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1 INTRODUCTION 1
4 SUMMARY 75
5 REFERENCES 78
Diabetes mellitus:
major role in determine in whom diabetes will develop and in whom it will
antibodies against the β-cells, thus also leading to their destruction. In order
degeneration.
reason is that obesity decreases the number of insulin receptors in the insulin
target cells through the body, thus making the amount of insulin that is
called juvenile diabetes. Patients with this disease are not obese, and they
have a high incidence of ketosis and acidosis, various anti B cell antibodies
are present in plasma, but the current thinking is that type I diabetes is
one –in – three chances that the other twin will do so also. In other words,
the concordance rate is about 33%. The main genetic abnormality is in the
diabetes if given early in the disease before all B cells are lost. Attempts
or isolated islet cells, but results to date have been poor, largely because B
disease than in IDDM. Concordance rates for NIDDM in identical twins are
100%. Currently, a genetic marker has not been discovered for NIDDM. The
delivered to the liver, adipose tissue, and skeletal muscle are thought to
affect the normal functioning of the insulin receptor (Haring HU. 1991).
This in turn may decrease the number of glucose transports that are
delivered to the cell surface, thereby decreasing the delivery of glucose into
mechanisms, if is known that restriction of caloric intake and weight less are
insulin from beta cell and may also increase the target tissues, sensitivity to
Gestational diabetes
Insulin
preproinsulin (Chan SJ. Keimp, stenor DF, e.al 1976) cleavage at the link
and B connected by two disulfide bonds. This entire process occurs within
Cleavage first proinsulin and next to insulin occurs within are released into
the circulation when the granule is dissolved at the plasma membrane of the
bonds. The α chain contains 2 amino acids and the β chain 30 amino acids.
insulin within the β cells of the islet of Langerhans is the single chain
proinsulin is split into insulin and C-peptide, both of which are then released
Dominiczalc, et al 1999).
Insulin receptor
(called receptor sites) are found only on certain cell types (liver cells,
1981). One subunit is a tyrosine – specific protein kinase (Roth. RA. Cassell
It is low relative to both the blood glucose and insulin levels. Insulin
Antibodies to receptor
The presence of circulating antibodies to the insulin receptor has also
been reported (R). Type II diabetes caused by such an antibodies to insulin
receptor sites is called type B diabetes. Type B diabetes usually has
symptoms of autoimmune disorders such as antinuclear antibodies
arthralgia, and enlargement of the parotid gland. Type B Diabetes has a
lower incidence than type A
Insulin resistance
Insulin resistance is a condition in which the body produces insulin but
does not use it properly. When people are insulin resistant, their muscle, fat,
and liver cells do not respond properly to insulin. As a result, their bodies
need more insulin to help glucose enter cells. The pancreas tries to keep up
with this increased demand for insulin by producing more. Eventually, the
pancreas fails to keep up with the body’s need for insulin. Excess glucose
builds up in the bloodstream, setting the stage for diabetes. Many people
with insulin resistance have high levels of both glucose and insulin
circulating in their blood at the same time.
Etiology of diabetes mellitus
Environmental, genetic and autoimmune factors involved in the
etiology of diabetes (Michael, R.C., 1992).
1. Induction of diabetes mellitus by environmental agents
Both type I and type II diabetes are at least partly inherited Type I
diabetes appears to be triggered by some mainly viral infections or less
likely stress-related or environmental factors. There is a genetic element in
individual susceptibility to some of these triggers which has been traced to
particular HLA genotypes who have inherited the susceptibility type I
diabetes mellitus seems to require an environmental trigger. A small
proportion of people with type I diabetes carry a mutated gene that cause
maturity onset diabetes of the young (Mody)
There is a stronger inheritance pattern for type II diabetes. Those with
first degree relatives with type II have a much higher risk of developing
type II concordance among monozygotic twins is close to 100% and 25%
of these with the disease have a family history of diabetes. This is found
approximately 85% of the patients diagnosed. So some experts believe that
inheriting a tendency towards obesity may also contribute.
3. Polyuria
Excess urine formation with increase in frequency of vooling urine is
called polyuria. It is due to the osmatic diuresis caused by increase in blood
sugar level.
4. Polydipsia
The increase in water intake is called polydipsia. The excess loss of
water decreases water content and increases salt content in the body. This
stimulates the thirst center in hypothalamus. Thirst center in turn increases
the intake of water.
5. Asthenia
The loss of strength is called asthenia. The body becomes very weak.
There is loss of energy. Asthenia is because of lack of insulin, which causes
decrease in protein syntheses and increase in protein breakdown. Protein
depletion also occurs due to the utilization of proteins for energy in the
absence of glucose utilization.
6. Acidosis
During insulin deficiency glucose cannot be utilization by the peripheral
tissues for energy. So a large amount of fat is broken down to release
energy. It causes the formation of excess ketoacidosis leading to acidosis.
One more reason for acidosis is that, the ketoacidosis are
excreted in combination with sodium irons through urine (ketonuria).
Sodium in exchanged for hydrogen ions which diffuse from the renal tubules
into ECF adding to acidosis.
7. Polyphagia
Polyphagia means the intake of excess food. It is very common in
diabetes mellitus.
8. Acetone breathing
In cases of severe ketoacidosis, acetone is expired in the expiratory air,
giving the characteristic atone or fruity breath odor. It is a life-threatening
condition of severe diabetes.
9. Kussmaul breathing
Severe acidosis increases the rate and depth of respiration which is
known as Kussmaul breathing.
11. Coma
Due to Kussmaul breathing, large amount of carbon dioxide is lost
during expiration. It leads to drastic reduction in the concentration of
bicarbonate ions causing severe acidosis and coma. It occurs in severe cases
of diabetes mellitus.
Increases in blood sugar level develop hyperosomolarity of plasma
which also leads to coma. It is called hyperosmolar coma.(Medical
physiology.,sembulingam.,fourth edition 2006)
Diagnosis of DM
The acute state of IDDM is readily diagnosed from the history,
symptoms (hunger, thirst, frequent urination, weight loss) and the
following abnormal laboratory tests: plasma glucose (>200mg /dL, 11.1m
mol/L), glucosuria (usually 4+or 2g/day), and presence of ketone bodies in
urine and serum. The asymptomatic patient presents a diagnostic problem,
but the tests described in the following paragraphs are helpful.
O’Sullivan test
The oral glucose tolerance test (OGTT) is a standard for making the
diagnosis of type II diabetes. It is still commonly used for diagnosing
gestational diabetes and in conditions of pre-diabetes, such as polycystic
ovary syndrome with an oral glucose tolerance test.
NEUROPATHY:
Neuropathy is the most common complication of Diabetes mellitus.
It is apparent in about 25% of Diabetes and is recognized by a variety of
symptoms that include pain, numbness, tingling or burning sensation in
extremities, dizziness and double vision. These symptoms are caused by
decreased motor and sensory nerve deduction velocities cased by axonal
degeneration and demyelization secondary manifestations of neuropathy
include cardiac failure excessive sweating and male impotence (Editorial
Lancet. 1993)
ANGIOPATHY
Angiopathy refers to damage lining (basement membranes) of blood
vessels. Angiopathy increases the risk of coronary heart disease and stroked
and can lead to retinopathy and nephropathy.
NEPHROPATHY
Nephropathy refers to damage to the glomerulus’s (filtering
apparatus of the nephron) and capillaries associated with the glomerulus’s
capillaries associated with the glomerulus’s capillary damage is cased by
antipathy. The result is reduction in the filleting capability of the kidneys
proteinuria is often the fist sign of diabetic nephropathy. Approximately 25-
30%of individual treated for end-stage renal failure are diabetics.
INFECTION
Diabetics are highly susceptible to infection, ulceration, and gangrene
(especially in the extremities) skin disorders are also more common in
diabetics than in non-diabetics,
Hyperglycemia
Protein synthesis
Protein is decreased in all tissues due to
• Depressed production of ATP
• Absolute or relative deficiency of insulin
Fat metabolism
Stored lipids are hydrolyzed by increased lipolysis liberating
free fattyacids. Increased free fatty acid interferes at several steps of
carbohydrate and phosphorylation in muscles, further contributing to
hyperglycemia. Excessive production of ketone bodies increases the
concentration of ketone bodies in blood and excretion of ketone bodies in
urine and leads to acidosis.
CARBOHYDRASE INHIBITORS
Physiological Treatment
Exercise and physical activity.
In general, the more active you are, the lower your blood sugar.
Physical activity causes sugar to be transported to your cells, where it's used
for energy, thereby lowering the levels in your blood. Aerobic exercises such
as brisk walking, jogging or biking are especially good. But gardening,
housework and even just being on your feet all day also can lower your
blood sugar.
A healthy diet
Yet understanding what and how much to eat can be a challenging task.
Fortunately, a registered dietitian can help you put together a meal plan that
fits your health goals, food preferences and lifestyle. Once you've decided
on a meal plan, keep in mind that consistency is extremely important. To
keep your blood sugar at a consistent level, try to eat the same amount of
food with the same proportion of carbohydrates, proteins and fats at the
same time every day.
But even with all the information you need and the best intentions,
sticking to your diet can be one of the most challenging parts of living with
diabetes. The key is to find ways to stay motivated. Don't let others
undermine your determination to eat in the healthiest way possible. You
have to believe that what you're doing matters? And that you're worth it.
Healthy weight
Being overweight is the greatest risk factor for type 2 diabetes. That's
because fat makes your cells more resistant to insulin. But when you lose
weight, the process reverses and your cells become more receptive to
insulin. For some people with type 2 diabetes, weight loss is all that's needed
to restore blood sugar to normal. Furthermore, a modest weight loss of 10 to
20 pounds is often enough.
Usually, people with Type 1 diabetes don't use oral medications. These
medications work best in people with Type 2 diabetes who have had high
blood sugar for less than ten years and who have normal weight or obesity.
It's not uncommon for oral medication to control blood sugar well for years
and then stop working. Some people who begin treatment with oral
medications eventually need to take insulin.
Sulfonylureas
Side Effects
Biguanides
The generic (non-brand) name of this drug is metformin. It helps lower
blood sugar by making sure your liver doesn't make too much sugar.
Metformin also lowers the amount of insulin in your body. You may lose a
few pounds when you start to take metformin. This weight loss can help you
control your blood glucose. Metformin can also improve blood fat and
cholesterol levels, which are often high if you have Type 2 diabetes.
Side Effects
Alpha-glucosidase inhibitors
Side Effects
Taking this medication may cause stomach problems such as gas,
bloating and diarrhea that most often go away after you take the medication
for awhile.
Thiazolidinediones
Side Effects
Edema, weight gain, decreased hematocrit and hemoglobin,
elevated alanine aminotransferase activity, hypoglycemia- during
combination therapy with sulfonylureas or insulin. Swelling in the legs or
ankles.
Meglitinides
Side Effects
• weight gain
• low blood sugar
Transplantation
In recent years, researchers have focused increasing attention on
transplantation for people with type 1 diabetes. Current procedures include:
Detoxification
It consists of the use of the short periods of fasting or controlled diets
and supports itself of toxic substances.
Mud therapy
Generally earth provides us with food, our main source of energy.
During element earth in the form mud or clay packs. Even mud baths are
uses food poisons from the body, for cooling the nerved system and for
activating vast the metabolic process of the entire body. When the digestive
system, and earth of impurities and toxemia in the body. Hence improving
elimination and re Mud bath treatment is used. There are many ways taking
mud treatment ordinary mud. The clay should be of such a consistency that
it could be body by loose cloths wrapping. The clay, in winter should be
sufficiently war.
Chromotherapy
Chromo therapy is a natural method of treatment of various
diseases, which their natural balance. Hence, we can say, it is a therapeutic
method, which spectrum with specific curative properties. By using the
property to region the harmony and order of the organism. The colour
illumination helps in physical well-being.
Medicinal plants
Cinnamomum zeylanicum
Cinnamomum (verum, synonym c. zeylanicum) is a small
evergreen tree belonging to the family Lauraeae, native to sri Lanka.
(Enzyclopaedia Britanica 2008). Or the spices obtained from tree’s
bark .
Scientific classification
Kingdom : Plantae
Division : Magnoliphita
Class : Magnoliopsida
Order : Laurales
Family : Lauraceae
Genus : cinnamomum
Species : C.verum
Binomial name
Cinnamomum verum
Synonyms
C. zeylanicum Blume
In Tamil - lavangapattai
In Malayalam - karugapatta
In Telugu - Dhalchi8na chalka (bark)
In Hindi - Dalchini
In English - Cinnamon
Applications of cinnamon
Cinnamon bark is widely used as a spice. It is principally employed in
cookery as a condiment and flavoring material. It is used in the
preparation of chocolate, especially in Mexico, which is the main
importer of true cinnamon. (www.fao.org.) It is also used in the
preparation of some kinds of desserts, such as apple pie, donuts and
cinnamon buns as well as spicy candies, tea, hot cocoa and liqueurs.
True cinnamon, rather than cassia, is more suitable for use in sweet
dishes. In the Middle East, it is often used in savory dishes of chicken
and lamb. In the United States, cinnamon and sugar are often used to
flavor cereals, bread-based dishes and fruits, especially apples; a
cinnamon-sugar mixture is even sold separately for such purposes.
Cinnamon can also be used in pickling.
Cinnamon bark is separately for such purposes. Cinnamon can also
be used in pickling. Cinnamon bark is one of the few spices that can
be consumed directly. Cinnamon powder has long been an important
spice in Persian cuisine, used in a variety of thick soups, drinks and
sweets. It is often mixed with rosewater or other spices to make a
cinnamon-based curry powder for stews or just sprinkled on sweets
treats.
In medicine it acts like other volatile oils and once had a reputation as
cure for colds. It has also been used to treat diarrhea and other
problems of the digestive system. (Shan B, Cai YZ, et al 2005)
Cinnamon is high in antioxidant activity (Felter, Harvey, 2007) the
essential oil of cinnamon also has antimicrobial properties (Lopez P,
2005) which can aid in the preservation of certain foods.
Animals
Experimental Design
Experimental animals are divided into five treatment groups.
Group- I
Normal
Six albino rats are maintained in normal condition.
Group – II
Diabetic
The rats were made diabetic by administration of 2% Alloxan
monohydrate. The rats were fasted for 16 hours but had been allowed free
access to water. Alloxan monohydrate was dissolved in sterile normal saline
immediately before use and injected intraperinotical cavity in a dose 2%
Alloxan monohydrate solution in saline. The single dose of alloxan
produces persistence hyperglycemia after 24 hours and it was observed that
the condition was maintained for 6 days.
Group –III
Cinnamomum zeylanicum control
The rats were in normal condition control rats also maintain same
procedure control rats receiving cinnamomum zeylanicum extract. 160
mg/kg body weight of rats. This herbal dissolved in 20ml of water and orally
administered for every 24 hours for 20 days
Group –IV
Treatment diabetic
Alloxan diabetic rats receiving cinnamomum zeylanicum extract
2ml per day orally administrated for every 24 hours for 20 days.
Group – V
Glibenclamide Treatment
Diabetic rats given with glibenclamide (600microgram/kg body
weight) in aqueous solution daily introgastric tube for 20 days.
The animal were dosed through provided the incubation everyday
before any food was given. Food and water were provided the duration of
treatment was 20 days. After the treatment period, the rats were sacrificed,
and blood was drawn from ventricles and serum separated for various
biochemical estimations. On the final day of experiment, liver tissue was
collected. Liver was excised from each animal; the tissue was washed with
ice cold saline and homogenized in Tris HCL buffer pH-7.5. The serum
obtained was used immediately for the estimation of blood glucose, total
serum protein, serum cholesterol, serum triglycerides, glycosylated
hemoglobin, urea, and insulin. Liver tissue was used for assay the enzyme
activated of Glutamate Pyruvate Transaminase (GPT), Hexokinase, glucose-
6 phosphatase and fructose 1, 6 bis phosphatase. The glycogen obtained after
over nights precipitation was then estimated.
Matsui (1972).
Reagents
filtered.
4.Procedure
precipitate protein and then centrifuged. 1.0ml of the supernatant was mixed
with 4 ml of O-toluidine reagent and was kept in a boiling water bath for
about 15 min. and the green colour developed was read at 600 nm in a
treated similarly.
Lowry(1951).
Reagents
hydrochloric acid were added. The mixture was refluxed gently for
about 10h. After cooling, 150g of lithium sulphate, 50ml of water and
a few drops of bromine were added. The mixture was boiled for
were cooled, made upto 1 litre and then filtered. The above stock
Procedure
A serum was mixed with 4.5ml of alkaline copper reagent and then
phenol reagent was then added. The blue colour developed was read at
Principle
used. The use of several distinct Mabs avoids hyperspecificity and allows
high sensitive assays with extended standard range and short incubation
time.
antibodies.
and incubated. The reaction is stopped with H2SO4 and the microtitre plate is
MATERIALS REQUIRED:
raddish peroxidase.
insulin.
4. Solution-A
5. Solution-B
haemolysis.
Sample preparation
Tube Dilution
The serum sample was diluted with the diluted buffer (in 11
dilution).Separate tips were used for each sample and then discarded as bio
hazardous waste.
Microwell dilution
required volume of wash buffer (50 ml per each strip) was prepared.
TEST PROCEDURE
2. 100µ l of the sample dilution buffer was added into A-I well as a
blank, 100 µ l of the negative control was added into B-I and C-I
I, F-I respectively.
4. The pellets were sealed with cover and incubated at 37°C ± 2°C for
30 minutes.
5. The plates were taken out from the incubator after the incubation
time was over and washed five times with 1X washing solution.
wells
7. The plate was sealed and incubated at 34°C± 2°C for 30 minutes.
10. After incubation 50 µ l of the stop solution was added. Then plates
Reagents
water
Procedure
0.1ml of blood was added to 3.3ml of water and mixed with 0.3ml of
10% sodium tungstate and 0.3ml of 0.67N sulphuric acid reagents. The
reagents were added in that order and kept in a boiling water bath for 30
min. cooled and the colour developed was measured at 480nm in a shimadzu
manner.
Jung method (1970) using the Ferric sulphate colour reaction in the presence
of uranyl acetate.
Reagents
several times with distilled water to get rid of ammonia and was
dissolved in cholesterol grade glacial acetic acid and made upto one
litre with acetic acid. 100mg of uranyl acetate was then added to it
and the contents were well shaken and left overnight. The reagent
3. Cholesterol standard
Reagent grade cholesterol was recrystallised from ethanol. The stock
Procedure
sample, mixed well allowed to stand for 5 minutes and centrifuged. 3.0ml of
cholesterol was mixed, and 3.0ml aliquots were taken. Blank tube contained
ferrous sulphate reagent was added to all the tubes and mixed well. The
spectrophotometry.
ESTIMATION OF TRIGLYCERIDES
Reagents
1. Isopropanol
Procedure
To an aliquot of serum / lipid extract, evaporated dryness, 0.1ml of
was added to all tubes and shaken well for 15 minutes. Centrifuged another
2.0ml of the supernatant fluid was transferred to labelled tubes. The tubes
were placed in a water bath at 650 for 15 minutes for saponification after
reagent and 0.5ml of acetyl acetone reagent, after mixing. The tubes were
kept in a waterbath at 650C for one hour, the contents were cooled and
40µ g triolein was treated similarly along with a blank containing only the
reagents. All the tubes were cooled and read at 405nm. The values were
Principle
five minutes with a weakly binding cation exchange resin. The labile
binding. During this mixing non glycosylated hemoglobin binds to the ion
exchange resin leaving HbA1C free in the supernatant. After the mixing
period, a filter separator is used to remove the resin from the supernatant.
Reagents
1. Lysing Reagent
3. Control Lyophilized
4. Resin separators
Precautions
numbers
of the assay
Procedure
well mixed sample. Mixed well the sample and allowed to stand at room
water bath. Added 0.1ml of hemolysate to it. Place a resin separator in the
tube, so that the rubber sleeve was at the upper mark of the tube (3 cm above
the resin level). Contents are mixed on vortex mixer continuously for 15
minutes. Allowed push down the resin separator in the tube until the resin
was firmly packed. Poured the supernatant directly into a cuvette and
Pipette 5ml of deionized water into a test tube. Then add 0.02ml of
hemolysate (from step I). Mixed well and read absorbance against distilled
water.
Normal values:
Calculations:
Absorbance of GHb
Absorbance of THb
The tubes were kept in boiling water bath for 5 minutes. After cooling, the
tubes were shaken well and placed in a freezer overnight. The precipitated
centrifuged again. The final precipitate was dissolved in 3.0ml of water and
heated for 5 minutes in boiling water bath and different aliquots were used
Procedure
Suitable aliquots of glycogen were made upto 1.0ml with water. A set
alone were setup. All the tubes were cooled in an ice bath and 4.0ml of
anthrone reagent was added. The contents of the tube were mixed well. All
the tubes were covered with glass marbles and heated for 20 minutes in
boiling water bath. The tubes were cooled and the green colour developed
The enzyme activity was assayed by the method of Mohur and Cook
(1957).
Reagents
Hydrochloric acid.
4. Standard Pyruvate
Procedure
homogenate was added and incubated at 370C for exactly 30 min. The
reaction was arrested by adding 1.0ml of DNPH and left aside for 20min at
protein.
ASSAY OF HEXOKINASE
Reagents
Procedure
min. The reaction was initiated by the addition of 2.0ml tissue homogenate.
1.0ml aliquot of the reaction mixture was taken immediately (zero time) to
tubes containing 1.0ml of 10% TCA. A second aliquot was removed after
The difference between the two values gave the amount of glucose
ASSAY OF GLUCOSE-6-PHOSPHATASE
(1965).
Reagents
3. 10% TCA
Procedure
carried out at 37°C for 60 minutes. The reaction was terminated by the
addition of 1.0ml of 10% TCA. The suspension was centrifuged and the
Reagents
Procedure
chloride, 0.1ml of EDTA and 0.1ml of the enzyme source. The incubation
was carried out at 37°C for 15 minutes. The reaction was terminated by the
addition of 1.0ml of 10% TCA. The suspension was centrifuged and the
for 20 minutes and the blue colour developed was read at 620nm against a
protein.
Statistical Analysis
Analysis of Variance (ANOVA) using SPSS 12.0 version (SPSS, Cary, NC,
values are expressed as mean ± SD and P < 0.05 was considered significant.
Result and discussion
The body weight of the alloxan induced diabetic group II rats was
found to be reduced. On treatment with Cinnamomum zeylanicum and
Glibenclamide on Group IV and V, the body weight was gained comparing
to the normal and control rats of Group I and III. This shows Cinnamomum
zeylanicum exhibited considerable gain of body weight.
The table 1 and fig 3,4,5 shows the level of blood glucose, serum
protein, and plasma insulin of different group of rats. Animal treated with
alloxan induced diabetes group II shows a significant elevated in blood
glucose when compared to group I and III of normal, control treated with
Cinnamomum zeylanicum extract. Alloxan , a β- islet cell cytotoxin ,
destroying the pancreatic β-cell leads to reduced secretion of insulin by the
pancreatic islet cell (Colca et al., 1983). Cinnamomum zeylanicum treated
group IV diabetic rats might enhance glucose utilization because of
significantly reduces the blood glucose levels in treated rats, This might be
due to restoration of delays insulin response or inhibition of intestinal
absorption of glucose due to reduction in the activity of indestinal
glycosidases like sucrase, maltase and lactase in the small intestine in the
cinnamon treated rat.(Sung Hg; kim , et al 2005) The similar reaction
might carried out in group V treated with Glibenclamide . There was a
marked reduction in the plasma protein content of untreated diabetic rats
group II when compared to that of normal and control rats of group I and III.
On administration of Cinnamomum zeylanicum extract to diabetic rats
restore the protein level almost equal to group V treated with Glibenclamide.
It might be due to the increased uptake or glucose by the cell by stimulating
the insulin receptor(IRS) I. (Mohamed H .Mahfouz et al 2010 ) This may
inhibit the protein catabolism leads to positive nitrogen balance(Miura and
kako.1995)
The diabetic rat shows a significant decrease in plasma insulin. On
treatment with an extract to Cinnamon diabetic rat group IV restore the
plasma insulin significantly compares to Glibeclamide treated group V. the
treatment of cinnamomum zeylanicum extract to normal control rat of group
III did not show significant effect of plasma insulin from the existing beta
cells of pancreas. Anti diabetic effect of cinnamon might be due to the
increase insulin like activity of cinnamon.(Richa Soni and vibha Bhatnagar
2009)
Table 2 and Fig 6,7,8 depicts the level of serum, cholesterol and
triglycerides. Urea, cholesterol and triglycerides levels which has increased
after induction of diabetes was found to be decreased in group IV after
treatment with Cinnamomum zeylanicum extract almost equal to
Glibenclamide treated group V rats. There are no any significant changes in
the level of urea, cholesterol and triglycerides in the administration of
Cinnamomum zeylanicum of group III rats. High cholesterol level
associated with coronary heart disease (CHD) observed in diabetic patients.
The occurrence of coronary heart disease in assay of liver enzyme GPT
indicated a decrease in their activity. It may due to the Cinnamoum
zeylanicum extract in the treatment rats stimulate the pancreatic insulin
mimetic effect. which is the inhibitor of lipolytic action .The
Phytochemical analysis shows that flavanoid present in the cinnamon
methyl hydroxyl chalcone which activate the insulin action and reduces the
lipolytic action(khar et al) . Urea is the catabolic product of protein.
elevated urea nitrogen in diabetes may be due to enhanced catabolism of
both liver and plasma proteins (Almal, vistrup et al). After the treatment
with Cinnamomum zeylanicum in group IV treated rat, it was restores to
normal compares with glibenclamide treated group V. It shows the herbal
may stimulate the glucose metabolism.
The level of glycogen in blood, GPT in liver tissue and glycosylated
haemoglobin were represented in table 3 and fig(9,10,11). Alloxan
administration resulted in significant fall of glycogen level in group II
diabetic animals when compares to normal. On treatment with
Cinnamomum zeylanicum and glibenclamide shows an elevated in the
stored glycogen level.
Liver glycogen may be considered as the best marker for assessing
hypoglycemic activity of any drug. This indicates that the peripheral free
glucose is being stores in liver in the form of glycogen by improving
glycogenesis.(Saltiela.et al 1986) The fall of liver glycogen content
observed in diabetic rats may be due to lack of insulin in the diabetic state,
result in the inactivation of liver glycogen synthase activity.
Chan SJ, Deimp P, Steiner DF: Cell-free synthesis of rat pre pro
insulin; characterization and partial amino acid sequence
determination, proc Nah Acad DciUSA 73: 1964, 1976
Toon, J.W., kim, C.J., Pack, C.Y. and MC Arthur , R.G.1987. Clin
Invest. Med., 10, 457-469.
Farell, M.A., Quiggins. P.A., Ellor, J.D. 1993. Diabetes care, 16.
253-256.