inhibition of α-glucosidase and glucose intestinal absorption by thymelaea hirsuta fractions...

$: Inhibition of α-glucosidase and glucose intestinal absorption by Thymelaea hirsuta fractions (毛花瑞香成分对α-糖甙酶以及肠道葡萄糖吸收的抑制作用)$
ORIGINAL ARTICLE

Inhibition of α-glucosidase and glucose intestinalabsorption by Thymelaea hirsuta fractionsSanae ABID,1 Abdenbi LEKCHIRI,2 Hassane MEKHFI,1 Abderrahim ZIYYAT,1

Abdekhaleq LEGSSYER,1 Mohamed AZIZ,1 and Mohamed BNOUHAM1

1Laboratory of Physiology and Ethnopharmacology, and 2Laboratory of Genetics and Biotechnology, Department of Biology, Faculty ofSciences, University Mohamed Ist, Oujda, Morocco

Correspondence

Mohamed Bnouham, BP: 717,Department of Biology, Faculty ofSciences, University Mohamed Ist, Oujda60 000, Morocco.Tel: +21 2 6762 7496Fax: +21 2 3650 0603Email: [email protected]

Received 16 March 2013; revised 29August 2013; accepted 8 November 2013.

doi: 10.1111/1753-0407.12106

Abstract

Background: Thymelaea hirsuta (L.) Endl. (Thymelaeaceae) is a medicinalplant used in Morocco to treat diabetes. In previous studies T. hirsuta hasshown a potent antihyperglycemic effect. Our aim was to study the effect ofthe plant on α-glucosidase inhibition and intestinal glucose absorption.Methods: Five fractions of T. hirsuta were tested, in vitro, in vivo and, insitu, to elucidate the inhibition of α-glucosidase and intestinal glucose uptake.Results: The fractions induced, in vitro, a significant inhibition ofα-glucosidase. The ethyl acetate fraction (EATh) had high activity and itsinhibition mode was non-competitive. The EATh at 50 and 100 mg/kg doses,decreased significantly, in vivo, the postprandial hyperglycemia after sucroseloading in normal and diabetic mice. Moreover, 50 mg/kg of EATh signifi-cantly decreased intestinal glucose uptake, in situ, in rats.Conclusion: The antihyperglycemic effect of T. hirsuta can be explained, inpart, by the inhibition of intestinal α-glucosidase and intestinal glucoseabsorption.

Keywords: diabetes, intestinal glucose absorption, streptozotocin, Thymelaeahirsuta, α-glucosidase inhibitor.

Introduction

Diabetes mellitus is a metabolic disorder characterizedby a persistent hyperglycemia, caused by the impairmentof pancreatic insulin secretion and/or insulin cellularresistance. Currently, it is estimated that 220 millionpeople worldwide have diabetes and that the number willincrease to 300 million by 2025.1 Increased sugar uptakeand physical inactivity are considered causal factors.

This illness has become a global health problem, dueto increasing occurrence and concomitant micro andmacrovascular complications such as retinopathy, neu-ropathy, cardiovascular diseases and concomitant dia-betic mortality.

Several studies have suggested that a cause of chroniccomplications is postprandial hyperglycemia.2,3

Therefore, controlling blood glucose level is the treat-ment aim of diabetes. One of the therapeutic approachesto this disease is the inhibition of postprandial hypergly-cemia. This approach targets inhibition of intestinalα-glucosidase (delaying digestion of polysaccharides tomonosaccharide) and reduction of intestinal glucoseabsorption.

Currently, the search for natural antihyperglycemicproducts has received attention because they have fewerside-effects than synthetic drugs and are more economic.

In Moroccan folk medicine, the aerial parts (flowers,leaves, branches) of Thymelaea hirsuta (L.) Endl.

Significant findings of the study: The ethyl acetate fraction of T. hirsuta inhibits α- glucosidase and intestinalglucose transporters.What this study adds: For the first time, a mechanism for the antihyperglycemic action of T. hirsuta, has beendemonstrated.

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Journal of Diabetes •• (2014) ••–••

1© 2013 Ruijin Hospital, Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd

mailto:[email protected]

(Thymelaeaceae), widely distributed in the Mediterra-nean area, are used to prevent and treat diabetes.4,5 Pre-vious studies in our laboratory have demonstrated theantihyperglycemic activity of a polyphenol-rich fractionof this plant (PrF-TH).6,7 Moreover, this plant has dem-onstrated hypoglycemic, antidiabetic,8 antioxidant,9 anti-melanogenesis,10 and antiseptic activities.11

No information in the literature was found on itsmechanism of action concerning its antihyperglycemicactivity. Thus the aim of the present study is to evaluatethe inhibitory effects of fractions of the aerial part of T.hirsuta on α-glucosidase, in vitro, and, in vivo, in miceand intestinal absorption of glucose, in situ, in rats.

Methods

Chemicals and reagents

α-glucosidase was purchased from Sigma-Aldrich (USA).D (+)-glucose was obtained from Sigma-Aldrich (Seelze).Sucrose was purchased from Prolabo (groupe Rhone-Poulenc) (European Economic Community, EEC).Glucose Autokit was purchased from BioSystems (Bar-celona, Spain). Streptozotocin was purchased fromSigma-Aldrich (St. Louis, MO, USA) and Acarbose(Glucor 50) was purchased from Bayer Schering Pharma(Casablanca, Morocco). Pentobarbital was obtainedfrom CEVA santé animale (La Ballastière). Dimethyl-sulfoxide (DMSO) (C6H6OS) was obtained from Prolabo(Paris, France). Hexane (C6H14), dichloromethane(CH2Cl2) and methanol (CH3OH) were purchased fromSigma-Aldrich (Steinheim, Germany) and ethyl acetate(C4H8O2) was obtained from Scharlau chemie (Spain). Allother reagents were obtained from commercial sources.

Plant material

Plant material was bought from the herb market in Oujda(Oriental Morocco). The plant material was previouslyidentified and authenticated by a botanist according tothe Voucher specimen deposited in the department ofBiology, Faculty of Sciences, Oujda, Morocco.

The fresh herb was first washed with water, and driedat 40°C overnight in the oven before starting the Soxhletextraction.

Soxhlet extraction

200 g of dried and powdered aerial parts of T. hirsuta wereextracted with different solvents of increasing polarity(hexane, dichloromethane, ethyl acetate, methanol anddistillated water successively). The fractions obtainedwere then evaporated in a rotavaporator. The yield ofeach fraction is shown in Fig. 1.

Inhibition assay, in vitro, for α-glucosidase activity

The enzymatic activities of α-glucosidase were deter-mined colorimetrically by monitoring the release ofglucose from the sucrose. The amount of liberatedglucose was measured by the glucose oxidase methodusing a commercially available Autokit.12

The hexane (HTh), dichloromethane (DTh), ethylacetate (EATh), methanol (MTh) and aqueous (ATh)fractions of T. hirsuta were suspended in DMSO anddistillated water.

The assay mixtures contained 0.1 mL of sucrose(50 mmol/L), 0.1 mL of enzyme solution (10 IU), in1 mL of phosphate buffer (50 mmol/L) at pH 7.5.

In a first series, 10 μL (165 μg/mL) of each fractionand the same volume of distilled water, 0.3% DMSO, orAcarbose (57 μg/mL) were used as control, negativecontrol and positive control, respectively. In a secondseries the same procedure was followed but with avolume of 20 μL (328 μg/mL) of each fraction, control,negative control and positive control (144 μg/mL).

The mixture was incubated for 20 min at 37°C; thereaction was stopped by heating at 100 °C for 5 min in awater bath. The absorbance was measured at 500 nm byspectrophotometry (SPECTRONICR 20 GENESYS;Spectronic Instruments, New York, NY, USA).

The inhibitory activity was calculated using the fol-lowing formula:12

Inhibitory activityOD OD ODcontrol Test control

(%)( ) .= − ×100

Each test was performed three times.

Kinetics of α-glucosidase inhibition by ethylacetate fraction

The test was performed using as substrate, increasingconcentrations of sucrose (2, 3, 4, 6 and 8 mmol/L) in theabsence or presence of EATh at two different concentra-tions (90 and 180 μg/mL). Optimal doses were determinedbased on results from the inhibitory activity assay asdescribed earlier and from a preliminary test ofα-glucosidase inhibition kinetics. The type of inhibitionexhibited by EATh was determined by Lineweaver-Burkplot analysis of the data, which were calculated from theresults according to Michaelis-Menten kinetics.13

Animals

Wistar rats (150–250 g) and mice (20–30 g) used in thisstudy were obtained from the animal house of theDepartment of Biology of the Faculty of Sciences

Thymelaea hirsuta: inhibition of postprandial hyperglycemia S. ABID et al.

2 © 2013 Ruijin Hospital, Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd

(Oujda, Morocco). They were kept in cages with accessto pellets and water and maintained under standardlaboratory conditions (light/dark cycle of 12/12 and tem-perature of 23 ± 2°C).

All animals were cared for in compliance with theGuide for the Care and Use of Laboratory Animals,published by the US National Institutes of Health (seehttp://grants.nih.gov/grants/olaw/Guide-for-the-Care-and-Use-of-Laboratory-Animals.pdf).

Induction of diabetes: Diabetes was induced by asingle intraperitoneal injection of streptozotocin (STZ)at 150 mg/kg (body weight) in mice. STZ was dissolvedin fresh and cold sodium citrate buffer (0.1 M citric acid,0.1 M trisoduim citrate dihydrate) at pH 4.5. Five daysafter, mice with blood glucose levels more than 1.46 g/Land with signs of polyuria and polydipsia were selectedfor the test. The percentage of mice developing diabeteswas 85.71%.

In vivo, α-glucosidase inhibition by ethyl acetatefraction, in normal mice

A protocol described by Ortiz-Andrade et al.14 was usedwith some modifications. Mice were deprived of food for

16 h before experimentation but allowed free access towater.

EATh was suspended in 5% DMSO in distillatedwater.

The animals were divided into five groups with sixanimals/group. Groups 1 and 2 were treated with distil-lated water and 5% DMSO respectively at 10 mL/kg.Groups 3 and 4 were treated with EATh at 100 and50 mg/kg respectively (in a volume of 10 mL/kg) using anintragastric tube. Group 5 was treated with Acarbose at10 mg/kg.

Thirty minutes after oral administration of distilledwater, DMSO, Acarbose or test samples, mice wereorally loaded with sucrose (2 g/kg of body weight) inaqueous solution (10 mL/kg). Blood samples were col-lected from the tail tip, under light anesthesia, at 0, 30, 60and 120 min after sucrose administration. Blood glucoseconcentration was determined by the glucose oxidaseperoxidase method.

In vivo, α-glucosidase inhibition by ethyl acetatefraction, in diabetic mice

Mice were also divided into five groups with five animalsper group. They were treated similarly to the normal mice.

Figure 1 Flow charts of the yield of eachfraction of aerial part of Thymelaea hirsuta.

S. ABID et al. Thymelaea hirsuta: inhibition of postprandial hyperglycemia


http://grants.nih.gov/grants/olaw/Guide-for-the-Care-and-Use-of-Laboratory-Animals.pdf

http://grants.nih.gov/grants/olaw/Guide-for-the-Care-and-Use-of-Laboratory-Animals.pdf

In situ, intestinal absorption of glucose inhibition

The technique used is a perfusion of intestinal segmentsof rats, in situ. Rats were deprived of food for 36 h beforeexperimentation but allowed free access to water.

HTh, DTh, EATh, MTh and ATh were suspended inDMSO in distilled water. The final percentage of DMSOin the perfusion solution was 0.36%.

In the experiment, the rats were primarily anesthetizedwith pentobarbital at 50 mg/kg then a 10-cm jejunumsegment, which was cut about 10 cm below the pyloruswas perfused, in situ, with the perfusion solution at0.53 mL/min. The composition of the perfusion solutionwas (g/L): 7.37 NaCl, 0.2 KCl, 0.065 NaH2PO4. 2H2O,0.213 MgCl2. 6H2O, 0.6 NaHCO3 and 1.02 CaCl2.2H2O. D-glucose (1 g/L) was added to the solution justbefore the start of the appropriate experiment and thepH was maintained at 7.5. Plant fractions were tested at50 mg/kg and added after the D-glucose.

After 60 min, the liquid leaving the intestinal segmentwas recovered and the amount of glucose of the initialand final solutions was measured by oxidase-peroxidasemethod. The glucose absorbed was estimated bysubtraction.

Statistical analysis

All data are presented as mean ± standard error of themean (SEM). Statistical analysis and comparison ofmeans was evaluated by a two-tailed P-value or Stu-dent’s t-test, P-values of less than 0.05 were considered tobe significant.

Results

Alpha-glucosidase inhibitory activity of fractions ofThymelaea hirsuta

The results from the inhibitory activity of T. hirsuta(Fig. 2) showed that the HTh, DTh, EATh, MThand ATh have, in vitro, a significant inhibition onα-glucosidase as compared to the control. Moreover, thenegative control (0.3% DMSO) showed no significanteffect on the activity of the enzyme.

At 165 μg/mL, the MTh appeared to be the mostactive. It showed a 79.3 ± 8.5% inhibitory activity; fol-lowed by EATh, DTh, ATh and HTh. Increasing thedose to 328 μg/mL shows that the inhibitory activity ofMTh, ATh and HTh was not significantly different tothat at 165 μg/mL. But at this dose (328 μg/mL), theEATh and DTh showed inhibitory activity significantlyhigher than the lower dose (165 μg/mL).

Compared to Acarbose at 144 μg/mL, the inhibitoryactivity of EATh at 328 μg/mL was significantly higher(90.2%) than that of Acarbose (67.2%).

Kinetic analysis of α-glucosidase inhibition by ethylacetate fraction

Figure 3A shows that the rate of glucose release is lower inthe presence of the two concentrations of EATh (90 and180 μg/mL) as compared to the control. The inhibitionmode of EATh against α-glucosidase activity was ana-lyzed using Lineweaver-Burk plots. Double-reciprocalplots of enzyme kinetics demonstrated a non competitive

Figure 2 Inhibitory activity of Thymelaeahirsuta fractions at two different concentra-tions (165 and 328 μg/ml). The assaymixture contained 0.1 ml sucrose (50 mmol/L), 0.1 ml enzyme solution (10 UI), in 1 ml ofphosphate buffer (50 mmol/L) pH 7.5 andplant fractions at two different doses (165and 328 μg/ml) or acarbose at (57 and144 μg/ml). The mixture was incubated at37°C for 20 minutes. Glucose released isdetected colorimetrically by adding a com-mercially available Autokit. The meaning iscompared with the control. n = 3; NS, notsignificant (P > 0.05); *P < 0.05; **P < 0.01;***P < 0.001. HTh, hexane fraction of T.hirsuta; DTh, dichloromethane fraction ofT. hirsuta; EATh, ethyl acetate fraction ofT. hirsuta; MTh, methanol fraction of T.hirsuta; ATh, aqueous fraction of T. hirsuta.



inhibition of α-glucosidase activity (Fig. 3B). The Kmvalue of hydrolysis of sucrose was 6.5 mmol/L and Vmaxwas 16.66 nmol/min.

In vivo, α-glucosidase inhibition by ethyl acetatefraction, in normal mice

To confirm the inhibitory effect of T. hirsuta on intestinalα-glucosidase, in vivo, we selected the more active frac-tion; EATh, and we tested its impact on serum glucoselevels with sucrose loaded normal mice. The results inFig. 4A show that in the control group, the postprandialhyperglycemia level caused by 2 g/kg sucrose loadingreaches 1.5 g/L 30 min after sucrose administration, andthen it decreased to 1.25 g/L 60 min after and to 1.06 g/L120 min after. However, in the presence of 50 and100 mg/kg of EATh, the elevation of serum glucose levelwas significantly suppressed (P < 0.01 and P < 0.001respectively) at 30 and 60 min (but not at 120 min) com-

pared with control. Acarbose at 10 mg/kg significantlydecreased (P < 0.01) the serum glucose level only at30 min, and this effect was statistically similar to that ofEATh at 50 mg/kg. 5% DMSO (negative control)showed no significant difference compared to the control(data not shown). Data indicate that this anti-postprandial hyperglycemia effect of EATh might beassociated with the inhibition of intestinal α-glucosidase.

In vivo, α-glucosidase inhibition by ethyl acetatefraction, in diabetic mice

Figure 4B shows that the serum glucose level of diabeticcontrol mice increased from 2.22 to 3.61 g/L 30 min afterthe administration of 2 g/kg of sucrose and then itdecreases to 3.5 g/L at 60 min and to 3 g/L at 120 min.However, in the presence of 100 mg/kg of EATh, theglycemia was changed from 2.42 to 2.54 g/L at 30 minafter sucrose loading; a significant diminution compared

(a)

(b)

Figure 3 Kinetics of α-glucosidase inhibi-tion by ethyl acetate fraction. (a) Releaserate of glucose depending on the concentra-tion of sucrose. (b) Lineweaver-Burk plot ofkinetic analysis of α-glucosidase inhibitionby EATh. The α-glucosidase was treatedwith different concentrations of sucrose(2–8 mmol/L) in the absence and presenceof the ethyl acetate fraction of Thymelaeahirsuta at two different concentrations (90and 180 μg/ml). The enzymatic reaction wascarried out by incubating the mixture at 37°Cfor 20 minutes. Glucose released wasdetected colorimetrically by adding a com-mercially available Autokit.



with the control (P < 0.05). At 50 mg/kg, the bloodglucose level was increased from 2.2 to 2.9 g/L 30 minafter sucrose administration; this change is significantlysimilar to that of EATh at 100 mg/kg and to Acarbose at10 mg/kg (from 1.98 to 2.8 g/L). This similitude with theAcarbose indicates that EATh may contain activeα-glucosidase inhibitors.

In situ, intestinal absorption of glucose inhibition

To investigate the inhibitory effect of T. hirsuta fractionson intestinal glucose uptake, we perfused a segment ofjejunum with glucose in the presence and absence of thefive plant fractions. Figure 5 shows that in absence of

T. hirsuta fractions, the amount of glucose uptake was7.05 mg/10 cm/h. In the presence of 50 mg/kg EATh, theamount of glucose uptake was significantly decreased(P < 0.05) to 4.7 mg/10 cm/h, and the percentage of inhi-bition was 33.4% in comparison with the control.However, HTh, DTh, MTh and ATh at 50 mg/kgexerted no significant effect on intestinal glucose uptake.On the other hand, 0.36% DMSO as a negative controlinduced no significant effect on intestinal glucose uptake.

Discussion

Recent studies indicate that postprandial hyperglycemiaincreases the macro and microvascular complication

(a)

(b)

Figure 4 Effect of EATh on serum glucoselevel after sucrose loading in normal (a) andstreptozotocine diabetic mice (b). Mice weredeprived of food for 16 h. It’s received EATh(50 and 100 mg/kg), Acarbose (10 mg/kg) oronly distillated water (control) and 30 minafter, sucrose was administrated at 2 g/kg.Blood samples were collected from the tailtip under light anesthesia at 0, 30, 60 and120 minutes after sucrose administration.Each plot represents the means ± SEM.(a) n = 6; (b) n = 5. *P < 0.05; **P < 0.01;***P < 0.001. EATh, ethyl acetate fraction ofT. hirsuta.



risks.15 Indeed, hyperglycemia impairs secretion and sen-sitivity of insulin, causes oxidative stress and induces thenon-enzymatic glycosylation of different proteins.16

Therefore, controlling postprandial hyperglycemiabecomes crucial in the management of type II diabetes toprevent vascular complications of this disease.2

Postprandial glycemia, in normal conditions, is moni-tored by two pathways, the digestion of polysaccharidesinto absorbable monosaccharides and the intestinalabsorption of these monosaccharides. After ingestion,polysaccharides are degraded to oligosaccharides byamylase and further degraded to absorbable monosac-charides by α-glucosidase, which is attached to the brushborder of intestinal cells. To reach the blood, glucose isactively transported into absorptive epithelial cells medi-ated by SGLT1 (sodium-glucose linked transporter 1)located in the brush border membrane (BBM) thencarried out of epithelial cells by the facilitated diffusionmechanism mediated by GLUT2 (Glucose transporter 2)located on basolateral membrane (BLM).17

In patients with type II diabetes the expression ofintestinal monosaccharide transporters SGLT1 andGLUT2 increases.18,19 Consequently, the absorption ofglucose increases and so does postprandial glycemia.20

One of the therapeutic approaches for controllingpostprandial glycemia is to prevent polysaccharide deg-radation via inhibition of α-glucosidase (α-glucosidaseinhibitors were approved as therapeutic drugs for diabe-tes in the 1990s). However, currently there is no anti-diabetic drug to inhibit glucose intestinal transporters.

In this work, we studied the effect of Thymelaeahirsuta on two pathways of postprandial hyperglycemia.We found that T. hirsuta had intensive inhibitory activityagainst α-glucosidase, in vitro and in vivo. For the first

time we have shown that, in vitro, HTh, DTh, EATh,MTh and ATh can significantly inhibit α-glucosidase.Moreover, the EATh demonstrated high inhibitoryactivity, followed by methanol, dichloromethane,aqueous, and hexane fractions. EATh also showed, at328 μg/mL, inhibitory activity more effective than Acar-bose at 144 μg/mL. And the type of inhibition for thisfraction was non competitive. This activity of EATh wasconfirmed, in vivo, in normal and diabetic mice. Indeed,EATh at 100 and 50 mg/kg, suppressed the increase ofblood glucose levels after 2 g/kg of sucrose loading innormal and STZ diabetic mice. This effect might berelated to the inhibition of intestinal α-glucosidase (thesame mechanism acarbose exhibits). On the other hand,the antihyperglycemic activity of this plant might bemore effective in vivo than in vitro. This result is similarto that reported by Patel et al. 2012.21 This effect may beexplained by double inhibition; the inhibition of sucrosedegradation by α-glucosidase and also the inhibition ofliberated glucose absorption, via intestinal SGLT1and/or GLUT2 transporters. This last hypothesis wasconfirmed in situ in rats. We have shown that EATh at adose of 50 mg/kg inhibits significantly (P < 0.05) theintestinal absorption of glucose (33.4%). But the mecha-nism by which this fraction inhibits glucose absorption isnot yet clear, so, other experiments are necessary toclarify this inhibition.

Thymelaea hirsuta contains sterols (cholesterol,campesterol, β-sitosterol, β-sitosterol- β-stigmasterol),coumarins (daphnoretin, daphnin, daphnetin, daphnetin-glucoside, umbelliferone, scopoletin and esculetin), ter-penes (lupeol, phytol, β-amyrine, betulin, erythrodiol,and lanosterol), a flavone (2-vicenin), the flavonol tiliro-side (3-p-coumaroylglucosylkaempferol), tannins, an

Figure 5 Effect of T. hirsuta fractions onintestinal glucose uptake in rats. A 10 cm ofrat jejunum was perfused, in situ, with asolution of perfusion containing glucose(1 g/l) and the fraction of T. hirsuta at 50 mg/kg. After 60 minutes, the glucose absorbedwas estimated. The results were expressedas mean ± SEM and the meaning is com-pared with the control. n = 6; NS, not signifi-cant; *P < 0.05. HTh, hexane fraction of T.hirsuta; DTh, dichloromethane fraction ofT. hirsuta; EATh, ethyl acetate fraction of T.hirsuta; MTh, methanol fraction of T. hirsuta;ATh, aqueous fraction of T. hirsuta.



aliphatic alcohol (C12H22O), a lactone (C19H18O6);long chain alkanes (27-31 carbons), long chain alcohols(22, 24, 26, 28 carbons) and 5,12-dihydroxy-6,7-epoxy-resiniferonol.7,22

Previous studies have shown that T. hirsuta is rich inpolyphenols9 and essential oil.11 Therefore, the polyphe-nols and essential oil compounds are most likely respon-sible for the antioxidant activity.9,11 In addition, theflavonoids (a polyphenolic class widespread in plants)are known for their hypoglycemic effects23,24 that may berelated to the ability to inhibit glucose absorption, toimprove glucose tolerance, to stimulate glucose uptake inperipheral tissues, and to regulate the activity and/or theexpression of the rate-limiting enzymes involved in thecarbohydrate metabolism pathway.25 Moreover, severalrecent experimental studies have demonstrated the roleof flavonoids in the inhibition of glucosidases.26,27

Therefore, the higher EATh activity might be due tothe presence of some flavonoids that were obtainedduring the extraction process with ethyl acetate.

Consequently, the antihyperglycemic effect of T.hirsuta could be explained by the presence of flavonoidsand/or other phytochemical constituents that can actseparately or synergistically. So, further phytochemicalstudies are necessary to isolate active compounds andthen to test their individual and synergistic actions.

In conclusion, the results of our study demonstratedthat Thymelaea hirsuta inhibits intestinal α-glucosidaseand intestinal glucose transport. Therefore, this Moroc-can plant can be ingested before or during meals in orderto decrease postprandial hyperglycemia. Additionalexperiments are needed to clarify the mechanism ofaction for glucose absorption inhibition and to identifythe active compounds.

Acknowledgements

This work was supported by grants from the CNRST ofMorocco, (Project URAC40) and project Morocco-Belgium CUD. The authors thank Professor AlisonBanks, Teacher at the American Language Center,Oujda, Morocco, for the English revision.

Disclosure

The authors declare no conflict of interests.

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