INTRODUCTION:
DIABETES:
Diabetes mellitus, or simply diabetes, is a group of metabolic
diseases in which a person has high blood sugar, either because the pancreas
does not produce enough insulin, or because cells do not respond to the insulin
that is produced.
Insulin produced by the pancreas lowers
blood glucose. Absence or insufficient production of insulin causes diabetes.[1]
TYPES:
The two types of diabetes are referred to as
type 1 and type 2. Former names for these conditions were insulin-dependent and
non-insulin-dependent diabetes, or juvenile onset and adult onset diabetes.
Type 1 diabetes is also called
insulin-dependent diabetes. It used to be called juvenile-onset diabetes,
because it often begins in childhood. Type 1 diabetes is an autoimmune
condition.
It's caused by the body
attacking its own pancreas with antibodies. In people with type 1 diabetes, the
damaged pancreas doesn't make insulin.
Type 2 DM results from insulin resistance,
a condition in which cells fail to use insulin properly, sometimes combined
with an absolute insulin deficiency. This form was previously referred to as
non insulin-dependent diabetes mellitus (NIDDM) or "adult-onset diabetes".[4]
TABLE.1.COMPARISION
OF TYPE 1 AND TYPE 2 DIABETES
|
Feature |
Type 1 diabetes |
Type 2 diabetes |
|
Onset |
Sudden |
Gradual |
|
Age at onset |
Mostly in children |
Mostly in adults |
|
Body habitus |
Thin or normal |
Often obese |
|
Ketoacidosis |
Common |
Rare |
|
Autoantibodies |
Usually present |
Absent |
|
Endogenous
insulin |
Low or absent |
Normal, decreased |
|
Concordance |
50% |
90% |
|
Prevalence |
~10% |
~90% [12,13] |
SYMPTOMS:
Polyuria (frequent urination), polydipsia (increased thirst), and polyphagia
(increased hunger).
DIAGNOSIS:
Diabetes is diagnosed by blood sugar
(glucose) testing.
TABLE. 2. DIAGNOSIS OF DIABETES
|
Condition |
2
hour glucose mmol/l(mg/dl) |
Fasting
glucose mmol/l(mg/dl) |
HbA1c % |
|
Normal |
<7.8
(<140) |
<6.1
(<110) |
<6.0 |
|
Impaired
fasting glycaemia |
<7.8
(<140) |
≥
6.1(≥110) & <7.0(<126) |
6.0–6.4 |
|
Impaired
glucose tolerance |
≥7.8
(≥140) |
<7.0
(<126) |
6.0–6.4 |
|
Diabetes mellitus |
≥11.1
(≥200) |
≥7.0
(≥126) |
≥6.5 [15] |
CAUSES:
The cause of diabetes depends on
the type.
Type 1 diabetes:
Type 1 diabetes is partly
inherited, and then triggered by certain infections, with some evidence
pointing at Coxsackie B4 virus. A genetic element in individual susceptibility to
some of these triggers has been traced to particular HLA genotypes (i.e., the
genetic "self" identifiers relied upon by the immune system).
However, even in those who have inherited the susceptibility, type 1 DM
seems to require an environmental trigger. The onset of type 1 diabetes is
unrelated to lifestyle.[10,18]
Type 2 diabetes:
Type 2 diabetes is due
primarily to lifestyle factors and genetics A number of lifestyle factors are
known to be important to the development of type 2 diabetes, including obesity
(defined by a body mass index of greater than thirty), lack of physical
activity, poor diet, stress, and urbanization. Excess body fat is associated
with 30% of cases in those of Chinese and Japanese descent, 60-80% of cases in
those of European and African descent, and 100% of Pima Indians and Pacific
Islanders. Those who are not obese often have a high waist–hip ratio. [7]
COMPLICATIONS:
The major complications of diabetes are
both acute and chronic.
·
Acute complications: dangerously elevated blood
sugar (hyperglycemia), diabetic ketoacidosis and nonketotic hyperosmolar coma.
·
Chronic complications: disease of the blood vessels
(both small and large) which can damage the feet, eyes, kidneys, nerves, and
heart may occur. [7,11]
TREATMENT:
Diabetes treatment depends on
the type and severity of the diabetes. Type 1 diabetes is treated with insulin,
exercise, and a diabetic diet. Type 2 diabetes is first treated with weight
reduction, a diabetic diet, and exercise[2]. When these measures
fail to control the elevated blood sugars, oral medications are used. If oral
medications are still insufficient, insulin medications and other injectable medications are considered. [9]
PLANT PROFILE:
Musa paradisiaca:
Musa paradisiaca is the accepted name for the hybrid between Musa acuminata
and Musa balbisiana
belongs to family Musacae. Linnaeus
originally used the name M. paradisiaca only for plantains or cooking
bananas, but the modern usage includes hybrid cultivars used both for cooking
and as dessert bananas. They are typically 2–9 meters (7–30 ft) tall when
mature. The above-ground part of the plant is a "false stem" or pseudostem,
consisting of leaves and their fused bases. [8,14]
Chemical
constituents:
Tannins, eugenol,
tyramine. High tannin content in the plant and unripe
fruits has antibiotic activity. Serotonin, levarterenol,
and dopamine are available in the ripe fruit and peel. Other chemical
constituents are alkaloids, steroidal lactones, and iron [5]
Cinnamon is a spice obtained from the inner
bark of several trees from the genus Cinnamomum that is used in both sweet and savoury foods. While Cinnamomum verum
is sometimes considered to be "true
cinnamon". All are members of the genus Cinnamomum in the family Lauraceae.
Chemical constituents:
C. verum bark yields 0.4–0.8% oil;
tannins, consisting of polymeric 5,7,3′,4′-tetrahydroxyflavan-3,4-diol
units; large amounts of catechins and proanthocyanidins (condensed tannins) and procyanidins; resins; mucilage; gum; sugars; calcium
oxalate; two insecticidal compounds (cinnzelanin and cinnzelanol); coumarin (lowest
concentration in Ceylon cinnamon); and others. C. verum
cinnamon bark oil contains as its major component cinnamic
aldehyde (usually 60–80%); other major constituents
include sesquiterpenoids (4–5%) (e.g., α-humulene and β-caryophyllene
that make up 3–4% of the total, limonene, and others), eugenol,
eugenol acetate, cinnamyl
acetate, cinnamyl alcohol, methyl eugenol,
benzaldehyde, cuminaldehyde,
benzyl benzoate, monoterpenes (e.g., linalool, pinene, phellandrene, and
cymene), carophyllene, safrole,
and others.
C. verum leaf oil contains high
concentrations of eugenol (Ceylon type 80–88%;
Seychelles type 87–96%); it also contains many of the major constituents present
in cinnamon bark oil (e.g., benzyl benzoate (6%), cinnamaldehyde,
cinnamyl acetate, eugenol
acetate, benzaldehyde, linalool, α-terpinene, and others), as well as other minor compounds,
including α-humulene, β-caryophyllene,
α-ylangene, methyl cinnamate,
and cinnamyl acetate.[6]
Coriandrum sativum:
Coriander (Coriandrum
sativum), also known as cilantro, Chinese parsley
or dhania,
is an annual herb in the family Apiaceae.
Chemical constituents:
The essential oil from the coriander herb
contained the highest amount of aliphatic aldehydes,
among which was decanal, E-2-dodecanol
and E-2-decenol had the highest
percentages. In addition to the above-mentioned aliphatic aldehydes,
the presence of linalool, phytol, and oleic acid was
found in the essential oil extracted from the coriander herb.
Fruits contain 0.2–2.6% (usually
0.4–1.0%) volatile oil. The major component of the oil is d-linalool (coriandrol),
which is present in 55–74%, depending on the ripeness of the fruits,
geographical locations, and other factors. Other compounds present in the oil
include decyl aldehyde, trans-tridecene-(2)-al-(1),
borneol, geraniol, geranyl acetate, camphor, carvone,
anethole, caryophyllene
oxide, elemol, and monoterpene
hydrocarbons (mainly γ-terpinene, and α-
and β-pinene, d-limonene, p-cymene,
β-phellandrene, and camphene, with relative
proportions varying considerably with sources). Other constituents present in
fruits include up to 26% fats made up of glycerides
(primarily of oleic, petroselinic and linolenic acids), a small amount of unsaponifiable
matter (containing β-sitosterol, δ-sitosterol, triacontane, triacontanol, tricosanol, etc.),
and Δ-octadecenoic acid; proteins (11–17%);
about 1.0% starch and 20% sugars; coumarins (psoralen, angelicin, scopoletin, umbelliferone, etc.);
flavonoid glycosides, including
quercetin-3-glucuronide, isoquercitrin, coriandrinol (β-sitosterol-d-glucoside),
and rutin; tannins; chlorogenic
and caffeic acids; and others.
Leaves contain less volatile oil than
fruits; about 5% fats; about 22% proteins; sugars; coumarins
and flavonoid glycosides similar to those in fruits; chlorogenic and caffeic acids;
vitamin C; and others. The volatile oil contains mainly decyl
and nonyl aldehydes, and
linalool, among others.
SCREENIG MODELS FOR DIABETIC MELLITUS:
TABLE.3.DIFFERENT MODELS FOR IDDM
|
Chemically induced |
STZ (Streptozotocin) induced diabetes, Alloxan
induced diabetes. |
|
Other diabetogenic
chemicals induce models |
Dithizone induced diabetes . Goldthioglucose induced diabetes. Monosodium glutamate induced
diabetes. |
|
Hormones induced diabetes |
Growth hormone induced
diabetes Corticosteroid induced
diabetes |
|
Virus induced diabetes |
EMC-D or M variant Mengo-2T
CB4 Reo Kilham rat virus |
|
Insulin Antibodies-induce
diabetes |
_____ |
|
Surgically induced diabetes |
_____ |
|
Genetic Models |
The NOD mouse The BB rat[16] |
MATERIALS AND
METHODS:
Preparation of
extract:
The
shade dried powdered material was subjected to successive extraction using
n-hexane, Ethyl acetate, Ethanol by continuous percolation process in soxhlet apparatus. The aqueous extract was prepared by the
maceration with water. Each extract was concentrated by distilling off the
solvent and evaporated to dryness. The extracts were dissolved in 1% carboxy methyl cellulose (CMC) and used for the present
study.
IN VITRO ANTIDIABETIC ACTIVITY (BY GLUCOSE
DIFFUSION INHIBITORY STUDY):
A
simple model system was used to evaluate the effects of plant extracts on
glucose movement in vitro. The model was adapted from a method which
involved the use of a sealed dialysis tube into which 15ml of a solution of
glucose and sodium chloride (0.15M) was introduced and the appearance of
glucose in the external solution was measured. The model used in the present
experiment consisted of a dialysis tube (6cmX15mm) into which 1ml of 50g/liter
plant extract in 1% CMC and 1ml of 0.15M sodium chloride containing 0.22M
D-glucose was added. The dialysis tube was sealed at each end placed in a 50ml
centrifuge tube containing 45ml of 0.15M sodium chloride. The tubes were placed
on an orbital shaker and kept at room temperature. The movement of glucose into
the external solution was monitored at set time intervals. Estimation of
glucose was estimated by popular known GOD/POD method.
Preparation
of diffusion tube:
A
centrifuge tube was taken which is closed at one end; to this on another side
the semi-permeable tube is attached. Egg membrane is taken for this purpose.
Egg membrane is isolated by submerging it in Conc. Nitric acid.
Estimation of glucose:
Photometric
estimation of glucose in plasma based on GOD/ POD method is done as described
in the manufacturer’s (Aspen Pvt. Ltd.) instruction manual as follows:
Principle:
Glucose is
oxidized by oxidase to gluconic
acid and H2O2 is liberated. The colorimetric indicator, quioneimine is generated from 4-aminopyrine and phenol by H2O2
under the catalytic action of peroxidase. Intensity
of color generated is directly proportional to glucose concentration.[17]
β-D-glucose + H2O + O2 Gluconic
acid + H2O2
Assay:
Wavelength------
500-540 nm
Temperature-----
370C
Light path-------- 1cm
|
Solutions |
Blank |
Sample\Standard |
|
Sample\Standard |
-- |
10µl |
|
Distilled
water |
10µl |
-- |
|
Reagent |
1000 µl |
1000 µl |
Mix,
incubate for approx. 15 min at 370C and read the absorbance against the blank
within the 30 min.
Calculation:
Absorbance
of Test
Glucose
Concentration = -----------------------------x Concentration of
(mg/dl)
Absorbance of Standard Standard
Statistical Analysis:
Data
are expressed as mean + S.E.M. Statistical comparison between groups were done
by one way analysis of variance (ANOVA) followed by Tukey
Kramer multiple comparison test to analyze the differences. p<0.001 were
considered as significant.
RESULTS AND DISCUSSION:
Effects of various extracts on glucose diffusion:
The effect
of various extracts on glucose diffusion inhibition was depicted in Fig 1 and
table-4.
At
the end of 27 hrs, glucose movement of control (without plant extract) in the
external solution had reached a plateau with a mean glucose concentration above
300mg/dl (316.66+1.76). It was evident from the graph that the ethanol and
aqueous extracts were found to be potent inhibitors of glucose diffusion
(p<0.001) compared to control. The ethanol extract was found to be more
potent than other extracts showing the lowest mean glucose concentration of
208+1.15 mg/dl at the end of 27 hrs. Thus the ethanol and aqueous extracts can
be selected for further in vivo studies.
CONCLUSION:
The present study was carried out to
estimate the efficiency of several plants which are used as spices in daily
dishes. When we used these spices as different extracts they showed
anti-hyperglycemic activity and it was done on the basis of their effectiveness
of chemical constituents. The study was performed by using the diffusion tube
method rather than using animals. Finally it is proven that ethanolic
extract showed better potent than other extracts. So, it may be beneficial to
use ethanolic extract than conventional
anti-diabetics taking advantage of less side effect. Since ethanolic
extract may interact metabolism of the drugs, it advised to go for aqueous
extract than any type of extract.
FIG.1.Effect of Different Extracts on
Diffusion of Glucose