Vol.3, No.4, 221-226 (2013) Journal of Diabetes Mellitus
http://dx.doi.org/10.4236/jdm.2013.34034
Anti-diabetic and antioxidant effects of virgin
coconut oil in alloxan induced diabetic male
Sprague Dawley rats
Bolanle Iranloye1*, Gabriel Oludare1, Makinde Olubiyi1,2
1Department of Physiology, College of Medicine, University of Lagos, Lagos, Nigeria;
*Corresponding Author:
2Department of Physiology, Kogi State University, Ayangba, Nigeria
Received 25 September 2013; revised 20 October 2013; accepted 28 October 2013
Copyright © 2013 Bolanle Iranloye et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
ABSTRACT
Oxidative stress has been discovered to be in-
volved in the progression of diabetes mellitus.
The antioxidant properties of virgin coconut oil
(VCO) among other functions might have a be-
neficial effect in ameliorating the disease. This
study w as aimed to determine the glycemic and
antioxidant effects of VCO in alloxan induced
diabetic rats. 24 male Sprague-Dawley rats w ere
divided into 4 group s as follows: control (C), dia-
betes untreated (DUT), diabetes treated with 7.5
ml/kg VCO (DT7.5) and diabetes treated with 10
ml/kg VCO (DT10). Alloxan (100 mg/kg b.w I.P)
was used to induce diabetes and VCO was ad-
ministered orally once daily for 4 w eeks. Fasting
blood glucose level w as measured on Day 0 (72
hours post alloxan injection) and after 4 weeks.
Glucose tolerance test was conducted on the
4th week as well as the determination of serum
insulin and liver antioxidant parameters using
standard biochemical methods. Values are means
± S.E.M., compared by ANOVA and Tukey’s post
hoc test. The result s show that VCO significantly
reduced the fasting blood glucose level in DT7.5
rats (132.4 ± 6.911) and DT10 rats (131.6 ± 12.2)
are compared with DUT rats (320.4 ± 22.99) and
improved the oral glucose tolerance. Serum in-
sulin was increased in DT10 rats. GSH activities
significantly increased p < 0.05 in DT10 rats (0.39
± 0.022) when compared to DUT rats (0.032 ±
0.004). CAT activities also significantly increased
p < 0.05 in DT7.5 (17.63 ± 0.61) and DT10 rats
(30.88 ± 0.97) w hen compared to DUT rats (10.98
± 0.6). SOD activities significantly increased p <
0.05 in DT7.5 (2.634 ± 0.04) and DT10 rats (2.258 ±
0.32) when compared to DUT rats (1.366 ± 0.05)
while MDA significantly reduced p < 0.05 in DT7.5
(49.16 ± 0.51) and DT10 (33.64 ± 0.42) rats when
compared to DUT rats (99.93 ± 4.79). This study
revealed that VCO has a hypoglycemic action,
enhances insulin secretion and also ameliorates
oxidative stress induced in type I (alloxan-in-
duced diabetic) male rats.
Keywords: Virgin Coconut Oil; Oxidative Stress;
Blood Glucose; Glucose Tolerance
1. INTRODUCTION
Diabetes mellitus characterized by hyperglycaemia, is
due to the deficiency of insulin secretion or its action. It
has been associated with a syndrome of disturbance in
the homeostasis of carbohydrate, fat and protein metabo-
lism [1]. Diabetes mellitus has been categorized into type
1 and type 2 diabetes. Type 1 diabetes refers to defi-
ciency of endogenous insulin which is caused by a cellu-
lar-mediated auto immune destruction of the beta cells in
the pancreas which produces insulin. And type 2 diabetes
is as a result of a decreased response to insulin by its
receptors, which is also referred to as insulin resistance
[1,2].
Oxidative stress contributes significantly to the patho-
physiology of several diseases which include diabetes
[3]. Alloxan, a chemical used in inducing diabetes acts
mainly by the generation of reactive oxygen species
(ROS) [3]. It preferentially accumulates in the GLUT2
glucose transporter in the pancreatic beta cells and sub-
sequently leads to the death of the cells. Therefore al-
loxan is a model compound when studying diabetes as a

B. Iranloye et al. / Journal of Diabetes Mellitus 3 (2013) 221-226
222
result of ROS mediated beta cell toxicity.
Historically, coconut oil has been renowned for its
medicinal and nutritional value. Studies on the biological
effects of coconut oil have proven that it ameliorates
oxidative stress by boosting the antioxidant defense sys-
tem, mopping up free radicals and reducing lipid peroxi-
dation [4,5]. It has also been reported to suppress micro-
bial and viral activities [6], promote weight loss and en-
hance thyroid function [7]. Other researches have also re-
ported that coconut oil possesses anti-inflammatory and
anti-ulcerogenic effect [8], while also having the ability
to increase the level of high density lipoprotein (HDL)
cholesterol and to reduce the level of low density lipo-
protein (LDL) in serum and tissues [4].
Copra oil and virgin coconut oil (VCO) are the two
main types of coconut oil. Copra oil is extracted from the
dried endosperm of the coconut fruit while VCO is pro-
duced by a “wet” extraction process from the fresh en-
dosperm of the coconut fruit [9]. The mode of extraction
of VCO makes it more beneficial than copra oil. This is
because no chemicals are used and there is little or no
application of heat during its extraction. Therefore it re-
tains more of the natural active components which in-
clude polyphenols which have been proven to boost the
antioxidant defense system [4].
The present study therefore, determined the possible
role of the antioxidant effect of VCO on oxidation/per-
oxidation linked with diabetes mellitus in alloxan in-
duced diabetic rats as well as its possible effect on glu-
cose homeostasis.
2. MATERIALS AND METHODS
2.1. Animals
Male Sprague-Dawley rats weighing 120 - 150 g were
obtained from the Laboratory Animal House of the Col-
lege of Medicine of the University of Lagos. The rats
were allowed to acclimatize for two weeks before the
commencement of the experiment and were fed with
standard rat chow and water ad libitum at 20˚C - 25˚C
under a 12 h light/dark cycle. All animal handling and
experiment protocols complied with the international
guidelines for laboratory animals as supported by the
College of Medicine of the University of Lagos ethical
committee.
2.2. Experimental Groups
Rats were randomly divided into 4 groups (n = 6):
Group 1, control (C) received 0.5 ml distilled water;
Group 2, diabetic untreated (DUT); Group 3, diabetic
treated with 7.5 ml/kg body weight of VCO (DT7.5) and
Group 4, diabetic treated with 10 ml/kg body weight of
VCO (DT10). Seventy two hours following the induction
of diabetes, VCO was administered orally for 4 weeks
daily at the appropriate dose for Groups 3 and 4 animals.
2.3. Induction of Diabetes
Following 2 weeks acclimatization of the rats, Alloxan
monohydrate (manufactured by Denixco Private limited,
India) was used to induce type 1 diabetes in Groups 2, 3
and 4. A dose of 100 mg/kg body weight of Alloxan
monohydrate was administered only once intraperito-
neally. A mild pressure was applied at the spot of injec-
tion to enhance absorption. After 3 days of administra-
tion the fasting blood glucose level of these rats were
measured. Rats with fasting blood glucose level above
200 mg/dl were considered diabetic.
2.4. Measurement of Blood Glucose
Blood glucose level was measured using One Touch
Ultra test strips (Lifescan Inc. Milpitas, USA). Blood
was obtained from the rats at the tip of rat’s tail. The
blood was dropped on the test strips already inserted in a
One Touch Ultra Easy Glucometer (Lifescan Inc.
Milpitas, USA). The glucose levels of the animal were
displayed on the glucometer in about 5 seconds. Blood
glucose level was measured at the beginning of the ex-
periment and after 4 weeks.
2.5. Preparation of Virgin Coconut Oil
Mature coconuts were bought from Mushin Market,
Lagos, Nigeria. VCO was extracted using the wet extrac-
tion method [4]. The solid endosperm of mature coconut
was crushed and made into thick slurry. About 500 ml of
water was added to the slurry obtained and squeezed
through a fine sieve to obtain coconut milk. The resultant
coconut milk was left for about 24 hours to facilitate the
gravitational separation of the emulsion. Demulsification
produced layers of an aqueous phase (water) on the bot-
tom, an emulsion phase (cream) in the middle layer and
an oil phase on top. The oil on top was scooped and
warmed for about 3 minutes to remove moisture. The
obtained oil was then filtered and stored at room tem-
perature.
2.6. Oral Glucose Tolerance Test (OGTT)
On the 4th week of the experiment, all groups were
subjected to oral glucose tolerance test (OGTT). The rats
were fasted overnight for sixteen-hour (16-h) and subse-
quently challenged with a glucose load of 2 ug/kg body
weight. Blood glucose levels were determined at 0 h
(pre-glucose treatment) and at 30, 60, 90, 120 and 180
min (post glucose treatment). The glucose levels were
measured using a complete blood glucose monitoring
system (One-Touch Ultra Easy Glucose Meter, Lifescan

B. Iranloye et al. / Journal of Diabetes Mellitus 3 (2013) 221-226 223
Inc. Milpitas, USA).
2.7. Sample Collection
The rats were anesthetized by intramuscular injection
of 50 mg/kg of ketamine. The liver was removed and
homogenized in phosphate buffer, pH 7.4 and stored at
−20˚C. Blood samples were also collected from the ven-
tricle of the heart, allowed to clot and spun at 3000 rmp
to obtain serum sample for insulin assay.
2.8. MDA L evel
As a marker of lipid peroxidation, the level of malon-
dialdehyde (MDA) in the liver homogenate was meas-
ured [10]. 1 ml of the tissue homogenate was thoroughly
mixed with 2 ml of TCA-TBA-HCl solution and heated
for 15 minutes in a water bath. After cooling, the pre-
cipitate is removed by centrifugation and the absorbance
measured at 535 nm is taken as an index of lipid peroxi-
dation.
2.9. SOD, CAT and GSH Activities
At the end of the 4 week period of the experiment, the
activity of the superoxide dismutase (SOD) enzyme in
the liver homogenate was determined [11]. The reaction
was carried out in 0.5m sodium carbonate buffer pH 10.2
and was initiated by the addition of 3 × 10−4 epinephrine
in 0.005 N HCl. The absorbance was read at 320 nm.
Catalase (CAT) activity was determined by measuring
the exponential disappearance of H2O2 at 240 nm and
expressed in units/mg of protein [12]. Reduced glu-
tathione (GSH) content of the liver homogenate was de-
termined [13], based on the reaction of Ellman’s reagent
5,5’dithiobis-2-nitrobenzoic acid (DNTB) with the thiol
group of GSH at pH 8.0 to produce 5-thiol-2-nitroben-
zoate which is yellow at 412 nm. Absorbance was re-
corded using UV-Visible Spectrophotometer in all meas-
urement. The protein concentrations of the samples were
measured using the method of Bradford [14].
2.10. Serum Insulin Level
Enzyme-Linked Immunosorbent Assay (ELISA) was
used to measure the level of insulin in the serum sample
obtained from the animal. The protocol used was as de-
scribed by the manufacturer of the assay kit (Enzo-Life
Science).
2.11. Statistical Analysis
Data were presented as mean and Standard Error of
Mean (SEM). One-way ANOVA and Tukey’s post hoc
test was used to determine the specific pairs of groups
that were statistically different at p < 0.05. Analysis was
performed with GraphPad software.
3. RESULTS
3.1. Fasting Blood Glucose
Fasting blood glucose was measured at 72 hours post
alloxan injection. Hyperglycemia was observed in DUT,
DT7.5, and DT10 rats. After four weeks of coconut oil
treatment, DT7.5 and DT10 rats showed a significant re-
duction (p < 0.05) in fasting blood glucose level com-
pared with DUT rats (Figures 1 and 2).
3.2. Oral Glucose Tolerance Test (OGTT)
After 4 weeks administration of coconut oil, glucose
concentration (pre glucose challenge) in both DT7.5 and
DT10 rats showed a significantly reduced glucose con-
centration when compared with DUT rats. As expected,
there was an initial increase in blood glucose 30 minutes
post glucose challenge which reduced over time as pre-
sented in Figure 2. Three hours post glucose challenge
showed that DT7.5 and DT10 significantly reduced blood
glucose level when compared with DUT rats. The effect
Figure 1. Fasting blood glucose level (mg/dl) of diabetic rats
induced with alloxan. Values are expressed as mean ± S.E.M.
*p < 0.05 is significant compared with Group 1 (control).
Figure 2. Effect of 4 weeks VCO supplementation on fasting
blood glucose level (mg/dl) in alloxan induced diabetic rats.
Values are expressed as mean ± S.E.M. *p < 0.05 is significant
compared with Group 1 (control). #p < 0.05 is significant com-
pared with Group 2 (diabetes untreated).

B. Iranloye et al. / Journal of Diabetes Mellitus 3 (2013) 221-226
224
of DT10 was more effective than that of DT7.5 (Figure 3). antioxidative defence capacity, thus the generation of
ROS by alloxan leads to the death of these cells. This is
possible due to the reduction product of the reaction,
dialuric acid, which generates hydrogen peroxide, su-
peroxide radicals and hydroxyl radicals. These radicals
are responsible for the death of the beta cells and the
ensuing state of insulin-dependent alloxan diabetes [3].
3.3. Antioxidant Enzymes Activities and
MDA Levels
MDA level was significantly increased in DUT rats
when compared to control (p < 0.05), however, MDA
levels were significantly reduced in DT7.5 and DT10 rats
compared with DUT rats. Though a significant reduction
in DT7.5 rats was observed when compared with DUT
rats, the value observed compared with the control still
shows lipid peroxidation (Table 1). In the antioxidant
enzymes, SOD activity was significantly reduced in DUT
rats when compared with control. DT7.5 and DT10 sig-
nificantly increased the activity of SOD when compared
with DUT rats. The enhancement in SOD activity how-
ever was still significantly lower compared with the con-
trol values. The activity of GSH was significantly re-
duced in DUT rats when compared with control. How-
ever, DT10 rats significantly increased the activity of
GSH while DT7.5 had no effect on the activity of GSH
when compared with DUT rats. Lastly, CAT activity was
reduced in DUT treated rats when compared with control
rats. DT7.5 and DT10 significantly increased the activity
of CAT when compared with DUT rats. DT10 enhanced
this activity more than the control rats while this activity
was still decreased in DT7.5 rats compared to control rats
(Table 1).
This study reports marked hyperglycemia 72 hours
post alloxan injection (100 mg/kg body weight). This is
supported by other previous studies and reports [15-17].
Four weeks of treatment with VCO decreased the fasting
blood glucose level in DT7.5 and DT10 rats when com-
pared with DUT rats. Supporting the report that coconut
oil has a hypoglycemic effect [18,19]. Since, alloxan
generates ROS to impair the beta cell function; it is pos-
sible that VCO alleviates blood glucose level due to its
antioxidant property. It is possible that the beta cells re-
sponse to oxidative stress might have been enhanced thus
enabling the cells to carry out their function of insulin
production. Consequently, this increase in insulin pro-
duction will lead to reduced blood glucose.
Oral glucose tolerance test is used to measure insulin
function or the degree of peripheral utilization of glucose
[20]. In this study, following glucose administration,
there was a minimal rise in the blood glucose level which
fell below the control value after 2 hours in the control
rats. In DUT, DT7.5 and DT10 rats there was a marked rise
in blood glucose level after the glucose challenge and the
blood glucose level failed to return to the control value
3.4. Serum Insulin Level
Table 2 shows the serum insulin level of male rats
treated with VCO. DUT rats shows a significantly re-
duced insulin level when compared control. DT10 alone
significantly increased the level of insulin when com-
pared with DUT rats. Though the values of DT7.5 were
increased it was however not significant and the values
obtained was still significantly lower than those of the
control rats.
4. DISCUSSION
Figure 3. Effect of virgin coconut oil (VCO) on oral glucose
tolerance test (OGTT). Values are expressed as mean ± S.E.M.
*p < 0.05 is significant compared with Group 1 (control). #p <
0.05 is significant compared with Group 2 (diabetes untreated).
Alloxan, used in inducing diabetes is a toxic glucose
analogue that generates ROS in the presence of intracel-
lular thiols [3]. The beta cells of the pancreas have a low
Table 1. Effect of VCO on the activity of superoxide dismutase, glutathione, catalase and malondialdehyde levels.
Control (C)Diabetes untreated (DUT)Diabetes + 7.5 ml/kg VCO (DT7.5) Diabetes + 10 ml/kg VCO (DT10)
MDA (U/mg protein) 31.78 ± 2.1899.93 ± 4.79* 49.16 ± 0.51*# 33.64 ± 0.42#
SOD (U/mg protein) 3.91 ± 0.14 1.37 ± 0.05* 2.63 ± 0.04*# 2.26 ± 0.32*#
GSH (U/mg protein) 0.11 ± 0.0070.03 ± 0.004* 0.04 ± 0.008* 0.39 ± 0.022*#
CAT (U/mg protein) 25.87 ± 0.9610.98 ± 0.60* 17.63 ± 0.61*# 30.88 ± 0.97*#
V
alues are expressed as mean ± S.E.M. *p < 0.05 is significant compared with control. #p < 0.05 is significant compared with diabetes untreated group.

B. Iranloye et al. / Journal of Diabetes Mellitus 3 (2013) 221-226 225
Table 2. Effect of virgin coconut oil (VCO) on serum insulin
level.
Insulin level (μiu/ml)
Control (C) 3.05 ± 0.25
Diabetes untreated (DUT) 1.19 ± 0.04*
Diabetes + 7.5 ml/kg VCO (DT7.5) 1.90 ± 0.40*
Diabetes + 10 ml/kg VCO (DT10) 2.50 ± 0.03#
Values are expressed as mean ± S.E.M. *p < 0.05 is significant compared
with Control. #p < 0.05 is significant compared with Diabetes untreated
group.
even after 3 hours indicating impairment in glucose tol-
erance which is an indication of diabetes. In DT7.5 and
DT10 rats there was a significant improvement in glucose
tolerance compared with the DUT rats, supporting the
view that ingestion of VCO improves glucose tolerance
in diabetic rats [21]. In addition, the 10 ml/kg dosage of
VCO proved to have a greater effect as the blood glucose
level in DT10 rats after 3 hours of glucose challenge was
closer to the control value than in DT7.5 rats.
It has been reported that the lauric oil in VCO pos-
sesses insulino-tropic properties [18]. Serum insulin was
increased in DT10 rats with a non significant increase in
DT7.5 rats compared with DUT rats. Since the dosage of
7.5 ml/kg body weight of VCO could not elevate serum
insulin, it implies that the 10 ml/kg body weight dose is
more effective in the control of glucose homeostasis than
the 7.5 ml/kg body weight. This is evidenced by the re-
duction in blood glucose level and the improvement in
glucose tolerance compared to DUT rats as discussed
earlier.
Antioxidant enzymes are critical part of cellular pro-
tection against reactive oxygen species and ultimately
oxidative stress. Oxidative stress is determined by the
balance between the generation of ROS such as super-
oxide anion (2 O) and the antioxidant defense systems
such as superoxide dismutase (SOD). Antioxidants en-
zymes involved in the elimination of ROS include SOD,
CAT and GSH, respectively. The present study showed a
decrease in the activity of all measured antioxidants en-
zymes in DUT rats. This indicates a decrease in the anti-
oxidant defense system. However treatment with VCO in
DT7.5 and DT10 rats increased the activities of the anti-
oxidant enzymes. Since oxidative stress contributes sig-
nificantly to the pathophysiology of diabetes [22], sub-
stances that suppress oxidative stress might be therapeu-
tically beneficial. Studies have shown that exogenously
administered antioxidants have protective effects on dia-
betes, thus providing insight into the relationship be-
tween free radicals and diabetes [20,22-24]. The reduc-
tion in fasting blood glucose of rats treated with VCO
after 4 weeks and a decrease in the OGTT of the rats
compared with the diabetic untreated rats can be associ-
ated to the antioxidant effect of VCO.

5. CONCLUSION
VCO alleviates hyperglycemia and improves glucose
tolerance probably by its antioxidant effect which con-
sequently leads to improvement of insulin secretion as
examined in this study. The study also shows that a dos-
age of 10 ml/kg body weight of VCO is quite beneficial
and more effective than that of 7.5 ml/kg body weight.
This was evident because the 7.5 ml/kg body weight did
not increase insulin secretion and possibly because of the
higher OGTT values.
REFERENCES
[1] American Diabetes Association (2010) Diagnosis and
classification of diabetes mellitus. Diabetic Care, 33.
[2] World Health Organization (2011) Diabetes fact sheet.
Sheet number 312 August.
[3] Lenzen, S. (2008) The mechanisms of alloxan- and strep-
tozotocin-induced Diabetes. Diabetologia, 51, 216-226.
http://dx.doi.org/10.1007/s00125-007-0886-7
[4] Nevin, K.G. and Rajamohan, T. (2006) Virgin coconut oil
supplemented diet increases the antioxidant status in rats.
Food Chemistry, 99, 260-266.
http://dx.doi.org/10.1016/j.foodchem.2005.06.056
[5] Dosumu, O.O., Duru, F.I.O., Osinubi, A.A., Oremosu,
A.A. and Noronha, C.C. (2010) Influence of virgin coco-
nut oil (VCNO) on oxidative stress, serum testosterone
and gonadotropic hormones (FSH, LH) in chronic ethanol
ingestion. Agriculture and Biology Journal of North Ame-
rica, 1, 1126-1132.
[6] Van Immerseel, F., De Buck, J. and Boyen, F. (2004)
Medium-chain fatty acids decrease colonization and in-
vasion through hilA suppression shortly after infection of
chickens with Salmonella enterica serovar enteritidis. Ap-
plied and Environmental Microbiology, 70, 3582-3587.
http://dx.doi.org/10.1128/AEM.70.6.3582-3587.2004
[7] Takeuchi, H., Sekine, S., Kojima, K. and Aoyama, T.
(2008) The application of medium-chain fatty acids: Edi-
ble oil with a suppressing effect on body fat accumulation.
Asia Pacific Journal of Clinical Nutrition, 17, 320-324.
[8] Anosike, C.A. and Obidoa, O. (2010) Anti-inflammatory
and anti-ulcerogenic effect of ethanol extract of coconut
(Cocos nucifera) on experimental rats. African Journal of
Food, Agriculture, Nutrition and Development, 10, 10-16.
[9] Cretney, J. and Tafunai, A. (2004) Tradition, trade, and
technology: Virgin coconut oil in samoa. In Chains of
Fortune: Linking Women Producers and Workers with
Global Markets, 45-74.
[10] Uchiyama, M. and Mihara, M. (1978) Determination of
malonaldehyde precursor in tissues by thiobarbituris acid
test. Analytical Biochemistry, 86, 271-278.
http://dx.doi.org/10.1016/0003-2697(78)90342-1
[11] Sun, M. and Zigmam S. (1978) An improved spectro-

B. Iranloye et al. / Journal of Diabetes Mellitus 3 (2013) 221-226
226
photomeric assay for superoxide dismutase based on epi-
nephrine autooxidation. Analytical Biochemistry, 90, 81-
89. http://dx.doi.org/10.1016/0003-2697(78)90010-6
[12] Aebi, H. (1984) Catalase in vitro. Methods in Enzymology,
8, 121-126.
http://dx.doi.org/10.1016/S0076-6879(84)05016-3
[13] Van Dooran, R., Liejdekker, C.M. and Handerson, P.T.
(1978) Synergistic effects of phorone on the hepatotoxic-
ity of bromobenzene and paracetamol in mice. Toxicology,
11, 225-233.
http://dx.doi.org/10.1016/S0300-483X(78)91389-6
[14] Bradford, M.M. (1976) A rapid and sensitive method for
the quantification of microgram quantities of protein util-
izing the principle of protein-dye binding. Analytical Bio-
chemistry, 72, 248-254.
http://dx.doi.org/10.1016/0003-2697(76)90527-3
[15] Szkudelski, T. (2001) The mechanism of alloxan and
streptozotocin action in B cells of the rat pancreas. Phy-
siological Research, 50, 536-546.
[16] Lenzen, S., Tiedge, M., Jorns, A. and Munday, R. (1996)
Alloxan derivatives as a tool for the elucidation of the
mechanism of the diabetogenic action of alloxan. In:
Shafrir, E., Ed., Lessons from Animal Diabetes. Birk-
häuser, Boston, 113-122.
http://dx.doi.org/10.1007/978-1-4612-4112-6_8
[17] Jorns, A., Munday, R., Tiedge, M. and Lenzen, S. (1997)
Comparative toxicity of alloxan, N-alkylalloxans and nin-
hydrin to isolated pancreatic islets in vitro. Journal of
Endocrinology, 155, 283-293.
http://dx.doi.org/10.1677/joe.0.1550283
[18] Garfinkel, M., Lee, S., Opara, E.C. and Akwari, O.E.
(1992) Insulinotropic potency of lauric acid. A metabolic
rationale for medium chain fatty acids (MCF) in TPN
formulation. Journal of Surgical Research, 52, 328-333.
http://dx.doi.org/10.1016/0022-4804(92)90111-C
[19] Sadikot, S.M. (2005) Coconut for health nutrition. Jakarta,
APCC, 6.
[20] Kim, S.S., Gallaher, D.D. and Csallany, A.S. (2000) Vi-
tamin E and probucol reduce urinary lipophilic aldehydes
and renal enlargement in streptozotocin induced diabetic
rats. Lipids, 35, 1225-1237.
http://dx.doi.org/10.1007/s11745-000-0639-2
[21] Siddalingaswamy, M., Rayaorth, A. and Khanum, F.
(2011) Anti-diabetic effects of cold and hot extracted vir-
gin coconut oil. Journal of Diabetes Mellitus, 1, 118-123.
http://dx.doi.org/10.4236/jdm.2011.14016
[22] Maritim, A.C., Sanders, R.A. and Watkins, J.B. (2003)
Diabetes, oxidative stress and antioxidants: A review. Jour-
nal of Biochemical and Molecular Toxicology, 17, 24-38.
http://dx.doi.org/10.1002/jbt.10058
[23] Mekinova, D., Chorvathova, V., Volkovova, K., Staru-
chova, M., Grancicova, F., Klvanova, J., Nevin, K.G. and
Rajamohan, T. (2004) Beneficial effects of virgin coconut
oil on lipid parameters and in vitro LDL oxidation. Clini-
cal Biochemistry, 37, 830-835.
http://dx.doi.org/10.1016/j.clinbiochem.2004.04.010
[24] Borenshtein, D.R., Ofri, M., Werman, A., Stark, H.J.,
Tritschler, W. and Moeller Madar Z. (2001) Cataract de-
velopment in diabetic sand rats treated with alpha-lipoic
acid and its gamma-linolenic acid conjugate. Diabetes/
Metabolism Research and Reviews, 17, 44-50.
http://dx.doi.org/10.1002/1520-7560(0000)9999:9999<::
AID-DMRR153>3.0.CO;2-S