Received: 5 July 2016 | Revised: 12 August 2016 | Accepted: 17 August 2016

DOI 10.1111/jfbc.12336

FULL ARTICLE

b-Glucan, but not Lactobacillus plantarum P-8, inhibits lipid

accumulation through selected lipid metabolic enzymes in
obese rats

Hsiu-Chuan Lee1 | Wei-Ting Yu1 | Yu-Ru Guo1 | Shih-Yi Huang1,2

1
School of Nutrition and Health Sciences,
Taipei Medical University, Taipei, Taiwan
2
Graduate Institute of Metabolism and
Obesity Science, Taipei Medical University,
Taipei, Taiwan
Correspondence
Shih-Yi Huang, School of Nutrition and
Health Sciences, Taipei Medical University,
250 Wu-Xing Street, Taipei 110, Taiwan.
Email: Sihuang@tmu.edu.tw
Funding information
Ministry of Science and Technology,
Taiwan, Grant/Award Number: NSC101-
2320-B-038-020-MY2; NSC102-2313-
B-038-003-MY2, and MOST103-2320-
B-038-012-MY3
Abstract
We compared the effects of barley b-glucan and Lactobacillus plantarum P-8 on changes in body
weight, white adipose tissue, and the activities of specific lipid metabolic enzymes in diet-induced
obese rats. Obese rats were administered barley b-glucan (B), L. plantarum P-8 (P), or both for
8 weeks. The results showed that the dietary intervention reduced the body weight and white adi-
pose tissue accumulation, and altered gut microbiota in the distal faeces of the B group.
Furthermore, acetate and propionate levels considerably increased in the caecal digest and rectal
feces of the B group. In addition, b-glucan, but not L. plantarum P-8, increased the activities of
hepatic acetyl CoA carboxylase, fatty acid synthase, and carnitine palmitoyl transferase and
reduced epididymal fat lipoprotein lipase activity, thus resulting in decreased white adipose tissue
accumulation in the obese rats. However, b-glucan and L. plantarum P-8 showed no synergistic
effects.
Practical applications
b-Glucan ameliorates hyperlipidaemia, increases hepatic acetyl CoA carboxylase, fatty acid syn-
thase, and carnitine palmitoyl transferase activities, and reduces epididymal fat lipoprotein lipase
activity, thus resulting in reduced white adipose tissue accumulation in obese rats. b-Glucan
reduces of reducing lipid levels and regulating specific lipid metabolic enzymes.

KEYWORDS
beta-glucan, Lactobacillus plantarum, obesity, short chain fatty acids

1 | INTRODUCTION
Incidences of overweight and obesity have been increasing, and have
thus become a major health concern worldwide (WHO, 2016). The
World Health Organization indicated that at least 2.3 billion adults
were overweight, and more than 700 million were obese, in 2015.
Obesity increases the risk of several metabolic disorders, including
complex dyslipidaemia, hypertension, atherosclerosis, glucose intoler-
ance, and type 2 diabetes mellitus, as well as the risk of mortality
(Ogden, Carroll, & Flegal, 2014). Thus, obesity prevention is being con-
sidered in public health strategies and during functional food
development.
Recent studies have suggested that gut microbiota and dietary
fibre are critical for harvesting energy from the diet (Tilg, Moschen, &
Kaser, 2009) and are involved in diseases such as obesity and meta-
bolic disorders (Tilg & Moschen, 2014). Gut microbiota ferment indi-
gestible polysaccharides into short-chain fatty acids (SCFAs), which are
then partially absorbed into the colon and mainly excreted in faeces
(Wong, de Souza, Kendall, Emam, & Jenkins, 2006). An increase
observed in the faecal SCFA levels of germ-free mice colonised with
the microbiota of obese mice indicates that gut microbiota-produced
SCFAs may have a critical role in obesity development (Turnbaugh
et al., 2006). Decreased levels of gut microbiota such as Methanobrevi-
bacter smithii and reduction in the Bacteroidetes/Firmicutes ratio have
been strongly associated with obesity in humans (Ley et al., 2005;
Turnbaugh et al., 2009).
Dietary fibre consumption has been demonstrated to produce
beneficial health effects and improvements in healthy participants and

J Food Biochem. 2017;41:e12336. wileyonlinelibrary.com/journal/jfbc V

C 2016 Wiley Periodicals, Inc. | 1 of 9
https://doi.org/10.1111/jfbc.12336
2 of 9 | LEE ET AL.

patients with metabolic syndrome (Carlson, Eisenmann, Norman, Ortiz, TA BL E 1 Compositions of experimental diets
& Young, 2011; Hu, 2003). Oat or barley b-glucans may reduce total
Groups Normal diet High-fat diet
cholesterol (TC) levels in participants with hypercholesterolemia (FDA,
Energy (%)
1997, 21 January). Gut microbiota-produced SCFAs from dietary fibre
Protein 19 19
may affect energy homeostasis, neurotransmission, and even disease Fat 10.2 44.8
development (Wu, Tremaroli, & Backhed, 2015). b-glucan has dual Carbohydrate 70.8 36.2
kcal/g 3.6 4.6
health benefits, accelerating bile acid excretion (Ellegard & Andersson,
2007) and functioning as a prebiotic to produce SCFA and regulate Subgroups N C P B M

energy homeostasis (Wong et al., 2006). Several interventional studies Ingredients (g/Kg)
Casein 177 224 223 223 223
on probiotics have reported that gut microbiota-produced SCFAs affect
L-cystine 3 3 2 2 2
lipid metabolism and reduce body weight in patients with obesity Cornstarch 541 187 187 151 137
(Druart et al., 2014; Salazar et al., 2015). Maltodextrin 30 30 30 30 30
Sucrose 100 215 214 214 214
Studies have suggested that SCFA production by gut microbiota is Cellulose 50 50 50 50 50
associated with dietary fibre consumption, and that these SCFAs may be Soybean oil 22 22 21 21 21
Lard 22 216 214 214 214
involved in the initiation of satiety, energy homeostasis, inflammation,
AIN 93M mineral mix 35 35 35 35 35
and chronic metabolic dysfunction (Byrne, Chambers, Morrison, & Frost, Calcium phosphate, dibasic 2 2 2 2 2
2015b; Druart et al., 2014). Most of the relevant studies have focused AIN 93 vitamin mix 15 15 15 15 15
Choline bitartrate 3 3 3 3 3
on the prebiotic potential of indigestible fructo-oligosaccharides (i.e., inu-
b-Glucan 0 0 0 40 40
lin) and galacto-oligosaccharides for increasing the total quantity of gut L. plantarum 0 0 4 0 4
microbiota. The role of mixed-linkage b-glucans fermented by gut micro- N 5 normal; C 5 control; P 5 Lactobacillus plantarum; B 5 (1,3/1,4)
biota in increasing SCFA levels has gained little attention (Zhong, Marun- b-glucan; M 5 Lactobacillus plantarum plus b-glucan.
gruang, Fak, & Nyman, 2015). Thus, with respect to the food matrix,
b-glucan-containing foods may contribute to optimal growth conditions
for various gut microbial strains and increase SCFA production (Arena fat diet supplemented with barley b-glucan at 1 g/d (B), L. plantarum P-8
et al., 2014; Nielsen et al., 2016). (1 3 109 colony-forming units [CFU]) at 0.1 g/d (P), L. plantarum P-8 at
Beneficial bacteria, such as the members of the Lactobacillus and 0.1 g/d plus b-glucan at 1 g/d (M), or no supplements, as a control (C),
Bifidobacterium genera, may have anti-obesity (Park, Oh, & Cha, 2014; for 8 weeks. The composition of the treatment diets was based on the
Yoo et al., 2013) and anti-inflammatory (Zhong et al., 2015) properties. American Institute of Nutrition-93M diet (MP Biomedicals, LLC Santa

However, few studies have evaluated the synergistic effects of prebiot- Ana, CA, USA), containing 10% and 45% soybean oil (Table 1). Barley

ics and probiotics on metabolic dysfunction diseases and the status of (1!3,1!4)-b-glucan (GlucagelTM; 75%; average molecular weight, 740

microbiota-produced SCFAs in the gut. Therefore, the aim of this study kDa) was purchased from DKSH Taiwan Ltd, Taiwan. L. plantarum P-8

is to evaluate the effects of barley b-glucan and Lactobacillus plantarum (LABCOTTM lactic acid bacteria GFB007) was purchased from GeneFerm

P-8 on gut microbiota, SCFA production, body fat distribution, and the Biotechnology Co., Ltd, Tainan, Taiwan. During the experiment, the food

activities of specific lipid metabolic enzymes in diet-induced obese rats.
2 | MATERIALS AND METHODS
2.1 | Animal protocols and experimental design
Fifty 6-week-old male Sprague Dawley rats (BioLASCO Taiwan, Taipei,
Taiwan), each weighing 150–180 g, were housed in a temperature- and
humidity-controlled room with a 12-h light–dark cycle (light period,
08:00–20:00; temperature 228C–248C; humidity, 60%; two rats per
cage). The rats were allowed to adapt for 2 weeks and fed Rodent Lab-
oratory Chow 5001.
The rats were then assigned to the following diet groups for 12
weeks: a normal diet group with fat constituting 10% of total energy
(n 5 10) and a high-fat diet group intended to induce obesity with fat
constituting 45% of total energy (n 5 40) (Ghibaudi, Cook, Farley, van
Heek, & Hwa, 2002). The rats fed the high-fat diet were considered
obese when their body weight was >10% of that of the rats fed the nor-
mal diet (Abdul Kadir, Rahmat, & Jaafar, 2015). The 40 obese rats were
then divided into four groups each of which was provided either a high-
intake and body weight were recorded and then used to determine the
food efficiency of diet-induced obesity. All animals were provided the
aforementioned diets and water ad libitum. These conditions were main-
tained throughout all the experiments. All animal procedures complied
with the guidelines of the Institutional Animal Care and Use Committee
of Taipei Medical University (LAC-101-0190).
Fresh rectal faeces from the obese rats were collected after mas-
saging their stomachs at the beginning of week 0 and the end of week
8 of the intervention. The fresh rectal faeces (approximately 10 g) col-
lected from the treated mice were frozen in liquid nitrogen and then
stored in a 2808C freezer for gut microbiota and SCFAs analyses.
At the end of the experiment, all the rats were euthanised using
carbon dioxide, and their livers, kidneys, and caeca were excised and
weighed prior to further biochemical analysis. Furthermore, adipose tis-
sues, including inguinal, retroperitoneal, epididymal, perirenal, and mes-
enteric fat were collected and weighed prior to further analysis.
Abdominal blood was collected for biochemical analyses. Caecal epi-
thelial tissue, colonic mucin, and rectal faeces were collected to analyse
SCFA concentrations. All chemicals used in this study were obtained
from Sigma-Aldrich (St. Louis, MO, USA).
LEE ET AL. | 3 of 9

2.2 | Biochemical assays tration was determined using a DC protein assay kit II (Bio-Rad Labora-
tories, Berkeley, CA, USA); bovine serum albumin (Pierce, Rockford, IL,
To evaluate the safety of the experimental diets, overnight tail-vein
USA) was used to generate a standard curve. The ELISA microplates
blood samples were collected in ethylenediaminetetraacetic acid
were read using an ELISA reader (Dynatech Laboratories, Chantilly, VA,
(EDTA) tubes, centrifuged at 3,000 g for 10 min to obtain plasma, and
USA), with a maximum absorbance of 450 nm.
maintained at 2808C at the end of the experiment. The activities of
The lipoprotein lipase (LPL) activity of epididymal fat in the adipose
glutamate oxalate transferase (GOT) and glutamate pyruvate transfer-
tissue specimens was evaluated by using a fluorescent method, accord-
ase (GPT) and levels of blood urea nitrogen, creatinine, triglycerides
ing to the manufacturer’s instructions (LPL activity Kit, Roar Biomedi-
(TGs), TC, low-density lipoprotein cholesterol (LDLc), and high-density
cal, New York, NY). A total of 0.2 g of tissues was mixed and
lipoprotein cholesterol (HDLc) were measured from the plasma sam-
homogenised with 2 mL of a homogenising buffer (containing 0.3 M
ples. GOT and GPT activities and blood urea nitrogen and creatinine
mannitol, 10 mM HEPES, 1 mM EGTA, pH 7.2) in an ice bath. The
levels were analysed by using an automatic chemistry analyser (Hitachi
homogenates were then centrifuged at 1,200 g and 48C for 10 min,
7170S). TG and TC levels were measured with an Ortho Clinical Diag-
and the supernatant was centrifuged at 13,000 g and 48C for 12 min.
nostics VITROS® 950 automated analyser (Johnson & Johnson, New
The pellets were then resuspended in 0.07 M sucrose, 0.22 M manni-
Brunswick, NJ, USA), and LDLc and HDLc levels were determined by
tol, 0.02 M HEPES buffer (pH 7.4), and 0.01 M EDTA. The superna-
using a TBA-c16000 automated analyser (Toshiba, Tokyo, Japan). A
tants were used for LPL activity assay (Notarnicola, Miccolis, Tutino,
modified version of Kumar’s experimental method (Kumar, Grover, &
Lorusso, & Caruso, 2012). An aliquot of the supernatant (100 lL) was
Batish, 2011) was used to extract faecal cholic acid, the concentration
incubated with 100 mL of prediluted substrate emulsion at 378C for
of which was measured using a bile acid kit (BXC0581A, Fortress Diag-
1 h. The hydrolysed TGs were measured at 370-nm excitation and
nostics, Antrim, UK). Faecal water content was calculated using the fol-
450-nm emission. The fluorescence intensity values of the samples
lowing equation: water content (%) 5 (wet weight2dry weight)/wet
were compared with the values of a standard curve in each run. LPL
weight 3 100.
activity was expressed as hydrolysed substrate nmol/min/mg protein,
and evaluated using the Lowry method. All measurements were per-
2.3 | Selected lipid metabolic enzyme activities formed in duplicate.
The activities of hepatic lipid-regulating enzymes, namely acetyl CoA
carboxylase (ACC), fatty acid synthase (FAS), and carnitine palmitoyl 2.4 | Faecal sample culture
transferase (CPT)21, were assayed using a previously described spec-
The faeces were collected from the obese rats and frozen at weeks
trophotometric method (Numa, Bortz, & Lynen, 1965; Small, Burdett, &
0 and 8, on the same day as the gut microbiota and SCFAs analyses. In
Connock, 1985). Five hundred mg fresh liver samples were mixed and
the gut microbiota analysis, 1 g of the faecal sample was dissolved in
homogenised with 5 mL of a homogenising buffer (containing 0.3 M
9 mL of saline and homogenised. Subsequently, the faecal water was vor-
mannitol, 10 mM HEPES, 1 mM EDTA, pH 7.2) at 48C. The hepatic
texed for 10 min and dilutions were prepared. The faecal water samples
homogenates were centrifuged at 1,200 g and 48C for 10 min, and the
were then incubated in duplicate at various concentrations. The faecal
supernatant was again centrifuged at 7,200 g and 48C for 12 min. Pel-
samples were cultured on media specific for Escherichia coli (Endo agar),
lets were then resuspended in 0.07 M sucrose, 0.22 M mannitol,
Lactobacillus (MRS agar), Bifidobacterium (BIM agar), and total anaerobic
0.02 M HEPES buffer (pH 7.4), and 0.01 M EDTA. The resulting post-
bacteria (CDC agar) for 48 h at 378C under anaerobic conditions. Follow-
nuclear supernatants were assayed for ACC, FAS, and CPT-1 activities.
ing the incubation, the various groups of bacteria on the media were
FAS activity was measured as malonyl CoA-dependant oxidation by
counted. The results are expressed as CFU per gramme of wet faeces.
following the decrease in the absorbance at 340 nm resulting from
NADPH oxidation in the presence of acetyl-CoA. The FAS activity was
2.5 | SCFA analysis
expressed as the nmol of NADPH that was reduced per min per mg
protein (nmol/min/mg protein). ACC activity was determined as The caecal epithelial tissue and faecal samples were collected to ana-
described previously (Numa et al., 1965). CPT-1 activity was deter- lyse SCFA concentrations. SCFA extraction procedures were modified
mined on the basis of the method developed by Small et al. (1985) as described previously (Ezz El-Arab, 2009). All faecal samples for each
with minor modifications. The tissue homogenates were centrifuged at group and time interval were ground and thoroughly mixed for SCFA
800 g and 48C for 10 min, and the supernatant was centrifuged at analysis. A portion of the faecal sample (100 mg) was mixed with 500
7,200 g at 48C for 12 min. The pellets were then resuspended in mL of deionised water and 4-methyl-n-valeric acid (as an internal stand-
0.07 M sucrose, 0.22 M mannitol, 2 mmol/L HEPES buffer (pH 7.4), ard), added to a 2-mL Eppendorf tube, and mixed for 2 min. The mixed
and 1 mmol/L EDTA. The assay was based on the moiety CoA of pal- sample was centrifuged at 10,000 rpm and 48C for 1 min. The superna-
mitoyl CoA released by CPT-1 and reacted with 5,50 -dithiobis-(2-nitro- tant was transferred to another 2-mL Eppendorf tube. Subsequently,
benzoic acid) at 378C. The changes in the absorbance at 412 nm were 20 mL of 20% trichloroacetic acid solution was mixed with the superna-
measured at 20-s intervals for 5 min. The activity was expressed as tant, and the mixture was centrifuged at 10,000 rpm at 48C for 25 min.
CoASH nmol/min/mg protein (Small et al., 1985). The protein concen- SCFAs were extracted from the supernatant two times by using 1 mL
4 of 9 | LEE ET AL.

TA BL E 2 Dietary intake and weight of selected adipose tissues in each group

N C P B M

Dietary intake (g) 20.8 6 0.8 20.8 6 1.2 21.0 6 0.7 20.0 6 1.1 20.9 6 0.5

Body weight gain (g) 68.9 6 10.0 124.6 6 10.6* a

130.1 6 11.1 a
76.1 6 5.3 b
113.3 6 9.9a
Liver weight (g) 13.5 6 0.7 14.5 6 0.9 16.9 6 1.3 14.2 6 0.8 12.8 6 0.7

Total body fat (g) 45.8 6 3.5 98.3 6 6.6*ab 112.8 6 10.8a 87.6 6 5.9b 101.4 6 7.6ab
% of body weight 8.0 6 0.4 13.3 6 0.6*ab 14.5 6 1.1a 12.5 6 0.5b 13.7 6 0.7ab
Retroperitoneal fat (g) 3.11 6 0.53 3.11 6 0.24 2.45 6 0.17 2.28 6 0.19 3.41 6 0.41
Epididymal fat (g) 9.8 6 1.0 20.8 6 1.5* 23.0 6 2.0 19.5 6 1.7 21.1 6 1.8
Perirenal fat (g) 17.5 6 1.4 38.7 6 2.7*a 49.0 6 5.8b 35.4 6 3.5a 42.9 6 3.5a
Inguinal fat (g) 5.2 6 0.4 12.3 6 1.3*a 16.1 6 1.5b 11.5 6 0.7a 11.2 6 1.1a
Mesenteric fat (g) 10.3 6 0.9 23.5 6 2.4*a 22.9 6 2.0ab 18.9 6 1.6b 22.3 6 1.9ab

Note. Data are expressed as the mean 6 SEM, n 5 8–10.

N 5 normal; C 5 control; P 5 Lactobacillus plantarum; B 5 (1,3/1,4) b-glucan; M 5 Lactobacillus plantarum plus b-glucan.
The superscript symbol “*” means significantly different from the normal group (p < .05). Values in the same row with different superscript letters signif-
icantly differ at p < .05 by one-way ANOVA with least significant difference.

of ether. The ether layer was collected and mixed with 25 mL of 5 M
NaOH solution and acetone. The processed samples were lyophilised
and stored for SCFA analysis. All measurements were performed in
duplicate.
Chromatographic analysis was performed using the Trace Gas
Chromatography (GC) system (Thermo Finnigan Trace GC, Milan, Italy),
equipped with a flame ionisation detector. A GC capillary column
(NukolTM 24107, Sigma-Aldrich) with a column size of 30 m, inner
diameter of 0.25 mm, and a 0.25-lm-thick film coating was used.
Nitrogen was supplied as the carrier gas at a flowrate of 0.5 mL/min,
with a split ratio of 1:10. The GC oven temperature was initially main-
tained at 1308C then increased 68C/min to 2008C and maintained for
7.5 min. The temperature of the flame ionisation detector and injection
port was 2308C. The flowrates of hydrogen and air were 30 and
300 mL/min, respectively. The volume of the injected sample for GC
was 2 lL. Independently replicated determinations were performed
three times for each sample.
renal and inguinal fat were significantly higher in the P group than in
the C group (p < .05); however, the weights of total body fat and
mesenteric fat were significantly lower in the B group than in the C
group (p < .05). Overall, the weights of total body fat and selected
adipose tissue fat were significantly higher in the high-fat diet group
than in the normal diet group (p < .05).
3.2 | Lipid profile and safety
We observed no significant differences in the plasma and liver levels of
TC, HDLc, and LDLc among the groups at the end of the experiments;
however, the plasma TG level was significantly higher in the C group
than in the normal diet, B, and P groups (Table 3). Moreover, the daily
faecal weight was significantly higher in the B and M groups than in the
C group (p < .05 for both). Although blood urea nitrogen and creatinine
levels were significantly lower in the C group than in the normal diet
group, the levels were within the normal range. Liver and kidney function
indices after the intervention indicated that the diet was safe (Table 3).

2.6 | Statistical analysis 3.3 | Effects on gut microbiota

Data are expressed as the mean 6 standard error of the mean for each
group. A p value of <.05 was considered statistically significant. One-
way ANOVA was used to compare the mean values, and significant dif-
ferences among groups were determined using Duncan’s multiple
range test (PASW statistics 18, SPSS, Inc., Hong Kong).
We observed that the numbers of E. coli CFUs were significantly higher
in the rectal faeces of the treated groups than in those of the non-
treated groups (all p < .05). We also observed a significant increase in
the number of Bifidobacterium CFUs in the rectal faeces of the M group
at the end of the treatments (Table 4).

3 | RESULTS 3.4 | SCFA levels

3.1 | Obesity status and growth of rats
To investigate the obesity status and growth of rats during the
experiment, we evaluated the dietary intake, body weight, and
selected adipose tissues (Table 2). We measured the body weight of
all rats to evaluate the obesity status. We observed no differences in
food intake and liver weight among the obese rat groups. After
treatment, the final body weight gain of the B group was signifi-
cantly lower than that of the C group (p < .05). The weights of peri-
After 8 weeks, the levels of SCFAs, particularly acetate and propionate,
in the caecal faeces were significantly higher in the M group than in
the other treated groups (p ˂.05). However, no differences in SCFA lev-
els were observed in the rectal faeces of the P, B, and M groups. The
SCFA levels in the rectal faeces of the P, B, and M groups were signifi-
cantly higher than those of the C group (p < .05). After 8 weeks, com-
pared with other treated groups, the propionate and butyrate levels
were significantly higher in the B and M groups, respectively. More-
over, the levels of total SCFAs, acetate, propionate, and butyrate in the
LEE ET AL. | 5 of 9

TA BL E 3 Effects of 8-week consumption of L. plantarum and b-glucan on selected biochemical parameters

Groups/parameter N C P B M

Plasma
TC (mg/dL) 49.8 6 3.3 56.6 6 4.1 60.0 6 3.9 52.0 6 6.7 47.6 6 4.0
TG (mg/dL) 122 6 11 182 6 26*a 159 6 24ab 108 6 12b 112 6 10b
HDLc (mg/dL) 14.5 6 0.6 15.7 6 1.0 15.9 6 1.0 14.6 6 1.7 12.8 6 0.7
LDLc (mg/dL) 3.60 6 0.22 4.30 6 0.37 4.38 6 0.32 4.00 6 0.37 3.50 6 0.22
GOT (U/L) 99.9 6 12.7 91.5 6 6.1 91.5 6 7.1 86.1 6 4.2 96.3 6 17.9
GPT (U/L) 34.2 6 3.6 32.4 6 1.5 40.0 6 7.0 32.0 6 2.4 43.5 6 12.6
BUN (mg/dL) 11.7 6 0.5 9.7 6 0.3* 10.0 6 0.6 10.5 6 0.7 10.8 6 0.2
Creatinine (mg/dL) 0.40 6 0.01 0.37 6 0.01*a 0.38 6 0.01a 0.37 6 0.01b 0.40 6 0.01b
Liver
TC (mg/g) 3.09 6 0.87 2.25 6 0.16a 3.74 6 0.50b 3.24 6 0.67ab 2.98 6 0.62ab
TG (mg/g) 7.5 6 1.5 9.7 6 1.2a 13.3 6 2.2b 9.4 6 0.6a 10.2 6 0.9ab
Feces
Weight (g/d/rat) 2.93 6 0.84 3.87 6 0.58a 3.77 6 0.86a 7.29 6 2.07b 6.67 6 0.71b
Cholic acid (mmol/d/rat) 2.76 6 0.78 1.69 6 0.80 0.93 6 0.30 2.22 6 1.35 1.24 6 0.41
Water content (%) 0.38 6 0.09 0.33 6 0.05 0.28 6 0.06 0.29 6 0.09 0.24 6 0.09

Note. Data are expressed as the mean 6 SEM, n 5 8–10.

TC 5 total cholesterol; TG 5 triglyceride; HDLc 5 high-density lipoprotein cholesterol; LDLc 5 low-density lipoprotein cholesterol; GOT 5 glutamate
oxaloacetate transaminase; GPT 5 glutamate pyruvate transaminase; BUN 5 blood urea nitrogen. N 5 normal; C 5 control; P 5 Lactobacillus plantarum;
B 5 (1,3/1,4) b-glucan; M 5 Lactobacillus plantarum plus b-glucan.
The superscript symbol “*” means significantly different from the normal group (p < .05). Values in the same row with different superscript letters signif-
icantly differ at p < .05 by one-way ANOVA with least significant difference.

colonic mucin were higher in the P and M groups than in the other or a combination of both. The B and M groups exhibited the lowest
treated groups (p < .05) (Table 5). body weight gain and the highest daily faecal output (Kalra & Jood,
1998, 2000). However, the P and M groups showed significant body

3.5 | Selected hepatic lipogenic and lipolytic enzyme
activities
The activities of hepatic ACC, FAS, and CPT-1 were significantly higher
in the B group than in the other treated groups (all p < .05; Figure 1).
However, the LPL activity in the epididymal fat tissue significantly
decreased in the P, B, and M groups (all p < .05; Figure 2).
4 | DISCUSSION
In this study, we observed that body weight gain and body fat distribu-
tion differed among obese rats fed a high-fat diet supplemented with
barley b-glucan (primarily (1!3,1!4)-b-glucan; 90%), L. plantarum P-8,
weight gain and body fat accumulation in specific adipose tissues (i.e.,
perirenal, inguinal, and mesenteric fat). The fat-regulating properties of
L. plantarum P-8 have been reported in murine models (Kim et al.,
2014; Park et al., 2014): Lipolytic enzymes such as CPT-1 were regu-
lated by L. plantarum LG42, resulting in a significant decrease in the fat
pad weight of epididymal adipose tissue (Park et al., 2014). Similar lipid
reduction is caused by Lactobacillus strains and occurs in hosts with
dysfunctional metabolisms (i.e., elevated serum insulin, TNFa, or IL-1b
levels) (Fak & Backhed, 2012; Wang et al., 2014). However, in our
study, we did not observe a similar decrease in white adipose tissue
accumulation in the P and M groups. According to our study protocol,
we fed most of our rats with the high-fat diet for 12 weeks, followed
by the applicable treatment administration. After administration, the

TA BL E 4 Effects of 8-week consumption of L. plantarum and b-glucan on the gut microbiota in rectal feces

N C P B M

Endo Baseline 7.45 6 0.20 7.05 6 0.24 6.75 6 0.20 7.00 6 0.14 6.83 6 0.11
8th week 7.79 6 0.17 8.00 6 0.14* 7.85 6 0.35* 7.82 6 0.15* 7.21 6 0.21*
MRS Baseline 7.63 6 0.13 7.40 6 0.08 7.74 6 0.13 7.40 6 0.11 7.46 6 0.12
8th week 7.76 6 0.20 7.22 6 0.14 7.13 6 0.09* 7.57 6 0.15 7.60 6 0.24
BIM Baseline 7.57 6 0.22 7.33 6 0.18 7.41 6 0.14 7.30 6 0.16 7.17 60.10
8th week 7.67 6 0.20 7.28 6 0.11 7.24 6 0.15 7.37 6 0.09 7.69 6 0.13*

CDC Baseline 8.35 6 0.22 8.08 6 0.17 8.11 6 0.09 8.23 6 0.11 8.17 6 0.14
8th week 8.18 6 0.21 8.10 6 0.13 8.36 6 0.28 8.41 6 0.13 8.056 0.14

Note. Data are expressed as the mean 6 SEM, n 5 8–10. Values are expressed as log (colony-forming units per gram) of wet feces. Endo agar was used
for isolating Escherichia coli, MRS agar was used for isolating Lactobacillus, BIM agar was used for isolating Bifidobacterium, and CDC agar was used for
isolating total anaerobic bacteria.
N 5 normal; C 5 control; P 5 Lactobacillus plantarum; B 5 (1,3/1,4) b-glucan; M 5 Lactobacillus plantarum plus b-glucan.
The superscript symbol “*” means significantly different from the baseline in the same treatment (p < .05).
6 of 9 | LEE ET AL.

TA BL E 5 Levels of SCFAs in cecal and rectal feces and colon mucin of rats after administration

N C P B M

Cecum feces (mM/g wet)

Total SCFAs 49.5 6 3.7 58.9 6 5.0a 61.8 6 4.2a 53.2 6 2.9a 90.3 6 6.8b
Acetate 21.7 6 2.0 33.2 6 3.3*a 32.5 6 3.0a 32.6 6 1.4a 53.2 6 4.2b
Propionate 11.8 6 1.2 12.5 6 1.0a 13.1 6 0.8a 11.6 6 0.9a 20.9 6 1.9b
Butyrate 16.0 6 1.4 13.1 6 1.6ab 16.3 6 1.3b 9.0 6 1.6a 16.2 6 2.3bc
Rectal feces (mM/g wet)
Total SCFAs 11.8 6 1.0 14.4 6 1.5a 21.9 6 2.5b 23.4 6 2.3b 22.8 6 1.1b
Acetate 9.4 6 0.7 13.2 6 1.5a 20.3 6 2.3b 19.5 6 1.8b 19.5 6 1.1b
Propionate 1.0 6 0.1 0.7 6 0.1a 0.6 6 0.1a 1.7 6 0.2b 1.2 6 0.1a
Butyrate 1.5 6 0.2 0.5 6 0.0a 0.9 6 0.2ab 2.2 6 0.8bc 2.6 6 1.7c

Colon mucin (mM/g)

Total SCFAs 19.1 6 1.7 27.8 6 5.6a 46.2 6 9.8b 22.2 6 2.4a 13.6 6 1.7c
Acetate 16.0 6 1.4 22.6 6 4.5a 35.7 6 8.2b 17.1 6 1.9a 9.9 6 1.4c
Propionate 2.1 6 0.3 3.5 6 0.8a 7.0 6 1.5b 3.9 6 0.6a 2.5 6 0.3c
Butyrate 1.0 6 0.1 1.6 6 0.4a 3.5 6 0.7b 1.1 6 0.3a 1.2 6 0.2a

Note. Data are expressed as the mean 6 SEM, n 5 8–10.

SCFAs 5 short-chain fatty acids; N 5 normal; C 5 control; P 5 Lactobacillus plantarum; B 5 (1,3/1,4) b-glucan; M 5 Lactobacillus plantarum plus b-glucan.
The superscript letter “*” means significantly different from the normal group (p < .05). Values in the same row with different superscript letters signifi-
cantly differ at p < .05 by one-way ANOVA with least significant difference.

hepatic TC and TG levels did not differ between the control and normal
groups. These findings are inconsistent with those of other studies,
probably because this level of obesity (more than 10% of body weight)
does not cause the onset of abnormal lipid metabolism in the liver
(Abdul Kadir et al., 2015). High-fat diets are a major cause of obe-
sity; but in mammals, despite long-term intake of a high-fat diet sig-
nificantly increasing abdominal fat weight (Woods, Seeley, Rushing,
D’Alessio, & Tso, 2003), biochemical parameters remain within nor-
mal ranges (Table 3).
Oat and barley b-glucans have been shown to reduce TC levels in
people diagnosed with hypercholesterolaemia (FDA, 1997, 21 January)
and to increase bile acid excretion (Bae, Kim, Lee, & Lee, 2010; Ellegard
& Andersson, 2007). High molecular weight b-glucan (1,200 kDa) has
higher viscosity than low molecular weight b-glucan (400 kDa) and
thus may trap more unabsorbed cholesterol and its derivatives (e.g.,
bile salts) than low molecular weight b-glucan does. However, the
lipid-lowering effects of high and low molecular weight b-glucans were
reported to be similar (Keenan et al., 2007). Notably, b-glucan demon-
strated multiple cholesterol-lowering effects not only in the structural
trapping of bile acid but also in the elevation of CYP7A1 activity (Yang,
Kim, Lee, Lee, & Moon, 2003) and LDL receptor regulation (Watkins,
2004), which accelerate bile acid excretion and cholesterol utilisation,
respectively. In this study, TC and faecal cholic acid levels did not differ
among the treatment groups. However, serum TG levels were signifi-
cantly lower in the B and M groups than in the C group. No differences
in other biochemical parameters were observed in the P group.
In our study, the dietary intervention with b-glucan did not affect
food intake and white adipose tissue weight; nevertheless, a decreasing
trend in food efficiency and white adipose tissue weight was observed.
By contrast, after the dietary intervention with L. plantarum, an increas-
ing trend in body weight and food efficiency was observed. These
results are inconsistent with those of studies that used murine models
for examining the anti-obesity effects of L. plantarum (Lee, Paek, Lee,
Park, & Lee, 2007; Park et al., 2014; Yoo et al., 2013). Regarding stud-
ies of humans, the number of Firmicutes, such as Lactobacillus, have
been found to be higher in patients with obesity than in participants

F I G U R E 1 The percentage yields of different extracts obtained F I G U R E 2 Results of TPC and TFC of different extracts obtained
from the powdered roots of N. leucophylla from stems of N. leucophylla
LEE ET AL.
with a normal weight; one study indicated that some Lactobacillus
strains may contribute to gut microbiota-induced obesity (Kadooka
et al., 2010; Million, Maraninchi, et al., 2012). The inconsistent results
may be due to different degrees of weight gain caused by variation in
host-specific factors (i.e., animal species and host physical status), as
well as the different Lactobacillus species (Million, Angelakis, et al.,
2012) and their secondary metabolites (i.e., SCFAs, t10, c12-
conjugated linoleic acid, and cholic acid) (Byrne, Chambers, Morrison, &
Frost, 2015; Lee et al., 2007). In our study, the P and M groups exhib-
ited higher body weight gain and white adipose tissue accumulation
(inguinal and perirenal fat) than the C group did. The levels of total
SCFAs, particularly butyrate, in rectal faeces and the colonic mucin
were proportionally associated with weight gain and adipose tissue
accumulation in the P and M groups. Several mechanisms through
which bacterial metabolites affect the regulation of energy homeostasis
and obesity have been suggested (Erejuwa, Sulaiman, & Ab Wahab,
2014). Bacteria-produced SCFAs are thought to activate a series of
G-protein–coupled receptors (GPR41 and GRP43) in gut epithelial cells.
The activation of SCFA-linked G-protein-coupled receptors, which con-
siderably increase energy harvest and deposition in hosts, can be attrib-
uted to gut microbiota (Erejuwa et al., 2014). These results support the
alternative view that gut microbiota may have a key role in modulating
the harvest of energy from macronutrients, and may be a factor that
affects the metabolic status of the host, regulating additional energy
expenditure and accumulation (Cani & Everard, 2016).
Regarding gut SCFA levels, we analysed the relationship among
SCFAs in caecal faeces, rectal faeces, and colonic mucin. Gut
microbiota-produced SCFAs fulfil a relatively small portion of the
energy requirement; however, studies have suggested that these
metabolites may affect energy homeostasis (Moreno-Indias, Cardona,
Tinahones, & Queipo-Ortuno, 2014; Moreno-Indias and Tinahones,
2015). SCFAs regulate cell differentiation, activate intestinal neuro-
transmitter release (de Theije et al., 2014; Zaibi et al., 2010), and regu-
late energy homeostasis through gluconeogenesis and lipogenesis in
specific organs such as the liver and muscles (Udayappan, Hartstra,
Dallinga-Thie, & Nieuwdorp, 2014). In our study, we observed that the
total SCFA levels in caecal and rectal faeces were significantly higher in
the M group than in the C group. Butyrate levels in the colonic mucin
layer were significantly higher in the P and M groups than in the B
group. Therefore, we propose that SCFAs, particularly butyrate, pene-
trate the intestinal epithelium and directly provide a signal that acti-
vates signalling cascade events, thereby enabling the cellular activities
of lipogenic and lipolytic enzymes. The LPL activity of the M group was
inversely correlated with gut SCFA levels. In addition, SCFA levels in
the colonic mucin were higher in the P and M groups than in the other
treated groups. Furthermore, the B and M groups had lower SCFA lev-
els in the colonic mucin than other treated groups did. Although a trend
of increasing SCFA levels in the colon mucin and of increasing hepatic
ACC and FAS activities was observed in the P and M groups, the SCFA
levels produced by 109 CFU of L. plantarum P-8 did not reach the
threshold for activating enzymes involved in energy homeostasis. Thus,
SCFAs in various locations (faeces and mucin) and under different die-
| 7 of 9
tary treatments (probiotic and prebiotics) may independently contrib-
ute to weight gain and weight production. Moreover, some
Lactobacillus spp. have modulating properties that release the fasting-
induced adipocyte factor from intestinal cells, thereby inhibiting LPL
activity and resulting in increased liver-derived TG storage (Backhed,
Manchester, Semenkovich, & Gordon, 2007).
Our study has a few limitations. First, although probiotics (e.g.,
L. plantarum P-8) have been used to reduce weight gain in some murine
species, the subspecies of Lactobacillus involved in energy homeostasis
in rats does not exhibit consistent properties in this respect. Second,
we did not quantify the changes in mucosal receptors and proinflam-
matory factors. Although the results regarding bacteria-produced
SCFAs indicated that SCFAs have a crucial role in energy homeostasis,
the expression levels of possible mucosal receptors (i.e., GPR41 and
GRP43) and proinflammatory factors should be quantified. Additional
studies investigating the inflammatory status (i.e., insulin, CRP, TNFa,
and selected IL levels) are necessary. Third, we did not analyse the gly-
caemic status of the rats, although the rats fed the high-fat diet for 8
weeks had normal liver and kidney functions and exhibited no extreme
changes in their liver lipid profiles. Notably, obesity-related metabolism
may trigger abnormal blood sugar and lipid regulation leading to the
onset of metabolic syndrome. Fourth, some activities of lipolytic and
lipogenic enzymes were inconsistent among the treated groups (i.e.,
the P and B groups). The physical network of SCFAs and related energy
homeostasis parameters (i.e., intestinal mucosal barriers and carbohy-
drate and lipid metabolic enzymes) could be interpreted as indicating
that an unknown upstream neurotransmitter regulates macronutrient
metabolism. A well-designed study on L. plantarum should be con-
ducted to evaluate the effects of SCFAs on the activities of intestinal
mucosal barriers and lipid metabolic enzymes.
In summary, our results indicate that administering b-glucan and L.
plantarum P-8 to obese rats produces different energy harvesting
effects. b-Glucan, but not L. plantarum P-8, can increase the activities
of hepatic FAS, ACC, and CPT and reduce the activity of epididymal fat
LPL, resulting in decreased white adipose tissue accumulation in obese
rats. However, b-glucan and L. plantarum P-8 demonstrated no syner-
gistic effects. Further evidence demonstrating the ability of SCFAs to
reduce body weight and white adipose tissue accumulation under a
high-fat diet is necessary.
ACKNOWLEDG MENTS
This research was partially supported by grants (NSC101-2320-B-
038-020-MY2; NSC102-2313-B-038-003-MY2, and MOST103-
2320-B-038-012-MY3) from the Ministry of Science and Technol-
ogy, Taiwan.
CONFLIC T OF I NTE RE ST
The authors declared that they have no conflict of interest.
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