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					Diabetes mellitus – CLS 452                                                              Independent Study


                                           Diabetes Mellitus



 Abstract : The objective of this project is to Review all the sides of commonly and widely spread disorder
           among the world which is diabetes mellitus . Here we will discuss the background of it and main
           topics which involves , also the classification in details and several causes including the Genetic
           bases .complications and test performance , treatment and some helpful advise for controlling the
           disease .




1.History
Diabetes mellitus is one of the oldest diseases in human. It was Discovered in Egypt
about 1500 BC and this discovery is the first documented of Diabetes mellitus .
 in 1000 BC the Greece accredited the symptoms of DM as patient have a large
quantity of urine, affected by nausea, burning thirst and people with this disease
describe by short life , unpleasant and painful , within a short time they expire.
In 1921 Banting and Best in Canada discover insulin and use it to treat dog with
diabetes. After one year The first human with diabetes treated with insulin. He was 14
years old boy.
In 1982 Human Insulin produced by bacteria instead the insulin previously purified
from pigs and cattle.
In 1993 , The Diabetes Control and Complication Trial note that good control will
decrease complications [1].
Global Prevalence of Diabetes Estimates for the year 2000 and projections for 2030
and the result was The prevalence of diabetes for all age-groups in the world was to
be 2.8% in 2000 and 4.4% in 2030. The total number of people with diabetes is
projected to rise from 171 million in 2000 to 366 million in 2030 as shown in table 1
[2]
    .


Table 1. Global Prevalence of Diabetes Estimation :
      In 2000, people with diabetes                 In 2030, people with diabetes
                ( millions)                                  ( millions)
                   171                                          366

Table 2. In Saudi Arabia , the prevalence was as follow according to years [3] :

                       Year                                                     Prevalence
                       1982                                                         6%
                       1987                                                         8%
                       1997                                                        26 %
                       2000                                                        24 %




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2. Introduction :

Diabetes mellitus is a chronic disease caused by malfunction of pancreas in producing
of insulin or by effectiveness of insulin which will lead to accumulation of glucose
and raise level of it in blood vessels , this defect will affect the blood vessels and
nerves with the time [4] .
 in normal people, after intake food, the body breaks it down into glucose, which the
blood carries to cells. People who have diabetes have defect in pancreas which does
not make enough insulin or because the cells in the muscles, liver, and fat do not use
insulin, or both. As a result, the amount of glucose in the blood raises while the cells
are starved of energy. With the time ( in years ) , high blood glucose, also called
hyperglycemia, damages nerves and blood vessels, which can lead to complications
such as heart disease, stroke, kidney disease, blindness, nerve problems, gum
infections, and amputation of extremities [5]. diabetes complications in general are
serious and premature death, but it can control the disease and lower the risk of
complications[1] [6]. Genetics and life style such as obesity are the main cause of
diabetes in general [7] .


3. The Hormones involves in Diabetes Mellitus
3.1 The Role of Insulin and relation of it with diabetic :
Pancreas is a part of endocrine glands and produce Insulin hormone from the Islets of
Langerhans especially Beta cells that also produce amylin beside insulin (Insulin and
amylin are 65-80% of total products of Islets of Langerhans ) . islets. Humans have
roughly one million islets. In standard histological sections of the pancreas , See
figure 1 for pancreas [8].




                                 Figure 1 , pancreas [8]




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                              figure 2 , Islets of Langerhans [ 9 ]



Insulin is composed of two peptide chains referred to as the A chain and B chain. A
and B chains are linked together by two disulfide bonds, and an additional disulfide is
formed within the A chain. In most species, the A chain consists of 21 amino acids
and the B chain of 30 amino acids . Insulin is the principal hormone that regulates
uptake of glucose from the blood into most cells, muscle and fat cells, Therefore m
defect of insulin or the effectiveness of its receptors plays a big role in diabetes
mellitus . most of the carbohydrate in food is converted within a few hours to the
glucose, which used by the body as source of energy. Insulin is released into the blood
in response to hi levels of blood glucose after food intake. Insulin is used by about 2\3
of the body's cells to absorb glucose from the blood , for conversion to other needed
molecules and storage. Insulin is also important for conversion of glucose to glycogen
for internal storage in liver and muscle cells. Low glucose levels result both in the
reduced release of insulin from the beta cells and in the reverse conversion of
glycogen to glucose when glucose levels fall. This is mainly controlled by the
hormone glucagon which acts in an opposite manner to insulin. Glucose thus
recovered by the liver re-enters the bloodstream; muscle cells lack the necessary
export mechanism [10].



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The insulin mRNA is translated as a single chain precursor called preproinsulin, and
removal of its signal peptide during insertion into the endoplasmic reticulum
generates proinsulin. Proinsulin consists of three domains: an amino-terminal B chain,
a carboxy-terminal A chain and a connecting peptide in the middle known as the C
peptide. Within the endoplasmic reticulum, proinsulin is exposed to several specific
endopeptidases which excise the C peptide, thereby generating the mature form of
insulin. Insulin and free C peptide are packaged in the Golgi into secretory granules
which accumulate in the cytoplasm.

When the beta cell is appropriately stimulated, insulin is secreted from the cell by
exocytosis and diffuses into islet capillary blood. C peptide is also secreted into blood,
but has no known biological activity.

The insulin receptor on surface of the cells is a tyrosine kinase. In other words, it
functions as an enzyme that transfers phosphate groups from ATP to tyrosine residues
on intracellular target proteins. Binding of insulin to the alpha subunits causes the beta
subunits to phosphorylate themselves (autophosphorylation), thus activating the
catalytic activity of the receptor. The activated receptor then phosphorylates a number
of intracellular proteins, which in turn alters their activity, thereby generating a
biological response. The insulin particularly will facilitates entry of glucose into
muscle, adipose and several other tissues by mechanism of which cells can take up
glucose is by facilitated diffusion through a family of hexose transporters. In many
tissues , For example muscle; the major transporter used for uptake of glucose (called
GLUT4) is made available in the plasma membrane through the action of insulin. In
the absense of insulin, GLUT4 glucose transporters are present in cytoplasmic
vesicles, where they are useless for transporting glucose. Binding of insulin to
receptors on such cells leads rapidly to fusion of those vesicles with the plasma
membrane and insertion of the glucose transporters, thereby giving the cell an ability
to efficiently take up glucose. When blood levels of insulin decrease and insulin
receptors are no longer occupied, the glucose transporters are recycled back into the
cytoplasm .and it should be noted here that there are some tissues that do not require
insulin for efficient uptake of glucose: important examples are brain and the liver.
This is because these cells don't use GLUT4 for importing glucose, but rather, another
transporter that is not insulin-dependent.

Insulin also will stimulates the liver to store glucose in the form of glycogen. A large
fraction of glucose absorbed from the small intestine is immediately taken up by
hepatocytes, which convert it into the storage polymer glycogen. Insulin has several
effects in liver which stimulate glycogen synthesis. First, it activates the enzyme
hexokinase, which phosphorylates glucose, trapping it within the cell. Coincidently,
insulin acts to inhibit the activity of glucose-6-phosphatase. Insulin also activates
several of the enzymes that are directly involved in glycogen synthesis, including
phosphofructokinase and glycogen synthase.

3.2 Insulin and Lipid Metabolism

The metabolic pathways for utilization of fats and carbohydrates are deeply and
intricately intertwined. Considering insulin's profound effects on carbohydrate
metabolism, it stands to reason that insulin also has important effects on lipid
metabolism. Important effects of insulin on lipid metabolism include the following
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Insulin promotes synthesis of fatty acids in the liver. As discussed above, insulin is
stimulatory to synthesis of glycogen in the liver. However, as glycogen accumulates
to high levels (roughly 5% of liver mass), further synthesis is strongly suppressed.

When the liver is saturated with glycogen, any additional glucose taken up by
hepatocytes is shunted into pathways leading to synthesis of fatty acids, which are
exported from the liver as lipoproteins. The lipoproteins are ripped apart in the
circulation, providing free fatty acids for use in other tissues, including adipocytes,
which use them to synthesize triglyceride.

Insulin inhibits breakdown of fat in adipose tissue by inhibiting the intracellular lipase
that hydrolyzes triglycerides to release fatty acids.

Insulin facilitates entry of glucose into adipocytes, and within those cells, glucose can
be used to synthesize glycerol. This glycerol, along with the fatty acids delivered from
the liver, are used to synthesize triglyceride within the adipocyte. By these
mechanisms, insulin is involved in further accumulation of triglyceride in fat cells [11].



3.3 The role of Glucagon and relation of it with diabetes :

Glucagon has a major role in maintaining normal concentrations of glucose in blood,
and is often described as having the opposite effect of insulin. That is, glucagon has
the effect of increasing blood glucose levels.

Glucagon is a linear peptide of 29 amino acids. and it is structurally related to the
secretin family of peptide hormones. Glucagon is synthesized as proglucagon and
proteolytically processed to yield glucagon within alpha cells of the pancreatic islets.
Proglucagon is also expressed within the intestinal tract, where it is processed not into
glucagon, but to a family of glucagon-like peptides (enteroglucagon).



The major effect of glucagon is to stimulate an increase in blood concentration of
glucose. As discussed previously, the brain in particular has an absolute dependence
on glucose as a fuel, because neurons cannot utilize alternative energy sources like
fatty acids to any significant extent. When blood levels of glucose begin to fall below
the normal range, it is imperative to find and pump additional glucose into blood.
Glucagon exerts control over two pivotal metabolic pathways within the liver, leading
that organ to dispense glucose to the rest of the body,Glucagon stimulates breakdown
of glycogen stored in the liver. When blood glucose levels are high, large amounts of
glucose are taken up by the liver. Under the influence of insulin, much of this glucose
is stored in the form of glycogen. Later, when blood glucose levels begin to fall,
glucagon is secreted and acts on hepatocytes to activate the enzymes that
depolymerize glycogen and release glucose. Glucagon also activates hepatic
gluconeogenesis. Gluconeogenesis is the pathway by which non-hexose substrates
such as amino acids are converted to glucose. As such, it provides another source of
glucose for blood. This is especially important in animals like cats and sheep that

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don't absorb much if any glucose from the intestine - in these species, activation of
gluconeogenic enzymes is the chief mechanism by which glucagon does its job.

Glucagon also appears to have a minor effect of enhancing lipolysis of triglyceride in
adipose tissue, which could be viewed as an addition means of conserving blood
glucose by providing fatty acid fuel to most cells [11 ].



4. Classification of diabetes :

There is couple types of diabetes classified as type 1 , type 2 , gestational type and
others type . when the pancreas can not produce the insulin; this type known as
insulin-dependent and it is Type 1 . but when the body can not respond properly to the
action of insulin produced by the pancreas, this will be named as non-insulin-
dependent and it is Type 2. it is more common ( 90% of all diabetes cases) [3]. Few
pregnant women ( 2-5%) develop a temporary type of diabetes called ‗gestational
diabetes‘. but usually disappears after delivery . women who have this type are under
risk to develop type 2 later [11]. Other types of diabetes related to specific genetic
conditions and account for 1-5% of all diagnosed cases [5].


4.1 Type 1 Diabetes mellitus :
Known as insulin-dependent and diabetes mellitus ( IDDM) , also named by juvenile-
onset diabetes. It is caused by an auto-immune reaction where the body‘s defence
system destroy the beta cells in Islets of Langerhans . The reason is not understood
till now. So , patient here will produce a little amount of insulin and some cases will
not. It usually occurs in children or young adults. Patients here need to insulin dose
daily and If not have access to insulin, they die [11].


4.2 Type 2 Diabetes mellitus :
Known as non-insulin dependent diabetes . also named by adult-onset diabetes.
Patient usually not need for insulin dose . It can be control when life style is observe
such as diet, daily exercise, oral medication, and possibly insulin in demand .but if not
diagnosed and treated ; it will cause serious complication and early death
It is most common in people above 45 years who are overweight. But know
becoming more common in children and young adults cause overweight is hi between
these age . 90 % of patient with diabetes are fall in this type as I mention previously
[12]
     . See figure below [12].




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                                     Obesity



                                                   Enlarged
                      Overeating
                                                   fat cells




                       Increased                     Insulin
                        appetite                   resistance



                                     Type 2
                                    diabetes




4.3 Gestational diabetes :

It is a form of glucose intolerance appear in some women during pregnancy. It is
more common in overweight women and women with a family history of diabetes.
During pregnancy, gestational diabetes requires treatment to normalize maternal
blood glucose levels to avoid complications in the infant. After pregnancy, 5-10% of
women with gestational diabetes are at risk to have type 2 diabetes. Women who have
had gestational diabetes have a 20% to 50% chance of developing diabetes in the next
5-10 years [5].


4.4 Other Types of Diabetes :

Here ,the patient have signs of more than one type. Such as latent autoimmune
diabetes in adults (LADA), also called type 1.5 diabetes or double diabetes, people
have signs of both type 1 and type 2 diabetes. Diagnosis usually occurs above of age
30 . the patient here almost still have the productivity of insulin when diagnosed of
LADA , like what happen in type 2 diabetes . but this type in an developing with
years and the pancreas will stop making insulin . so , the patient will have to use
insulin to regulate blood glucose level . and that‘s why some experts describe LADA
by a ― slowly developing kind of type 1 diabetes ‖


Other types of diabetes caused by genetic defects of the beta cell, such as maturity-
onset diabetes of the young (MODY) and neonatal diabetes mellitus . or genetic
defects in insulin action, resulting in the body‘s inability to control blood glucose
levels. Or genetic syndromes associated with diabetes, such as Down syndrome . or
diseases of the pancreas or conditions that damage the pancreas, such as pancreatitis
and cystic fibrosis . and excess amounts of certain hormones resulting from some
medical conditions such as cortisol which affect the action of insulin [4].



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5. Signs , Symptoms and Complications

5.1 Signs and Symptoms :

Before the explain of signs and symptoms , there is important question to ask , who
gets diabetes ? and the answer is Anyone, anywhere, at any age can get diabetes . in
type 1, there is some risk factors such as genetic , environmental factor and family
history . in type 2 , people over age 40 ( 90 % of diabetes over age 40 have type 2 ) ,
obesity ( more than 80 % of people with type 2 are overweight ) , family history ,
physical inactivity , pregnant women with gastationl type have a risk to develop type
2 , and finally the race [11].

many cases with Diabetes undiagnosed because symptoms almost are harmless. But
most important is the fact which is early detection will decrease the complications of
diabetes by looking for warning signs that sometimes appear as follow regarding to
the type of DM . type 1 diabetes is usually sudden and including symptoms like ,
Abnormal thirst and a dry mouth ,Frequent urination , tiredness, Unexplained weight
loss , Slow-healing wounds and Blurred vision .Type 2 diabetes have same symptoms
but its usually less obvious and gradual , therefore hard to detect. That‘s why people
with type 2 diagnosed after few years later when symptoms appear [11].



5.2 Complications of diabetes :

Without control and management it can lead to complications such as cardiovascular
disease, kidney failure, blindness and nerve damage.



( I ) Short-term complications:

1 - Low blood sugar (hypoglycaemia)

People who takes insulin will blood sugar falling too low (because they have
misestimated the insulin they need, or have not eat enough). Hypoglycaemia can be
corrected rapidly by eating sugar. If it is not corrected it can lead to the consciousness
condition .

2 - Ketoacidosis

When the body breaks down fats, acidic waste products called ketones are produced.
The body cannot tolerate large amounts of ketones and will try to get rid of them
through the urine. However, the body cannot release all the ketones and they build up
in your blood, causing ketoacidosis. Ketoacidosis is a severe condition caused by lack
of insulin. It mainly affects people with type 1 diabetes.

3- Lactic acidosis


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Lactic acidosis is the build up of lactic acid in the body. Cells make lactic acid when it
use glucose for energy. If too much lactic acid still in the body, the balance tips and
the person will feel sick. Lactic acidosis is rare and mainly affects people with type 2
diabetes.

4 - Bacterial/fungal infections

People with diabetes are at risk to have bacterial and fungal infections. Bacterial
infections include sties and boils. Fungal infections include athlete‘s foot, ringworm
and vaginal infections.

( II ) Long-term complications:

1- Eye disease (retinopathy)

Eye disease, or retinopathy, About 2% of all people who have had diabetes for 15
years become blind, while about 10% develop a severe visual impairment .

2 - Kidney disease (nephropathy)

About 1\3 of all people with diabetes develop kidney disease and approximately 20%
of people with type 1 diabetes develop kidney failure.

3 - Nerve disease (neuropathy)

Diabetic nerve disease, or neuropathy affects at least half of all people with diabetes.
There are different types of nerve disease which can result in a loss of sensation in the
feet or in some cases the hands, pain in the foot and problems with the functioning of
different parts of the body including the heart, the eye, the stomach, the bladder. A
lack of sensation in the feet can lead to people with diabetes injuring their feet. These
injuries can lead to ulcers and possibly amputation.

4- Diseases of the circulatory system

Disease of the circulatory system, or cardiovascular disease, accounts for 75% of all
deaths among people with diabetes. The risk of heart disease is 2-4 times higher than
those who do not have diabetes. It is the main cause of disability and death for people
with type 2 diabetes in industrialized countries.

5 - Amputation

Diabetes is the most common cause of amputation that is not the result of an accident.
People with diabetes are 15 to 40 times more likely to require lower-limb amputation
compared to the general population [11].




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6. Diagnosis :


First thing we have to take pre-diabetes cases detecting in consideration as long as
importing fact that early diagnosed person will have a good chance to control the
disease .
In pre-diabetes, blood glucose levels elevate but not consider a marker for diagnosis
of diabetes. However, a lot of people with pre-diabetes will have type 2 diabetes
within 10 years. Individuals with pre-diabetes have an increased risk of heart disease
and stroke. With modest weight loss and moderate physical activity, people with pre-
diabetes can delay or prevent type 2 diabetes.

6.1 The test for diabetes and pre-diabetes diagnosis is as follow :

1- A fasting plasma glucose (FPG) test :
measures blood glucose in a person who has not eaten anything for at least 8 hours.
This test is used to detect diabetes and pre-diabetes.

2-An oral glucose tolerance test (OGTT) :
 measures blood glucose after a person fasts at least 8 hours and 2 hours after the
person drinks a glucose-containing beverage. This test can be used to diagnose
diabetes and pre-diabetes.

3-A random plasma glucose test :
 also called a casual plasma glucose test, measures blood glucose without regard to
when the person being tested last ate. This test, along with an assessment of
symptoms, is used to diagnose diabetes but not pre-diabetes.
Test results indicating that a person has diabetes should be confirmed with a second
test on a different day .

6.2 FPG Test :

The FPG test is the preferred test for diagnosing diabetes because of its convenience
and low cost. However, it will miss some diabetes or pre-diabetes that can be found
with the OGTT. The FPG test is good when doing in the morning. Results and their
meaning are shown in Table 3. People with a fasting glucose level of 100 to 125
(mg/dL) have a form of pre-diabetes called impaired fasting glucose (IFG). Having
IFG means a person has an increased risk of developing type 2 diabetes but does not
have it yet. A level of 126 mg/dL or above, confirmed by repeating the test on another
day, means a person has diabetes.




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Table 3. FPG test


                                                     Plasma Glucose Result (mg/dL)
                    Diagnosis
                     Normal                                   99 or below
                                                               100 to 125
   Pre-diabetes (impaired fasting glucose)

                    Diabetes *                               126 or above

*confirmed by repeating this test in another day .

Table 4. OGTT


                                              2-hour Plasma Glucose Result (mg/dL)
                Diagnosis
                 Normal                                    139 or below
      Pre-diabetes (impaired glucose                        140 to 199
                tolerance)
                 Diabetes*                                  200 or above



6.3 OGTT :

This is more sensitive than the FPG test for diagnosing pre-diabetes, but it is less
convenient to doing. The OGTT requires fasting for at least 8 hours before the test.
The plasma glucose level is measured immediately before and 2 hours after a person
drinks a liquid containing 75 grams of glucose dissolved in water. Results and their
meaning are shown in Table 4. If the blood glucose level is between 140 and 199
mg/dL 2 hours after drinking the liquid, the person has a form of pre-diabetes called
impaired glucose tolerance (IGT). Having IGT, like having IFG, means a person has
an increased risk of developing type 2 diabetes but does not have it yet. A 2-hour
glucose level of 200 mg/dL or above, confirmed by repeating the test on another day,
means a person has diabetes.




*confirmed by repeating this test in another day .

Gestational diabetes is also diagnosed based on plasma glucose values measured
during the OGTT, preferably by using 100 grams of glucose in liquid for the test.
Blood glucose levels are checked four times during the test. If blood glucose levels


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are above normal at least tow time during the test, the woman has gestational diabetes.
Table 3 shows the above-normal results for the OGTT for gestational diabetes.


Table 5. Gestational diabetes: Above-normal results for the OGTT

     Plasma Glucose Result (mg/dL)                            When
             95 or higher                                    Fasting
               180 or higher                                At 1 hour
               155 or higher                                At 2 hours
               140 or higher                                At 3 hours




6.4 Random Plasma Glucose Test :

A random, or casual, blood glucose level of 200 mg/dL or higher, plus the presence of
the following symptoms, can mean a person has diabetes with increased urination ,
increased thirst and unexplained weight loss . Other symptoms can include fatigue,
blurred vision, increased hunger, and sores that do not heal. The doctor will check the
person‘s blood glucose level on another day using the FPG test or the OGTT to
confirm the diagnosis [4] .


6.5 Who should be tested for diabetes and pre-diabetes?
People aged 45 or older should consider getting tested for pre-diabetes or diabetes.
People younger than 45 should consider testing if they are overweight, obese, or
extremely obese and have one or more of the risk factors as being physically inactive
, having a parent, brother, or sister with diabetes , giving birth to a baby weighing
more than 9 pounds or being diagnosed with gestational diabetes , having high blood
pressure— 140/90 mmHg or above or being treated for high blood pressure , having
an HDL, or ―good,‖ cholesterol level below 35 mg/dL or a triglyceride level above
250 mg/dL ,
having polycystic ovary syndrome, also called PCOS , having IFG or IGT on
previous testing , having a condition called acanthosis nigricans, characterized by a
dark, velvety rash around the neck or armpits , having a history of cardiovascular
disease; disease affecting the heart and blood vessels .

If results of testing are normal, testing should be repeated at least every 3 years.
Doctors may recommend more frequent testing depending on initial results and risk
status. People whose test results indicate they have pre-diabetes should have their
blood glucose checked again in 1 to 2 years and take steps to prevent type 2 diabetes
developing .

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When a woman is pregnant, the doctor will assess her risk for developing gestational
diabetes at her first prenatal visit and order testing as needed during the pregnancy.
Women who develop gestational diabetes should also have follow-up testing 6 to 12
weeks after the baby is born [4] .


7. Treatment , Monitoring and Control

7.1 Treatment :

The treatment of diabetes is usually a complex program involving a specific diet, a
specific exercise prescription, and medications. These treatments are most effective
when carried out with a team of health care providers knowledgeable in the care of
people with diabetes. As opposed to high blood pressure, asthma, and even high
cholesterol, with diabetes, self-management is the fundamental key to success. Many
other conditions can result in good outcomes by taking a medication at the appropriate
times. With diabetes, so much more is required since everything from stress,
depression, food, exercise, other illness, and a host of other factors effect blood
glucose levels. Learning about all of these factors and knowing what to do when
blood glucose levels are above or below target can take quite a bit of time. The
rewards, however, are great.

Patients who do best are those who measure their blood glucose frequently, pay
attention to which factors affect blood sugar, and try to avoid anything that causes a
disruption in diabetes control in the future. No one is always successful in keeping
blood glucose in the "normal" range, and it must always be remembered that there is
no such thing as being "perfect" if you have diabetes. Fluctuations in blood glucose
will occur no matter how careful you are.

7.2 Self-management :

For a person with diabetes, self-management skills are the key to success. Although
eating at the same time each day the same amount of food, exercising everyday, and
taking the medication exactly as prescribed may be helpful, doing all of these things
perfectly for the rest of one's life is not realistic. Rather, the goal of therapy is to know
what to do when the daily routine is disrupted: such as a late dinner, a ten-mile bike
ride that was not planned, or a birthday celebration with cake and other goodies.
Certain life situations also require self-management expertise--acute illness such as
nausea and vomiting (gastroenteritis), surgery, pregnancy, and menopause all have
their own challenges for people with diabetes. It is beyond the scope of this essay to
deal with the daily complexities for everyone with diabetes, but especially for those
on insulin and those with type 1 diabetes more training will be required.

7.3 Health care team :

Ideally, it would be best if an entire team of health care professionals were available
for everyone with diabetes. This is not always possible but at the very least, all of
these people should be available for consultation if needed. These team members
include:
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   1. Physician: Often an endocrinologist but may be a general internist or family
      practice physician. In the U.S. endocrinologists see a very small number of the
      adults with diabetes due to the small number of specialists and large number
      of patients with diabetes.
   2. Nurse Specialist: Usually a registered nurse with special expertise in diabetes
      care. All providers, but especially nurses and nutritionists, may be certified in
      diabetes education (CDE). A CDE ensures you are receiving up-to-date
      information about diabetes care and education.
   3. Nutritionist: In the opinion of many, the most important person on the team. A
      nutritionist with a CDE is an expert about the two most important factors of
      blood glucose control: food and medications. Current nutrition therapy has
      become quite sophisticated but outstanding nutritionists can simplify the
      information, especially for those learning how to match food with insulin.
   4. Mental Health Professionals: Both psychologists (using mostly counseling
      techniques) and psychiatrists (doctors who can also prescribe drugs) should be
      available as any mental health disorder can affect diabetes control.
   5. Pharmacist: Due to the complexity of medications with diabetes, the
      pharmacist has become a critical member of the team.
   6. Podiatrist: A doctor with special expertise in disorders of the feet, common for
      people with diabetes.

7.4 Pain and fatigue :

If controlled well, diabetes will not cause pain or fatigue. Poorly controlled diabetes
will result in these symptoms and will resolve with proper treatment. For patients with
type 2 diabetes fatigue will often improve if insulin is started and blood glucose
improves.

For most people, these symptoms mean another problem is present. For those with
type 1 diabetes the most common condition is hypothyroidism. It is estimated that 10-
20% of people with type 1 diabetes develop some type of thyroid problem.

7.5 Exercise and therapy :

Exercise is a key component of a treatment plan for anyone with diabetes. For those
with type 2 diabetes, exercise improves insulin's effect on the muscle and will result
in blood glucose lowering. For many newly diagnosed individuals, a regular exercise
program with proper diet can result in the need for no further therapy. However, if
your HbA1c remains above 7%, diet and exercise alone will not be sufficient.

For those on insulin, especially those with type 1 diabetes, exercise needs to be
planned to prevent problems with hypoglycemia. Exercise will result in a lowering of
blood glucose and either additional carbohydrate or less insulin will be required. More
frequent home blood glucose monitoring may be required. This is a large topic
beyond the scope of this essay and should be discussed in detail with your healthcare
team.




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7.6 Medications :

For type 2 diabetes there are 4 classes of medications:

   1. Insulin secretagogues (for example, glyburide, glipizide, repaglinide,
      glimiperide to name a few)--These agents increase stimulate the pancreas to
      make more insulin.
   2. Biguanides--There is only one available, metformin. This drug makes the liver
      more sensitive to insulin. It lowers HbA1c levels 1.5-2%, similar to that of
      insulin secretagugues.
   3. Alpha-glucosidase inhibitors (acarbose and miglitol)--These drugs slow down
      the absorption of carbohydrate.
   4. Thiazolidinediones (also called "glitazones") (pioglitazone, rosiglitazone)--
      These drugs result in insulin becoming more sensitive at the muscle.

Insulin is used for both type 1 and type 2 diabetes. Insulin can be classified as basal
(or background) insulin, or mealtime (or prandial) insulin. In general, the basal
insulins are the long-acting and intermediate-acting insulins, and the mealtime
insulins are the short-acting and rapid-acting insulins.

7.7 Long acting :

   1. Glargine: no peak, lasts 24 hours
   2. Ultralente: broad peak, 10-16 hours, lasts 20-24 hours

7.8 Intermediate acting :

   1. NPH: peaks 5-8 hours, lasts 12-16 hours
   2. Lente: similar to NPH

7.9 Short-acting :

   1. Regular: peaks 2-3 hours, lasts 6-8 hours

7.10 Rapid-acting :

   1. Lispro: peaks 1 hour, lasts 4-5 hours
   2. Aspart: peaks 1 hour, lasts 4-5 hours

7.11 Surgery :

People with diabetes have more frequent surgery than those without. However, only
rarely do we use surgery to actually TREAT diabetes. This occurs with either a
kidney-pancreas transplant, or more rarely, a pancreas transplant by itself. Pancreas
transplants are only done for those with type 1 diabetes. For those who do not need a
kidney transplant, pancreas transplants may be considered if frequent, life-threatening
hypoglycemia is occurring. In the near future we hope that islet cell transplants will
become available. Islets are the tiny cells in the pancreas that make insulin.


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7.12 Social impacts :

There are a variety of important social impacts of the management and treatment
programs for diabetes. Much of this depends on the age of the patient. For children, it
is critical for teachers and other adults to be familiar with routine diabetes care, but
particularly the treatment of mild hypoglycemia. For teens, social issues become more
complicated, but it is important for at least some friends to be aware of the diabetes.
For young adults, other issues pertaining to one's job, dating situations, and overall
comfort level with sharing information about diabetes become important points. Many
sensitive issues, particularly regarding family planning, questions regarding sexual
issues, and the effects of diabetes on mental health will require discussion with a
health care provider knowledgeable about these topics as they relate to diabetes. For
older adults, many of these same issues are present but now it is common for patients
to also address the social impact of the various complications of diabetes. This is
obviously a complicated topic that deserves a great amount of attention from a
provider with understanding of the impact of all of the elements of diabetes on
someone's life.



7.13 Long-term management :

Ongoing monitoring can be divided into two major categories.

First, monitoring for the diabetes itself needs to be considered. Although this is
usually done with two major mechanisms, there other important tests are occasionally
needed. Home blood glucose monitoring is the standard for assessing diabetes control
at home. Although there is still controversy as to how often someone with type 2
diabetes who does not take insulin should measure their blood glucose, all patients
who take insulin should monitor on a regular basis, both to assess any patterns in
glucose levels, but also to make changes at the time if the glucose level is too high or
too low.

The other way diabetes is monitored is with HbA1c described above. This test allows
both patients and their physicians to assess overall blood glucose control during the
past 3 months. The goal for the majority of people should be a HbA1c below 7%,
which would be an average blood glucose level of 150 mg/dL.

Monitoring also needs to         include    assessment   of   complications.    Current
recommendations include:

   1. a yearly dilated eye exam to exam the retina,
   2. a yearly test for kidney disease with protein (or microalbumin) from a urine
      test,
   3. a yearly lipid panel with the primary goal to maintain LDL cholesterol below
      100 mg/dL
   4. at least a yearly comprehensive foot exam to assess risks for foot ulcer, and
   5. regular blood pressure measurements with a goal to maintain a blood pressure
      below 130/80.

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7.14 Unproven remedies :

There are numerous misconceptions about treatments for diabetes, but the most
common ones involve insulin therapy.

First, some people think that starting insulin therapy will lead to blindness or some
other major problem. The thinking here occurs often due to the fact a relative or friend
had a similar problem just after starting insulin. In truth, insulin has been shown to
PREVENT these problems and there is no cause and effect relationship between the
timing of insulin therapy and the start of a complication.

The other problem is that many people feel they can avoid insulin if they "behave"
and are careful with the diet. The reality is that over time, insulin secretion normally
diminishes so that no matter what is done with pills, diet, and exercise, the only way
to maintain the goal of a HbA1c of less than 7% will be with insulin therapy. Insulin
is not dangerous if used correctly. Furthermore, the vast majority of patients don't
complain about insulin use once they start. A more common complaint regards the
finger pokes for home glucose monitoring.

It needs to be emphasized: the goal of therapy is to bring the blood glucose levels
down to the target range. Having the primary goal of avoiding insulin will eventually
lead to a poor outcome.

7.15 How to make Insulin ?
Recombinant DNA technology is used to make human insulin. The chemical
components of human insulin have been slightly modified to make insulin analogs.
Rapid acting insulin analogs start to work within minutes, allowing you to take your
insulin 15 minutes before a meal. Rapid-acting insulin acts more similar to the way
insulin is released after meals in people without diabetes. Long-acting insulin analogs
are modified so they are absorbed slowly and work longer [12].




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8. Body Mass Index (BMI) :




A graph of body mass index is shown above. The dashed lines represent subdivisions
within a major class. For instance the ―Underweight‖ classification is further divided
into ―severe,‖ ―moderate,‖ and ―mild‖ subclasses. taken from World Health
Organization database [13] .

BMI is a statistical measurement which compares a person's weight and height.
Though it does not actually measure the percentage of body fat, it is a useful tool to
estimate a healthy body weight based on how tall a person is. Due to its ease of
measurement and calculation, it is the most widely used diagnostic tool to identify
obesity problems within a population. However, it is not considered appropriate to use
as a final indication for diagnosing individuals [14] .

9.Genetics and diabetes

9.1 Genetics and type 1 diabetes :

Researchers believed that Genetics play a role, which is indicated by the disease
occurring multiple times in a family.
A family history of type 1 diabetes is a major indicator that a person may also develop
the disorder. The risk of a child developing type 1 diabetes in association with a
parent with the disease is the following:
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      1 in 17 when the father has diabetes

      1 in 25 when the mother has diabetes and gave birth to the child before age 25

      1 in 100 when the mother has diabetes and gave birth to the child after age 25

      1 in 4 to 1 in 10 when both parents have diabetes



The high rate of occurrence of diabetes within families helped encourage research into
genetic links to the disease. Scientists are trying to determine which genes are
involved in individuals with type 1 diabetes and how genetic mutations interfere with
the production of insulin. To date, they have not found a single gene responsible for
type 1 diabetes. However, there are about 19 sections of the human genome that
appear to be related to a susceptibility to type 1 diabetes.

One section of the genome contains several genes involved in building human
leukocyte antigens (HLA). The proteins formed by these genes help the immune
system recognize the body‘s own cells. When HLA genes malfunction, an
autoimmune disorder may occur.

There are many types (alleles) of HLA genes. According to the American Diabetes
Association, 95 percent of people with type 1 diabetes have HLA-DR3, HLA-DR4 or
both alleles. The HLA genes involved in diabetes also vary by ethnicity and race.
HLA-DR3 and HLA-DR4 are most common in white diabetic patients, but HLA-DR7
is common in patients of African descent and HLA-DR9 is common in patients of
Japanese descent.

The inherited HLA-DR gene makes individuals more susceptible to type 1 diabetes,
but it is not the only factor. Other genes, including other HLA genes (HLA-DQ) and
IDDM2 (the insulin gene), are also likely to be involved. Researchers are continuing
to study additional gene clusters and chromosomes to determine their role in type 1
diabetes.

The genetic factor is a complicated issue in the development of type 1 diabetes. Most
people with the disease do not have a parent or sibling with it. Also, identical twins
have identical genes, but there is only a 50 percent chance of both twins developing
the disease. This means that factors in addition to genetics play a role in the
development of the disease.

A form of type 1 diabetes that can develop in adults is known as latent autoimmune
diabetes of adulthood (LADA). It is not known how the genetic risk factors for LADA
may differ from those of standard type 1 diabetes.

9.2 Genetics and type 2 diabetes :

genetic link to type 2 diabetes appears much stronger than for type 1. Identical twins
share the same genetic code, but should one identical twin develop type 2 diabetes,

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the risk for the other twin is 60 to 75 percent, according to the American Diabetes
Association.
Evidence for the genetic basis of the disease is also provided by its frequency among
racial and ethnic groups. In the United States, type 2 diabetes occurs most frequently
among African Americans, Hispanics/Latinos, Native Americans, Alaska Natives,
Asian Americans and Pacific Islanders.
Some researchers believe that this prevalence is due to the presence of a ―thrifty‖ gene
or set of genes inherited amongst these ethnic groups. In theory, the thrifty gene
originally altered the use of insulin to enable people to store energy in the body more
efficiently to survive periods of food scarcity. Surviving food scarcity periods is
generally no longer an issue in modern Western societies, and the thrifty gene has
shifted from being a survival mechanism to being a risk factor for diabetes.
Research indicates that in most cases of type 2 diabetes there is more than one gene
involved and that the gene combinations may differ between families. In addition, the
genes may have only slight variations, and it is possible that the variations are
common in the human population. These factors make research into the genetics of
type 2 diabetes difficult.
These genes appear to affect the way insulin acts on tissues, creating insulin
resistance. This condition impairs the ability of cells to use the insulin that is present,
and it accumulates in the bloodstream, causing hyperinsulinemia. In addition, other
genes may affect the insulin-making beta cells of the pancreas, limiting their ability to
produce enough insulin to overcome the resistance.
Scientists in recent years have linked several genes to development of type 2 diabetes.
For example:

      A gene variant called TCF7L2 could predispose close to 38 percent of
       Northern European populations and many black Americans to type 2 diabetes.
       It might increase their risk of diabetes by 80 percent. However, these
       researchers found that moderate exercise and weight loss – the same
       preventive treatments touted in the landmark Diabetes Prevention Program –
       could virtually erase the additional risk in people with this genetic makeup.

      A gene called ARNT (aryl hydrocarbon receptor nuclear translocator) has
       been found to be expressed abnormally in the beta cells of people with type 2
       diabetes. The discovery provides new insight into the development of the
       disease, and potentially a treatment.

The identification of some genes involved in type 2 diabetes has led to the
development of genetic tests for the disease. These tests examine samples of blood or
cells from the inside of the cheek for the responsible gene. Interpreting the results is
complicated, and genetic counseling is recommended to patients interested in
undergoing genetic screening.
Genetics can also contribute to factors that may lead to type 2 diabetes. Obesity,
which is caused by both genetic and environmental factors, increases insulin
resistance and the risk of type 2. Other risk factors for type 2 diabetes that may
involve a genetic component include:

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      Unhealthy levels of cholesterol and triglycerides (hyperlipidemia)
      Metabolic syndrome
      High blood pressure

Though a family history of type 2 diabetes is one of the strongest risk factors for
developing the disease, this genetic predisposition is far more significant for those
who consume an unhealthy, high-calorie diet and get little exercise.
Gestational diabetes, the form that affects some women during pregnancy, is also a
metabolic disorder and may have a similar genetic composition to type 2 diabetes.

9.3 Genetics and other type of diabetes :

Several genes have been linked to some of the less common forms of diabetes and
associated conditions. Researchers have identified certain genes that may be a factor
in syndromes of extreme insulin resistance, diabetes-deafness syndromes and
maturity-onset diabetes of the young (MODY).

MODY is a rare form of diabetes that is caused by inherited genetic defects. It
accounts for less than 5 percent of diabetes cases, according to the American Diabetes
Association. In most cases, MODY occurs in three or more generations of a family
and often develops in the teen years or early 20s. Children of patients with MODY
have a 50 percent risk of developing the condition. The disorder is sometimes
considered a variation of type 2 diabetes but can be misdiagnosed as type 1.

There are several types of MODY. Each appears to be caused by a single-gene
mutation. The genetic defects primarily affect the function of beta cells (pancreas
cells that produce insulin), causing the development of this disease. The six forms of
MODY and the associated genetic mutation are:

      MODY1 (hepatic nuclear factor-4alpha or HNF-4alpha)
      MODY2 (pancreatic glucokinase or GCK)
      MODY3 (HNF-1alpha)
      MODY4 (insulin promoter factor-1 or IPF-1)
      MODY5 (HNF-1beta)
      MODY6 (neurogenic differentiation factor-1 or neuroD1)

Other rare forms of diabetes can also be caused by single genes. The action of insulin
and cellular sensitivity to insulin may be affected by the insulin receptor gene. A
genetic mutation can also affect a molecule called PPAR-gamma, which affects
insulin action and is a target for some antidiabetic agents, medications for type 2
diabetes.

Certain genetic defects of the beta cell can lead to Wolfram syndrome. This disorder
is also known by the acronym DIDMOAD (diabetes insipidus, diabetes mellitus, optic
atrophy and deafness), which refers to many of the conditions that occur in
conjunction with it. The gene responsible, WSF1, is active in the pancreas and nerve
cells.

Several diabetic disorders involve defects in the insulin receptor gene. Indicators are
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hyperinsulinemia and the skin condition acanthosis nigricans. These disorders
include:

      Type A insulin resistance. A condition in which the body‘s cells lose their
       ability to use insulin. Insulin resistance can cause an increased production of
       male hormones in girls, leading to polycystic ovarian syndrome.

      Leprechaunism (also called Donohue syndrome). A rare fatal form of mental
       and physical retardation that often causes death within the first year of life.

      Rabson-Mendenhall syndrome. Another rare congenital disorder involving
       severe insulin resistance and poor prognosis.

There are also numerous genetic syndromes that can lead to secondary diabetes or
prediabetes. Although many subcategories exist, the main classifications include:

      Pancreatic deficiencies
      Mutant insulin syndromes
      Glucokinase gene mutations
      Mitochondrial DNA gene mutation
      Chromosomal defects
      Hereditary neuromuscular disorders [15] .



10. conclusion :

Diabetes is a slow killer with no known curable treatments. However, its
complications can be reduced through proper awareness and timely treatment. Three
major complications are related to blindness, kidney damage and heart attack. It is
important to keep the blood glucose levels of patients under strict control for avoiding
the complications. One of the difficulties with tight control of glucose levels in the
blood is that such attempts may lead to hypoglycemia that creates much severe
complications than an increased level of blood glucose. In our communities in Saudi
Arabia ; we have a large percentage of diabetic patient , actually every family in
general have a member with this disorder , so; proper education and care for the
family and friends can decrease the risk of disease and quick processing to deal with
the patient .




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References :

1-Rowena taylor , History of Diabetes . The National Institute of Clinical Excellence
(NICE) , UK ( 2004 ) .
http://www.drtaylor.co.uk/diabetes/info/diabetes/History.pdf

2- Wild S, Roglic G, Green A, Sicree R, King H. Article of Global Prevalence of
Diabetes: Estimates for the year 2000 and projections for 2030. Diabetes
Care. ch.27: P.1047-1053, volume 27, number 5, May 2004
http://www.who.int/diabetes/facts/en/diabcare0504.pdf

3 - Nasser M. Al-Daghri , Metabolic basis of coronary artery disease, PhD. Thesis .
Birmingham university (2002) .ch.1.2 , P.8–17 .
4-diabetes action online , world health organization (WHO) .
http://www.who.int/diabetes/en/

5 –Henry JB. Clinical diagnosis and management by laboratory methods. 20th ed.
Philadelphia: WB Saunders; 2001. p. 215 and 561. ISBN 0-7216-8864-0.


6 – American Diabetes Association: Clinical Practice Recommendations.
Diabetes Care, ch.25: P.1-47, Volume 30 , January 2007 .
http://care.diabetesjournals.org/content/vol30/suppl_1/

7–The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus:
Report of the Expert Committee on the Diagnosis and Classification of
DiabetesMellitus. Diabetes Care ,ch. 20:P.1183–1197, 1997 .
http://care.diabetesjournals.org/cgi/content/full/25/suppl_1/s5

8 - Elayat AA, el-Naggar MM, Tahir M , An immunocytochemical and morphometric
study of the rat pancreatic islets, Department of Anatomy, Faculty of Medicine, King
Abdulaziz University, Jeddah, Saudi Arabia. 1995 . P:629-637 , Jurnal of Anatomy
,pubmed central , PMCID : PMC1167020 .
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1167020

9 – Assady, S., Maor, G., Amit, M., Itskovitz-Eldor, J., Skorecki, K.L., and
Tzukerman, M. (2001). Insulin production by human embryonic stem cells. Diabetes.
50. http://www.diabetes.org/Diabetes_Rapids/Suheir_Assady_ 06282001.pdf

10 – Diabeticsanonymous organization .
http://www.diabeticsanonymous.org/pathphysiology.html

11- Gabir M, Hanson Rl , Dabelea D, Imperatore G, Roumain J, Bennett PH,
Knowler WC. Article of Plasma glucose and prediction of microvascular disease and
mortality. Evaluation of 1997 American Diabetes Association and 1999
World Health Organization criteria for diagnosis of diabetes. Diabetes Care
; ch.23: P.1113–1118 , Volume 23, Issue 8 , 2000 .
http://care.diabetesjournals.org/cgi/content/abstract/23/8/1113


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12 - Eleano N. Whitney , Corinne B. Cataldo , Sharon R. Rolfes . Understanding
Normal and Clinical Nutrition (2002) , 6th edition .ch.25 : P.745-768 .
13 – Body Mass Index .
graphhttp://www.who.int/bmi/index.jsp?introPage=intro_3.html
14 – General Overview about Body Mass Index , May 5, 2005 .
http://www.medicinenet.com/script/main/art.asp?articlekey=56149&page=2

15 - Laura Dean, Johanna McEntyre . The Genetic Landscape of Diabetes ( Book at
NCBI ).
http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=diabetes




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                                   Content
Head                                                                     Page
1.History …………………………………………………………………...……….....1
2. Introduction………..………………………………………………………..……....2
3. The Hormones involves in Diabetes Mellitus ……….……..…..….…………….....2
        3.1 The Role of Insulin and relation of it with diabetis……….…………….…2
        3.2 Insulin and Lipid Metabolism…………………………………...………...4
        3.3The role of Glucagon and relation of it with diabetes……..…….………....5
4. Classification of diabetes ………………………………………..………………....6
        4.1 Type 1 Diabetes mellitus ……………………………………..……….…..6
        4.2 Type 2 Diabetes mellitus………………………………………………... ..6
        4.3 Gestational diabetes :…..………………………………...………….….. ..7
        4.4 Other Types of Diabetes…………………………………...……….……...7
5. Signs , Symptoms and Complications……….…………………………… ………..8
        5.1 Signs and Symptoms:…………………………………………...….…… ..8
        5.2 Complications of diabetes …………………………..…………..………...8
        5.3 Short-term complications…………………..……………………..…….....8
        5.4 Long-term complications…………………………………………..…… ..9
6. Diagnosis :………………………………………………….…………………….....9
        6.1 The test for diabetes and pre-diabetes diagnosis …….……….………… 10
        6.2 FPG Test ………………………………………………………..………..10
        6.3 OGTT …………………………………………………………….…… ..11
        6.4 Random Plasma Glucose Test ………...………………………….…… ..12
        6.5 Who should be tested for diabetes and pre-diabetes ……………...……..12
7. Treatment , Monitoring and Control ……………………..…………………….....12
        7.1 Treatment………………………………………..……..….……………..12
        7.2 Self-management………………………………….…….………………..13
        7.3 Health care team…………………………………….……………………13
        7.4 Pain and fatigue……………………………………….…….………...….14
        7.5 Exercise and therapy………………………………….……..….….…….14
        7.6 Medications………………………………………………..…….……….14
        7.7 Long acting…………………………………………….……..…………..15
        7.8 Intermediate acting……………………………………..……….………..15
        7.9 Short-acting ……………..………………………………..……….……..15
        7.10 Rapid-acting …………………………………………….……..….……15
        7.11 Surgery …………………………………………………..………..……15
        7.12 Social impacts………………………………………………….….……15
        7.13 Long-term management……………………….……………….….……16
        7.14 Unproven remedies……………………………….…………….……....16
        7.15 How to make Insulin ……………………………………..…………….17
8. Body Mass Index (BMI) ………………………………………………….………17
9.Genetics and diabetes ……………………………………………………...............18
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       9.1 Genetics and type 1 diabetes ……………………...……………………..18
       9.2 Genetics and type 2 diabetes ………………………...…………………..19
       9.3 Genetics and other type of diabetes …………………………………..…20
10. conclusion ………………………………………………………………………..22
References…………………………………………………………………...……….23
Content ………………………………………………………………...………...…..25

                              **END**




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