enzymes with cutoffs of 20 U/l for female and30U/l
for male patients.
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The 40 eligible participants were randomly assignedto two groups
equal in number, groups 1 and 2. It wasa randomized trial using
sealed envelope allocationsequence method. Group 1 received a
program ofmoderate intensity aerobic exercise. Group 2 followed
aprogram of low-caloric diet program. Each patient
hadbeenre-evaluatedafter8weeksof their treatmentprogramfor BMI,
body fat content, WC, ALT, and AST.
Equipment
(1)
Assessment equipment:(a) Height and weight scale: RGZ 220
(China).(b) Tape measurement: 150 cm.(c) Body Stat 1500: SN 213056
(UK).(d) Liver enzyme measuring machine: Microlab
300 SN 11-5046 (France).(e) Liver enzyme measuring kits:
BioSystems
(Spain).(f) Ultrasonography: SonoScope SN 3322415
made in China.
Therapeutic equipment:
(2)
Electronic treadmill: Grand Fit AC 999 (China).obic exercise is
defined as any activity that uses large
Aer
muscle groups working continuously for a long durationand
rhythmic in naturewithmoderate intensity.Aerobicmeans ‘with
oxygen’, involves or improves oxygenconsumption by the body, and
refers to the use ofoxygen in a muscle’s energy-generating process.
Manytypes of exercises are aerobic and by definition areperformed
at moderate levels of intensity for extendedperiods of time
[11].
Training programThe purpose of training program was explained
toeach patient. Each patient participated in theexercise training
program on electronic treadmillwith moderate intensity for 30–50min
three times aweek day after day for 8 weeks.
Phases of exercise
(1)
Warming up phase: 5–10min with mild intensity[30–40% maximum heart
rate (HRmax)].HRmax=211–0.64 age [12].
(2)
Training phase: each patient trained for 20–30minwith moderate
intensity (60–70% HRmax).
(3)
Cooling down phase: 5–10min with mild intensity(30–40% HRmax).
Low-caloric diet programIn a professional review, a low-caloric
diet of about1200–1500 kcal/day is recommended for patients
withNonalcoholic Steatohepatitis (NASH) [13]. A diet of
1400 kcal/day could be effective in improving histologyin
patients with biopsy-proven NASH [14].
In this study, four different graduated low-caloricdiet programs
were established. Every 2 weeks thediet program had been changed
gradually from1800 kcal/day to 1500 to 1200 to 1000 kcal.
Following is an example for 1800 kcal/day diet program:
Breakfast: One leaf of dark bread+three spoonfuls ofbeans with
olive oil+light cheese+two vegetables.Snack: One fruit+small cup of
coffee or tea with ateaspoonful of sugar.Lunch: Nine spoonfuls of
rice or macaroni+green salad+250 g of any type of skimmed protein
(fish, tuna,meat, chicken, and, liver).Snack: One fruit+a cup of
cinnamon with a teaspoonfulof sugar.Dinner: Half loaf of dark
bread+boiled egg+grilled orboiled eggplant+two vegetables.Snack:
One fruit+a cup of green tea.
Calorie intake was gradually reduced every 2 weeksuntil reaching
1000 kcal/day at the last 2 weeks.
Statistical analysisResults
areexpressedasmean±SDornumberandpercent.Comparison between
categorical data [n (%)] was madeusing the χ2-test. According to
test of normality,comparison between different variables in the
twogroups was performed using either the unpaired t-testor the
Mann–Whitney test whenever it was appropriate.Within-group
comparison (pretreatment vs. post-treatment) was performed using
either the paired t-testor the Wilcoxon signed-ranks test whenever
it wasappropriate. Statistical package for the social
sciences(SPSS) (IBM corporation in Armonk, New York,USA) computer
program (version 19 Windows) wasused for data analysis. A P value
less than or equal to0.05 was considered significant.
ResultsThere were no statistically significant
differencesbetween the two groups at baseline in the meanvalues of
age, height, and weight.
Comparison between the mean values of body massindex in the two
studied groups measured before andafter treatmentWithin-group
comparison
In the exercise group, there was a statisticallysignificant
difference in the mean value of BMImeasured before treatment
(44.24±5.47 kg/cm2)
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when compared with its corresponding value aftertreatment
(43.56±5.46 kg/cm2) (P=0.002).
In the diet group, there was no statistically
significantdifference between the mean value of BMI measuredbefore
treatment (43.41±4.97 kg/cm2) and its corres-ponding value after
treatment (42.24±5.17 kg/cm2)(P=0.436).
The percentage of decrease in BMI in both the exerciseand diet
groups was 1.54 and 2.17%, respectively.
Between-group comparison
Before treatment, there was no statistically
significantdifference between the mean value of BMI inthe exercise
group (44.24±5.47 kg/cm2) and itscorresponding value in the diet
group (43.41±4.97 kg/cm2) (P=0.615). After treatment, there wasno
statistically significant difference betweenthe mean value of BMI
in the exercise group(43.56±5.46 kg/cm2) and its corresponding
value inthe diet group (42.24±5.17 kg/cm2) (P=0.436) (Fig. 1).
Figure 2
Mean values ofWC in both groupsmeasured pre- and
post-treatment
Table 1 Comparison between mean values of body massindex and
waist circumference in the two studied groupsmeasured before and
after treatment
Exercise (n=20) Diet (n=20) P value
BMI
Comparison between mean values of waistcircumference in the two
studied groups measuredbefore and after treatmentWithin-group
comparison
In the exercise group, there was a statisticallysignificant
difference in the mean value of WCmeasured before treatment
(124.50±10.50 cm) whencompared with its corresponding value after
treatment(120.30±10.29 cm) (P=0.001).
In the diet group, there was a statistically
significantdifference between the mean value of WCmeasured before
treatment (124.00±6.81 cm) and itscorresponding value after
treatment (119.55±7.90 cm)(P=0.001).
The percentage of decrease in WC in both the exerciseand diet
groups was 3.37 and 3.59%, respectively.
Figure 1
Mean values of BMI in both groupsmeasured pre- and
post-treatment
Between-groups comparison
Before treatment, there was no statistically
significantdifference between the mean value ofWC in the
exercisegroup (124.50±10.50 cm) and its corresponding valuein the
diet group (124.00±6.81 cm) (P=0.859). Aftertreatment, there was no
statistically significantdifference between the mean value of WC in
theexercise group (120.30±10.29 cm) and its corres-ponding value in
the diet group (119.55±7.90 cm)(P=0.797) (Fig. 2 and Table 1).
Comparison between mean values of fat content in thetwo studied
groups measured before and aftertreatmentWithin-group
comparison
In the exercise group, there was a statistically
significantdifference in the mean value of fat measured
beforetreatment (56.82±12.42 kg) when compared with
itscorresponding value after treatment (54.17±12.26
kg)(P=0.001).
In the diet group, there was a statistically
significantdifference between the mean value of fat measured
Pretreatment 44.24±5.47 43.41±4.97 0.615 (NS)
Post-treatment 43.56±5.46 42.24±5.17 0.436 (NS)
Mean difference 0.68 1.17
% Change 1.54↓↓ 2.7↓↓
t-Value 3.624 1.624
P value 0.002 (S) 0.121 (NS)
WC
Pretreatment 124.50±10.50 124.00±6.81 0.859 (NS)
Post-treatment 120.30±10.29 119.55±7.90 0.797 (NS)
Mean difference 4.20 4.45
% Change 3.37↓↓ 3.59↓↓
t-Value 12.178 10.156
P value 0.001 (S) 0.001 (S)
Data are expressed as mean±SD. WC, waist circumference.P0.05,
NS. ↓↓Decrease.
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before treatment (53.79±11.77 kg) and its corres-ponding value
after treatment (49.27±12.00 kg)(P=0.001).
The percentage of decrease in fat in both theexercise and diet
groups was 4.66 and 8.40%,respectively.
Between-group comparison
Before treatment, there was no statistically
significantdifference between the mean value in the exercisegroup
(56.82±12.42 kg) and its corresponding valuein the diet group
(53.79±11.77 kg) (P=0.433). Aftertreatment, there was no
statistically significantdifference between the mean value of the
exercisegroup (54.17±12.26 kg) and its corresponding valuein the
diet group (49.27±12 kg) (P=0.210) (Fig. 3and Table 2).
Comparison between the mean values of alanineaminotransferase
(serum glutamic-pyruvictransaminase) in the two studied groups
measuredbefore and after treatmentWithin-group comparison
In the exercise group, there was a statisticallysignificant
difference in the mean value of ALTmeasured before treatment
(33.90±17.53 IU/l) whencompared with its corresponding value after
treatment(28.90±14.80 IU/l) (P=0.001).
Figure 3
Mean values of fat content in both groups measured pre- and
post-treatment
Table 2 Comparison between mean values of fat in the twostudied
groups measured before and after treatment
Fat Exercise (n=20) Diet (n=20) P value
Pretreatment 56.82±12.42 53.79±11.77 0.433 (NS)
Post-treatment 54.17±12.26 49.27±12.00 0.210 (NS)
Mean difference 2.65 4.52
% Change 4.66↓↓ 8.40↓↓
t-Value 11.329 7.114
P value 0.001 (S) 0.001 (S)
Data are expressed as mean±SD. P0.05, NS. ↓↓Decrease.
In the diet group, there was a statistically
significantdifference between the mean value of ALT measuredbefore
treatment (33.80±11.47 IU/l) and its corres-ponding value after
treatment (27.10±8.68 IU/l)(P=0.001).
The percentage of decrease in ALT in both the exerciseand diet
groups was 14.75 and 19.82%, respectively.
Between-group comparison
Before treatment, there was no statistically
significantdifference between the mean value of ALT inthe exercise
group (33.90±17.53 IU/l) and itscorresponding value in the diet
group (33.80±11.47IU/l) (P=0.598). After treatment, there was
nostatistically significant difference between the meanvalue of ALT
in the exercise group (28.90±14.8 IU/l)and its correspondingvalue
in thedietgroup(27.10±8.68IU/l) (P=0.882) (Fig. 4).
Comparison between mean values of aspartateaminotransferase
(serum glutamic oxaloacetictransaminase) in the two studied groups
measuredbefore and after treatmentWithin-group comparison
In the exercise group, there was a statisticallysignificant
difference in the mean value of ASTmeasured at after treatment
(40.00±13.97 IU/l)when compared with its corresponding value
aftertreatment (32.50±13.37 IU/l) (P=0.001).
In the diet group, there was a statistically
significantdifference between the mean value of AST measuredbefore
treatment (38.85±15.73 IU/l) and itscorresponding value after
treatment (31.05±11.42IU/l) (P=0.001).
The percentage of decrease in AST in both theexercise and diet
groups was 18.75 and 20.08%,respectively.
Figure 4
Mean values of ALT (SGPT) in both groups measured pre- and
post-treatment
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Figure 5
Mean values of AST (SGOT) in both groups measured pre- and
post-treatment
Table 3 Comparison between mean values of
alanineaminotransferase (serum glutamic-pyruvic transaminase)
andaspartate aminotransferase (serum glutamic
oxaloacetictransaminase) in the two studied groups measured
beforeand after treatment
Exercise(n=20)
Diet (n=20) Zvaluea
P value
ALT
Pretreatment 33.90±17.53 33.80±11.47 −0.528 0.598(NS)
Post-treatment
28.90±14.80 27.10±8.68 −0.149 0.882(NS)
Meandifference
5.0 6.7
% Change 14.75↓↓ 19.82↓↓
Z valueb −3.933 −3.924
P value 0.001 (S) 0.001 (S)
AST
Pretreatment 40.00±13.97 38.85±15.73 −0.054 0.957(NS)
Post-treatment
32.50±13.37 31.05±11.42 0.002 0.991(NS)
Meandifference
7.5 7.80
% Change 18.75↓↓ 20.08↓↓
Z valueb −3.832 −3.709
P value 0.001 (S) 0.001 (S)
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Between-group comparison
Before treatment, there was no statistically
significantdifferencebetween themeanvalueofAST in theexercisegroup
(40.00±13.97 IU/l) and its corresponding valuein the diet group
(38.85±15.73 IU/l) (P=0.957). Aftertreatment, therewasno
statistically significantdifferencebetween the mean value of serum
glutamic-pyruvictransaminase in the exercise group (32.50±13.37
IU/l)and its corresponding value in the diet group(31.05±11.42
IU/l) (P=0.991) (Fig. 5 and Table 3).
Data are expressed as mean±SD. ALT, alanine
aminotransferase;AST, aspartate aminotransferase. aMann–Whitney
test.bWilcoxon’s signed-rank test. P0.05, NS.↓↓Decrease.
Discussion
The results of this study showed that there was nosignificant
difference between the effects of moderateintensity aerobic
exercise versus low-caloric diet onliver enzymes in fatty liver
patients.
All patients had mild fatty liver with liver enzymesabove 20U/l
for female and 30U/l for male with BMIgreater than or equal to 30
kg/m2. There were no otherdiseases or problems affecting the
patient except fattyliver.
Sample size of the study was calculated by means ofpower
analysis to avoid errors. Duration of the studywas determined
according the previous studies as asuitable time for the treatment
program [15].
Rohollah et al. [15] in their experimental researchreported that
8-week aerobic exercise showed adecrease in the levels of ALT and
AST.
Rusu et al. [16] reviewed that there is no consensusas to what
diet or lifestyle approach is the best forNAFLD patients. However,
patients with NAFLDmay benefit from a moderate-to-low
carbohydrate(40–45% of total calories) diet, coupled withincreased
dietary Mono Unsaturated Fatty Acids(MUFA) and n-3 Poly Unsaturated
Fatty Acid(PUFAs) and reduced Saturated Fatty Acid (SFAs).
More Clinical Randomized Trial (CRT) is needed toclarify the
specific effects of different diets and dietarycomponents on the
health of NAFLD patients. Asmall clinical randomized trial showed
that short-term carbohydrate restriction is more efficacious
inreducing intrahepatic TG.
Petersen et al. [17] showed that a low-fat diet reducedcalorie
intake (daily intake 1200 kcal/day) andeffectively reduced body
weight and intrahepaticlipid content with improvement in insulin
resistancein NAFLD patients.
Wang et al. [18] reported that central obesity isstrongly
associated with hepatic steatosis (HS).Modification of lifestyle
including dietary restrictionfor weight loss and control of risk
factors such as type 2diabetes mellitus and dyslipidemia is
recommended asthe first and most important approach to managepeople
with NAFLD.
Huang et al. [14] conducted a study on reducing
insulinresistance and included the following recommendationsfor
caloric intake: 40–50% carbohydrates, with emphasison complex
carbohydrates with fibers, 35–40% from
fatwithemphasisonmonounsaturatedandpolyunsaturatedfats, and 15–20%
from protein. After 12 months, there
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was histological improvement in nine of 15 patients
withbiopsy-proven NASH, as measured by steatosis gradeand NASH
score.
Solga and Alkhuraishe [19] showed that the lowcaloric diet and
diet low in saturated fats is oftenrecommended. However, little is
known about theeffects of changes in dietary composition on
liverhistopathology in NAFLD.
In contrast, Capristo et al. [20] reported thatrecommendation of
a low-fat diet could actuallyworsen NAFLD histopathology.
Johnson et al. [6] showed that aerobic exercise trainingreduces
hepatic and visceral lipids in obese patients withsedentary
lifestyle. Thus, regular exercise may mitigatethe metabolic and
cardiovascular consequences ofobesity, including fatty liver, and
this is notcontingent upon weight loss.
Sreenivasa et al. [21] showed that moderate aerobicexercise
helped normalize ALT in NASH but thisnormalization did not occur in
the 15 patients whofailed to comply with the exercise program.
Stewart et al. [22] stated that aerobic exercise
increasesinsulin sensitivity independent of weight loss,
anddecreases peripheral lipolysis that probably interfereswith the
development of steatosis, inhibitinghepatic lipid synthesis and
stimulating fatty acidoxidation. A number of studies suggested
thatNAFLD improves after weight loss. Improvementsin liver
biochemistry and ultrasonography have beenfound with modest weight
reduction, but few studieshave evaluated the effect of weight
reduction onhepatic histology.
Suzuki et al. [23] reported body weight loss and
lifestylemodifications with changes in serum ALT levels. Theyfound
that weight loss and regular exercise resulted inimprovement in
serum ALT. They suggested thatreducing body weight by at least 5%
with subsequentweight control and exercising regularly may
bebeneficial in treating fatty liver.
Adams et al. [24] reported that studies showed that asedentary
lifestyle with reduced physical activity,independent of diet, is
another determinant offatty liver. Although these risk factors
maysuccessfully be modified by moderate lifestyleintervention, the
existence of other risk factorsmost probably may necessitate more
intensetreatment.
Keating et al. [25] showed clear evidence for theimportance of
exercise therapy on liver fat but notALT levels. This benefit is
apparent with minimalor no weight loss and at exercise levels below
currentexercise recommendations for obesity management.
Kakarla et al. [26] reported that the exercise training
byinducing antioxidant capacity protects against oxidativestress.
Similar changes were reported in male animals,which clearly
envisage no sex difference in theantioxidant enzyme system with
regard to age andexercise. In conclusion, it can be stated that
12weeks of treadmill exercise training has beneficialeffect in
improving the antioxidant defense capacityof the liver tissue by
augmenting superoxide dismutase,catalase, glutathione reductase
activities, andglutathione levels in older rats, thereby
preventingoxidative damage to the liver tissue.
Shelby [27] reported that some findings suggestedthat short-term
high-caloric feeding increases intrahepatic triglyceride (IHTG),
whereas short-term low-caloric feeding decreases IHTG despite
little changein total body weight, suggesting that ongoing
excesscaloric delivery directly contributes to thedevelopment of
NAFLD. Weight loss with low fator low carbohydrate diets can
improve IHTG;however, specific macronutrients such as
fructose,trans-fatty acids, and saturated fat may contributeto
increased IHTG independent of total calorieintake. N-3
polyunsaturated fatty acids andmonounsaturated fatty acids may play
a protectiverole in NAFLD. The mechanisms behind theseeffects are
not fully understood. Diet has animportant role in the
pathophysiology of NAFLD.Patients with NAFLD must be advised to
reducecalorie intake with either low fat or lowcarbohydrate diets
as well as limit intakes offructose, trans-fatty acids, and
saturated fat.
Kirk et al. [10] reported that moderate calorierestriction
causes temporal changes in liver andskeletal muscle metabolism; 48
h of calorierestriction affects the liver (IHTG content,
hepaticinsulin sensitivity, and glucose production),
whereasmoderate weight loss affects muscle (insulin-mediatedglucose
uptake and insulin signaling).
Petersen et al. [17] stated that weight loss as well asexercise
is associated with improvement in insulinsensitivity and logical
treatment modalities forpatients with NAFLD who are overweight or
obese.Weight reduction is with caloric restriction andphysical
exercise.
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Suzuki et al. [23] showed that weight reduction andlifestyle
modification with diet changes and increasedphysical activity are
recommended as the first step inthe control of NAFLD. Achieving and
maintainingweight reduction may improve NAFLD, but the resultof
several reports is inconsistent.
Palmer and Schaffner [28] showed that, in overweightadults free
fromprimary liver disease, a weight reductionof greater than or
equal to 10% corrected abnormalhepatic test results decreased
hepatosplenomegaly, andresolved some stigmata of liver disease. In
similarlystudied overweight patients with primary liver
disease,some findings improved, but the changes did notcorrelate
with a greater than or equal to 10% weightloss. Increased ALT
activity was the most frequenthepatic enzyme abnormality in this
population. Forevery 1% reduction in body weight, ALT
activityimproved by 8.1%.
In contrast, Jian-Gao et al. [29] reported that a studyindicated
that it might be difficult to resolvesteatohepatitis by merely
short-term low caloric diettherapy, long-term appropriate diet
control orconcurrent administration of medications that candirectly
reduce the severity of liver damage may bereasonable alternatives
for the treatment of NASHpatients with obesity.
In contrast, Selezneva et al. [30] reported that low-caloric
diet had poor compliance and little effect onALT and AST during
short-term diet intervention inNASH patients. Diet modifications
should bereconsidered in NASH patients in favor of fewercalories
restricted and easy to follow diet.
In rehabilitation clinics, doctors should advise obesemild fatty
liver disease patients with mild elevatedliver enzymes to follow
regular moderate aerobicexercise or follow low-caloric diet
according togeneral health status, lifestyle, co-operation,
andpsychological state of each patient. Both low-caloric diet and
moderate aerobic exercise improveliver histology and help in
normalizing liverbiochemistry.
ConclusionIt was concluded that there was no
significantdifference between results of both groups. After
thetreatment both low caloric diet and moderate aerobicexercise
showed a decrease in AST, ALT,WC, and fatcontent with no
significant changes in the BMIcompared with that before
treatment.
Financial support and sponsorshipNil.
Conflicts of interestThere are no conflicts of interest.
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Appendix IConsent form
I am freely and voluntarily consent to participate in this
resMohammed Mohammed Abdeen Sallam.
Through description of the study procedure has been explconsent
and discontinue participation in this research stu
Participant:
Date:
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60:S353.
earch study under the direction of the researcher/Fatma
ained to me and I understand that I may withdraw mydy at any
time without prejudice to me.