Consumption of Mesona chinensis Attenuates Postprandial Glucose

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The American Journal of Chinese Medicine, Vol. 42, No. 2, 315–336
© 2014 World Scientiﬁc Publishing Company
Institute for Advanced Research in Asian Science and Medicine
DOI: 10.1142/S0192415X14500219
Consumption of Mesona chinensis
Attenuates Postprandial Glucose and
Improves Antioxidant Status Induced
by a High Carbohydrate Meal in
Overweight Subjects
Charoonsri Chusak,*,‡ Thavaree Thilavech†,‡ and Sirichai Adisakwattana*,‡
*Department
of Nutrition and Dietetics, Faculty of Allied Health Sciences
†
Program in Biomedical Sciences, Graduate School
‡
Research Group of Herbal Medicine for Prevention
and Therapeutic of Metabolic Diseases
Chulalongkorn University, Thailand
Abstract: Edible plants constitute a potential source for controlling postprandial hyperglycemia and oxidative stress. The objective of this study was to investigate in vitro antioxidant
and intestinal -glucosidase inhibitory activities of Mesona chinensis (MC). In addition, the
acute effect of MC on postprandial glucose and plasma antioxidant status after the consumption of a high carbohydrate (HC) meal by overweight subjects was also determined.
The results showed that total phenolic and ﬂavonoid contents in the extract were
212:37 5:64 mg gallic acid equivalents/g dried extract and 23:44 2:50 mg catechin
equivalents/g dried extract, respectively. MC extract markedly inhibited the intestinal maltase
and sucrose with the IC50 values of 4:66 0:22 mg/mL and 1:30 0:43 mg/mL, respectively. However, MC extract had no inhibitory activity against pancreatic -amylase. In
addition, MC extract had antioxidant properties including DPPH radical scavenging activity,
superoxide radical scavenging activity (SRSA), hydroxyl radical scavenging activity
(HRSA), trolox equivalent antioxidant capacity (TEAC), ferric reducing antioxidant power
(FRAP), oxygen radical absorbance capacity (ORAC), and ferrous ion cheating activity
(FICP). The signiﬁcant decrease in postprandial plasma glucose, triglyceride and malondialdehyde levels, and the increase in plasma antioxidant capacity (FRAP and ORAC)
were observed in overweight subjects receiving a HC meal together with MC extract (1 g).
The ﬁnding supports that MC helps normalize and enhance antioxidant defense induced by a
HC meal, suggesting that MC may have the potential for the prevention of chronic conditions
and diseases associated with overweight and obesity.
Correspondence to: Dr. Sirichai Adisakwattana, Department of Nutrition and Dietetics, Faculty of Allied Health
Sciences, Chulalongkorn University, 154 Rama 1 Rd., Wangmai Pathumwan, Bangkok, Thailand 10330. Tel:
(þ66) 2-218-1067, E-mail: [email protected]
315
316
C. CHUSAK et al.
Keywords: Mesona chinensis; Antioxidant; -Glucosidase; High Carbohydrate Meal;
Overweight.
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Introduction
Syndrome X is a group of metabolic abnormalities related to abdominal obesity, dyslipidemia, hypertension, and hyperglycemia. Excessive accumulations of abdominal fat, inner
abdomen, and visceral fat create the form of overweightness and/or obesity that leads to an
increased risk of cardiovascular diseases and type 2 diabetes (Boyko et al., 2000; Grundy
et al., 2004). Consumption of carbohydrate-rich diets result in marked increase in postprandial glucose that causes oxidative stress by increasing the production of reactive
oxygen species through several biochemical pathways (Hill and Prentice, 1995; Gregersen
et al., 2012). Increased oxidative stress has been associated with impaired endothelial
function and atherosclerosis, leading to coronary artery disease (Sies and Stahl, 1995;
Burton-Freeman, 2010; Hanhineva et al., 2010). In people who are overweight and obese,
attenuating postprandial glucose excursion by inhibiting -glucosidase and the reduction of
oxidative stress by increasing antioxidant dietary intakes could be a possible strategy to
reduce the incidence of diabetes and its complications (Liao et al., 2006; Satoh et al., 2006;
O’Keefe et al., 2008; Adisakwattana et al., 2010).
A number of studies have shown the beneﬁcial effect of plant-based diets for the
inhibition of -glucosidase in vitro and in vivo that delays postprandial hyperglycemia
(Mai et al., 2007; Ranilla et al., 2010; Adisakwattana et al., 2011). Furthermore, plantbased diets also contain variable chemical families and amounts of antioxidants. Polyphenols, naturally occurring compounds found in plant-based diets, are considered
important to human health. In the last decade, there has been much interest in the
potential health beneﬁts of dietary plant polyphenols as antioxidants and -glucosidase
inhibitors (Hanhineva et al., 2010). It is believed that dietary plant polyphenols may help
to delay postprandial hyperglycemia and increase plasma antioxidant capacity in humans
with minimal side effects. Mesona chinensis (MC) Benth (Chinese Mesona) belongs to
the same mint family as Lamiaceae. It is an economically valued agricultural plant in
Southeast Asia and China (Zhao et al., 2011). MC is most commonly consumed as an
herbal drink and a gelatin-type dessert (Grass jelly). This plant-based diet has also been
used as an ancient folk medicine to treat hypertension, diabetes and liver diseases (Shen
et al., 2000). Previous studies have shown that MC contains 17 amino acids (seven
essential amino acids), carbohydrates, fat, ﬁber, polyphenols, and ﬂavonoids (Liu et al.,
2005; Hailan et al., 2011). However, there is currently no evidence of the effects of MC
on postprandial glycemia and antioxidant status in humans. The objective of this study,
therefore, was to investigate the effects of MC extract on the inhibition of intestinal
-glucosidase and antioxidant activity in vitro. In addition, this work was also designed
to investigate the acute effect of MC extract on postprandial glucose and plasma antioxidant status in overweight subjects after the consumption of a high carbohydrate
(HC) meal.
MESONA CHINENSIS ON BODY WEIGHT
317
Materials and Methods
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Chemicals and Reagents
Fluorescein sodium salt, 2,2 0 -Azobis (2-methylpropionamidine) dihydrochloride,
6-Hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid, bovine xanthine oxidase, 2,2 0 Azino-bis (3-ethylbenzothiazoline-6-sulfonic acid diammonium salt, 2,4,6-Tris(2-pyridyl)s-triazine, rat intestinal acetone powder, porcine pancreatic-amylase, 2,2 0 -diphynyl-1picrylhydrazyl, 2-thiobarbituric acid, tris(hydroxymethyl)aminomethane, 2,2 0 -bipyridyl,
hydroxylamine hydrochloride, Folin–Ciocalteu’s phenol reagent, and (þ)-catechin hydrate
were purchased from Sigma–Aldrich (St. Louis, MO, USA). Trichloroacetic acid (TCA)
was purchased from Merck (Darmstadt, Germany). Gallic acid was purchased from Fluka
(St. Gallen, Switzerland). 2-Deoxy-D-ribose was purchased from Affymetrix Inc. (Santa
Clara, CA, USA). Glucose and triglyceride liquicolor were purchased from HUMAN
GmbH (Wiesbaden, Germany). All other chemicals used were of analytical grade.
Plant Preparation and Extraction
The dried whole plants were purchased from a speciﬁc herbal drugstore in Bangkok,
Thailand. The dried plants (300 g) were boiled in distilled water (4 L) at 90 C for 4 h. After
boiling, the residue of the plant was ﬁltered with a colander. The aqueous solution was
dried using a spray dryer SD-100 (Eyela World, Tokyo Rikakikai Co., LTD, Japan). The
condition of the spray dryer was inlet temperature 178–180 C, outlet temperature 85–
95 C, blower 0.80–0.90 m3/min, and atomizing at 90 kPa. The powder extract was kept in
a dry place.
Measurement of Total Phenolic and Flavonoid Content
The content of total phenolics and total ﬂavonoids in the extract was determined using the
Folin–Ciocalteu’s phenol reagent and aluminum chloride colorimetric method with a
previously published report, respectively (Adisakwattana et al., 2010). The content of total
phenolics was expressed as mg gallic acid equivalents/g dried extract. The content of total
ﬂavonoids was expressed as mg catechin equivalents/g dried extract. The extract was
freshly dissolved in distilled water before use.
Intestinal -Glucosidase and Pancreatic -Amylase Inhibitory Activity
The intestinal -glucosidase inhibitory activity was done according to a previous study
(Adisakwattana et al., 2011). 100 mg of rat intestinal acetone powder was brieﬂy homogenized in 3 mL of 0.9% NaCl solution. After centrifugation (12,000 g 30 min), the
crude enzyme solution (10 L) was incubated with 80 L maltose (25.9 mM) or sucrose
(60 mM) in 0.1 M phosphate buffer pH 6.9, and 10 L of the sample at various concentrations in distilled water at 37 C for 30 min (maltase assay) and 60 min (sucrase assay).
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C. CHUSAK et al.
The mixtures were suspended in boiling water for 10 min to stop the reaction. The concentrations of glucose released from the reaction mixtures were determined by the glucose
oxidase method.
The pancreatic -amylase inhibition assay was performed according to a previous
report (Adisakwattana et al., 2011). Porcine pancreatic -amylase was dissolved in 0.1 M
phosphate buffer saline, pH 6.9. The various concentrations of the sample were added to a
solution containing the starch (1 g/L) in 0.1 M phosphate buffer with a pH of 6.9. The
reaction was initiated by adding pancreatic -amylase (3 units/mL) to the incubation
medium (ﬁnal volume: 500 L). After 10 min the reaction was stopped by adding 500 L
dinitrosalicylic (DNS) reagent (1% 3,5-dinitrosalicylic acid, 0.2% phenol, 0.05% Na2SO3,
and 1% NaOH in aqueous solution) to the reaction mixture. The mixtures were heated at
100 C for 10 min to develop the yellow–brown color. Thereafter, 500 L of 40% potassium sodium tartarate solution was added to the mixtures to stabilize the color. After
cooling to room temperature in a cold water bath, absorbance was recorded at 540 nm using
a spectrophotometer.
DPPH Radical Scavenging Activity
2,2-Diphenyl-1-picrylhydrazyl (DPPH) radical scavenging activity was measured according to a previous literature (Mäkynen et al., 2013). Brieﬂy, the sample (100 L) was added
to 100 L DPPH solution (0.2 mM in ethanol) and incubated for 30 min at room temperature. The decrease in the solution absorbance was measured at 515 nm. The DPPH
radical scavenging activity was calculated from a standard curve using ascorbic acid. The
DPPH radical scavenging activity was expressed as an equivalent of ascorbic acid (mg
ascorbic acid/g dried extract). Ascorbic acid was used as a positive control for this study.
Trolox Equivalent Antioxidant Capacity (TEAC) Assay
The Trolox equivalent antioxidant capacity (TEAC) assay was measured according to a
previously published report (Mäkynen et al., 2013). Brieﬂy, a 2,2 0 -azinobis(3-ethylbenzothiazoline-6-sulfonate) free radical (ABTS þ ) solution was prepared by mixing 7 mM
ABTS þ in 0.1 M phosphate buffer saline (pH 7.4) with 2.45 mM K2S2O4 in distilled
water. The solution was kept for 16 h at room temperature in the dark. The ABTS þ was
diluted with 0.1 M phosphate buffer saline (pH 7.4) to absorbance between 0.900 and 1.000
at 734 nm. 10 L of the extract (1 mg/mL) was mixed with 90 L the diluted ABTS þ
solution. After 6 min, the absorbance was measured at 734 nm. The TEAC value was
calculated from the calibration curve of Trolox. The TEAC value was expressed as mg
Trolox equivalents/mg dried extract.
Ferric Reducing Antioxidant Power (FRAP) Assay
The FRAP assay was measured according to a previously published report (Mäkynen et al.,
2013). The FRAP reagent contained 0.30 M sodium acetate buffer solution (pH 3.6),
MESONA CHINENSIS ON BODY WEIGHT
319
10 mM 2,4,6-tripyridyl-S-triazine (TPTZ) in 40 mM HCl and 20 mM FeCl3 in the ratio
10:1:1 and freshly prepared. 90 L of the FRAP reagent was mixed with 10 L of the
extract (1 mg/mL). The mixture reaction was incubated at room temperature and kept in the
dark. After 4 min, the absorbance was measured at 595 nm. The FRAP value was calculated from the calibration curve of FeSO4. The FRAP value was expressed as mM FeSO4
equivalents/mg dried extract.
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Hydroxyl Radical Scavenging Activity
The HRSA measurement was done according to a previously described method (Halliwell
et al., 1987). The reaction mixture was generated by adding 30 L of 2-deoxy-2-ribose
(17 mM), 30 L of the extract, 30 L of 1.2 mM EDTA, 60 L of 0.3 mM FeCl3, 30 L of
34 mM hydrogen peroxide (H2O2), and 60 L of 0.6 mM ascorbic acid. The reaction was
performed at 37 C for 1 h. Thereafter, 150 L of 1% (w/v) thiobarbituric acid (TBA) and
300 L of 2.8% (w/v) TCA were added to the mixture, which was then incubated at 100 C
for 15 min. After cooling, the absorbance was measured at 532 nm against a blank containing deoxyribose and buffer. Trolox was used as a positive control for this study.
Superoxide Radical Scavenging Activity
The measurement of superoxide radical scavenging activity (SRSA) was done according to
a previous method (Kweon et al., 2001) with slight modiﬁcation. In brief, 7.5 L of the
sample, 150 L of 0.30 mM xanthine, 50 L of 0.15 mM NBT, 50 L of 0.60 mM EDTA,
and 7.5 L of xanthine oxidase (0.05 unit/mL) were mixed in a microplate. After incubation for 40 min at 37 C, the absorbance was measured at 560 nm against an appropriate
blank to determine the quantity of formazan generated. A Trolox was used as a positive
control for this study.
Ferrous Ion Chelating Activity
The ferrous ion chelating activity (FICP) was measured according to a previous report with
a minor modiﬁcation (Yamaguchi et al., 2000). In brief, 25 L of 1 mM FeSO4 solution
and an equal volume of extract was mixed with 100 L of Tris-HCl buffer (pH 7.4), 100 L
of 2,2 0 -bipyridyl solution (0.1% in 0.2 M HCl), 40 L of 10% (w/v) hydroxylamine-HCl,
and 150 L of ethanol, respectively. After the total volume of the reaction mixture was
adjusted to 1 mL by distilled water, the absorbance was recorded at 522 nm. The FICP was
calculated from the calibration curve of EDTA. The activity was expressed as mg of EDTA
equivalents/mg dried extract.
Oxygen Radical Absorbance Capacity (ORAC) Assay
The ORAC assay was done according to a previous method with slight modiﬁcation (Wang
et al., 2011). The sample (25 L) was mixed with 48 nM sodium ﬂuorescein (150 L) in
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C. CHUSAK et al.
75 mM phosphate buffer saline. After incubation for 10 min at 37 C, AAPH (25 L)
solution was then added to the mixture. The ﬂuorescence intensity (excitation ¼ 485 nm;
emission ¼ 535 nm) was measured every minute until 1 h. The quantitation of the antioxidant capacity was calculated using the area under the curve (AUC). The ORAC value
was calculated from AUC of Trolox. The ORAC value was expressed as mol Trolox
equivalents/mg dried extract.
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Human Study
Men (n ¼ 11) aged 20–40 years that were free of any serious illness, did not use tobacco
products and were not taking any medications or nutritional supplements were recruited for
the study. Other inclusion characteristics were BMI of 23–30 kg/m2, resting blood pressure
< 160=100 mm Hg, fasting blood glucose < 100 mg/dL, fasting total cholesterol < 200 mg/
dL, fasting triglyceride < 150 mg/dL. The study was approved by the ofﬁce of Ethics
Review Committee for Research Involving Human Research Subjects, Human Science
Group, Chulalongkorn University (COA No. 178/2555). A randomized, controlled, 3period crossover study with two weeks’ separation between testing sessions was conducted. The three test conditions were a HC meal, a HC meal plus 0.5 g of MC extract and
a HC meal plus 1 g of MC extract. A HC meal consisted six tablespoons of Ensure®
(230 mL) and three slices of white bread with one tablespoon of condensed milk. The
consumption of the meal was approximately 69% of calories as carbohydrate, 15% as
protein, and 16% as fat. Participants were instructed to avoid high antioxidant foods for
48 h prior to testing. After 8 h of fasting, the participants were allowed 15 min to consume
the meal. The ﬁrst postprandial blood sample was collected at the end of the 30 min eating
period. Subsequently, blood was collected every 30 min for 4 h. For each sample, blood
was centrifuged and portions of plasma were kept and stored at 20 C.
Assay Methods
Plasma glucose was determined by using a glucose oxidase method (HUMAN GmbH,
Germany). Serum triglyceride was determined by using a triglyceride enzymatic colorimetric method (HUMAN GmbH, Germany).
Plasma FRAP Assay
Plasma FRAP was determined according to a previously published report (Benzie and
Strain, 1996). The plasma was diluted to 1:5 with 0.1 M phosphate buffer saline (pH 7.4).
The FRAP reagent contained 0.3 M of sodium acetate buffer saline (pH 3.6), 10 mM TPTZ
in 40 mM HCl, and 20 mM FeCl3. 90 L of FRAP reagent was mixed with 10 L of the
diluted plasma. The reaction mixture was incubated in the dark at room temperature for
30 min and the absorbance was read at 595 nm. The FRAP value was calculated from the
calibration curve of FeSO4 and expressed as mM FeSO4 equivalents.
MESONA CHINENSIS ON BODY WEIGHT
321
Plasma ORAC Assay
Plasma ORAC assay was determined according to a previously published report with
slight modiﬁcations (Wang et al., 2011). The plasma was diluted to 1:10 with 0.1 M
phosphate buffer saline (pH 7.4). The diluted plasma (25 L) was mixed with 4.8 nM
sodium ﬂuorescein in 75 mM phosphate buffer saline (150 L). After incubation at 37 C
for 10 min, 25 L of 64 mM AAPH was added to the mixture. The ﬂuorescence intensity
(excitation ¼ 485 nm; emission ¼ 535 nm) was measured every 2 min for 1 h. The quantitation of the antioxidant capacity was calculated by using the AUC following equation:
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AUCantioxidant ¼ AUCS AUCb
where AUCS was the AUC of the diluted plasma and AUCb was the area under the curve of
the blank (0.1 M PBS). The ORAC value was calculated from the calibration curve of
Trolox and expressed as mol Trolox equivalents.
Plasma MDA Assay
Plasma malondialdehyde (MDA) was determined according to a previously published
report (Wolff and Dean, 1987). The plasma (160 L) was mixed with 160 L of 10%
thichloroacetic acid (TCA) and 30 L of 50 M 2,6-di-tert-butyl-4-methylphenol (BHT).
The mixture was centrifuged at 13,000 rpm for 10 min at 4 C to precipitate proteins. After
0.67% thiobarbituric acid (150 L) was added to the supernatant (150 L), the mixture
solution was incubated at 95 C for 10 min. Then, the solution was cooled at room temperature and was read at 532 nm. MDA was used for a calibration curve. Plasma MDA
concentration was calculated from the calibration curve of MDA.
Statistical Analysis
The IC50 values were calculated from plots of the log concentration of inhibitor concentration vs. percentage inhibition curves. Data were expressed as mean standard error of
the mean (SEM), n ¼ 3. In the human study, postprandial incremental areas were calculated by the trapezoidal method as the AUC above the baseline value. One-way repeated
measure ANOVA was used for comparison of the time point within groups, followed by
Post hoc test by Least Square Signiﬁcance (LSD) for multiple comparisons. p value < 0:05
was considered to be a statistically signiﬁcant difference.
Results
Phytochemical Analysis
Phenolic compounds and ﬂavonoids are considered as major contributors to antioxidant
activity as well as the intestinal -glucosidase and pancreatic -amylase inhibitory activity.
Therefore, the dried extract was examined for total phenolic content and ﬂavonoids. The
322
C. CHUSAK et al.
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Table 1. The IC50 Values for Intestinal
®-Glucosidase (Maltase and Sucrase),
and Pancreatic ®-Amylase by MC
MC
IC50 Values
Intestinal maltase
Intestinal sucrase
Pancreatic -amylase
4.66 0.22
1.30 0.43
NI
Note: Results are expressed as means SEM, n ¼ 3. Intestinal maltase and sucrase
inhibitory activities are expressed as the
IC50 value (mg/mL). NI ¼ no inhibition.
results showed that the total phenolic and ﬂavonoid content of MC extract was
212:37 5:64 mg gallic acid equivalents/g dried extract, and 23:44 2:50 mg catechin
equivalents/g dried extract, respectively.
The Intestinal -Glucosidase and Porcine -Amylase Inhibitory Activity
MC extract was investigated for inhibitory activity against the intestinal -glucosidase
(maltase and sucrase). The results exhibited that MC extract markedly inhibited the
intestinal maltase and sucrase in a concentration-dependent manner (data not shown). As
shown in Table 1, the IC50 values of MC extract on intestinal sucrase and maltase were
1:30 0:43 mg/mL and 4:66 0:26 mg/mL, respectively. Nevertheless, MC extract did
not show any effect on pancreatic -amylase inhibition.
Antioxidant Capacities
The effects of MC extract on different antioxidant capacities are shown in Table 2. On the
DPPH assay, MC extract had signiﬁcant radical scavenging activity, with increasing
concentration in the range of 0.05–1.00 mg/mL. The IC50 values of MC extract and
ascorbic acid were found to be 0:14 0:02 mg/mL and 0:02 0:01 mg/mL, respectively,
indicating that MC extract had seven times less potency than ascorbic acid. According to
Table 2. The DPPH, TEAC, FRAP, ORAC, HRSA, SRSA, and FICP of MC
Antioxidant Activity
MC
DPPH
TEAC
FRAP
ORAC
HRSA
SRSA
FICP
0.14 0.02
0.41 0.02
1.42 0.06
25.98 1.30
0.09 0.01
0.38 0.03
0.33 0.01
Note: Data are expressed as mean SEM, n ¼ 3. DPPH radical scavenging activity, SRSA (superoxide radical
scavenging activity), and HRSA (hydroxyl radical scavenging activity) were expressed as the IC50 value
(mg/mL). TEAC was expressed as mg trolox equivalents/mg dried extract. FRAP was expressed as mM FeSO4
equivalents/mg dried extract. ORAC was expressed as mol trolox equivalents/mg dried extract. FICP was
expressed as mg EDTA equivalents/mg dried extract.
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MESONA CHINENSIS ON BODY WEIGHT
323
the results from the TEAC assay, MC extract had the ability of 0:41 0:02 mg Trolox
equivalents/mg dried extract. A FRAP assay determined the reducing ability of an antioxidant reacting with a ferric tripyridyltriazine (Fe 3þ –TPTZ) complex and producing a
colored ferrous tripyridyltriazine (Fe 2þ –TPTZ). MC extract had a FRAP value of
1:42 0:06 mM FeSO4 equivalents/mg dried extract. Moreover, the ORAC value of the
extract was 25:98 1:30 as mol Trolox equivalents/mg dried extract. The hydroxyl
radical is one of the representative reactive oxygen species generated in the body. The
results showed that the IC50 values of MC and Trolox were 0:09 0:01 mg/mL and
0:03 0:01 mg/mL, respectively. This suggests that MC extract had three times less
potency than Trolox. In addition, MC extract had the superoxide radicals scavenging
activity in a concentration-dependent manner with the IC50 value of 0:38 0:03 mg/mL,
while the IC50 value of Trolox was found to be 1:40 0:21 mg/mL. The results showed
that MC extract had 3.65 times more potency than Trolox. Furthermore, MC extract had
the FICP with 0:33 0:01 mg EDTA equivalents/mg dried extract.
Human Study
The screening and visit baseline characteristics of the participants are presented in Table 3.
The effects of MC extract, together with a HC meal, on the incremental postprandial
glucose are presented in Fig. 1A. The basic carbohydrate meal caused a rapid rise of
glucose, with the peak concentration at 30 min, followed by a rapid fall below the baseline
level within 210 min. Ingestion of MC extract together a HC meal results in a lower
glucose concentration and a slow decline during the 210 min. Comparing at individual
time points with a HC meal, the incremental plasma glucose concentration was signiﬁcantly decreased at 120 min ( p ¼ 0:041), 150 min ( p ¼ 0:020), 180 min ( p ¼ 0:021),
and 240 min ( p ¼ 0:008) after consuming the HC meal plus 0.5 g of the extract.
Meanwhile, the incremental plasma glucose concentration was signiﬁcantly decreased at
Table 3. Baseline Characteristics of Eleven
Participants in the Study
Variable
Age (years)
Weight (kg)
Height (cm)
BMI (kg/m 2 )
Plasma glucose (mg/dL)
Total cholesterol (mg/dL)
Serum triglyceride (mg/dL)
Creatinine (mg/dL)
SGOT (U/L)
SGPT (U/L)
25.0
73.15
172.64
24.71
94.0
194.0
89.7
0.97
20.08
12.08
0.68
2.98
1.86
0.34
2.51
5.86
7.43
0.02
1.04
1.90
Note: Data are expressed as mean SEM,
n ¼ 11.
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C. CHUSAK et al.
(A)
(B)
Figure 1. The effects of MC on the incremental plasma glucose concentration (A) and the incremental AUCs of
plasma glucose concentration (B) induced by a HC meal in overweight subjects (n ¼ 11). Values are means with
standard error of the means (SEMs). Mean value was signiﬁcantly different from that of a HC meal: *p < 0:05.
90 min ( p ¼ 0:000), 120 min ( p ¼ 0:017), 180 min ( p ¼ 0:023), and 240 min ( p ¼ 0:003)
after consuming a HC meal plus 1 g of the extract. As shown in Fig. 1B, the incremental AUCs of plasma glucose concentration was signiﬁcantly reduced after consumption of a HC meal plus 1 g of the extract ( 38:98 16:97 min mg=dL) compared
to a HC meal (47:20 21:06 min mg=dL) ( p ¼ 0:009). However, there was no signiﬁcant difference between a HC meal plus 0.5 g of the extract and a HC meal alone
(13:01 14:39 min mg=dL).
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MESONA CHINENSIS ON BODY WEIGHT
325
(A)
(B)
Figure 2. The effects of MC on the incremental plasma FRAP level (A) and the incremental AUCs of FRAP level
(B) induced by a HC meal in overweight subjects (n ¼ 11). Values are means with SEMs. Mean value was
signiﬁcantly different from that of a HC meal: *p < 0:05.
As shown in Fig. 2A, consumption of a HC meal with MC extract results in higher
plasma FRAP concentrations at 90 min. Comparing with a HC meal at the individual time
points, only at 90 min after administration of a HC meal plus 0.5 g of the extract, the
incremental plasma FRAP level ( p ¼ 0:006) signiﬁcantly increased. In the meantime, the
incremental plasma FRAP level in a HC meal plus 1 g of the extract was signiﬁcantly
increased at 30 min ( p ¼ 0:013), 90 min ( p ¼ 0:002), 150 min ( p ¼ 0:042) and 210 min
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( p ¼ 0:008), respectively. In Fig. 2B, the incremental AUCs for plasma FRAP level
were signiﬁcantly higher in a HC meal plus 0.5 g of the extract ( p ¼ 0:002; 128:29 72:60 min mol=L), as well as a HC meal plus 1 g the extract ( p ¼ 0:016; 162:22 116:34 min mol=L), when compared to HC meal (220 59:47 min mol=l).
The individual time points of the incremental postprandial plasma ORAC level were
signiﬁcantly increased at 30 min ( p ¼ 0:05), 60 min ( p ¼ 0:016), 90 min ( p ¼ 0:028), and
240 min ( p ¼ 0:034) after consumption of a HC meal plus 0.5 g of the extract (Fig. 3A).
(A)
(B)
Figure 3. The effects of MC on the incremental plasma ORAC level (A) and the incremental AUCs of ORAC
level (B) induced by a HC meal in overweight subjects (n ¼ 11). Values are means with SEMs. Mean value was
signiﬁcantly different from that of a HC meal: *p < 0:05.
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In addition, the group administered a HC meal together with 1 g of the extract also signiﬁcantly increased the incremental postprandial plasma ORAC level at 90 ( p ¼ 0:018),
210 ( p ¼ 0:016), and 240 min ( p ¼ 0:030), respectively. As shown in Fig. 3B, the
incremental AUCs of plasma ORAC level in the groups receiving a HC meal plus 0.5 g of
the extract ( p ¼ 0:036; 78:40 20:49 min mol=L) and a HC meal plus 1 g of the extract
(A)
(B)
Figure 4. The effects of MC on the incremental plasma MDA level (A) and the incremental AUCs of MDA level
(B) induced by a HC meal in overweight subjects (n ¼ 11). Values are means with SEMs. Mean value was
signiﬁcantly different from that of a HC meal: *p < 0:05.
328
C. CHUSAK et al.
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( p ¼ 0:033; 61:07 18:75 min mol=L) were signiﬁcantly higher than of a HC meal
(154:91 86:45 min mol=L).
Comparing at individual time points with a HC meal, a signiﬁcant decrease in the
incremental postprandial plasma MDA level at 30 min ( p ¼ 0:007), 180 min ( p ¼ 0:046)
and 210 min ( p ¼ 0:010) was observed after ingestion of a HC meal plus 1 g of the extract
(Fig. 4A). No signiﬁcant changes in the plasma MDA level were seen after a HC meal plus
(A)
(B)
Figure 5. The effects of MC on the incremental serum triglyceride concentration (A) and the incremental AUCs of
serum triglyceride concentration (B) induced by a HC meal in overweight subjects (n ¼ 11). Values are means
with SEMs. Mean value was signiﬁcantly different from that of a HC meal: *p < 0:05.
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MESONA CHINENSIS ON BODY WEIGHT
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0.5 g of the extract. As shown in Fig. 4B, only the administration of MC extract (1 g)
showed a signiﬁcant decrease in the incremental AUCs of plasma MDA (0:124 0:11 min mol=L), as compared to a HC meal (0:312 0:10 min mol=L) ( p ¼ 0:043).
In addition, there was no signiﬁcant change in the incremental AUCs of a HC meal plus
0.5 g of the extract (0:074 0:15 min mol=L).
Figure 5A shows the effects of MC on the incremental postprandial serum triglyceride
concentration. After the consumption of a HC meal, the postprandial triglyceride concentration peaks at 180 min, while MC extract (0.5 g and 1.0 g) suppressed the postprandial triglyceride concentrations at 210 min ( p ¼ 0:003 and p ¼ 0:006) and 240 min
( p ¼ 0:008 and p ¼ 0:012), respectively. As shown in Fig. 5B, an intake of a HC
meal plus 0.5 g ( p ¼ 0:031) and 1 g ( p ¼ 0:033) of the extract signiﬁcantly reduced
the incremental AUCs of serum triglyceride concentration (32:39 17:43 min mg=dL
and 39:92 20:03 min mg=dL, respectively) as compared to a HC meal (123:98 37:06 min mg=dL).
Discussion
The intestinal -glucosidases are the key enzymes of dietary carbohydrate digestion. Starch
is primarily digested in the small intestine through the action of pancreatic -amylase,
yielding both linear maltose and branched isomaltose oligosaccharides, which are further
hydrolyzed by intestinal -glucosidase (sucrase and maltase) to release absorbable
monosaccharides (Inzucchi, 2002). The inhibition of these enzymes signiﬁcantly suppresses postprandial hyperglycemia and may have beneﬁcial effects on insulin resistance
and glycemic index control in diabetic patients (Inzucchi, 2002). The administration of
acarbose results in a 20% reduction in the postprandial peak of glycemia and a 25%
reduction in the incidence of diabetes (Chiasson, 2006). Additionally, the long-term
administration of -glucosidase inhibitor may decrease the level of HbA1c , resulting in a
signiﬁcant reduction in the incidence of diabetic complications such as micro- and macrovascular diseases (Scorpiglione et al., 1999). The most common side effects of acarbose are
mild-to-moderate gastrointestinal disturbance such as ﬂatulence, meteorism and abdominal
distention that occurs in a dose-dependent pattern (Hanefeld et al., 1991). Our results
indicate that MC extract showed a marked inhibition against intestinal -glucosidase,
especially for sucrose, whereas it had no inhibitory activity on pancreatic -amylase.
Excessive inhibition of pancreatic -amylase causes gastrointestinal side effects related to
abnormal bacterial fermentation of undigested carbohydrates in the large intestine (Kwon
et al., 2008). It has been suggested that plant-based foods have lower inhibitory activity
against pancreatic -amylase and stronger inhibitory activity against intestinal -glucosidase, indicating that they may be effective agents for the control of postprandial hyperglycemia with fewer side effects than acarbose (Kwon et al., 2008). It is noteworthy that
polyphenols and ﬂavonoids have been shown to inhibit intestinal -glucosidase activity in
vitro (Koh et al., 2009; Fontana Pereira et al., 2011). The earlier studies report a strong
correlation between the polyphenolic content in the extracts and the ability to inhibit
intestinal -glucosidase (Mai et al., 2007; Ramkumar et al., 2010). According to the results
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obtained, the ﬁndings suggest that MC contains high polyphenolic compounds and ﬂavonoids that may be related to its intestinal -glucosidase inhibitory activity. It has been
shown recently that ﬂavonoids inhibit the enzymes through hydrogen bonding interactions
between the hydroxyl groups of the ﬂavonoids and the catalytic residues of the binding site
(Xiao et al., 2013). The molecular interaction of ﬂavonoids in the extract on a speciﬁc
binding site on intestinal -glucosidase remains unknown. However, it can be assumed that
ﬂavonoids in the MC extract may interact with enzymes via these interactions.
Free radicals play an important role in the development of pathogenesis in several
human diseases, such as rheumatoid arthritis, diabetes and its complications, cancer, and
various neurodegenerative and pulmonary diseases (Bjelakovic et al., 2008). Antioxidants
from human diets have the ability to neutralize free radicals and can protect the cells from
damaging oxidation. The literature has documented antioxidant activity of Mesona procumbens Hemsl. (Hsian-tsao) through a thiocyanate method (Hung and Yen, 2002). In
addition, the extract of Mesona procumbens leaf gum has also shown antioxidant activity
including the radical-scavenging effects, FICP, and reducing power (Lai et al., 2001). The
results showed that the extract was more effective in scavenging superoxide radicals than
chelating ferrous ion or scavenging DPPH radicals. The current study was the comprehensive investigation to determine the antioxidant activity of MC extract, including DPPH
radical scavenging activity, TEAC, FRAP, ORAC, hydroxyl, and superoxide radical
scavenging activities, as well as metal chelating activity. Several studies reveal that phenolic compounds and ﬂavonoids have been reported to be major phytochemicals responsible for antioxidant activity (Zheng and Wang, 2001; Palacios et al., 2011). In addition,
ﬂavonoids found in the edible plants act as antioxidants by trapping free radicals (Cao
et al., 1997). Previous studies demonstrated the strong correlation between phenolic
compounds, ﬂavonoids, and antioxidant activity (Rice-Evans et al., 1996; Mäkynen et al.,
2013). The ﬁndings show that MC contains high levels of phenolic compounds and ﬂavonoids. These results appear to suggest that phenolic compounds and ﬂavonoids in the
extract may contribute to the antioxidant activity of MC.
The increased oxidative stress in the overweight and obese plays a pivotal role in the
pathogenesis of metabolic syndromes. Excessive free radicals generally cause the tissue
damage and regulate the inﬂammatory status in adipocytes (Zhu et al., 2006). Being
overweight and obesity are independent risk factors for plasma lipid peroxidation and poor
glycemic control that can cause protein oxidation (Osawa and Kato, 2005; Ahmed et al.,
2005). Interestingly, the consumption of carbohydrate-rich meals has been shown to
increase postprandial glucose and oxidative stress by active oxidative metabolism and
formation of reactive oxygen species induced oxidative stress (Hill and Prentice, 1995;
Gregersen et al., 2012). An increase in oxidative stress has been associated with a corresponding increase in diverse diseases, including endothelial dysfunction, diabetic complications, atherosclerosis, and hypertension (Johnson, 2012; Popolo et al., 2013; Sun
et al., 2013). A previous study reveals that the consumption of small amounts of antioxidant rich food has been associated with inadequate antioxidant defenses in Spanish
obesity (Schröder et al., 2004). Additionally, the consumption of a HC meal results in
a greater and more prolonged oxidative stress in obese subjects than in normal subjects
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MESONA CHINENSIS ON BODY WEIGHT
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(Patel et al., 2007). According to the results from in vitro, we assume that the consumption
of MC extract together with a HC meal may decrease postprandial glucose and increase
antioxidant status in overweight subjects. Our ﬁndings exhibited that MC extract markedly
decreased postprandial glucose induced by a HC meal in overweight men. In healthy
humans, the postprandial plasma glucose concentration typical peaks approximately 30–
60 min after intake of a HC meal. It consequently returns to baseline within 120–180 min
(Brynes et al., 2003). The results showed that consumption of MC extract (1 g) could not
attenuate the peak of postprandial plasma glucose within 30 min, but the postprandial
plasma glucose was suppressed after 60 min of administration. It can be suggested that the
underlying mechanism of MC extract on the postprandial plasma glucose lowering effect
may be involved in the inhibition of -glucosidase in vitro. Hanhineva et al. (2010)
suggested that dietary polyphenol may inﬂuence carbohydrate metabolism and glucose
homeostasis at many levels. The possible mechanisms of dietary polyphenol include the
inhibition of -glucosidase and glucose absorption in the small intestine, the stimulation of
insulin secretion from pancreatic β-cell or the activation of glucose uptake via glucose
transporter at adipose tissues and skeletal muscles (Rutter, 2001; Hanhineva et al., 2010;
Nicolle et al., 2011). It is possible that MC extract may have other mechanisms on the
plasma glucose lowering effect. Further studies are required to explore the extract
responsible for the stimulation of insulin secretion and the activation of glucose uptake.
Interesting reports have shown that the attenuated and prolonged postprandial plasma
glucose reduces the independent risk factors for macrovascular complications (Ceriello,
2010). A previous study has shown that consumption of a HC meal results in increasing
postprandial triglyceride concentrations after 3–4 h (Wolever et al., 2013). A HC meal can
induce hypertriglyceridemia because it increases the production rate and decreases the
clearance rate of VLDL particles. These results cause the alteration of serum lipid proﬁles
(Hellerstein, 2002). The attenuation of carbohydrate-induced postprandial triglyceride may
reduce the risk of cardiovascular disease via the reduction of VLDL particles (Parks, 2001).
In the present study, postprandial triglyceride exhibited a similar pattern to a previous
study. The rise in postprandial triglyceride was attenuated by the extract 3 h after consumption. Our data suggest that MC extract has beneﬁcial effects on delaying postprandial
triglyceride that may reduce the risk of developing macrovascular complications in overweight or obesity.
The postprandial state has been described as pro-oxidative, with the magnitude of the
oxidative stress response linked to a HC meal (Ceriello et al., 1999). The previous studies
have demonstrated that the consumption of a HC diet markedly reduces postprandial
endogenous antioxidant levels such as sulfhydryl (-SH) groups, uric acid and vitamin C, as
well as plasma antioxidant status. Contrastingly, it can increase a marker of oxidative
damage called as malondialdehyde (MDA) (Ceriello et al., 1999; Mah et al., 2011).
Skulas-Ray et al. (2011) demonstrated that adding 14 g of high antioxidant spice blend to a
meal exerted postprandial plasma FRAP and ORAC in overweight men. Moreover,
Micallef et al. reported that the consumption of 400 mL/day of red wine enriched
with anthocyanin signiﬁcantly increased plasma thiol and decreased plasma MDA in young
and old subjects (Micallef et al., 2007). Roussel et al. (2009) demonstrated that the
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C. CHUSAK et al.
consumption of polyphenol-rich extract of cinnamon signiﬁcantly increased plasma thiol
and FRAP levels associated with the reduction of plasma MDA concentration in the
overweight and obese after 12 weeks of study. This evidence suggests that cinnamon
extract has a protective effect against lipid and protein oxidation, together with an
increasing antioxidant status (Roussel et al., 2009). The increasing postprandial oxidative
stress may impair the pathogenesis and complications of several chronic diseases such as
cardiovascular disease and diabetes mellitus. Interestingly, it has been reported that an
increase in plasma antioxidant status associated with the reduction of lipid peroxidation
may help to reduce the incidence of CVD in healthy adults (Ashfaq et al., 2006; Halliwell
and Chirico, 1993). From the current study, consumption of MC together with a HC meal
reduces postprandial glucose and increases antioxidant status as well as decreases MDA
levels, suggesting that MC extract acts in protecting lipid oxidation. These ﬁndings raise
the possibility that polyphenol-rich MC extract may therefore be a natural anti-atherosclerotic component of the diet. However, the limitation of this study was the relatively
small sample size and the selection of only overweight men. Further study is needed to
characterize these effects in long-term consumption, large sample sizes, and more diverse
populations such as obesity and people with cardiovascular risk factors.
Conclusions
MC (Chinese mesona) extract demonstrates beneﬁcial effects on intestinal -glucosidase
inhibitory activities as well as antioxidant activity. MC also reduces postprandial glucose
and increases antioxidant status in a HC meal of overweight people. The available
evidence appears to suggest that MC could be a potential alternative for food and pharmaceutical applications for the prevention of cardiovascular diseases and diabetes and its
complications.
Acknowledgments
We wish to thank Amway Thailand for the partial ﬁnancial support (Amway for Nutrition
Research Grant). The authors would also like to thank the Special Task Force for Activating Research (STAR) under 100 years Chulalongkorn University Fund and the Research
Group of Herbal Medicine for Prevention and Therapeutic of Metabolic Diseases for
ﬁnancial support.
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