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ORIGINAL PAPER
Oat Prevents Obesity and Abdominal Fat Distribution,
and Improves Liver Function in Humans
Hong-Chou Chang &Chien-Ning Huang &Da-Ming Yeh &
Shing-Jung Wang &Chiung-Huei Peng &Chau-Jong Wang
Published online: 31 January 2013
#Springer Science+Business Media New York 2013
Abstract Obesity is associated with a great diversity of dis-
eases including non-alcoholic fatty liver disease. Our recent
report suggested that oat, rich in beta-glucan, had a metabolic-
regulating and liver-protecting effect in an animal model. In
this study, we performed a clinical trial to further confirm the
effect of oat. Subjects with BMI ≧27 and aged 18–65, were
randomly divided into a control (n=18) and an oat-treated (n=
16) group, taking a placebo or beta glucan-containing oat
cereal, respectively, for 12 weeks. Our data showed that
consumption of oat reduced body weight, BMI, body fat and
the waist-to-hip ratio. Profiles of hepatic function, including
AST, but especially ALT, were useful resources to help in the
evaluation of the liver, since both showed decrements in
patients with oat consumption. Nevertheless, anatomic
changes were still not observed by ultrasonic image analysis.
Ingestion of oat was well tolerated and there was no adverse
effect during the trial. In conclusion, consumption of oat
reduced obesity, abdominal fat, and improved lipid profiles
and liver functions. Taken as a daily supplement, oat could act
as an adjuvant therapy for metabolic disorders.
Keywords Oat .Obesity .Abdominal body fat .Fatty liver
Abbreviation
ALT Alanine transaminase
AST Aspartate transaminase
BMI Body mass index
BUN Blood urea nitrogen
FFA Free fatty acids
FS Fatty liver scores
γ-GT gamma-glutamyl transpeptidase
HDL-C High-density lipoprotein cholesterol
LDL-C Low-density lipoprotein cholesterol
TG Triacylglycerol
Chiung-Huei Peng and Chau-Jong Wang contributed equally to this
work and therefore, share the corresponding authorship.
H.-C. Chang :C.-N. Huang
Institute of Medicine, Chung-Shan Medical University,
Number 110, Section 1, Chien-Kuo North Road,
Taichung 402, Taiwan
C.-N. Huang
Department of Internal Medicine, Chung Shan Medical University
Hospital, Number 110, Section 1, Chien-Kuo North Road,
Taichung 402, Taiwan
D.-M. Yeh
School of Medical Imaging and Radiological Sciences,
Chung Shan Medical University,
Number 110, Section 1, Chien-Kuo North Road,
Taichung 402, Taiwan
D.-M. Yeh
Department of Medical Imaging, Chung Shan Medical University
Hospital, Number 110, Section 1, Chien-Kuo North Road,
Taichung 402, Taiwan
S.-J. Wang
Division of Research and Development, STANDARD Foods Co.,
Taipei, Taiwan
C.-H. Peng (*)
Division of Basic Medical Science, Hungkuang University,
Number 34, Chung Chie Road, Shalu County,
Taichung 433, Taiwan
e-mail: a222907@sunrise.hk.edu.tw
C.-J. Wang
Institute of Biochemistry and Biotechnology, Chung-Shan Medical
University, Number 110, Section 1, Chien-Kuo North Road,
Taichung 402, Taiwan
C.-J. Wang (*)
Department of Medical Research, Chung Shan Medical University
Hospital, Number 110, Section 1, Chien-Kuo North Road,
Taichung 402, Taiwan
e-mail: wcj@csmu.edu.tw
Plant Foods Hum Nutr (2013) 68:18–23
DOI 10.1007/s11130-013-0336-2
Introduction
Obesity, generally measured by body mass index (BMI), is
associated with a great diversity of diseases involving the
cardiovascular and metabolic systems. In recent years, there
has been increased recognition that body fat deposition and
abdominal obesity play a critical role in the pathogenesis of
related disorders [1].
There is a metabolic link among abdominal fat, high
triacylglycerol (TG), high low-density lipoprotein cholester-
ol (LDL-C), low high-density lipoprotein cholesterol (HDL-
C) and flux of free fatty acids (FFA) [2]. Since the liver
regulates the plasma lipid level through low density lipo-
protein (LDL) clearance and high density lipoprotein (HDL)
recruitment, non-alcoholic fatty liver is generally considered
to be the liver component of metabolic syndrome, which is
defined by over waist circumference, dyslipidaemia, hyper-
glycaemia, and hypertension [3,4]. It showed that obesity
induced steatosis, lymphocyte infiltration, and the subse-
quent development of hepatic illness [5]. As commonly
found in ultrasound screening, liver disorders are often
accompanied with an elevation of AST (aspartate transam-
inase) and ALT (alanine transaminase) [4]. In addition,
gamma-glutamyl transpeptidase (γ-GT) was often accom-
panied with hepato-cholecystic disorders and may be in-
volved in the promotion of carcinogenesis [6].
Previous reports have suggested that oat has metabolic-
regulating effects. Oat bran decreased the total choles-
terol level in serum, and decreased cholesterol and TG
contents in the liver [7]. Whole-grain oat cereal reduced
LDL-C in overweight and obese adults [8]. Oat contains
vitamins, minerals, antioxidants, and phenolic com-
pounds, and is rich in beta-glucan [9]. Oat-derived
beta-glucan increased HDL-C, while diminished LDL-C
and non-HDL cholesterol in overweight individuals
[10]. It has been suggested that daily intake of at least
3 g of oat beta-glucan reduces total cholesterol and
LDL-C in normo- or hyper-cholesterolemic subjects
[11]. Using the high-fat-diet (HFD)-fed rat model, we
recently demonstrated that oat reduced body weight and
fat, and improved the serum lipid profile via increasing
liver LDL clearance, inhibiting hepatic lipogenesis, and
stimulating lipolysis. [12].
Although many previous reports have shown that oat
improved lipid profiles and reduced body weight, few
of them emphasized the effects of oat on liver function,
hepatic steatosis, and body fat distribution. In this
study, we performed a clinical trial to further confirm
the effect of oat on metabolic regulation. We examined
whether oat could attenuate obesity, body fat deposi-
tion, waist circumstance, and improve serum parameters
and liver function to prevent hepatic steatosis in obese
subjects.
Materials and Methods
Subjects The study was approved by the Institute Review
Board of Chung Shan Medical University Hospital (CSMUH
No: CS09072). All participants gave their informed consent in
writing. Subjects with BMI ≧27andaged18–65 were
recruited for the study. Those who had one of the following
were excluded: a drinking habit (≧20 g alcohol daily), ALT 3-
fold higher or bilirulin above 2 mg/dl, kidney dysfunction,
cardiovascular disease, endocrine or severe systemic distur-
bance, mental disorder, or taking any OTC or prescribed
medication and nutraceutics. Forty subjects fulfilled the above
criteria were recruited for the study (Table 1).
Study Design The study was conducted from July 2009 to
June 2010. Before and after the experiment, the basal serum
parameters (glucose, TG, cholesterol, LDL-C, HDL-C, FFA,
AST and ALT), BMI, waist-to-hip ratio, body fat and the fatty
liver score (FS, described below) were measured as curative
indexes. The subjects were double-blinded, randomized and
divided into two groups (20 subjects in each), one taking beta-
glucan-containing oat cereal and the other a placebo (with a
similar external but without beta-glucan), respectively. One
cereal pack (37.5 g) was prescribed to be mixed with 250 mL
Table 1 Baseline demographic data of the subjects
Control
(n=18)
Oat-treated
(n=16)
pvalue
Biometrics
Age (y/o) 37.67± 10.59 39.44 ±11.69 0.65
Height (m) 1.65± 0.12 1.64±0.08 0.61
Weight (kg) 81.63± 17.39 78.36 ±11.74 0.53
BMI (kg/m
2
) 29.54± 2.54 29.18±2.34 0.66
Body fat (%) 37.46± 5.55 36.64±6.72 0.70
Waist-to-hip ratio 0.93± 0.04 0.94± 0.02 0.43
Systolic pressure (mmHg) 122.78±13.05 124.00 ±12.24 0.78
Diastolic pressure (mmHg) 76.44 ±8.75 78.88±7.97 0.41
Diabetes indicators
TCHO (mg/dl) 191.17± 29.51 189.31± 22.46 0.84
LDL-C (mg/dl) 133.11±23.13 126.25 ±24.69 0.41
HDL-C (mg/dl) 42.72± 6.70 45.75± 10.06 0.30
TG (mg/dl) 135.83± 57.86 132.81± 69.63 0.89
FFA (U/min/mg protein) 0.79 ±0.31 0.82 ±0.47 0.85
Glucose (mg/dl) 100.67± 34.31 94.62 ±8.12 0.50
Uric acid (mg/dl) 6.17±1.46 5.84± 1.34 0.51
Hepatic function
AST (U/L) 20.17± 10.51 27.06 ±19.74 0.21
ALT (U/L) 28.72± 26.80 42.44±34.14 0.20
FS 4.78± 2.41 3.75± 2.89 0.27
Data are presented as mean ± SD and analyzed by the Student's t-test.
p<0.05 was considered statistically significant
Plant Foods Hum Nutr (2013) 68:18–23 19
hot water and replaced some staple food of meals twice daily.
The calorific capacity in each pack was 144.8 kcal, with car-
bohydrate 25.3 g; protein 4.0 g; lipid 2.5 g; fiber 3.7 g and beta-
glucan 1.5 g. Body weight, waist-to-hip ratio and body fat were
measured at weeks 0, 2, 6, 8 and 12. Serum parameters and
safety evaluations, including heart rate, respiration, blood pres-
sure, γ-GT, creatinine, blood urea nitrogen (BUN), albumin,
uric acid, blood and urine routine were alsomeasuredat weeks
0, 6 and 12. The recruited subjects were asked to take 3-day
records of daily meals and physical activity at each of the time
points before the trial, first six weeks and last six weeks,
respectively. At the end of the study, 34 subjects had complet-
ed all the experiments: 18 controls (6 males and 12 females)
and 16 (6 males and 10 females) in the beta-glucan group. Six
subjects withdrew from the trial: one with hyperglycemia, one
with higher TG, and four did not adhere to the following
appointments.
Serum Parameters Serum glucose, TG, total cholesterol,
LDL-C, HDL-C, AST, ALT, BUN, creatinine, γ-GT, albu-
min and uric acid were analyzed on a Beckman Synchron
CX9 clinical system. FFA was analyzed using a Free Fatty
Acid Quantification Kit (ab65341, abcam).
Body Fat and Waist-to-Hip Ratio Body fat was measured
with a Tanita TBF-300GS analyzer. Waist-to-hip ratio was
calculated by the waist circumference (just above the upper
hip bone) divided by the hip circumference at its widest part.
Ultrasonic Image and Fatty Liver Scores (FS) The liver
ultrasonic image examination was performed with the Aloka
system (Prosound SSD-4000, with 5.0-MHz convex transduc-
er). Five items, including hepatic clearance, far gain attenuation,
and opaque of the bladder wall, portal area and hepatic vein,
were evaluated. Each item was classified as 0, 1, or 2 to indicate
normal, mild to moderate, or severe, respectively. FS was cal-
culated as the sum of the scores of the five items [13]. In general,
the recruited subjects showed mild liver steatosis (Table 1).
Statistical Analysis Using an unpaired Student t-test for the
control and oat-treated groups, and a paired Student t-test
for the pre- and post-trial, a pvalue of less than 0.05 was
considered statistically significant. All the analyses were
performed with SigmaPlot 11.0.
Results
Oat Reduced Body Weight and BMI Weight and BMI were
slightly increased in the control group, but significantly
lowered by 2.08±2.05 kg and 0.81 ±0.80 kg/m
2
, respective-
ly, in the oat-treated group (Table 2). Almost 90 % of the
Table 2 Treatment effects
Control (n=18) Oat-treated (n=16)
6wk–0wk pvalue* 12 wk –0wk pvalue* 6 wk –0wk pvalue* 12 wk –0wk pvalue* pvalue**
Biometrics
Weight (kg) −0.21± 1.09 0.422 0.52± 1.74 0.225 −1.54± 1.64 0.002* −2.08±2.05 0.001* 0.000**
BMI (kg/m
2
)−0.18± 0.37 0.050* 0.15 ±0.62 0.317 −0.59±0.65 0.002* −0.81± 0.80 0.001* 0.000**
Body fat (%) 0.07± 1.32 0.820 0.39 ±1.94 0.406 −0.34 ±1.97 0.495 −0.93 ±1.73 0.048* 0.045**
Waist-to-hip tatio 0.01± 0.01 0.029* 0.01 ±0.03 0.013* −0.01 ±0.02 0.094 −0.01±0.02 0.115 0.003**
Diabetes indicators
TCHO (mg/dl) −11.22±39.43 0.244 −3.94 ±11.36 0.159 −11.75± 19.69 0.031* −19.69±21.71 0.002* 0.011**
LDL-C (mg/dl) −4.28± 13.76 0.205 −0.83±14.56 0.811 −9.44±18.10 0.055 −13.50± 14.81 0.002* 0.017**
HDL-C (mg/dl) 0.94± 4.28 0.362 1.61± 5.75 0.251 2.94 ±4.78 0.027* 0.94± 6.29 0.560 0.746
TG (mg/dl) −2.61± 45.52 0.811 8.50± 51.99 0.497 −26.38± 48.18 0.045* −15.81± 49.91 0.224 0.175
FFA(U/min/mg protein) −0.02±0.42 0.856 −0.15± 0.37 0.109 −0.08± 0.50 0.548 −0.14 ±0.38 0.156 0.946
Glucose (mg/dl) 7.89± 8.60 0.001* 11.44± 20.52 0.030* 1.50± 7.71 0.449 5.38 ±6.57 0.005* 0.266
Uric acid (mg/dl) −0.02± 0.61 0.878 −0.32±0.86 0.136 0.06± 0.60 0.713 −0.22± 0.64 0.190 0.711
Hepatic function
AST (U/L) 0.78 ±4.85 0.505 0.17±5.50 0.351 −4.25±15.18 0.280 −6.69±15.17 0.027* 0.083
ALT (U/L) 2.11±8.53 0.309 2.67 ±11.80 0.899 −7.81±18.41 0.110 −14.25±22.42 0.098 0.009**
FS −1.00± 1.75 0.027* −0.81± 1.60 0.060 0.748
Data are presented as mean ± SD and analyzed by paired t-test
*p<0.05 indicates the significance of each difference at 6 or 12 weeks compared with the baseline
**p<0.05 indicates the significance of each 12 wk –0 wk difference between the control and oat-treated groups
20 Plant Foods Hum Nutr (2013) 68:18–23
oat-treated subjects had reduced body weight and BMI (data
not shown).
Oat Reduced Body Fat and Waist-to-Hip Ratio During the
trial, the body fat and waist-to-hip ratio of more than 60 %
of the oat-treated subjects was reduced (data not shown).
The mean difference significantly decreased by 0.93±
1.73 % and 0.01±0.02, respectively, in the oat-treated group
(Table 2).
Oat Decreased Serum Cholesterol and Improved the Lipo-
protein Profiles Serum cholesterol was significantly de-
creased in the oat-treated subjects (Table 2). Although
HDL-C was not altered, oat decreased LDL-C. The serum
TG and FFA were not significantly reduced after oat treat-
ment, while serum glucose was slightly altered in both
groups.
Oat Reduced ALT and AST, and Improved FS In the oat-
treated subjects, AST significantly decreased from 27.06±
19.74 to 20.38±7.94 U/L, while no significance was found
compared with the control. ALT decreased 36 %, but no
significance was found between the pre- and post-trial.
However, compared with the control, ALT was significantly
decreased with oat treatment (Table 2). As seen in the
ultrasonic images, FS of the control and oat-treated groups
decreased 21 and 22 %, respectively (Table 2), without a
significant difference.
Oat did not Change the Safety Evaluation Markers With the
exception of the body temperature of the control group, the
safety evaluation markers were not altered after the trial.
However, γ-GT decreased 25 % in the oat-treated group,
with a marginal pvalue of 0.052, close to the criteria of
significance (Table 3). Hence, the oat treatment showed no
harm in terms of vital signs and blood safety markers.
Discussion
In the present study, we demonstrated the anti-obesity and
liver-protection benefit of oat for the human body. Oat
reduced weight and body fat, especially inhibiting abdomi-
nal fat distribution. Oat decreased serum cholesterol and
LDL-C, thereby improving the lipoprotein profiles. The
liver function indexes were ameliorated by oat treatment,
and thus the occurrence or aggravation of fatty liver was
avoided. While exerting a benefit on metabolic regulation,
oat did not burden any of the systemic life signs.
Although BMI is widely used in body weight classifica-
tion and was adopted in this study [14], it may have limi-
tations and lead to a mis-estimation of the prevalence of
overweight and obesity. For some special populations who
have shorter lower limbs, using standing height alone to
calculate BMI may overestimate the number of individuals
that are overweight and obese, and at risk for type 2 diabetes
mellitus and cardiovascular disease [15].
Table 3 Safe evaluation markers
Control (n=18) Oat-treated (n=16)
pre-trial post-trial pvalue pre-trial post-trial pvalue
Heart rate (BPM) 72.67 ±8.26 76.44 ±8.85 0.059 72.25± 9.19 75.50±6.13 0.214
Respiration rate (BPM) 17.44±1.15 17.50 ±1.65 0.912 16.88± 1.59 16.75± 1.77 0.847
Systolic pressure (mmHg) 122.78±13.05 118.44± 8.61 0.170 124.00 ±12.24 119.12±7.23 0.150
Diastolic pressure (mmHg) 76.44± 8.75 74.89± 5.10 0.444 78.88 ±7.97 78.62 ±8.79 0.922
Body temperature (°C) 36.79± 0.27 36.60±0.19 0.033* 36.69± 0.34 36.53±0.22 0.129
WBC (*10
3
/μl) 6.55± 1.34 6.26±1.08 0.353 6.25 ±1.50 5.99± 1.66 0.217
RBC (*10
6
/μl) 4.83± 0.49 4.94±0.56 0.110 5.06 ±0.85 5.08± 0.89 0.718
Hb (mg/dl) 14.30± 1.70 14.60±1.93 0.152 14.91 ±1.60 14.98± 1.94 0.749
BUN (mg/dl) 11.87 ±1.95 11.46±2.33 0.493 11.49± 3.09 12.28± 2.81 0.309
Creatinine (mg/dl) 0.86± 0.18 0.84±0.15 0.331 0.86 ±0.16 0.86± 0.15 0.855
Albumin (g/dl) 4.39±0.31 4.33± 0.18 0.305 4.49± 0.31 4.41±0.27 0.227
γ-GT (U/L) 31.78± 18.03 31.33±17.54 0.806 35.62± 30.65 26.75±19.35 0.052
TSH (μIU/ml) 1.33± 0.69 1.66±0.82 0.063 1.40 ±0.72 1.33± 0.74 0.574
T4 (μg/dl) 7.10± 1.19 6.78±1.13 0.212 6.68 ±0.98 6.66± 1.04 0.926
WBC white blood cell, RBC red blood cell, Hb hemoglobulin, TSH thyroid stimulating hormone, T4 thyroxine
Data are presented as mean ± SD and analyzed by paired ttest
*p<0.05 indicates the significance
Plant Foods Hum Nutr (2013) 68:18–23 21
On the other hand, central obesity but not generalized
obesity, predicts a high prevalence of hepatic steatosis and
related disorders, including impairment of glucose tolerance
and type 2 diabetes. The analysis revealed that the quanti-
tative insulin-sensitivity index, waist circumference and
waist-to-height ratio had a significant association with the
development of fatty liver, whereas BMI did not. Hence, in
this study, we measured waist circumference and used the
waist-to-hip ratio as the index, which should more adequate-
ly reflect the regulatory effect of oat on abdominal fat
distribution and central obesity [16].
OurdatashowedthatALTwassignificantlyloweredinthe
oat-treated group compared with the control, implicating that
oat is beneficial for preventing fatty liver. However, the ultra-
sound image changes were not parallel with the functional
index. As a marker of liver disorders, ALT is associated with
the pathogenesis of metabolic syndrome, type 2 diabetes
mellitus and subsequent cardiovascular disease [17]. In the
absence of a detectable ultrasonic change, ALT and AST are
associated with hyperinsulinemia and insulin resistance, indi-
cating that a mild stage of steatosis is sufficient to mediate the
association between insulin resistance and liver enzymes [18].
In this trial, the duration of oat treatment was only 12 weeks.
Some liver improvement was assumed to be too mild for
detection by ultrasound, thus liver enzymes might be able to
reflect early changes. Considering the sub-cellular distribution
and biochemical properties of hepatic enzymes, ALT is supe-
rior for monitoring early or mild liver changes [18].
We demonstrated the benefits of oat beta-glucan on meta-
bolic regulation in this study. Oat beta-glucan may form a
viscous layer at the small intestine, which attenuates the
uptake of dietary cholesterol and reabsorption of bile acid.
The reduced bile acid levels activate the conversion from
cholesterol to bile acid, thus decreasing the hepatic cholesterol
content, and stimulating LDL receptor synthesis and plasma
LDL-C clearance [11]. However, controversy still exists. Con-
sumption of beta-glucan-enriched meals did not significantly
lower serum cholesterol and LDL-C in some studies. [19].
While assessing its metabolic regulating effect, the physico-
chemical properties of oat beta-glucan should be considered.
The lowering of LDL-C by oat beta-glucan may depend on
viscosity, which is dictated by molecular weight and solubility
in the intestine [20]. The oat-induced LDL-C reduction sig-
nificantly diminished when molecular weight was reduced
[21]. Our data revealed that oat effectively reduced obesity,
as well as the serum lipid and liver function indexes. The
effect could be exerted by the proper molecular weight of
beta-glucan. Initial moisture levels and extrusion temperatures
affected the water solubility and viscosity of oat product [22].
Processing conditions also influence the amount of beta-
glucan [23]. Although beta-glucan is a major polysaccharide
of oat, we still cannot rule out whether other functional com-
ponents participate in the metabolic regulation [9].
In conclusion, we found that oat decreased obesity, ab-
dominal fat, serum cholesterol, LDL-C, and liver functions.
Taken as a daily supplement, oat could act as an adjuvant
therapy for metabolic disorders.
Acknowledgments We thank STANDARD Foods Co., Taiwan for
providing all experimental diets.
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