Journal of Ethnopharmacology 72 (2000) 69 76

www.elsevier.com/locate/jethpharm

Effects of A6errhoa bilimbi leaf extract on blood glucose

and lipids in streptozotocin-diabetic rats
P. Pushparaj a, C.H. Tan a, B.K.H. Tan b,*
a

Department of Biochemistry, Faculty of Medicine, National Uni6ersity of Singapore, Singapore 119260, Singapore
Department of Pharmacology, Faculty of Medicine, National Uni6ersity of Singapore, 10 Kent Ridge Crescent,
Singapore 119260, Singapore

Received 18 June 1999; received in revised form 5 December 1999; accepted 28 February 2000

Abstract
The present study was designed to investigate the hypoglycemic and hypolipidemic activities of an ethanolic extract
of A6errhoa bilimbi Linn. leaves (Oxalidaceae, Common name: Bilimbi) in streptozotocin (STZ)-diabetic rats. The
optimal hypoglycemic dose (125 mg kg 1) was determined by performing the oral glucose tolerance test (OGTT) in
both normal and STZ-diabetic rats. To investigate the effect of repeated administration of an ethanolic extract of
A6errhoa bilimbi (ABe) leaves, diabetic rats were treated with vehicle (distilled water), ABe (125 mg kg 1) or
metformin (500 mg kg 1) twice a day for 2 weeks. Like metformin, ABe significantly lowered blood glucose by 50%
and blood triglyceride by 130% when compared with the vehicle. ABe also significantly increased the HDL-cholesterol
concentrations by 60% compared with the vehicle. ABe thus significantly increased the anti-atherogenic index and
HDL-cholesterol/total cholesterol ratio. However, like metformin, ABe did not affect total cholesterol and LDLcholesterol concentrations, but significantly reduced the kidney lipid peroxidation level. These data show that ABe has
hypoglycemic, hypotriglyceridemic, anti-lipid peroxidative and anti-atherogenic properties in STZ-diabetic rats.
2000 Elsevier Science Ireland Ltd. All rights reserved.
Keywords: A6errhoa bilimbi Linn.; Diabetes mellitus; Hypoglycemia; Hypolipidemia; Streptozotocin; Sprague Dawley rat

1. Introduction
The use of medicinal plants for the treatment of
diabetes mellitus dates back from the Ebers papyrus of about 1550 BC. Many traditional plant
treatments for diabetes mellitus are used through* Corresponding author. Tel.: +65-8743272; fax: +657730579.
E-mail address: phctankh@nus.edu.sg (B.K.H. Tan).

out the world. After the introduction of insulin

therapy the use of the traditional treatments for
diabetes mellitus greatly declined in the occidental
societies, although some traditional practices are
continued for prophylactic purposes and as adjuncts to conventional therapy (Swanston Flatt et
al., 1990). Few of the traditional plant treatments
for diabetes have received scientific scrutiny, and
the World Health Organization has recommended
that this area warrants attention (WHO, 1980).

0378-8741/00/$ - see front matter 2000 Elsevier Science Ireland Ltd. All rights reserved.
PII: S 0 3 7 8 - 8 7 4 1 ( 0 0 ) 0 0 2 0 0 - 2

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P. Pushparaj et al. / Journal of Ethnopharmacology 72 (2000) 6976

This paper describes the study of A6errhoa bilimbi

Linn. (Oxalidaceae, common name: Bilimbi), a
common plant in Asia, which has been widely
used in traditional medicine as a cure for cough,
cold, itches, boils, rheumatism, syphilis, diabetes,
whooping cough, and hypertension (Goh et al.,
1995). In addition, A. bilimbi has been widely
reported for its multiple ethnopharmacological
properties such as anti-inflammatory, anti-scorbutic, astringent, anti-bacterial, and postpartum protective properties (Goh et al., 1995). In Indonesia
it has a considerable medicinal reputation as a
potent folk remedy in the treatment of diabetes
mellitus (Wee Yeow Chin, 1992). A preliminary
study in our laboratory showed the reduction of
blood glucose and food intake in diabetic rats
given with extracts of A. bilimbi fruits and leaves
(Tan et al., 1996).
This study was thus initiated with the aim of
evaluating the effects of an ethanolic extract of A.
bilimbi leaves on the blood glucose level and
serum lipid profile in streptozotocin-diabetic
SpragueDawley (SD) rats.

2. Materials and methods

2.1. Materials
The plant was collected from a private garden
and identified as A6errhoa bilimbi by Dr Ruth
Kiew, Keeper of Herbarium and Library, Singapore Botanic Gardens. A dried specimen was
deposited in the herbarium (Voucher specimen
No. BT 2).

2.2. Preparation of the plant extract

The fresh leaves of A. bilimbi (1 kg) were
blended and extracted with 80% ethanol (10 l)
until exhaustion. The mixture was filtered with
Whatman No. 1 filter paper (Whatman International, UK). The filtrate was centrifuged for 10
min at 10 000 g to remove particulate substances. The clear supernatant was concentrated
at 40C by a rotavapor (Buchi Labortechnik,
Switzerland) to 1 l. The concentrate was freezedried, yielding about 40 g of yellowish-green pow-

der. The extract was suspended in distilled water

before use.

2.3. Animals
All experiments were performed on male
SpragueDawley (SD) rats aged 10 weeks (200
250 g) obtained from the Laboratory Animal
Holding Unit, National University of Singapore,
Singapore. The animals were acclimatized for 12
weeks before being used for the experiments.
Standard pelleted diet (Glen Forest, WA, Australia) and water were given ad libitum. Animals
were maintained under a constant 12-h light and
dark cycle and an environmental temperature of
2123C (Niyonzima and Vlietinck, 1993).

2.4. Induction of experimental diabetes mellitus

The overnight fasted SD rats were made diabetic with streptozotocin (STZ) (Sigma, St Louis,
MO; 60 mg kg 1, i.p). The STZ was freshly
dissolved in citrate buffer (0.01 M, pH 4.5) and
maintained on ice prior to use; the injection volume was 1 ml kg 1 (Hamilton et al., 1998).
Diabetes was confirmed in the STZ-treated rats
by measuring the fasting blood glucose concentration 72 h after injecting STZ. The SD rats with
blood glucose level above 350 mg dl 1 were considered to be diabetic and were used in the experiment (Lisa et al., 1998). Animals had free access
to food and water after the STZ injection.

2.5. Experimental procedure

2.5.1. The OGTT in normal and STZ-diabetic
SD rats
Prior to an oral glucose tolerance test (OGTT)
rats were fasted for 16 h. Distilled water (control),
a reference drug metformin (500 mg kg 1), or
each of three different doses of ABe (125, 250 and
500 mg kg 1) were then orally administered to
groups of 45 rats each. Thirty minutes later,
glucose (3 g kg 1) was orally administered to
each rat with a feeding syringe (Al-awadi et al.,
1985). Blood samples were collected from the tail
vein by tail milking at 30 (just before the ABe
and metformin administration), 0 (just before the

P. Pushparaj et al. / Journal of Ethnopharmacology 72 (2000) 6976

oral administration of glucose), 60, 120, and 180

min after glucose load for the assay of glucose
(Trinder method, Sigma Diagnostics, Sigma, St
Louis, MO).
The OGTTs were performed in STZ-diabetic
rats using the same procedure as described for the
normal rats. Six animals were used for distilled
water (control), metformin (positive control) and
ABe-treated groups.

2.5.2. Repeated administration of the ABe in

STZ-diabetic SD rats
One week after STZ induction of diabetes in
male SD rats, the fasting blood glucose levels
were measured. The hyperglycemic rats (blood
glucose \350 mg dl 1) were divided on day zero
into three groups (each with 5 6 rats). The fasting blood glucose level, total cholesterol, triglycerides, HDL-cholesterol, and LDL-cholesterol
concentrations were also measured on day zero.
Distilled water, metformin (500 mg kg 1) and
ABe (125 mg kg 1) were then administered orally
twice a day to control, positive control and the
treatment groups, respectively for 2 weeks. Body
weight, food and water intakes were monitored
daily for 2 weeks. On day 15, after 16 h fasting,
the rats were decapitated and the blood was collected for estimation of the fasting blood glucose,
total cholesterol, triglycerides, LDL-cholesterol,
and HDL-cholesterol (using diagnostic kits,
Boehringer Mannheim, Germany). The organs
such as liver and kidney were isolated, weighed
and stored at 70C for the assay of hepatic
cytochrome P450 and thiobarbituric acid reactive
substances (TBARS) in both liver and kidney.
2.6. Li6er microsomal cytochrome P450 content
2.6.1. Preparation of li6er microsomes
After 14 days of treatment, all the rats were
decapitated and their livers and kidneys were
removed quickly, rinsed in ice-chilled normal saline and weighed. Liver microsomes were prepared, using the ultra-centrifugation method (El
Defrawy El Masry et al., 1974). The rat liver (2 g)
was homogenized in ice cold 1.15% KCl (20 ml)
using a glass Potter-Elvejhem homogeniser. The
homogenate obtained was centrifuged at

71

10 000 g for 10 min at 4C and the supernatant

obtained recentrifuged at 100 000 g for 45 min
at 4C. The microsomal pellet was resuspended in
a volume of glycerol buffer [200 mM potassium
phosphate buffer, pH 7.4; 50% (v/v) and 1.15%
(w/v) potassium chloride (5:8:7)] equivalent to
twice the liver weight. The pellet was further
homogenized with seven strokes of the pestle after
which aliquots of the microsomal suspension were
stored at 70C. Protein content in each microsomal suspension was determined by Lowrys
method (Lowry et al., 1951).

2.6.2. Assay of li6er microsomal cytochrome P450

content
An aliquot of microsomal preparation of 1 mg
protein ml 1 was obtained by adding 0.5 ml of 1
M potassium phosphate buffer and the required
volume of 1.15% KCl. A modified technique
(Omura and Sato, 1964) was adopted in this assay
to eliminate the absorption peak at 420 nm due to
contamination by hemoglobin in the sample. The
microsomal preparation was placed in two cuvettes and initially saturated with carbon monoxide. A small amount of sodium dithionite (not
more than 2 mg) was added to the sample cuvette
only. The microsomal P450 content was then determined from the difference in absorbance values
between the dithionite-reduced and control microsomal preparations using a Shimadzu UV-dualbeam spectrophotometer. The molar extinction
coefficient of microsomal P450 at the lmax of 450
nm was 91 mM 1 cm 1.
2.7. Assay of TBARS
The liver and kidney samples were minced and
homogenized by a polytron homogeniser in icecold 1.15% KCl to make a 25% (w/v) homogenate. The determination of the lipid
peroxidation level in the liver and kidneys was
performed by the thiobarbituric acid method
(Uchiyama and Mihara, 1978). Briefly to 0.1 ml
of 25% homogenate, 0.2 ml of 8.1% sodium dodecyl sulfate (SDS), 1.5 ml of 1% phosphoric acid
and 0.2 ml of distilled water were added, followed
by 1 ml of 0.6% 2-TBA. The mixture was heated
for 45 min in a boiling water bath. After the

P. Pushparaj et al. / Journal of Ethnopharmacology 72 (2000) 6976

72

reaction, the mixture was cooled in an ice bath;

the cold TBA reactants were extracted with 4.0 ml
of n-butanol. After centrifugation at 1000 g for
10 min, the absorbance of the n-butanol layer was
determined at 535 nm. The TBARS values thus
obtained were expressed as nmol of malonaldehyde per 25 mg wet tissue.

Table 1
The mean percentage changes in the blood-glucose levels over
the 0-h control, ABe and metformin-treated normal and diabetic rats after oral glucose load (3 g kg1) in the oral glucose
tolerance test (OGTT)a
Group

Percentage change in blood glucose level

60 min

A. Normal rat
Control
76 916
ABe 125 mg
39 98.3
kg1, p.o.
250 mg
679 16.1
kg1, p.o.
500 mg
609 7.9
kg1, p.o.
Metformin
29 9.7*
500 mg
kg1, p.o.
B. STZ-diabetic rat
Control
ABe 125 mg
kg1, p.o.
250 mg
kg1, p.o.
500 mg
kg1, p.o.
Metformin
500 mg
kg1, p.o.
a

120 min

38 9 11.2
7 9 1.2*

419 12.2
29 6.9

11911.5

89 9.9

32914.6

159 3.9

26912.3

64 99.6
23 93.5

34 98.8
3 91.7*

47 9 6.5

1798.5

369 8.5
2 9 6.7***

180 min

39 12.1
2699.6**

669 5.5*

89 6
18
94.3**
129 6.6
18
95.6**
66
91.7**

Values are expressed as the mean9S.E.M. for 46 rats in

each group. The percentage change in blood glucose at 60, 120
and 180 min was calculated from the corresponding 0-h value
(just before the oral administration of glucose) in each group.
* PB0.05 compared with the corresponding control.
** PB0.01 compared with the corresponding control.
*** PB0.001 compared with the corresponding control.

2.8. Statistical analysis

The results are presented as means9 S.E.M.
The changes in body weight, food and water
intakes during the 14 days of treatment period
were compared by two-way ANOVA. The data
on blood glucose, total cholesterol, triglycerides,
LDL-cholesterol, HDL-cholesterol, TBARS, and
anti-atherogenic index were analysed by the Students t-test (two-tailed). P-values of B 0.05 were
considered to be statistically significant.
3. Results

3.1. Effects of ABe on glucose tolerance in

normal and STZ-diabetic SD rats
The blood glucose levels of the normal rats
reached a peak 60 min after the oral administration of glucose and gradually decreased to the
pre-glucose load level (Table 1A). Of the three
different doses, viz. 125, 250 and 500 mg kg 1,
the lowest dose, i.e. 125 mg kg 1 caused a significant attenuation in the blood glucose at 180 min
when compared to the vehicle-treated control
group (PB 0.05). Metformin (500 mg kg 1) produced a significant decrease (P B0.01) in blood
glucose level 180 min after the administration of
an oral glucose load.
In the diabetic rats, the fasting blood glucose
levels were 45 times higher than that of the
normal SD rats. The ABe at a dose of 125 mg
kg 1 produced a significant attenuation in the
blood glucose (PB 0.05) at 120 and 180 min
(PB 0.01) after the oral glucose load (Table 1B).
There was no significant attenuation in the rats
administered 250 mg of ABe kg 1, even at 180
min. However, ABe at a dose of 500 mg kg 1
caused a significant attenuation (PB 0.01) in the
blood glucose only at 180 min when compared to
the vehicle-treated group. Metformin (500 mg
kg 1) caused significant attenuation at 60 min
(PB 0.001), 120 min (PB 0.01) and 180 min (PB
0.01) when compared to the vehicle-treated group.
Of the three doses of ABe tested, the lowest dose
(125 mg kg 1) was found to be most effective in
improving glucose tolerance (P B0.01). Hence it
was selected for the 2-week study.

P. Pushparaj et al. / Journal of Ethnopharmacology 72 (2000) 6976

73

Table 2
Body weight, water and food intakes in STZ-diabetic rats before and after oral treatment with vehicle (distilled water), ABe (125
mg kg1) and metformin (500 mg kg1) twice a day for 2 weeksa
Treatment group

Vehicle
ABe
Metformin

Body weight (g)

Water intake (ml rat1 day1)

Food intake (g rat1 day1)

Before

After

Before

After

Before

After

222911
259918
258913

205 914
282931*
323947*

149 9 27
92.6 9 30
101.1 9 27

131 9 23
89 9 12*
77.6 926*

37 95
28 9 7
26 9 6

44.4 95
34 94*
29 91.1*

Values are expressed as mean 9S.E.M. (n= 5 or 6).

* Significantly different from vehicle at PB0.001.

3.2. Effects of 2 -week administration of ABe and

metformin on STZ-diabetic SD rats
The body weights in the ABe-treated and the
metformin-treated groups were increased significantly (PB0.001) on day 14 when compared with
the vehicle-treated group (Table 2). The food
intake was significantly lowered in the ABetreated and metformin-treated groups (P B0.001)
when compared with the vehicle-treated group.
Similarly, the water intake was significantly reduced (PB0.001) in both ABe-treated and metformin-treated groups (Table 2).
As shown in Table 3, the daily administration
of the ABe (125 mg kg 1 twice a day) for 14 days
in STZ-diabetic SD rats caused a significant reduction in the blood glucose level when compared
with the vehicle-treated control (P B0.01) rats
and day zero value (P B0.05). Similarly, repeated
administration of metformin (500 mg kg 1 twice
a day) for 14 days caused a significant reduction
(PB 0.01) in the blood glucose level in STZ-diabetic SD rats when compared to vehicle and day
zero values. There was a significant decrease in
serum triglycerides (P B 0.05) and a significant
increase in HDL-cholesterol (P B0.05) in the
ABe-treated SD rats when compared to the vehicle-treated control SD rats. However, ABe did not
decrease the serum cholesterol and LDL-cholesterol significantly (P\ 0.05). The daily administration of metformin (500 mg kg 1 twice a day)
for 14 days to STZ-diabetic SD rats caused a
significant decrease in the serum triglycerides
(PB 0.01) when compared to the vehicle-treated
control rats. Metformin, however, did not de-

crease serum cholesterol and LDL-cholesterol. It

also failed to increase the HDL-cholesterol. The
anti-atherogenic index was significantly increased
in the ABe-treated group (PB 0.001) when compared to the vehicle-treated group of rats. However, there was no significant difference in the
anti-atherogenic index of the metformin and the
vehicle-treated groups (P\ 0.05). The HDLcholesterol/total cholesterol ratio was significantly
increased in the ABe-treated group when compared to the vehicle-treated group (PB 0.01).
However, there was no significant difference (P\
0.05) in the HDL-cholesterol/total cholesterol ratio in the metformin-treated group when
compared to the vehicle-treated group.
As shown in Table 4, there was no significant
difference in the hepatic microsomal cytochrome
P450 content between ABe- and vehicle-treated
control STZ-diabetic SD rats (P\ 0.05). However
there was a significant reduction in the hepatic
microsomal cytochrome P450 content in the metformin-treated group when compared to the vehicle-treated group (PB0.05). The TBARS levels
were significantly reduced in the kidneys of both
ABe- and metformin-treated STZ-diabetic SD rats
(PB 0.01). However there was no significant difference in TBARS levels in the livers of both ABeand metformin-treated diabetic rats when compared to the vehicle-treated control diabetic rats.

4. Discussion
Our present studies show that ABe possesses
definite hypoglycemic, hypotriglyceridemic, anti-

74

Table 3
Metabolic variables in STZ-diabetic rats before and after oral treatment with vehicle (distilled water), ABe (125 mg kg1) and metformin (500 mg kg1) twice a day for 2 weeksa

Vehicle
ABe
Metformin

Fasting blood glucose

(mg dl1)

Total cholesterol
(mg dl1)

Triglycerides
(mg dl1)

Before

After

Before

After

Before

498.49 57.1
394.3 9 46.5
509.7 920.4

522.99 62.6
258.6940.2b,e
202.4931.2c,f

81.598.2
70.5913.1
57.599.1

110913.1
78.996.5
72.499.4

173.799.7
130.6924.5
194.197.0

LDL-cholesterol
(mg dl1)

HDL-cholesterol
(mg dl1)

Antiatherogenic index
(%)

HDL-C/TC ratio

After

Before

After

Before

After

Before

After

Before

185.89 37.6
44.2910.2b,e
59.1914.2b,f

26 9 6.1
21.491.8
19.797.9

24.193.0
21.897.7
2192.3

20.593.4
14.293.5
219 2.3

18.39 0.9
35.89 4.4b,e
25.394.8

44.4 917.7
28.195.4
59 9 8.0

20.792.3
0.390.08
90.39 17.0d,f 0.29 0.03
68.79 30.4 0.3690.03

After
0.2 90.02
0.46 90.05c,f
0.49 0.11

Values are expressed as mean 9 S.E.M. (n=5 or 6).

Significantly different from vehicle at PB0.05.
Significantly different from vehicle at PB0.01.
d
Significantly different from vehicle at PB0.001.
e
Significantly different from zero day at PB0.05.
f
Significantly different from zero day at PB0.01.
a

b
c

Table 4
Liver cytochrome P450 content and lipid peroxidation level in the kidney and liver of STZ-diabetic rats after 2 weeks of oral treatment twice a day with vehicle (distilled
water), ABe (125 mg kg1) and metformin (500 mg kg1)a
Treatment group

Vehicle
Abe
Metformin

Liver cytochrome P450 content

(nmol mg1 protein)

1.2 9 0.07
1.1 90.08
1.01 90.03*

Values are expressed as mean 9S.E.M. (n = 5 or 6).

* Significantly different from vehicle at PB0.05.
** Significantly different from vehicle at PB0.01.

Lipid peroxidation level (nmol of malonaldehyde per 25 mg of tissue)

Liver

Kidney

3.3 90.25
2.99 0.04
2.89 0.13

4.8 9 0.2
3.5 90.17**
3.3 9 0.25**

P. Pushparaj et al. / Journal of Ethnopharmacology 72 (2000) 6976

Treatment
group

P. Pushparaj et al. / Journal of Ethnopharmacology 72 (2000) 6976

atherogenic, and anti-lipid peroxidative properties

in STZ-diabetic rats after 2 weeks of treatment.
The hypoglycemic activity of ABe was observed
at the lowest dose (125 mg kg 1) in normal as
well as STZ-diabetic rats and was similar to the
action of metformin. Metformin, a biguanide,
(Bailey and Flatt, 1990) does not induce the secretion of insulin from the b-islet cells of pancreas,
but it increases glucose utilisation in the extrahepatic tissues, reduces hepatic gluconeogenesis
(Bailey, 1992) and increases the expression of
insulin receptors in the liver plasma membranes
(Kanigur-Sultuybek et al., 1995). Since ABe reduced the blood glucose potently in the STZ-diabetic SD rats like metformin, it may have
hypoglycemic principle(s) that are similar in action to metformin.
The daily administration of ABe (125 mg kg 1)
and metformin (500 mg kg 1) to STZ-diabetic
rats twice a day for 2 weeks caused a statistically
significant reduction in food and water intakes,
and an increase in the body weight in STZ-diabetic rats. This could be the result of improved
glycemic control produced by ABe and metformin. The ABe might reduce the triglycerides by
decreasing the serum non-esterified fatty acids
(NEFA) in the STZ-diabetic rats similar to masoprocol (nordihydroguaiaretic acid), a pure compound isolated from Larrea tridentata (Reed et
al., 1999). Since ABe increased HDL-cholesterol,
it significantly increased the anti-atherogenic index and HDL-cholesterol/total cholesterol ratio.
ABe thus has the potential to prevent the formation of atherosclerosis and coronary heart disease
which are the secondary diabetic complications of
severe diabetes mellitus (Fontbonne et al., 1989).
In contrast, metformin failed to increase the
HDL-cholesterol level and did not increase the
anti-atherogenic index and HDL-cholesterol/total
cholesterol ratio. However it has been reported
that metformin can reduce the blood lipid
parameters in non-diabetic patients with coronary
heart disease (Carlsen et al., 1996). Hence, ABe
may contain a hypolipidemic principle(s), which
could act in a way different from that of
metformin.

75

The cytochromes are the primary system (phase

I detoxification enzymes) responsible for chemical
defense in animals (Elizabeth Gillam, 1998). The
cytochrome P450 content in the liver has been
found to be increased in diabetic animals (Lucas
et al., 1998). The reduction in the insulin levels in
the diabetic state also causes an increase in the
level of cytochrome P450 enzymes (Woodcroft and
Novak, 1997). In this study cytochrome P450 content of the ABe-treated group was similar to that
of the vehicle-treated group. However a reduction
was found in the metformin-treated group. The
mechanism by which metformin reduces the cytochrome P450 content is not known.
The hyperglycemia in the STZ-treated rats
leads to the formation of hydrogen peroxide,
which subsequently generates free radicals such as
O2 and OH. These reactive compounds can
cause peroxidation of lipids, resulting in the formation of hydroperoxy fatty acids and endoperoxides. This increases the formation of
malonaldehyde (MDA) and thromboxane-B2
(TxB2). The accumulation of TxB2 along with
thromboxane-A2 (TxA2) can cause platelet aggregation and promote thrombosis (Sushil Jain et al.,
1998). Since ABe has the ability to reduce the
formation of TBARS, it could potentially prevent
platelet aggregation and thrombosis.
In conclusion, the hypoglycemic, hypotriglyceridemic, anti-lipid peroxidative as well as the antiatherogenic properties of ABe might be due to
different types of active principles, each with a
single or a diverse range of biological activities.
Further biochemical and pharmacological investigations are now in progress to isolate and identify
the active compound(s) in ABe.

Acknowledgements
The authors wish to thank the National University of Singapore for the research grant (RP
960329) and a research scholarship awarded to P.
Pushparaj. The authors also acknowledge the excellent technical assistance of Annie Hsu, Department of Pharmacology, National University of
Singapore, Singapore.

76

P. Pushparaj et al. / Journal of Ethnopharmacology 72 (2000) 6976

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