ARTICLE IN PRESS

Phytomedicine 14 (2007) 15–22

www.elsevier.de/phymed

Cinnamaldehyde—A potential antidiabetic agent

P. Subash Babu, S. Prabuseenivasan, S. Ignacimuthu
Division of Ethnopharmacology, Entomology Research Institute, Loyola College, Chennai 600 034, Tamil Nadu, India

Received 12 July 2006; accepted 30 October 2006

Abstract

Cinnamonum zeylanicum (cinnamon) is widely used in traditional system of medicine to treat diabetes in India. The
present study was carried out to isolate and identify the putative antidiabetic compounds based on bioassay-guided
fractionation; the compound identified decreased the plasma glucose levels. The active compound was purified by
repeat column and structure of cinnamaldehyde was determined on the basis of chemical and physiochemical evidence.
The LD50 value of cinnamaldehyde was determined as 1850737 mg/kg bw. Cinnamaldehyde was administered at
different doses (5, 10 and 20 mg/kg bw) for 45 days to streptozotocin (STZ) (60 mg/kg bw)-induced male diabetic
wistar rats. It was found that plasma glucose concentration was significantly (po0.05) decreased in a dose-dependent
manner (63.29%) compared to the control. In addition, oral administration of cinnamaldehyde (20 mg/kg bw)
significantly decreased glycosylated hemoglobin (HbA1C), serum total cholesterol, triglyceride levels and at the same
time markedly increased plasma insulin, hepatic glycogen and high-density lipoprotein–cholesterol levels. Also
cinnamaldehyde restored the altered plasma enzyme (aspartate aminotransferase, alanine aminotransferase, lactate
dehydrogenase, alkaline phosphatase and acid phosphatase) levels to near normal. Administration of glibenclamide, a
reference drug (0.6mg/kg bw) also produced a significant (po0.05) reduction in blood glucose concentration in STZ-
induced diabetic rats. The results of this experimental study indicate that cinnamaldehyde possesses hypoglycemic and
hypolipidemic effects in STZ-induced diabetic rats.
r 2006 Elsevier GmbH. All rights reserved.

Keywords: Cinnamonum zeylanicum; Bioassay-guided isolation; Cinnamaldehyde; Hypoglycemic effect; Streptozotocin

Introduction diabetes mellitus normally involves exercise, diet and

Diabetes mellitus is a chronic metabolic disorder
affecting approximately 4% population worldwide and
is expected to increase by 5.4% in 2025 (Kim et al., 2006).
It is characterized by abnormalities in carbohydrate, lipid
and lipoprotein metabolism, which not only lead to
hyperglycemia but also cause many complications, such
hyperlipidemia, hyperinsulinemia, hypertension and
atherosclerosis (Chait and Brunzell, 1996). Control of
Corresponding author. Tel.: +44 28178348; fax: +44 28174644.
E-mail address: eri_lc@hotmail.com (S. Ignacimuthu).
chemotheraphy. The conventional pharmacological treat-
ments for type II diabetes have a number of limitations,
such as adverse effects and high rates of secondary failure.
However, medicinal herbs are expected to have a similar
degree of efficacy without the troublesome side effects
associated with conventional drug treatment.
Presently, there is growing interest in herbal remedies
due to the side effects associated with the oral
hypoglycemic agents (therapeutic agent) for the treat-
ment of diabetes mellitus (Kim et al., 2006). More than
400 plants with glucose lowering effect are known
(Ernst, 1997). Nearly 100 polysaccharides from plants

0944-7113/$ - see front matter r 2006 Elsevier GmbH. All rights reserved.
doi:10.1016/j.phymed.2006.11.005
 ARTICLE IN PRESS
16 P. Subash Babu et al. / Phytomedicine 14 (2007) 15–22
have been reported for hypoglycemic activity. Some
botanical polysaccharides are considered as important
bioactive components responsible for hypoglycemic
effect (Wang and Ng, 1999). Also a number of plants
have hypolipidemic effect (Sharma et al., 2003). How-
ever, there is little information about plants with both
hypoglycemic and hypolipidemic effects.
Development and utilization of antidiabetic plants
have attracted increasing interest. The plant kingdom is
a wide field to search for natural effective oral
hypoglycemic or hypolipidemic agent that has slight or
no side effects. Hence, compounds with both hypogly-
cemic and hypolipidemic properties would be useful
antidiabetic agents (Luo et al., 2004).
A number of investigators have shown that cumarins,
flavonoids, terpenoids, and a host of other secondary
plant metabolites, including arginine and glutamic acid,
possess hypoglycemic effect in various experimental
models (Marles and Farnsworth, 1995; Ross, 2001).
Although the hypoglycemic effect of terpenoids appears
to involve stimulation of pancreatic b-cells and subse-
quent secretion of performed insulin, the metabolism of
cumarins probably involves hepatotoxity (Marles and
Farnsworth, 1995). In cinnamaldehyde, it undergoes
extensive metabolism. The alcohol is rapidly converted
to the aldehyde via alcohol dehydrogenase to cinnamal-
dehyde, which in turn, is converted to cinnamic acid. Thus
cinnamic acid is the major intermediate metabolite for
both chemicals. The major urinary metabolites are glycine
or glucuronic acid conjugates of benzoic acid, which are
formed as a result of b-oxidation of cinnamic acid.
Glycine and glucuronic acid conjugates of cinnamic acid
are formed in small amounts. A minor percentage of
cinnamaldehyde undergoes conjugation with glutathione
to form mercapturic acid derivatives (JECFA (Joint
Expert Committee on Food Additives), 2000).
It is well established that cinnamaldehyde really
possesses a wide variety of bioactive properties. A number
of traditional healers have claimed that cinnamon is
effective in the reduction of blood glucose level (Qin et al.,
2003; Alam et al., 2003) and promotes hypolipidemic
effect (Lee et al., 2003; Kannappan et al., 2006). However,
there are no reports available for hypoglycemic and
hypolipidemic effects of cinnamaldehyde from Cinnamo-
num zeylanicum. So the aim of this study was to
investigate the hypoglycemic and hypolipedemic effects
of cinnamaldehyde (using a bioassay guided separation) in
streptozotocin (STZ)-induced diabetic rats.
Materials and methods
Plant material
C. zeylanicum Blume. (Lauraceae) bark was collected
from Kanyakkumari district, Tamil Nadu, India and
shade dried. The species was identified and authenti-
cated by Dr. D. Narasimhan, Taxonomist, Department
of Botany, Madras Christian College, Chennai and the
voucher specimen (MPC-301) was deposited at the
Entomology Research Institute, Loyola College, Chen-
nai, Tamil Nadu, India.
Isolation and identification of the active compounds
Fresh bark (1.5 kg) was subjected to hydro-distillation
in a Clevenger-type apparatus for 4 h. The yield (v/w) of
volatile oil was 0.12%. The volatile oil was dried over
anhydrous sodium sulfate and stored in airtight screw
capped vials at 10 1C until use. Cinnamon oil (10 gm)
was chromatographed on a silica gel column (Merck
70–230 mesh, 400 gm, 3.5 i.d.  60 cm) and successively
eluted with stepwise gradient of hexane ethyl acetate
system (0%, 5%, 10%, 20%, 30%, 50%, 70% and
100%). Twenty-nine fractions were collected and each
fraction was spotted on a precoated Silica gel 60 F254,
0.25 mm thick TLC plate (Merck) and eluted in
hexane:ethyl acetate (4:1) and fractions with similar Rf
values in TLC pattern were pooled together. Fraction-3
(3.5 g) showed significant plasma glucose lowering
effect. For further separation bioactive substance was
chromatographed on a silica gel column and eluted with
a stepwise gradient of hexane–ethyl acetate (8:2) solvent
system, and an active isolate of 2.25 g was obtained. This
active isolate was subjected to spectral analysis. 1H and
13
C NMR spectra were recorded with a JEOL 300 MHz
FT NMR spectrometer (H1) 75, MHz (13C) and
chemical shifts were given in ppm. IR spectra were
taken on a Perkin Elmer FT-IR (Spectrum One)
spectrophotometer and mass spectra on a JEOL JMS-
DX30 spectrometer.
Experimental animals
Male wistar strain rats weighing about 200–250 g bred
in the Laboratory of Animal Medicine, Centre for
Animal Health Studies, Tamilnadu Veterinary and
Animal Sciences University, Madhavaram, Chennai,
Tamil Nadu, India were used. All the animals were kept
and maintained under laboratory conditions of tem-
perature (2272 1C), humidity (4575%) and 12 h
day:12 h night cycle; and were allowed free access to
food (standard pellet diet) and water ad libitum. The
animals were divided into 7 groups of 8 rats each.
Induction of diabetes
Diabetes mellitus was induced by single intraperito-
neal injection of freshly prepared STZ (60 mg/kg bw)
in 0.1 M citrate buffer (pH – 4.5) in a volume of
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P. Subash Babu et al. / Phytomedicine 14 (2007) 15–22
1 ml/kg bw. Diabetes was developed and stabilized
in these STZ treated rats over a period of 7 days
(Sarkar et al., 1996). The control animals were treated
with citrate buffer (pH – 4.5). After 7 days of
STZ administration, plasma glucose levels of each rat
were determined. Rats with a fasting plasma glucose
range of 280–350 mg/dl were considered diabetic
and included in the study. Blood was collected by
sinocular puncture.
Experimental design and treatment schedule
In the experiment, a total of 42 rats (12 normal; 30
STZ-diabetic surviving rats) were used. The rats were
divided into 7 groups of 6 rats each. Group 1 – normal
rats treated with vehicle alone (dimethylsulfoxide
[DMSO] 0.5%; 1 ml/kg bodyweight); Group 2 – normal
rats treated with cinnamaldehyde (20 mg/kg bw); Group
3 – STZ-treated diabetic rats; Groups 4, 5 and 6 – STZ-
treated diabetic rats treated with cinnamaldehyde 5, 10
and 20 mg/kg bw, respectively. Group 7 – STZ-treated
diabetic rats treated with glibenclamide (0.6 mg/kg bw)
for 45 days. After 45 days of treatment rats were
decapitated, their blood was collected and serum for the
measurement of cholesterol levels was obtained imme-
diately by centrifugation. Each liver was removed, dried
on tissue paper, weighed and stored at 80 1C for the
assay of liver glycogen.
Acute toxicity testing
A separate experiment was performed to know
whether any toxic effects were produced by cinnamal-
dehyde on liver and kidney. Rats fasted for 12 h were
randomly divided into drug-treated ‘test’ groups and
vehicle-treated ‘control’ group making up 7 groups of 6
rats per cage. Cinnamaldehyde (100, 200, 400, 800 1600
and 3200 mg/kg bw) was separately administered orally
to the rats in each of the test groups. Each of the rats in
the control groups was treated with vehicle alone
(DMSO 0.5%; 1 ml/kg bw). Then the rats in both the
test and control groups were allowed access to food and
water, and behavioral changes were observed over a
period of 24 h for sign of acute toxicity. The mortality
number caused by the compound within this period of
time was observed. Log dose–response plots were
constructed for the compound, from which the median
lethal dose (LD50) of the compound was determined
(Lorke, 1983).
Estimation of plasma glucose and hepatic glycogen
Fasting plasma glucose was estimated using glucose
oxidase–peroxidase method (Trinder, 1969). Hepatic
17
glycogen was estimated by the method of Morales et al.
(1973).
Determination of plasma insulin
Plasma insulin concentrations were determined by
radioimmunoassay kit (Pharmacia, Uppsala, Sweden)
with a beta metric counter (Cronex, Dupont, France).
The kit included human insulin as standard and 125I-
labeled human insulin antibody, which cross-reacts
similarly with rat insulin.
Determination of total hemoglobin and glycosylated
hemoglobin
Total hemoglobin was estimated by the cyanomethae-
moglobin method (Drabkin and Austin, 1932) and
glycosylated hemoglobin (HbA1C) was estimated by the
method of Sudhakar Nayak and Pattabiraman (1981),
as modified by Bannon (1982).
Measurement of cholesterol levels
Serum total cholesterol, triglycerides and serum
HDL-cholesterol were determined using commercial
kits (Dialab, Austria).
Plasma enzyme assessments
Alanine aminotransferase (ALT; EC 2.6.1.2)
and aspartate aminotransferase (AST; EC 2.6.1.1)
activities were assayed by the method of Reitman and
Frankel (1957). Lactate dehydrogenase (LDH, EC
1.1.1.27) activity was determined by the method of
Cabaud and Wroblewski (1958). Alkaline phosphatase
(ALP; EC 3.1.3.1) activity was measured at 405 nm
by the formation of paranitrophenol from para-nitro-
phenylphosphate as a substrate (Principato et al.,
1985). Acid phosphatase (ACP; EC 3.1.3.2) activity
was measured using the method of Moss (1984). Pro-
tein concentration was assayed by the method of
Lowry et al. (1951) using bovine serum albumin as a
standard.
Statistical analysis
Statistical analysis was performed using SPSS soft-
ware package, version 6.0. The values were analyzed by
one way analysis of variance (ANOVA) followed by
Duncan’s multiple range test (DMRT) (Duncan, 1957).
All the results were expressed as mean7SD for six rats
in each group. p-Values o0.05 were considered as
significant.
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18 P. Subash Babu et al. / Phytomedicine 14 (2007) 15–22

Results Plasma glucose levels measured in normal and

Identification of active compound
Using bioassay-guided fractionation one active isolate
was obtained. Structural determination of the active
isolate was done using different spectral techniques and
it was confirmed as trans-cinnamaldehyde. The yield of
cinnamaldehyde was 0.225 g per gram of cinnamon. The
compound was identified based on the following
evidence: C9H8O (MW, 132) EI-MS (70 eV): M+ 132,
103, 77, 63, 51, 39; IR (neat) max/cm: 3029, 1675, 1626,
1123, 747; 1H-NMR (CDCL3, 300 MHz): 6.69, 7.23,
9.70; 13C – NMR (CDCL3, 75 MHz): 193.62, 152.71,
133.94, 131.21, 129.03, 128.52, 128.43; the spectral data
corroborate with Lee (2002).
Oral administration of graded doses of cinnamalde-
hyde to male wistar rats, in our acute toxicity study
produced a median lethal dose value of 1850737 mg/kg
bw. Based on this observation the compound is
considered to be safe in mammals.
experimental rats after a single day and at the end of
7, 15, 30 and 45 days of treatment are given in Table 1.
STZ-treated diabetic rats showed significant increase in
the levels of blood glucose as compared to normal rats.
Oral administration of cinnamaldehyde 20 mg/kg bw
showed highly significant (po0.05) effect than 5 and
10 mg/kg bw doses. As the effect of cinnamaldehyde at a
dose of 20 mg/kg bw was more effective in 45 days
treatment, this dose was selected for further biochemical
studies.
Table 2 presents the effect of cinnamaldehyde on
changes in body weight, food uptake, plasma insulin,
total hemoglobin, HbA1C and liver glycogen in normal
and diabetic rats. In diabetic rats, there was a significant
(po0.05) decrease in body weight, liver glycogen,
plasma insulin and total hemoglobin and an increase
in food uptake and HbA1C as compared to normal rats.
Oral administration of cinnamaldehyde significantly
(po0.05) increased the body weight, plasma insulin,
liver glycogen and total hemoglobin and decreased food

Table 1. Effect of cinnamaldehyde on plasma glucose levels in normal and streptozotocin-induced diabetic male wistar rats

Groups Plasma glucose levels (mg/dl)

Diabetic 7th day 15th day 30th day 45th day

Normal 85.675.3 98.874.69b 89.276.22a 94.0374.08a 83.976.14a

Normal+cinnamaldehyde (20 mg/kg bw) 98.374.2 87.474.72a 88.573.81a 95.377.38a 87.677.47a
Diabetic control 341.9712.8 382.1719.3f 398.5712.4e 415.3715.20f 431.0717.31e
Diabetic+cinnamaldehyde (5 mg/kg bw) 317.779.7 291.375.05d 271.977.58d 263.279.25e 256.9711.38d
Diabetic+cinnamaldehyde (10 mg/kg bw) 328.777.4 306.279.1e 280.677.9d 238.379.8d 189.478.6c
Diabetic+cinnamaldehyde (20 mg/kg bw) 346.4711.7 274.376.3c 197.578.3c 163.3711.2c 127.476.3b
Diabetic+glibenclamide (0.6 mg/kg bw 305.3714.9 281.677.2cd 173.977.6b 148.377.2b 119.679.4b

Each value is mean7SD for six rats in each group.

Values not sharing a common superscript differ significantly at po0.05 (DMRT).

Table 2. Effect of cinnamaldehyde on body weight, hemoglobin, glycosylated hemoglobin, hepatic glycogen and plasma insulin in
normal and streptozotocin-induced diabetic male wistar rats

Groups Body weight (g/day) Food intake Total Glycosylated Hepatic Plasma
(g/day) hemoglobin hemoglobin glycogen insulin
Initial Final (mg/dl) (% total Hb) (g/100 g wet (mU/ml)
tissue

Normal 195.8715.6 205.4710.7c 45.373.6 14.0370.83c 0.5270.07ab 4.0970.37c 14.070.65c

Normal+cinnamaldehyde 190.675.6 198.678.6bc 48.874.7 14.2670.72c 0.4970.04a 4.4470.39d 15.470.79d
(20 mg/kg bw)
Diabetic control 195.278.3 165.776.5a 61.275.1 7.470.49a 0.9770.11d 1.9470.21a 8.2070.42a
Diabetic+cinnamaldehyde 193.7713.4 190.675.4b 46.873.5 12.5670.78b 0.5870.04bc 3.8770.28c 13.470.57c
(20 mg/kg bw)
Diabetic+glibenclamide (0.6 mg/ 198.675.7 193.479.2b 49.772.9 11.770.69b 0.6170.03c 3.1670.33b 12.770.58b
kg bw)

Each value is mean7SD for six rats in each group.

Values not sharing a common superscript differ significantly at po0.05 (DMRT).
 ARTICLE IN PRESS
P. Subash Babu et al. / Phytomedicine 14 (2007) 15–22 19

Table 3. Effect of cinnamaldehyde on serum total cholesterol, triglyceride, HDL cholesterol levels in normal and streptozotocin-
induced diabetic male wistar rats

Groups Total cholesterol (mg/dl) Triglycerides (mg/dl) HDL-cholesterol (mg/dl)

a ab
Normal 94.573.32 14.670.80 57.273.01c
Normal+cinnamaldehyde (20 mg/kg bw) 97.773.69a 13.571.08a 54.372.81b
Diabetic control 246.7713.2d 38.072.00d 38.571.33a
Diabetic+cinnamaldehyde (20 mg/kg bw) 113.574.80b 17.570.65c 54.372.42b
Diabetic+glibenclamide (0.6 mg/kg bw) 127.374.24c 15.270.47b 52.772.15b

Each value is mean7SD for six rats in each group.

Values not sharing a common superscript differ significantly at po0.05 (DMRT).

Table 4. Effect of cinnamaldehyde on plasma AST, ALT, LDH, ALP and ACP levels in normal and streptozotocin-induced
diabetic male wistar rats

Groups AST (U/dl) ALT (U/dl) LDH (U/l) ALP (U/l) ACP (U/l)

Normal 37.371.13a 54.573.24a 1167.5768.2a 53.772.82a 13.770.65a

Normal+cinnamaldehyde (20 mg/kg bw) 42.271.26b 52.174.16a 1092.7773.8a 57.873.16b 14.370.82a
Diabetic control 63.772.19e 89.474.85c 1563.5793.4c 82.773.48e 21.670.58d
Diabetic+cinnamaldehyde (20 mg/kg bw) 45.571.25c 62.873.07b 1291.2753.8b 65.972.35c 15.870.45b
Diabetic+glibenclamide (0.6 mg/kg bw) 47.571.84d 67.473.42b 1327.9767.3b 72.172.82d 17.370.50c

Each value is mean7SD for six rats in each group.

Values not sharing a common superscript differ significantly at po0.05 (DMRT).

uptake and HbA1C (40.2%) when compared to un-
treated diabetic rats.
Table 3 shows the levels of serum lipids in normal and
experimental rats. There was a significant decrease in the
level of serum HDL-cholesterol and a significant
increase in the levels of total cholesterol and triglycer-
ides in diabetic rats when compared to normal rats.
Administration of cinnamaldehyde brought back the
levels of serum lipids to near normal.
Table 4 shows that the activities of plasma enzymes
AST, ALT, LDH, ALP and ACP significantly (po0.05)
increased in diabetic rats compared to controls. Oral
administration of cinnamaldehyde for 45 days signifi-
cantly restores the enzyme levels to near normal in
diabetic rats.
Discussion
The aim of the present study was to evaluate the
antihyperglycemic and hypolipidemic effects of cinna-
maldehyde in STZ-induced diabetic rats. Diabetes
mellitus causes a disturbance in the uptake of glucose
as well as glucose metabolism. The use of a lower dose
of STZ (60 mg/kg) produced an incomplete destruction
of pancreatic b-cells even though the rats become
permanently diabetic (Aybar et al., 2002). After treat-
ment with a low dose of STZ there should be many
surviving b-cells, and regeneration is also possible
(Gomes et al., 2001). Hyperglycemia generates abnor-
mally high levels of free radicals by autoxidation of
glucose and protein glycation, and oxidative stress has
been reported to be a causal factor of cardiovascular
complications in STZ-induced diabetes mellitus (Okutan
et al., 2005). Hyperglycemia is associated with the
generation of reactive oxygen species (ROS) causing
oxidative damage particularly to heart, kidney, eyes,
nerves, liver, small and large vessels and gastrointestinal
system (Tunali and Yanardag, 2006). The increased
levels of plasma glucose in STZ-induced diabetic rats
were lowered by cinnamaldehyde administration. The
antihyperglycemic action of cinnamaldehyde results
from the potentiation of insulin from existing b-cells
of the islets of Langerhans. The plasma glucose lowering
activity was compared with glibenclamide, a standard
hypoglycemic drug. Glibenclamide has been used for
many years to treat diabetes, to stimulate insulin
secretion from pancreatic b-cells (Tian et al., 1998).
From the results of the present study, it appears that still
insulin producing cells are functioning and the stimula-
tion of insulin release could be responsible for most of
the metabolic effects. It may be suggested that the
mechanism of action of cinnamaldehyde is similar to
glibenclamide. Although a number of active principles
have also been observed with antidiabetic activity
(Villasenor et al., 2004; Sheehan and Zemaitis, 1983),
this is the first report that demonstrates antidiabetic
properties for cinnamaldehyde.
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20 P. Subash Babu et al. / Phytomedicine 14 (2007) 15–22
Decrease in body weight of diabetic rats is possible
due to catabolism of fats and protein, even though the
food intake is more in diabetic rats than control. Due to
insulin deficiency protein content is decreased in
muscular tissue by proteolysis (Vats et al., 2004). Oral
administration of cinnamaldehyde partially improves
body weight in diabetic rats. Lower levels of total
hemoglobin observed in diabetic rats might be due
to the increased formation of HbA1C. In uncontrolled or
poorly controlled diabetes, there is an increased
glycosylation of a number of proteins including
hemoglobin and a-crystallin of lens (Alberti and Press,
1982). HbA1C was found to increase in patients with
diabetes mellitus to approximately 16% and the
amount of increase was directly proportional to the
fasting blood glucose levels (Pari and Saravanan, 2002).
Oral administration of cinnamaldehyde decreases hy-
perglycemia and therefore levels of HbA1C decreased
(40.2%).
Insulin is a stimulator of glycogen synthase system
and when insulin is lacking this enzyme is not activated.
On the other hand insulin inhibits glycogenolysis and, if
there is a lack of insulin glycogenolysis, it is not under
inhibition of insulin and, therefore, glycogen content of
the liver decreases (Vats et al., 2004). Oral administra-
tion of cinnamaldehyde significantly increases hepatic
glycogen levels in STZ-diabetic rats, possibly because of
the reactivation of the glycogen synthase system as a
result of increased insulin secretion.
Lipids play a vital role in the pathogenesis of diabetes
mellitus. The most common lipid abnormalities in
diabetes are hypertriglyceridemia and hypercholestero-
lemia. In our study, we have noticed elevated levels of
serum lipids such as cholesterol and triglycerides in
diabetic rats. The levels of increased serum lipids in
diabetes represent a risk factor for coronary heart
disease (Al-Shamaony et al., 1994). Under normal
circumstances, insulin activates lipoprotein lipase and
hydrolyzes triglycerides (Shirwaikar et al., 2004). Insulin
increases uptake of fatty acids into adipose tissue and
increases triglyceride synthesis. Moreover, insulin in-
hibits lipolysis. In case of insulin deficiency, lipolysis is
not inhibited and we have increased lipolysis which
finally leads to hyperlipidemia. In insulin-deficient
diabetes, the concentration of serum free fatty acids is
elevated as a result of free fatty acid outflow from fat
depots, where the balance of the free fatty acid
esterification–triglyceride lipolysis cycle is displaced in
favor of lipolysis (Shirwaikar et al., 2004). HDL is an
antiatherogenic lipoprotein. It transports cholesterol
from peripheral tissues into the liver and thereby acts as
a protective factor against coronary heart disease. The
level of HDL-cholesterol, which increased after cinna-
maldehyde administration, might be due to the increase
in the activity of lecithin cholesterol acyl transferase
(LCAT), which may contribute to the regulation of
blood lipids (Patil et al., 2004). Administration of
cinnamaldehyde lowers serum lipids, and also increases
the serum HDL-cholesterol level in diabetic rats.
The increase in the activities of plasma AST, ALT,
LDH, ALP and ACP indicated that diabetes may be
induced due to liver dysfunction. Ohaeri (2001) also
found that liver was necrotized in STZ-induced diabetic
rats. Therefore, increase in the activities of AST, ALT,
LDH, ALP and ACP in plasma may be mainly due to
the leakage of these enzymes from the liver cytosol into
the blood stream (Navarro et al., 1993), which gives an
indication on the hepatotoxic effect of STZ. On the
other hand, treatment of the diabetic rats with
cinnamaldehyde caused reduction in the activity of
these enzymes in plasma compared to the mean values
of diabetic group and consequently may alleviate liver
damage caused by STZ-induced diabetes. These results
are in agreement with those obtained by El-Demerdash
et al. (2005) in rats.
Our finding shows that oral administration of
cinnamaldehyde produces significant antihyperglycemic
effect, lowers both total cholesterol and triglyceride
levels and, at the same time, increases HDL-cholesterol
in STZ-induced diabetic rats. This investigation reveals
the potential of cinnamaldehyde for use as a natural oral
agent, with both hypoglycemic and hypolipidemic
effects.
Acknowledgments
The authors are grateful to Indian Council of Medical
Research, New Delhi for providing Research Grant.
They also thank the Director, Dr. ALM. Post Graduate
Institute of Basic Medical Sciences, University of
Madras for permission to undertake part of the studies
at PGIBMS.
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