DIABETES MELLITUS

Introduction
Diabetes mellitus is taken from the Greek word diabetes, meaning siphon - to pass through
and the Latin word mellitus meaning sweet. A review of the history shows that the term
"diabetes" was first used by Apollonius of Memphis around 250 to 300 BC. Ancient Greek,
Indian, and Egyptian civilizations discovered the sweet nature of urine in this condition, and
hence the propagation of the word Diabetes Mellitus came into being. Mering and
Minkowski, in 1889, discovered the role of the pancreas in the pathogenesis of diabetes.
leading to the availability of an effective treatment for diabetes in 1922. Over the years,
exceptional work has taken place, and multiple discoveries, as well as management
strategies, have been created to tackle this growing problem. Unfortunately, even today,
diabetes is one of the most common chronic diseases in the country and worldwide.

Diabetes mellitus (DM) is a metabolic disease, involving inappropriately elevated blood

glucose levels. DM has several categories, including type 1, type 2, maturity-onset diabetes of
the result from defective insulin secretion (T1DM) and/or action (T2DM). T1DM presents in
children or adolescents, while T2DM is thought to affect middle-aged and older adults who
have prolonged hyperglycemia due to poor lifestyle and dietary choices. The pathogenesis for
T1DM and T2DM is drastically different, and therefore each type has various etiologies,

presentations, and treatments.

DIABETES MELLITUS

Diabetes is a metabolic disorder in which there are high levels of sugar in the blood, a
condition called hyperglycemia. Under normal conditions, food is broken down to glucose
which then enters the bloodstream and acts as fuel for the body. The pancreas produces a
hormonecalled insulin which helps to carry glucose from the bloodstream into muscle, fat

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and liver where it can be used as fuel. Diabetics are not able to move this sugar out of the
bloodstream because of two primary reasons:

1). their pancreas does not produce enough insulin and/or

2).their cells donot respond normally to insulin, a condition called insulin resistance. This is
whypeople with diabetes have high blood sugarlevels.

The term diabetes mellitus describes a metabolic disorder of multiple aetiology characterized
by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism
resulting from defects in insulin secretion, insulin action, or both.The effects of diabetes
mellitus include long–term damage, dysfunction and failure of various organs.

Pathophysiology

A patient with DM has the potential for hyperglycemia. The pathology of DM can be unclear
since several factors can often contribute to the disease. Hyperglycemia alone can impair
pancreatic beta-cell function and contributes to impaired insulin secretion. Consequentially,
there is a vicious cycle of hyperglycemia leading to an impaired metabolic state. Blood
glucose levels above 180 mg/dL are often considered hyperglycemic in this context, though
because of the variety of mechanisms, there is no clear cutoff point. Patients experience
osmotic diuresis due to saturation of the glucose transporters in the nephron at higher blood
glucose levels. Although the effect is variable, serum glucose levels above 250 mg/dL are
likely to cause symptoms of polyuria and polydipsia.

Insulin resistance is attributable to excess fatty acids and proinflammatory cytokines, which
leads to impaired glucose transport and increases fat breakdown. Since there is an
inadequate response or production of insulin, the body responds by inappropriately
increasing glucagon, thus further contributing to hyperglycemia. While insulin resistance is a
component of T2DM, the full extent of the disease results when the patient has inadequate
production of insulin to compensate for their insulin resistance.

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Chronic hyperglycemia also causes nonenzymatic glycation of proteins and lipids. The extent
of this is measurable via the glycation hemoglobin (HbA1c) test. Glycation leads to damage in
small blood vessels in the retina, kidney, and peripheral nerves. Higher glucose levels hasten
the process. This damage leads to the classic diabetic complications of diabetic retinopathy,
nephropathy, and neuropathy and the preventable outcomes of blindness, dialysis, and
amputation, respectively.

TYPES OF DIABETES

1) Type 1 diabetes(T1D)/ Juvenile diabetes/ Insulin dependent diabetes:

It is common among 10-14 years age group and account for 5%-10% of all diagnosed cases of
diabetes mellitus. ~90% is autoimmune mediated and 10% is idiopathic.

T1D affects both adults and children at any age and occurs when the person’s pancreas stop
producing insulindue to destruction of the pancreatic beta cells or by inactivity of these
insulin-producing cells. Affected individuals depend on dailyinjections of insulinto maintain
normal blood glucose levels. The causes of T1Dare not entirely understood however;
scientists believe that both genetic and environmental factors are involved.

2)Type 2 diabetes/ Non-insulin dependent diabetes mellitus (T2D or NIDDM):

This is the most common form of diabetes that most often occursin adulthood. However,
because of increased obesity rates and sedentary lifestyles,teens and young adults are also
being diagnosed with T2D or the precursor, prediabetes.

In T2D, fat, muscle and liver cells donot respond correctly to insulin. This is called insulin
resistance. As a result, blood sugar cannot enter these cells to be stored for energy and
buildsup in the blood. Insulin resistance is a gradual process that developsslowly over time.

It Account for about 90%-95% of all the diagnosed cases of diabetes.

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3)Gestational diabetes:

Thisrefers to diabetes that is first diagnosed during pregnancy. Weight gain and changing
hormones that occur during pregnancycanimpair insulin function,resulting in high blood
sugar. This form of diabetes usually disappears after pregnancy, however, women who have
had gestational diabetes have a 40-60% chance of developing T2Dwithin 5 to 10 years.

ASSOCIATION BETWEEN CHANGE IN PANCREATIC MORPHOLOGY AND VASCULAR

COMPLICATIONS WITHIN DIABETES MELLITUS

Dcreased pancreatic volume, increased pancreatic fat mass, and serrated pancreatic margins
are characteristic morphological changes of the pancreas in subjects with type 2 diabetes
mellitus. This retrospective study aimed to clarify the clinical signifcance of pancreatic
morphological changes in subjects with type 2 diabetes mellitus who underwent abdominal
magnetic resonance imaging. The mean age and HbA1c value were 59.1±16.3years old and
8.9±2.3%, respectively. Pancreatic body mass corrected for body surface area (BSA) in
subjects with diabetes mellitus was lower compared to those in normal glucose tolerance
(49.4±15.3 cm3 vs. 60.9±7.8 cm3), although it did not reach a statistic signifcance. There was a
negative correlation between BSA-corrected pancreatic volume and age, duration of
diabetes, glycoalbumin, mean and max IMT, and there was a positive correlation between
BSA-corrected pancreatic volume and HOMA2-β. Serration of the pancreatic limbus was more
often observed in subjects with diabetes mellitus compared to those in normal glucose
tolerance (74.1% vs. 14.3%). Subjects with serrated changes were older and had higher
HbA1c, and visceral fat area was signifcantly larger in subjects with serrated changes. BSA-
corrected pancreatic volume in subjects with serrated changes was signifcantly smaller, and
mean IMT was signifcantly thicker in subjects with serrulation. Furthermore, advanced
diabetic retinopathy and diabetic nephropathy were more often observed in subjects with
serrated changes. Taken together, decreased BSA corrected pancreatic volume and serrated
changes were associated with the progression of vascular complications in subjects with type
2 diabetes mellitus.

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Type 2 diabetes mellitus is a disease that causes βcell dysfunction due to genetic and
environmental factors; it is estimated that βcell function is reduced by 50% at the onset of
type 2 diabetes mellitus.

. Previous studies using ultrasonography and computed tomography (CT) to evaluate

pancreatic volume have shown a 722% decrease in pancreatic volume in subjects with type 2
diabetes compared to subjects without glucose intolerance.

Decreased βcell counts and fat deposition and fbrosis in the pancreas have been postulated
as reasons for the decreased pancreatic volume in type 2 diabetes.

Magnetic resonance imaging (MRI) has superior spatial resolution compared to CT, and it is
more sensitive to the intraabdominal fat than CT. Te use of MRI for the safe evaluation of
pancreatic morphology has led to studies in subjects with type 2 diabetes mellitus, and the
results of these studies showed that the pancreas is a characteristic pancreatic organ in type 2
diabetes mellitus. Imaging finding included decreased pancreatic volume, increased
pancreatic fat content, and serrated pancreatic limbus.

Tere was a signifcant correlation between pancreatic volume and homeostatic model
assessment βcell function (HOMAβ). Previous studies have suggested that morphological
changes in the pancreas in type 2 diabetes mellitus may have some effect on endogenous
insulin secretion.

Although there is concern about the possible association between morphological changes in
the pancreas and diabetesrelated complications, there have been no reports examining the
relationship between diabetesrelated complications and changes in pancreatic morphology.
This study aims to clarify the clinical signifcance of pancreatic morphological changes on
diabetesrelated complications and pathological progression in subjects with type 2 diabetes
who underwent abdominal magnetic resonance imaging(MRI).

Risk factors for Diabetes:

The following factors contribute to the risk of developing diabetes -

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Type 1 diabetes –

1).Family history of diabetes

2).Disease of the pancreas

3).Infection or illness that affects the pancreas

Type 2 diabetes –

1).Obesity

2).Family history of diabetes

3).History of gestational diabetes

4).Ethnic background

5).Old age

6).Hypertension

Gestational diabetes –

1).Family history of diabetes

2).Being overweight beforebecoming pregnant

3).Belonging to a high risk ethnic group (as mentioned above)

4).Having gestational diabetes during a previous pregnancy

5).Giving birth to a baby over 9 pounds

Symptoms:

1.Typ 1diabetes -Symptom of type 1 diabetes develop over a short period of time and include
weight loss, frequent urination, excessive thirst and hunger, weakness and fatigue, nausea
and vomiting.

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2.Type 2 diabetes –Symptoms develop slowly with some people showing no symptoms at all.
They include

any of the symptoms of type 1 diabetes, blurred vision, hard to heal skin, gum or bladder
infections, and tingling or numbness in the hands or feet.

3.Gestational diabetes –Symptoms may or may not develop during pregnancy and therefore
individuals need to be tested for the condition. Symptoms are same as for type 2 diabetes.

Complications of diabetes:

If not cared for appropriately, it may lead to the following complications –

1).Kidney disease ( Diabetic nephropathy)

2).Blindness (Diabetic retinopathy)

3).Heart disease and stroke. Diabetics are 2 to 4 times more likely to have a heart disease and
suffer a stroke.

4).Nerve damage (neuropathy). Too much sugar in the blood can injure the walls of the tiny
blood vessels (capillaries) that feed the nerves. This is especially true in the legs. This can
cause tingling, numbness, burning or pain. This usually begins at the tips of the toes or fingers
and spreads upward. Poorly controlled blood sugar could cause you to lose all sense of
feeling in the affected limbs over time.

Damage to the nerves that affect the digestive system can cause problems with nausea,
vomiting, diarrhea or constipation. For men, erectile dysfunction may be an issue.

5).Sores on feet and skin possibly resulting in amputations

6).Diabetic coma due to extremely high blood sugar

It also can be divided into two

A. Acute ፦ diabetic ketoacidosis.

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 . Hyperglycemic hyperosmolar state

B. Chronic ፦ A.microvascular complications ፦ retinopathy, macular edema, sensory and

motor neuropathy,autonomic neuropathy.

B.macrovascular complications ፦ coronary heart disease, peripheral arterial disease,

cerebrovascular disease.

How is Diabetes diagnosed?

1.Fasting blood glucose level –It is the preferred method of determining diabetes in children
and nonpregnant adults. Diabetes is diagnosed if blood glucose level is 126 milligrams per
decilitre (mg/dL) or higher after an 8-hour fast. Levels between 100-126 mg/dL are considered
prediabetes, a condition where individuals have high blood sugar but not high enough to be
classified as diabetes. Individuals with prediabetes have higher elevatedrisk of developing
T2D.

2.Hemoglobin A1c test –This is a blood test that shows how well you are controlling diabetes.
It shows the average level of blood glucose over the previous 3 months.

3.Oral glucose tolerance test (OGTT) –This is a test to check how well your body breaks down
sugar.

Diabetes is diagnosed if blood glucose level is 200mg/dL or higher after drinking a beverage
containing 75 grams of glucose dissolved in water.Gestational diabetes is diagnosed based on
blood glucose levels measured during the OGTT. Screening for type 2 diabetes in people who
have no symptoms is recommended for overweight children, overweight adults who have
other risk factors and adults over the age of 45.

Differential Diagnosis

In addition to T1DM, T2DM, any disorder that damages the pancreas can result in DM. There
are several diseases of the exocrine pancreas, including:

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 .Cystic fibrosis

. Hereditary hemochromatosis

. Pancreatic cancer

.Chronic pancreatitis

# Hormonal syndromes that can lead to impaired insulin secretion include:

. Pheochromocytoma

. Acromegaly

. Cushing syndrome

# Drug-induced insulin resistance is also in the differential of classical diabetes. These drugs
include:

. Phenytoin

. Glucocorticoids

. Estrogen

# Other diseases in the differential of diabetes mellitus include:

. Gestational diabetes

. Thyroid disorders

Treatment and management of diabetes:

Although there is no cure for diabetes, treatment and control of diabetes involves the
following:

1.Insulin injections

2.Weight loss

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3.Constant monitoring of blood glucose through frequent blood

glucose tests or self-monitoring equipments such as

glucometers.

4.Oral medications (recommended by physician) to lower blood glucose

5.Healthy diet including foods with fewer calories, an even amount of carbohydrates and
healthy monostaurated fats. Patients should work with their doctor or dietician to design a
meal plan to maintain near-normal blood glucose levels.

6.ExerciseIn all, a healthy lifestyle, insulin and oral medications to maintain normal glucose
levels are the foundations of diabetes management and treatment.

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 SUMMARY

Diabetes is a serious medical condition that affects millions of people worldwide. It can cause
various health complications and should be treated promptly to prevent long-term damage to
the body. By understanding the types, causes, symptoms, and treatment options for diabetes,
individuals can take steps to manage the condition effectively and lead a healthy life. If you
experience any symptoms of diabetes, it is crucial to seek medical attention immediately.

Remarkable morphological alterations do occur in the dentition of type I DM patients.

Type I diabetes mellitus Oral cavity can be considered as the mirror of the body as
manifestations of many systemic diseases reflect in it. Diabetes mellitus (DM), the most
common systemic disease of the millennium has broad spectrum of oral manifestations.
Advanced periodontal disease and dental caries, sialosis, xerostomia, dysgeusia, prolonged or
recurrent fungal and bacterial infections and burning mouth syndrome are well established
oral manifestations of this widely prevalent systemic disorder.

Among the two types of DM, type I DM is a disease, which commonly occurs in an age group
where the development of primary and permanent dentition takes place. It develops as a
result of synergetic effects of genetic, environmental, and immunological factors, which lead
to a progressive destruction of pancreatic beta cells, thereby causing decreased insulin
production.[3] As a result, through the direct effect of insulin deficiency and ensuing
hyperglycemia or via the more long-term effects of vascular disease, bone metabolism, and
mineral homeostasis are hampered.Hampering mineral homeostasis will have direct effect on
the hard tissues of the body namely, the bone and the teeth. These juvenile DM patients
have been found to have decreased vertical height of the alveolar bone and decreased
cephalometric measurements. Furthermore, in odontogenesis, mineralization defects are
proved and ameloblast's function is hampered due to the absence of secretory proteins,
resulting in enamel and dentin defects. As such metabolic disturbances can cause dental
anomalies, this study is aimed at identifying if any morphological alterations occur in the
dentition of type I DM patients.

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Dependable Diagnostic Biomarkers? Curr Rheumatol Rev. 2019;15(4):269-276. [PubMed]

2.Klein BE, Klein R, Moss SE, Cruickshanks KJ. Parental history of diabetes in a population-
based study. Diabetes Care. 1996 Aug;19(8):827-30. [PubMed]

3.Barnett AH, Eff C, Leslie RD, Pyke DA. Diabetes in identical twins. A study of 200 pairs.
Diabetologia. 1981 Feb;20(2):87-93. [PubMed]

4. Rudenski, A. S. et al. Natural history of pancreatic islet Bcell function in type 2 diabetes
mellitus studied over six years by homeostasis model assessment Diabet Med5(1), 36–41
(1988)

5. Alzaid, A., Aideyan, O. & Nawaz, S. Te size of the pancreas in diabetes mellitus. Diabet.
Med.10(8), 759763 (1993).

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