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Anti-diabetic and antioxidant effects of virgin coconut oil in alloxan induced diabetic male Sprague Dawley rats


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Oxidative stress has been discovered to be involved in the progression of diabetes mellitus. The antioxidant properties of virgin coconut oil (VCO) among other functions might have a beneficial effect in ameliorating the disease. This study was aimed to determine the glycemic and antioxidant effects of VCO in alloxan induced diabetic rats. 24 male Sprague-Dawley rats were divided into 4 groups as follows: control (C), diabetes 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 administered orally once daily for 4 weeks. Fasting blood glucose level was 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 results 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 insulin was increased in DT10 rats. GSH activities significantly increased p 10 rats (0.39 ± 0.022) when compared to DUT rats (0.032 ± 0.004). CAT activities also significantly increased p 7.5 (17.63 ± 0.61) and DT10 rats (30.88 ± 0.97) when 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 7.5 (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-induced diabetic) male rats.
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Vol.3, No.4, 221-226 (2013) Journal of Diabetes Mellitus
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.
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 was aimed to determine the glycemic and
antioxidant effects of VCO in alloxan induced
diabetic rats. 24 male Sprague-Dawley rats were
divided into 4 groups 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 weeks. Fasting
blood glucose level was 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 results 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) when 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
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
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
Copyright © 2013 SciRes. OPEN ACCESS
B. Iranloye et al. / Journal of Diabetes Mellitus 3 (2013) 221-226
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.
2.1. 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
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-
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
Copyright © 2013 SciRes. OPEN ACCESS
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 Level
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-
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 × 104 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
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.
3.1. 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).
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B. Iranloye et al. / Journal of Diabetes Mellitus 3 (2013) 221-226
Copyright © 2013 SciRes.
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 (Ta b l e 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
(Tabl e 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
Tab l e 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.
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 ± 2.18 99.93 ± 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 ± 0.007 0.03 ± 0.004* 0.04 ± 0.008* 0.39 ± 0.022*#
CAT (U/mg protein) 25.87 ± 0.96 10.98 ± 0.60* 17.63 ± 0.61*# 30.88 ± 0.97*#
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
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
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
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.
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.
[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.
[4] Nevin, K.G. and Rajamohan, T. (2006) Virgin coconut oil
supplemented diet increases the antioxidant status in rats.
Food Chemistry, 99, 260-266.
[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.
[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.
[11] Sun, M. and Zigmam S. (1978) An improved spectro-
Copyright © 2013 SciRes. OPEN ACCESS
B. Iranloye et al. / Journal of Diabetes Mellitus 3 (2013) 221-226
photomeric assay for superoxide dismutase based on epi-
nephrine autooxidation. Analytical Biochemistry, 90, 81-
[12] Aebi, H. (1984) Catalase in vitro. Methods in Enzymology,
8, 121-126.
[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.
[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.
[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.
[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.
[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.
[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.
[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.
[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.
[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.
[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.<::
Copyright © 2013 SciRes. OPEN ACCESS
... Coconut oil is largely consumed in the tropics and is renowned for its nutritional and medicinal value. Research has proven it possesses anti-diabetic properties [13] and ameliorative effects on reproductive dysfunction [14]. Lauric acid has been specifically reported to possess vaso-relaxant effects [15]. ...
... They cause an increase in circulating high-density lipoproteins (HDL) which may account for their health benefits [29]. In addition, lauric acid is the most abundant constituent of coconut oil, thus, reputable for its therapeutic properties, especially for diabetes [13] and reproductive disorders [30]. Lauric acid has also been specifically proven to possess vaso-relaxant and antioxidant properties [15]. ...
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Background Diabetes mellitus is a global health challenge and has been recognised as a risk factor for erectile dysfunction. Dissatisfaction with standard medications has been reported by some patients, hence therapeutic plants are being considered as a viable alternative therapy, with their active components being investigated to create a standard regimen. Lauric acid is the most abundant constituent of coconut oil and is proposed to be responsible for its therapeutic properties. The corpus cavernosum plays an important role in erectile function with its relaxation favouring erection. This study thus sought to investigate the possible relaxant action and mechanism of lauric acid on the corpus cavernosum of diabetic male Wistar rats. Diabetes was induced by intraperitoneal injection of streptozotocin after which graded doses of lauric acid were administered orally to three groups of diabetic rats, once daily for 4 weeks. At the end of the experiment, the corpus cavernosal tissues of the rat penis were extracted. Following phenylephrine or potassium chloride (KCl)—induced contraction, relaxation response to acetylcholine and sodium nitroprusside was used to evaluate endothelium-dependent and nitric oxide-mediated relaxation, respectively. Results Relaxation response to acetylcholine, following pre-contraction with phenylephrine, was significantly decreased in the cavernosal tissues of diabetic untreated rats and was not significantly improved in lauric acid treated diabetic groups. Relaxation response to acetylcholine, following pre-contraction with KCl, was significantly decreased in the diabetic untreated group but was significantly improved in lauric acid treated diabetic groups at the lowest dose. Decreased relaxation response to sodium nitroprusside, following pre-contraction with phenylephrine in tissues of diabetic untreated rats, was significantly improved in lauric acid-treated diabetic groups at lower doses. Decreased relaxation response to sodium nitroprusside, following pre-contraction with KCl, was significantly improved in lauric acid-treated diabetic groups at all doses. Conclusion Lauric acid improved relaxation of corpus cavernosum muscle in diabetic male rats by enhancing nitric oxide-mediated relaxing action of sodium nitroprusside and possibly inhibiting KCl-induced contraction.
... VCO with this range of antioxidant activity is beneficial in increasing antioxidant levels in the rat brain (in vivo test) (Yeap et al., 2015), preventing oxidative stress in rats (in vivo test) (Arunima & Rajamohan, 2013), and Fig. 9 Antioxidant activities of pure VCO, PVP/VCO fibers (with various ratios of 10:2, 10:3, 10:4, and 10:5), and vitamin C, as represented by the IC 50 value. Alphabet differences indicate significant differences (p < 0.05) from Tukey's one-way ANOVA analysis increasing insulin secretion to prevent diabetes in Sprague Dawley male rats (Iranloye et al., 2013). Furthermore, the antioxidant test indicated that loading VCO into the PVP fiber matrix did not alter its antioxidant activity. ...
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This study aimed to incorporate virgin coconut oil (VCO) into polyvinylpyrrolidone (PVP) fiber matrix using the rotary force spinning (RFS) method and evaluated their physicochemical properties, antioxidant activity, and release behavior. The PVP/VCO fibers were produced by varying the weight ratios of PVP:VCO of 10:2, 10:3, 10:4, and 10:5. Scanning electron microscopy (SEM) analysis revealed smooth, defect-free, and bead-free PVP/VCO fibers with diameters ranging from (1.28 ± 0.06) to (2.17 ± 0.41) µm. Fourier-transform infrared spectroscopy (FTIR) confirmed the successful loading of VCO into the PVP fiber matrix. X-ray diffraction (XRD) analysis indicated the amorphous nature of the PVP/VCO fibers. Differential scanning calorimetry (DSC) analysis demonstrated that PVP/VCO fibers exhibited higher thermal stability compared to pure PVP and VCO. The antioxidant activity of VCO, with IC50 value of (1.56 ± 0.30) mg mL⁻¹, was not significantly altered by the incorporation of VCO into the PVP fibers. The PVP/VCO fibers exhibited IC50 values ranging from (1.58 ± 0.06) to (2.25 ± 0.09) mg mL⁻¹. The release profile of VCO from the PVP/VCO fibers was influenced by the fiber diameter, with the samples containing weight ratios of 10:4 and 10:5 demonstrating optimal characteristics such as smaller diameter, higher thermal stability, higher antioxidant activity, and prolonged release behavior. This study holds promise for the development of novel oral delivery systems for VCO and contributes to the expanding research on the utilization of fiber structures in food supplement and drug delivery applications. Graphical Abstract
... MCFA was previously reported on its preferential metabolism in improving glucose homeostasis (Malaeb and Spoke, 2020). Previous studies on VCO containing high lauric acid content elucidated significant improvement in glucose tolerance of diabetic animals by regenerating β-cell (Maidin and Ahmad, 2015;Iranloye et al., 2013). Although lauric acid at 25 and 100 mg/kg did not significantly improve the FBG, the ameliorated glucose tolerance suggested their ongoing tissuerepairing phase. ...
Lauric acid, a 12‑carbon atom medium chain fatty acid (MCFA) has strong antioxidant and antidiabetic activities. However, whether lauric acid can ameliorate hyperglycaemia-induced male reproductive damage remains unclear. The study aimed to determine the optimal dose of lauric acid with glucose-lowering activity, antioxidant potential and tissue-protective effects on the testis and epididymis of streptozotocin (STZ)-induced diabetic rats. Hyperglycaemia was induced in Sprague Dawley rats by an intravenous injection of STZ at a dose of 40 mg/kg body weight (bwt). Lauric acid (25, 50 and 100 mg/kg bwt) was administered orally for eight weeks. Weekly fasting blood glucose (FBG), glucose tolerance and insulin sensitivity were examined. Hormonal profiles (insulin and testosterone), lipid peroxidation (MDA) and antioxidant enzyme (SOD and CAT) activities were measured in the serum, testis and epididymis. The reproductive analyses were evaluated based on sperm quality and histomorphometry. Lauric acid administration significantly improved FBG levels, glucose tolerance, hormones-related fertility and oxidant-antioxidant balance in the serum, testis and epididymis compared to untreated diabetic rats. Treatment with lauric acid preserved the testicular and epididymal histomorphometry, along with the significant improvements in sperm characteristics. It is shown for the first time that lauric acid treatment at 50 mg/kg bwt is the optimal dose for ameliorating hyperglycaemia-induced male reproductive complications. We conclude that lauric acid reduced hyperglycaemia by restoring insulin and glucose homeostasis, which attributes to the regeneration of tissue damage and sperm quality in STZ-induced diabetic rats. These findings support the correlation between oxidative stress and hyperglycaemia-induced male reproductive dysfunctions.
... The balance between the synthesis of ROS and defense capabilities are therefore indicative of the level of oxidative stress. GSH is one of the antioxidant enzymes responsible for eradicating ROS 78 . From the perspective of pharmaceutical toxicity, the viscera most often targeted is the liver. ...
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Objective: Diabetes mellitus is one of the most commonly arising endocrine conditions. The disorder gives rise to enduring damage to a number of body tissues and viscera as a result of related macrovascular and microvascular complications. In patients who are unable to maintain their nutritional status independently, medium-chain triglyceride (MCT) oil is frequently added as a supplement to parenteral nutrition. The aim of the present research is to establish whether MCT oil has a therapeutic influence on the hepatic damage occurring in male albino rats as a result of streptozotocin (STZ)-induced diabetes. Materials and methods: 24 male albino rats were randomized into four cohorts, i.e., controls, STZ-diabetic, metformin-treated and MCT oil-treated. The rodents were fed a high-fat diet for 14 days; a low dose of intraperitoneal STZ was then administered in order to induce diabetes. The rats were subsequently treated for 4 weeks with metformin or MCT oil. Analysis included an appraisal of liver histology and biochemical indices, i.e., fasting blood glucose (FBG), hepatic enzymes and glutathione (GSH), the latter obtained from hepatic tissue homogenate. Results: A rise in FBG and hepatic enzymes was observed, but in the STZ-diabetic cohort, hepatic GSH levels were diminished. Treatment with either metformin or MCT oil led to a decline in FBG and hepatic enzyme titers whereas GSH concentrations increased. Liver histology findings were notable amongst rodents within control, STZ-diabetic and metformin-treated groups. The majority of histological changes were resolved following therapy with MCT oil. Conclusions: The anti-diabetic and antioxidant characteristics of MCT oil have been substantiated by this work. MCT oil led to a reversal of the hepatic histological changes seen in STZ-induced diabetes in rats.
... The beta cell response to oxidative stress may have been enhanced to allow it to carry out its insulin-producing function. This increase in insulin production will cause a decrease in blood glucose 13 . ...
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Diabetes mellitus is a metabolic disease characterized by increased blood glucose levels. Currently, the treatment of diabetes mellitus uses synthetic or chemical drugs and natural ingredients such as virgin coconut oil. Virgin coconut oil (VCO) is extracted with minimal heating and no chemical purification process. This study aims to obtain data on the impact of VCO as an antidiabetic obtained from several research journals. This literature study uses a narrative review method obtained from the Google Scholar, Pubmed, and Science Direct databases. The results of this study indicate that VCO can be used as an alternative to lowering blood glucose levels because it has antidiabetic activity. Medium-chain fatty acid (MCFA) lauric acid in VCO can stimulate insulin production in pancreatic beta cells. This study concludes that virgin coconut oil can potentially reduce blood sugar levels.
... 100µL TMB substrate was added and incubated for 30 min at RT followed by 100µL stopping solution and OD read at 450 nm in the ELISA reader (Tecan Microplate Reader). Values were expressed in terms of ng/10µl with respect to standard [28]. ...
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Glycosaminoglycans (GAGs) are bioactive polysaccharides or glycoconjugates found in the fish waste having significant health impacts. In the present study it has been attempted to extract GAGs from mackerel fish waste through chemical and enzymatic methods. Further, the extracted GAGs (e-GAGs) were analyzed for their composition (uronic acid, total sugar & sulfate), chemical characterization was carried out through techniques of scanning electron microscopy (SEM) and Fourier transform infrared spectroscopy (FTIR) & Proton NMR. Further, probable major GAGs present was identified by enzymatic digestion. The biological potential of the extracted glycoconjugate was assessed further through in-vitro and in-vivo studies. In-vitro biological activity showed good lipase inhibition (IC50, 2.6 mg/mL) and bile acid binding properties (dose-dependent). Lipid accumulation lowered in the e-GAGs differentiated 3T3L1 preadipocyte cells have also been observed. The high fat fed animal (in-vivo) study showed ameliorative effect via reducing blood sugar∼1.28↓, lipid profile↓, plasma insulin∼3.5↓, improved glucose tolerance, and homeostatic model assessment for insulin resistance (HOMA-IR, ∼3.0↓). Furthermore, elimination of bile acid (BA) due to GAG-BA binding properties resultant in removal of elevated fecal triglyceride and cholesterol suggesting its lipid lowering activity. Regulation of various proteins linked to carbohydrate and lipid metabolism including fatty acid synthase (FAS), low density lipoproteins receptor (LDL-R), 7α-hydroxylase, glucose transporter-4 (GLUT4) and Peroxisome proliferator- activated receptor gamma (PPAR-γ) were significant (p < 0.05) with e-GAGs treatment when compared to HFD group. Thus, the e-GAGs showed potential hypolipidemic activity through elimination of bile acid binding property together with regulating the specific protein related to obesity and its associated complications.
Background and aim: Metabolic syndrome is associated with health conditions and neurological disorders. Brain-derived neurotrophic factor (BDNF) plays a protective role on the nervous system. Decreased levels of BDNF have been shown in MetS and neurodegenerative diseases. There is promising evidence regarding the anti-inflammatory antioxidant, and neuroprotective properties of virgin coconut oil (VCO). The aim of this study was to evaluate the effects of VCO consumption on serum BDNF levels, oxidative stress status, and insulin resistance in adults with MetS. Methods: This randomized controlled clinical trial was conducted on 48 adults with MetS aged 20-50 years. The intervention group received 30 ml of VCO daily to substitute the same amounts of oil in their usual diet. The control group continued their usual diet. Serum BDNF levels, total antioxidant capacity (TAC), malondialdehyde (MDA) as well as HOMA-IR and QUICKI index were measured after four weeks of intervention. Results: VCO consumption significantly reduced serum levels of MDA (p = .01), fasting insulin (p < .01) and HOMA-IR index (p < .01) and increased serum TAC (p < .01) and QUICKI index (p = .01) compared to the control group. Serum BDNF levels increased significantly in VCO group compared to the baseline (p = .02); however, this change was not significant when compared to the control group (p = .07). Conclusion: VCO consumption improved oxidative stress status and insulin resistance and had a promising effect on BDNF levels in adults with MetS. Further studies are needed to understand the long-term effects of VCO consumption.
Neurodegenerative disease (ND) is a clinical condition in which neurons degenerate with a consequent loss of functions in the affected brain region. Parkinson’s disease (PD) is the second most progressive ND after Alzheimer’s disease (AD), which affects the motor system and is characterized by the loss of dopaminergic neurons from the nigrostriatal pathway in the midbrain, leading to bradykinesia, rigidity, resting tremor, postural instability and non-motor symptoms such as cognitive declines, psychiatric disturbances, autonomic failures, sleep difficulties, and pain syndrome. Coconut oil (CO) is an edible oil obtained from the meat of Cocos nucifera fruit that belongs to the palm family and contains 92% saturated fatty acids. CO has been shown to mediate oxidative stress, neuroinflammation, mitochondrial dysfunction, apoptosis and excitotoxicity-induced effects in PD in various in vitro and in vivo models as a multi-target bioagent. CO intake through diet has also been linked to a decreased incidence of PD in people. During digestion, CO is broken down into smaller molecules, like ketone bodies (KBs). The KBs then penetrate the blood–brain barrier (BBB) and are used as a source of energy its ability to cross BBB made this an important class of natural remedies for the treatment of ND. The current review describes the probable neuroprotective potential pathways of CO in PD, either prophylactic or therapeutic. In addition, we briefly addressed the important pathogenic pathways that might be considered to investigate the possible use of CO in neurodegeneration such as AD and PD.
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Rice is a dietary staple foods and one of the most importand cereal crops, especially for people in Asia. The consumption of rice is associated with diabetes mellitus due to its high glycemic index. In other hand, some of rice components namely rice bran and rice bran oil contained some minor components which are reported to have some biological effects. Rice can be contaminated by some toxic elements such as arsenic and mercury coming from water and land in which it grows. Besides, some mycotoxins and mould can be present in rice. Therefore, some goverments control rice available in their market. Rice bran will produce rice bran oil and defatted rice bran. Defatted rice bran component consist a number of polysaccharide and dietary fiber that support in cancer and cardiovascular diet therapy. This reviews will cover some new research information on rice, rice bran and rice bran oil, especially in the biological activities and nutritional aspects to human. Such biological activities which are related to rice and its products are decreasing low density lipoprotein level, lowering cholesterol, reducing blood pressure and preventing colorectal cancer.
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Virgin coconut oil (VCO) has been shown to possess insulinotropic effects shown in isolated perfused mouse islet with hypolipidemic effects. Hot extracted virgin coconut oil (HEVCO) has been shown to possess better antioxidant properties than cold extracted virgin coconut oil (CEVCO). These properties were exploited to study the anti-diabetic effects of HEVCO and CEVCO in diabetic rats. Four groups 8 rats each, first group served as non-diabetic control remaining groups were made diabetic and force fed with 2ml alcoholic extracts of commercial coconut oil (CCO), CEVCO and HEVCO for 21 days. Blood glucose once in 5 days, body weight gain, food intake once in a week and water intake and urine output daily, were monitored. Animals were sacrificed at the end of 21 days. The results indicated HEVCO reduced blood glucose and lipids viz total cholesterol (TC), triglycerides (TG), High density lipoproteins (HDL), Low and Very Low Density Lipoprotein (LDL+ VLDL) and thiobarbutyric acid reactive substances (TBARS) increased the antioxidant status by elevating activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px), glutathione (GSH) concentration and decresed lipid peroxidation in liver than CEVCO. These beneficial effects may be attributed to increased polyphenolic and other antioxidants content present in HEVCO.
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The present study explored the effect of virgin coconut oil on oxidative stress, testosterone and gonadotropic hormones in alcohol-induced testicular injury. Twenty-five male rats were randomly assigned to one of five groups (n=5). The oil was processed from the mature endosperm of coconut and administered at 6.7 ml/kg body weight, while alcohol was given orally at 7 ml/kg body weight. After sacrifice, testicular malondialdehyde and serum hormone levels were determined. Testicular malondialdehyde levels increased significantly in animals treated with alcohol alone (p < 0.001), and animals treated with alcohol following virgin coconut oil treatment (p < 0.05) while the other groups showed a significant decrease (p < 0.05) when compared with the control. However, when compared with the group treated with alcohol alone, all the other groups showed a significant decrease (p < 0.05) in testicular malondialdehyde level. Serum testosterone levels increased significantly (p < 0.05) in rats treated with virgin coconut oil when compared with the alcohol-only treated group, while serum FSH and LH levels were not significantly different from the control values in all the treatment groups. Virgin coconut oil effectively lowered alcohol-induced oxidative stress by reducing testicular malondialdehyde levels and ameliorated the deleterious effect of alcohol on serum testosterone level, but showed no effect on serum FSH and LH levels.
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t The effect of the ethanol extract of coconut on egg albumin- induced inflammation in rat hind paw, hypotonicity induced haemolysis of human red blood cells and indomethacin – induced gastric ulcer in Wistar rats, was studied. Fifty adult rats of either sex of weight 120-200g were divided into ten experimental groups of five rats each; five groups were used for the inflammation test, while the other five groups were used for ulcer test. Inflammation was induced by injecting 0.1ml undiluted fresh egg albumin (philogistic agent) into the subplantar surface of the right hind paw of the rats. Ethanol extract of coconut with doses of 100, 200 and 400mg/kg, and indomethacin (100mg/kg) were administered intraperitoneally to separate groups of the rats one hour before inducing inflammation. The control group received equivalent volume of normal saline (vehicle). Ulcer was induced in the rats by the administration of indomethacin (50mg/kg) (p.o.) using standard procedures. Coconut extract with doses of 100, 200 and 400mg/kg, and ranitidine (100mg/kg) were administered orally to separate groups of the rats thirty minutes before inducing ulcer. The control group received equivalent volume of normal saline (vehicle). The percentage ulcer inhibition was taken as the measure of the protection against ulcer offered by the coconut extract. The effect of the coconut extract on haemolysis induced by distilled water was evaluated by incubating various concentrations of the extract with red blood cells and distilled water. The effect of the standard antiinflammatory drug, indomethacin was determined as a positive control. Changes in absorbance were used to assess the extent of haemolysis, hence membrane stabilization. From the results obtained, rats treated with 100 and 200mg/kg of the extract showed significant reduction of oedema at the later phase of inflammation and also reduced the ulcer induced by indomethacin, with 100mg/kg and 200mg/kg doses having an ulcer inhibition of 65.4% and 67.9% respectively; 400mg/kg of the extract increased the paw oedema of the animals and also evinced an increase in ulceration when compared to control. The coconut extract gave a dose dependent reduction in the haemolysis induced by distilled water. This suggests that the extract at low doses has potential anti-inflammatory and anti-ulcerogenic effect.
A protein determination method which involves the binding of Coomassie Brilliant Blue G-250 to protein is described. The binding of the dye to protein causes a shift in the absorption maximum of the dye from 465 to 595 nm, and it is the increase in absorption at 595 nm which is monitored. This assay is very reproducible and rapid with the dye binding process virtually complete in approximately 2 min with good color stability for 1 hr. There is little or no interference from cations such as sodium or potassium nor from carbohydrates such as sucrose. A small amount of color is developed in the presence of strongly alkaline buffering agents, but the assay may be run accurately by the use of proper buffer controls. The only components found to give excessive interfering color in the assay are relatively large amounts of detergents such as sodium dodecyl sulfate, Triton X-100, and commercial glassware detergents. Interference by small amounts of detergent may be eliminated by the use of proper controls.
In 1818, the Italian Brugnatelli obtained a substance from the oxidation of uric acid that he named ossieritrico. This name, from the Greek “to make red,” referred to the property of the substance to stain the skin a characteristic red color.1 Twenty years later, the German chemists, Wöhler and Liebig, studied uric acid oxidation in detail and obtained the same compound, which they named alloxan, apparently from conflation of the words allantoin and Oxalsäure.2 The early history of alloxan has been reviewed in detail elsewhere.3 Alloxan became generally accepted as the common name for this substance. The compound as synthesized via aqueous workup is a so-called hydrate, actually a gem-diol. The systematic name of this substance is 5,5,-dihydroxy-2,4,6 (1H, 3H, 5H)-pyrimidinetrione.
The in vitro toxicity of the diabetogenic agent alloxan as documented by the induction of beta cell necrosis was studied in isolated ob/ob mouse pancreatic islets. The effect of alloxan has been compared with that of a number of N-alkyl alloxan derivatives and with that of the structurally related compound, ninhydrin. Alloxan and its derivatives were selectively toxic to pancreatic beta cells, with other endocrine cells and exocrine parenchymal cells being well preserved, even at high concentration. In contrast, ninhydrin was selectively toxic to pancreatic beta cells only at comparatively low concentration, destroying all islet cell types at high concentrations. The ultrastructural changes induced by all the test compounds in pancreatic beta cells in vitro were very similar to those observed during the development of alloxan diabetes in vivo. The relative toxicity of the various compounds to pancreatic beta cells in vitro was not, however, related to their ability to cause diabetes in vivo. Indeed, the non-diabetogenic substances ninhydrin, N-butylalloxan and N-isobutylalloxan were very much more toxic to isolated islets than the diabetogemic compounds alloxan and N-methylalloxan. These results suggest that the differences in diabetogenicity among alloxan derivatives are not due to intrinsic differences in the susceptibility of the pancreatic beta cells to their toxicity, but may reflect differences in distribution or metabolism. High concentrations of glucose protected islets against the harmful effects of alloxan and its derivatives, but not those of ninhydrin. Low levels of glucose, and non-carbohydrate nutrients, afforded little protection, indicating that the effect of glucose is not due to the production of reducing equivalents within the cell. 3-O-Methylglucose, which protects against alloxan diabetes in vivo, did not protect against alloxan toxicity in vitro. Since 3-O-methylglucose is known to prevent uptake of alloxan by pancreatic beta cells, it appears that uptake of alloxan by the cell is not a prerequisite for the induction of beta cell necrosis.
Background Diabetes commonly leads to long-term complications such as cataract. This study investigated the effects of α-lipoic acid (LPA) and its γ-linolenic acid (GLA) conjugate on cataract development in diabetic sand rats.Methods Two separate experiments were conducted. In Experiment 1, sand rats were fed a ‘high-energy’ diet (70% starch), an acute model of Type 2 diabetes, and injected with LPA. In Experiment 2, the animals received a ‘medium-energy’ diet (59% starch), a chronic diabetic model, and were intubated with LPA or its GLA conjugate. Throughout the experiments, blood glucose levels and cataract development were measured. At the termination of the experiments, lens aldose reductase (AR) activity and lenticular reduced glutathione (GSH) levels were analyzed.ResultsLPA injection significantly inhibited cataract development and reduced blood glucose levels in rats fed the ‘high-energy’ diet. Lens AR activity tended to be lower, while lenticular GSH levels increased. In sand rats fed a ‘medium-energy’ diet (59% starch), LPA intubation had no effect on blood glucose levels and cataract development but GSH levels were increased. In contrast, sand rats intubated with GLA conjugate showed the highest blood glucose levels and accelerated cataract development. The conjugate treatment also decreased lenticular GSH content.Conclusions The hypoglycemic effects of LPA are beneficial in the prevention of acute symptoms of Type 2 diabetes. It remains to be shown that the antioxidant activity of LPA is responsible for prevention or inhibition of cataract progression in sand rats. Copyright © 2000 John Wiley & Sons, Ltd.
Virgin coconut oil (VCO) directly extracted from fresh coconut meat at 50°C temperature was tested for its effect on the activities of antioxidant enzymes and lipid peroxidation levels in male Sprague–Dawley rats, compared to copra oil (CO) and groundnut oil (GO) as control. Oils were fed to rats for 45 days along with a semi-synthetic diet and after the experimental period various biochemical parameters were done. Individual fatty acid analyses of VCO and CO were done using gas chromatography. Effect of polyphenol fraction isolated from the oils was also tested for the ability to prevent in vitro microsomal lipid peroxidation induced by FeSO4. The results showed that GO, rich in polyunsaturated fatty acids, reduced the levels of antioxidant enzymes and increased lipid peroxidation, indicated by the very high MDA and conjugate diene content in the tissues. PF fraction from VCO was found to have more inhibitory effect on microsomal lipid peroxidation compared to that from the other two oils. VCO with more unsaponifiable components viz. vitamin E and polyphenols than CO exhibited increased levels of antioxidant enzymes and prevented the peroxidation of lipids in both in vitro and in vivo conditions. These results showed that VCO is superior in antioxidant action than CO and GO. This study has proved that VCO is beneficial as an antioxidant.
Diabetes mellitus is characterized by complications affecting several organs, including the kidney. Lipid peroxidation increases in diabetes and has been implicated in the pathogenesis of diabetic complications. In this study, we examined the ability of two antioxidants, vitamin E and probucol, to reduce lipid peroxidation in vivo and renal hypertrophy, an early stage of diabetic nephropathy, in rats. Animals were divided into four groups: non-diabetic, diabetic, diabetic treated with vitamin E, and diabetic treated with probucol. Animals were given antioxidants by intraperitoneal injection after induction of diabetes by streptozotocin injection. After 7 wk, lipid peroxidation in vivo was measured by analyzing urinary excretion of lipophilic aldehydes and related carbonyl compounds (LACC) as 2,4-dinitrophenylhydrazones by high-performance liquid chromatography. A number of urinary lipophilic nonpolar and polar aldehydes and related carbonyl compounds were identified, almost all of which increased in diabetes. Antioxidant treatment resulted in significantly decreased excretion of urinary LACC excretion. Antioxidant treatment of diabetic rats reduced renal hypertrophy. There was a high correlation between kidney weight and urinary LACC. Since LACC are accepted markers of lipid peroxidation, these results indicate that antioxidants can reduce the elevated lipid peroxidation of diabetes and may slow the onset of diabetic nephropathy.