REGULATION OF BLOOD SUGAR

Seminar-5By

Dr.M.S.Bala Vidyadhar

CONTENTS Introduction

History & Basic considerations

Normal Physiology

Mechanisms of Blood Sugar Regulation

Hormonal Role

Alteration of blood glucose levels

Diabetes Mellitus

Public Health Scenario

Conclusion & References

Previous year questions

INTRODUCTION Blood sugar concentration, or glucose level, refers to

the amount of glucose present in the blood of a human.

Normally, in mammals the blood glucose level is

maintained at a reference range between about 3.6 and

5.8 mM (mmol/l).

It is tightly regulated as a part of metabolic

homeostasis.

HISTORY 1552 BC: Ebers Papyrus in ancient Egypt. First known written

description of diabetes.

1st Century AD: Arateus — “Melting down of flesh and limbs into urine.”

1776: Matthew Dobson conducts experiments showing sugar in blood and urine of diabetics.

Mid 1800s: Claude Bernard studies the function of the pancreas and liver, and their roles in homeostasis.

1869: Paul Langerhans identifies cells of unknown function in the pancreas. These cells later are named “Islets of Langerhans.”

HISTORY CONTD. 1889: Pancreatectomized dog develops fatal diabetes.

1921: Insulin “discovered” — effectively treated

pancreatectomized dog.

1922: First human treated with insulin. Eli Lilly begins

mass production.

1923: Banting and Macleod win Nobel Prize for work with

insulin.

1983: Biosynthetic insulin produced.

2001: Human genome sequence completed.

BASIC CONSIDERATIONS

Blood sugar/Glucose concentration:

The amount of Glucose ( in mg) in 1 dl of the human

blood. Measured as mg/ dl or mg %.

Normal Blood Glucose

Fasting state : 60 to 100 mg%

Postprandial : 100 to 140 mg %

Hyperglycemia:

It is a condition in which an excessive amount

of glucose circulates in the blood plasma. This is

generally a blood sugar level higher than

11.1 mmol/l (200 mg/dl).

Hypoglycemia:

It is a condition in  which blood sugar (or

blood glucose)  concentrations fall below a level 

necessary to properly support the body's need for energy 

and  stability throughout its cells.

We eat food containing carbohydrates

The carbohydrates are fully digested to glucose which is absorbed

CELL GROWTH AND ENERGY METABOLISM

TCA CycleKreb’s Cycle

CoA

Acetyl-CoA

Proteins

Amino acids

Fats

Fatty acids

CarbohydratesGlucose Pyruvate

ATP

INTERMEDIARY METABOLISM OF FUELS

NORMAL BLOOD GLUCOSE LEVEL

In normal persons, blood glucose level is controlled within a

narrow range.

In the early morning after overnight fasting, the blood

glucose level is low ranging between 70 and 110 mg/dL of

blood.

Between first and second hour after meals (postprandial),

the blood glucose level rises to 100 to 140 mg/dL.

Glucose level in blood is brought back to normal at the end

of second hour after the meals.

Blood glucose regulating mechanism is operated through liver

and muscle by the influence of the pancreatic hormones –

insulin and glucagon.

Many other hormones are also involved in the regulation of

blood glucose level.

Among all the hormones, insulin is the only hormone that

reduces the blood glucose level and it is called the anti-

diabetogenic hormone.

The hormones which increase blood glucose level are called

diabetogenic hormones or anti-insulin hormones.

NECESSITY OF REGULATION OF BLOOD GLUCOSE LEVEL Regulation of blood glucose (sugar) level is very

essential because:

Glucose is the only nutrient that is utilized for energy

by many tissues such as

I. brain tissues,

II. retina

III. germinal epithelium of the gonads.

ROLE OF LIVER

Liver serves as an important glucose buffer system.

When blood glucose level increases after a meal, the excess

glucose is converted into glycogen and stored in liver.

Afterwards, when blood glucose level falls, the glycogen in

liver is converted into glucose and released into the blood.

The storage of glycogen and release of glucose from liver are

mainly regulated by insulin and glucagon.

GLUCOSE HOMEOSTASIS – INSULIN AND GLUCAGON

HORMONAL REGULATION There are two types of mutually antagonistic metabolic

hormones affecting blood glucose levels:

1. Catabolic hormones (such as glucagon, growth

hormone, cortisol and catecholamines) which increase

blood glucose;

2. Anabolic hormone (insulin), which decreases blood

glucose.

ROLE OF PANCREAS The pancreas detects the change in blood glucose

concentration and releases the appropriate hormone:

ROLES OF INSULIN AND GLUCAGON IN REGULATING BLOOD GLUCOSE

GLUCAGON Glucagon binding to its' receptors on the surface of liver cells

triggers an increase in cAMP production leading to an

increased rate of glycogenolysis by activating glycogen

phosphorylase via the PKA-mediated cascade.

This is the same response hepatocytes have to epinephrine

release.

The resultant increased levels of G6P in hepatocytes is

hydrolyzed to free glucose, by glucose-6-phosphatase, which

then diffuses to the blood.

GLUCAGON CONTD.. The glucose enters extrahepatic cells where it is re-

phosphorylated by hexokinase.

Since muscle and brain cells lack glucose-6-phosphatase,

the glucose-6-phosphate product of hexokinase is retained

and oxidized by these tissues.

INSULIN Insulin stimulates extrahepatic uptake of glucose from the

blood and inhibits glycogenolysis in extrahepatic cells and

conversely stimulates glycogen synthesis.

As the glucose enters hepatocytes it binds to and inhibits

glycogen phosphorylase activity.

The binding of free glucose stimulates the

de_phosphorylation of phosphorylase thereby, inactivating

it.

When blood glucose levels are low, the liver does not compete

with other tissues for glucose since the extra-hepatic uptake of

glucose is stimulated in response to insulin.

Conversely, when blood glucose levels are high extra-hepatic

needs are satisfied and the liver takes up glucose for

conversion into glycogen for future needs.

Under conditions of high blood glucose, liver glucose levels

will be high and the activity of glucokinase will be elevated.

The G6P produced by glucokinase is rapidly converted to G1P

by phosphoglucomutase, where it can then be incorporated

into glycogen.

REGULATION OF GLUCOSE METABOLISM DURING EXERCISE

Glucagon secretion increases during exercise to promote

liver glycogen breakdown (glycogenolysis)

Epinephrine and Norepinephrine further increase

glycogenolysis

Cortisol levels also increase during exercise for protein

catabolism for later gluconeogenesis.

Thyroxine promotes glucose catabolism

Glucose uptake is enhanced by insulin.

Exercise may enhance insulin’s binding to

receptors on the muscle fiber.

Up-regulation (receptors) occurs with insulin after

4 weeks of exercise to increase its sensitivity

(diabetic importance).

Hormone Tissue of Origin Metabolic Effect

Effect on Blood

GlucoseInsulin

Pancreatic β-cells

1) Enhances entry of glucose into cells; 2) Enhances storage of glucose as glycogen, or

conversion to fatty acids; 3) Enhances synthesis of fatty acids and

proteins; 4) Suppresses breakdown of proteins into

amino acids, of adipose tissue into free fatty acids.

Lowers

Somatostatin

Pancreatic D- Cells

1) Suppresses glucagon release from α cells (acts locally);

2) Suppresses release of Insulin, Pituitary tropic hormones, gastrin and secretin

Raises

Glucagon

Pancreaticα-cells

1) Enhances release of glucose from glycogen; 2) Enhances synthesis of glucose from amino

acids Raises

Epinephrine Adrenal medulla 1) Enhances release of glucose from glycogen;

2) Enhances release of fatty acids from

adipose tissue.

Raises

cortisol Adrenal cortex 1) Enhances gluconeogenesis;

2) Antagonizes Insulin. Raises

ACTH Anterior pituitary

1) Enhances release of cortisol; 2) Enhances release of fatty acids from adipose

tissue. 3) Inhibiting uptake by extrahepatic tissues. Raises

Growth hormone

Anterior Pituitary 1)Antagonizes Insulin,

2) Inhibiting uptake by extrahepatic tissues. Raises

thyroxine Thyroid 1) Enhances release of glucose from glycogen; 2) Enhances absorption of sugars from

intestineRaises

INSULIN SYNTHESIS AND SECRETION

Insulin is small protein, with a molecular weight of about 6000

Daltons.

It is composed of two chains held together by disulfide bonds.

The amino acid sequence is highly conserved, and insulin from

one mammal almost certainly is biologically active in another.

Many diabetic patients are treated with insulin extracted from

pig pancreas.

Insulin is synthesized in beta cells in the pancreas.

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.

NORMAL PHYSIOLOGY Glucose controls Insulin and Glucagon release

LIVER AND KIDNEY Major source of net endogenous glucose production.

Accomplished by gluconeogenesis and glycogenolysis

when glucose is low

And of glycogen synthesis when glucose is high.

Can oxidize glucose for energy and convert it to fat

which can be incorporated into VLDL for transport.

METABOLIC EFFECTS OF INSULIN - IN THE LIVER

MUSCLE

Can convert glucose to glycogen.

Can convert glucose to pyruvate through glycolysis - further

metabolized to lactate or transaminated to alanine or

channeled into the TCA cycle.

In the fasting state, can utilize FA for fuel and mobilize

amino acids by proteolysis for transport to the liver for

gluconeogenesis.

Can break down glycogen

But cannot liberate free glucose into the circulation.

METABOLIC EFFECTS OF INSULIN - IN THE MUSCLE

ADIPOSE TISSUE Can store glucose by conversion to fatty acids and combine

these with VLDL to make triglycerides.

In the fasting state can use fatty acids for fuel by beta

oxidation.

METABOLIC EFFECTS OF GLUCAGON

INSULIN – ANABOLIC GLUCAGON - CATABOLIC

Metabolic Action Insulin Glucagon

Glycogen synthesis ↑ ↓

Glycolysis (energy release) ↑ ↓

Lipogenesis ↑ ↓

Protein synthesis ↑ ↓

Glycogenolysis ↓ ↑

Gluconeogenesis ↓ ↑

Lipolysis ↓ ↑

Ketogenesis ↓ ↑

BRAIN Converts glucose to CO2 and H2O.

Can use ketones during starvation.

Is not capable of gluconeogenesis.

Has no glycogen stores.

Brain is the major glucose consumer

Consumes 120 to 150 g of glucose per day

Glucose is virtually the sole fuel for brain.

BRAIN Brain does not have any fuel stores like glycogen.

Can’t metabolize fatty acids as fuel

Requires oxygen always to burn its glucose

Can not live on anaerobic pathways

One of most fastidious and voracious of all organs

Oxygen and glucose supply can not be interrupted

ALTERATIONS IN BLOOD SUGAR LEVELS

Based on the level of blood sugar in the body, two

major types of disorders occur:

1. Hyperglycemia

2. Hypoglycemia

HYPERGLYCEMIA A condition in which an excessive amount of glucose

circulates in the blood plasma (>10 mmol/L or 180 mg/dl).

Temporary hyperglycemia is often benign and asymptomatic.

Blood glucose levels can rise well above normal for short

periods without producing any permanent effects or

symptoms.

However, chronic hyperglycemia at levels more than slightly

above normal can produce a very wide variety of serious

complications over a period of years, including kidney

damage, neurological damage, cardiovascular damage,

damage to the retina etc.

Exerts high osmotic pressure in extracellular fluid, causing

cellular dehydration

Excess of glucose begins to be lost from the body in the urine:

GLYCOSURIA.

DIABETES MELLITUS Diabetes mellitus is a metabolic disorder characterized by

high blood glucose level, associated with other

manifestations.

‘Diabetes’ means ‘polyuria’ and ‘mellitus’ means ‘honey’.

The name ‘diabetes mellitus’ was coined by Thomas Willis,

who discovered sweetness of urine from diabetics in 1675.

In most of the cases, diabetes mellitus develops due to

deficiency of insulin.

CLASSIFICATION There are several forms of diabetes mellitus, which occur due

to different causes.

Diabetes may be primary or secondary.

Primary diabetes is unrelated to another disease.

Secondary diabetes occurs due to damage or disease of

pancreas by another disease or factor.

Recent classification divides primary diabetes mellitus into

two types, Type I and Type II.

TYPE I DIABETES MELLITUS Type I diabetes mellitus is due to deficiency of insulin because

of destruction of β-cells in Islets Of Langerhans.

This type of diabetes mellitus may occur at any age of life.

But, it usually occurs before 40 years of age and the persons

affected by this require insulin injection.

So it is also called Insulin-dependent Diabetes Mellitus

(IDDM).

When it develops at infancy or childhood, it is called juvenile

diabetes.

TYPE I DIABETES MELLITUS Type I diabetes mellitus develops rapidly and progresses

at a rapid phase. It is not associated with obesity, but may be associated

with acidosis or ketosis. Causes of type I diabetes mellitus:1. Degeneration of β-cells in the islets of Langerhans of

pancreas2. Destruction of β-cells by viral infection3. Congenital disorder of β-cells4. Destruction of β-cells during autoimmune diseases.5. It is due to the development of antibodies against β-

cells

OTHER FORMS OF TYPE 1 DIABETES MELLITUS

Latent autoimmune diabetes in adults (LADA):

1. LADA or slow onset diabetes has slow onset and slow

progress than IDDM and it occurs in later life after 35 years.

2. It may be difficult to distinguish LADA from type II diabetes

mellitus, since pancreas takes longer period to stop secreting

insulin.

Maturity onset diabetes in young individuals (MODY): It

is a rare inherited form of diabetes mellitus that occurs before

25 years. It is due to hereditary defects in insulin secretion.

TYPE II DIABETES MELLITUS Type II diabetes mellitus is due to insulin resistance (failure of

insulin receptors to give response to insulin).

So, the body is unable to use insulin.

About 90% of diabetic patients have type II diabetes mellitus.

It usually occurs after 40 years.

Only some forms of Type II diabetes require insulin. In most

cases, it can be controlled by oral hypoglycemic drugs.

So it is also called Non Insulin Dependent Diabetes Mellitus

(NIDDM).

TYPE II DIABETES MELLITUS Type II diabetes mellitus may or may not be associated with

ketosis, but often it is associated with obesity.

Causes for type II diabetes mellitus:

In this type of diabetes, the structure and function of β-cells

and blood level of insulin are normal.

But insulin receptors may be less, absent or abnormal,

resulting in insulin resistance.

Common causes of insulin resistance are:

1. Genetic disorders (significant factors causing type II

diabetes mellitus)

2. Lifestyle changes such as bad eating habits and

physical inactivity, leading to obesity

3. Stress.

TYPE II DIABETES MELLITUS

Other forms :

Gestational diabetes:

It occurs during pregnancy.

It is due to many factors such as hormones secreted

during pregnancy, obesity and lifestyle before and during

pregnancy.

Usually, diabetes disappears after delivery of the child.

However, the woman has high risk of development of

type II diabetes later.

Pre-diabetes:

It is also called chemical, subclinical, latent or borderline

diabetes.

It is the stage between normal condition and diabetes.

The person does not show overt (observable) symptoms

of diabetes but there is an increase in blood glucose level.

Though pre-diabetes is reversible, the affected persons

are at a high risk of developing type II diabetes mellitus.

DIFFERENCES BETWEEN TYPE I AND TYPE II DIABETES MELLITUS

SECONDARY DIABETES MELLITUS

Secondary diabetes mellitus is rare and only about 2% of

diabetic patients have secondary diabetes.

It may be temporary or may become permanent due to the

underlying cause.

Endocrine disorders such as gigantism, acromegaly and

Cushing’s syndrome. Hyperglycemia in these conditions causes excess stimulation

of β-cells. Constant and excess stimulation, in turn causes burning out

and degeneration of β-cells. The β-cell exhaustion leads to permanent diabetes mellitus.

CAUSES OF SECONDARY DIABETES MELLITUS

Damage of pancreas due to disorders such as chronic

pancreatitis, cystic fibrosis and hemochromatosis (high iron

content in body causing damage of organs).

Pancreatectomy (surgical removal)

Liver diseases such as hepatitis C and fatty liver

Autoimmune diseases such as celiac disease

Excessive use of drugs like antihypertensive drugs (beta

blockers and diuretics), steroids, oral contraceptives,

chemotherapy drugs, etc.

Excessive intake of alcohol and opiates.

SIGNS AND SYMPTOMS Various manifestations of diabetes mellitus develop because of

three major setbacks of insulin deficiency.

1. Increased blood glucose level (300 to 400 mg/dL) due to

reduced utilization by tissue

2. Mobilization of fats from adipose tissue for energy

purpose, leading to elevated fatty acid content in blood. This

causes deposition of fat on the wall of arteries and

development of atherosclerosis.

3. Depletion of proteins from the tissues.

GLUCOSURIA

Glucosuria is the loss of glucose in urine.

Normally, glucose does not appear in urine. When

glucose level rises above 180 mg/dL in blood,

glucose appears in urine.

It is the renal threshold level for glucose.

OSMOTIC DIURESIS

Osmotic diuresis is the diuresis

caused by osmotic effects.

Excess glucose in the renal tubules develops osmotic

effect.

Osmotic effect decreases the reabsorption of water from

renal tubules, resulting in diuresis.

It leads to polyuria and polydipsia.

ASTHENIA Loss of strength is called asthenia. Body becomes very weak

because of this.

Asthenia occurs due to protein depletion, which is caused by

lack of insulin.

Lack of insulin causes decrease in protein synthesis and

increase in protein breakdown, resulting in protein depletion.

Protein depletion also occurs due to the utilization of proteins

for energy in the absence of glucose utilization.

ACIDOSIS

During insulin deficiency, glucose cannot be utilized by the

peripheral tissues for energy.

So, a large amount of fat is broken down to release energy.

It causes the formation of excess ketoacids, leading to

acidosis.

One more reason for acidosis is that the ketoacids are excreted

in combination with sodium ions through urine (ketonuria).

Sodium is exchanged for hydrogen ions, which diffuse from

the renal tubules into ECF adding to acidosis.

ACETONE BREATHING In cases of severe ketoacidosis, acetone is expired in the

expiratory air, giving the characteristic acetone or fruity

breath odor.

It is a life-threatening condition of severe diabetes.

KUSSMAUL BREATHING Kussmaul breathing is the increase in rate and depth of

respiration caused by severe acidosis.

CIRCULATORY SHOCK Osmotic diuresis leads to dehydration, which

causes circulatory shock. It occurs only in severe

diabetes.

COMA

Due to Kussmaul breathing, large amount of carbondioxide 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.

Increase in the blood glucose level develops hyperosmolarity

of plasma which also leads to coma. It is called hyperosmolar

coma.

COMPLICATIONS OF DIABETES MELLITUS

Prolonged hyperglycemia in diabetes mellitus causes

dysfunction and injury of many tissues, resulting in some

complications.

Development of these complications is directly proportional to

the degree and duration of hyperglycemia.

However, the patients with well controlled diabetes can

postpone the onset or reduce the rate of progression of these

complications.

Initially, the untreated chronic hyperglycemia affects the blood vessels, resulting in vascular complications like atherosclerosis.

Vascular complications are responsible for the development of most of the complications of diabetes such as:

Complications contd.

Cardiovascular complications like:

i. Hypertension

ii. Myocardial infarction

Degenerative changes in retina called diabetic retinopathy.

Degenerative changes in kidney known as diabetic

nephropathy

Degeneration of autonomic and peripheral nerves called

diabetic neuropathy.

Complications contd.

ORAL MANIFESTATIONS Due to the systemic effects of diabetes mellitus, various

oral manifestations occur:

Gingivitis & periodontitis

Periradicular osteolytic inflammatory lesions

(abscesses, granulomas,etc)

Loss of teeth

Xerostomia and altered salivary composition

Lesions of oral mucosa and tongue.

GINGIVITIS & PERIODONTITIS Thickening of blood vessels

is a complication of diabetes that may increase risk for gum disease.

Blood vessels deliver oxygen and nourishment to body tissues, including the mouth, and carry away the tissues' waste products.

Diabetes causes blood vessels to thicken, which slows the flow of nutrients and the removal of harmful wastes.

This can weaken the resistance of gum and bone tissue to infection.

DIAGNOSTIC TESTS FOR DIABETES MELLITUS

Diagnosis of diabetes mellitus includes the determination

of:

1. Fasting blood glucose

2. Postprandial blood glucose

3. Glucose tolerance test (GTT)

4. Glycosylated (glycated) hemoglobin.

Determination of glycosylated hemoglobin is commonly

done to monitor the glycemic control of the persons already

diagnosed with diabetes mellitus.

Abnormal response in diagnostic tests:

Abnormal response in diagnostic tests occurs in conditions

like pre-diabetes.

There is an increased fasting blood glucose level or

impaired (decreased) glucose tolerance.

GLYCAEMIC INDEX The glycemic index or glycaemic index (GI) is a number

associated with a particular type of food that indicates the

food’s effect on a person’s blood glucose (also called blood

sugar) level.

The number typically ranges between 50 and 100, where 100

represents the standard, an equivalent amount of pure glucose.

The glycemic index is usually applied in the context of the

quantity of the food and the amount of carbohydrate in the

food that is actually consumed.

GLYCAEMIC INDEX CONTD.

Foods with carbohydrates that break down quickly during

digestion and release glucose rapidly into the bloodstream

tend to have a high GI.

Foods with carbohydrates that break down more slowly,

releasing glucose more gradually into the bloodstream, tend

to have a low GI.

Fruits like watermelon and ripe bananas have high glycemic

index whereas strawberries have low glycemic index.

TREATMENT FOR DIABETES MELLITUS Type I diabetes mellitus:

Type I diabetes mellitus is treated by exogenous

insulin.

Since insulin is a polypeptide, it is degraded in GI

tract if taken orally.

So, it is generally administered by subcutaneous

injection.

Type II diabetes mellitus:

Type II diabetes mellitus is treated by oral hypoglycemic

drugs.

Patients with longstanding severe diabetes mellitus may

require a combination of oral hypoglycemic drugs with

insulin to control the hyperglycemia.

Oral hypoglycemic drugs are classified into three

types.

Insulin secretagogues:

These drugs decrease the blood glucose level by

stimulating insulin secretion from β-cells.

Sulfonylureas (tolbutamide, gluburide, glipizide, etc.)

are the commonly available insulin secretagogues.

Insulin sensitizers:

These drugs decrease the blood glucose level by

facilitating the insulin action in the target tissues.

Examples are biguanides (metformin) and

thiazolidinediones (pioglitazone and rosiglitazone)

Alpha glucosidase inhibitors:

These drugs control blood glucose level by inhibiting

α-glucosidase.

This intestinal enzyme is responsible for the conversion of

dietary and other complex carbohydrates into glucose and

other monosaccharides, which can be absorbed from

intestine.

Examples of α-glucosidase inhibitors are acarbose and

meglitol.

HYPERINSULINISM

Hyperinsulinism is the hypersecretion of insulin.

Cause:

Hyperinsulinism occurs due to the tumor of β-cells in the

Islets of Langerhans.

Signs and Symptoms:

Hypoglycemia

Blood glucose level falls below 50 mg/dL.

Manifestations of central nervous system

Manifestations of central nervous system occur when the

blood glucose level decreases. All the manifestations are

together called neuroglycopenic symptoms.

Initially, the activity of neurons increases, resulting in

nervousness, tremor all over the body and sweating.

If not treated immediately, it leads to clonic convulsions and

unconsciousness. Slowly, the convulsions cease and coma

occurs due to the damage of neurons.

MANAGEMENT IN DENTAL CLINIC

The main objective is to maintain blood glucose levels as

close to normal as possible.

To minimize the risk of an intra-operative emergency,

clinicians need to consider some issues before initiating

dental treatment.

Medical history:

Glucose levels

Frequency of hypoglycemic episodes

Medication, dosage and times.

Consultation

MANAGEMENT IN DENTAL CLINIC

Scheduling of visits

Morning appt. (endogeneous cortisol)

Do not coincide with peak activity.

Diet

Ensure that the patient has eaten normally and taken

medications as usual.

Blood glucose monitoring

Measured before beginning. (<70 mg/dL)

Prophylactic antibiotics Established infection Pre-operation contamination wound Major surgery

During treatmentThe most complication of DM occur is hypoglycemia

episode.Hyperglycemia

After treatment Infection controlDietary intakeMedications : salicylates increase insulin secretion and

sensitivity avoid aspirin.

EMERGENCY MANAGEMENT

Initial signs : mood changes, decreased spontaneity,

hunger and weakness.

Followed by sweating, incoherence, tachycardia.

Consequenced in unconsiousness, hypotention,

hypothermia, seizures, coma, even death.

EMERGENCY MANAGEMENT

15 grams of fast-acting oral carbonhydrate.

Measurement of blood sugar levels.

Loss of conscious, 25-30ml 50% dextrose solution iv.

over 3 min period.

Glucagon 1mg.

EMERGENCY MANAGEMENT

Severe hyperglycemia

A prolonged onset

Ketoacidosis may develop with nausea, vomiting,

abdominal pain and acetone odor.

Difficult to different hypo- or hyper-glycemia.

Hyperglycemia need medication intervention and insulin

administration.

While emergency, give glucose first !

Small amount is unlikely to cause significant harm.

RECENT ADVANCES IN

RESEARCH

TYPE 1 1/2 DIABETES: MYTH OR REALITY?

There is a group of individuals (Type 1 1/2 diabetes), who

present like typical NIDDM, but have some of the

immunological and clinical features of IDDM.

Comparative studies in the area of cytokine production, T cell

reactivity and autoantibody clustering between classic Type 1

diabetes and Type 1 1/2 diabetes patients are needed as are

studies with the animal model of Type 1 1/2 diabetes,

Psammomys obesus.

Ref: Type 1 1/2 diabetes: myth or reality? Juneja r, palmer jp. Autoimmunity. 1999;29(1):65-83.

ESTIMATION OF BLOOD GLUCOSE LEVELS FROM GCF

The conventional laboratory methods employed to detect blood glucose are time consuming and require elaborative equipments.

The advent of blood glucose monitors allows the clinician to detect blood glucose at chair side.

Studies suggest a significant correlation was found between gingival crevicular blood glucose levels and capillary finger stick blood glucose levels in diabetics and non- diabetics.

The result suggests that Gingival Crevicular blood is an efficient diagnostic tool for estimation of blood glucose levels in patients with or without diabetes mellitus.

Ref: Estimation of Blood Glucose levels from GCF in patients with or without Diabetes Mellitus Tajinder Bansal, Ruchika Bansal, Deepa Jatti, Jithender Reddy Kubbi, Irfana Khursheed J Adv Med Dent Scie Res 2014;2(3):4-9.

PRE-DIABETES Prediabetes is the medical stage in which not all of the

symptoms required to label a person as diabetic are present, but

blood sugar is abnormally high. This stage is often referred to as

the "grey area.“

Impaired fasting glycaemia

Impaired glucose tolerance

The American College of Endocrinology (ACE) and

the American Association of Clinical Endocrinologists (AACE)

have developed lifestyle intervention guidelines for preventing

the onset of type 2 diabetes.

PUBLIC HEALTH SCENARIO

DIABETES MELLITUS Diabetes is part of a larger global epidemic of non communicable

diseases.

It has become a major public health challenge globally.

This disease affects 6.6% (285 million people) of the world’s

population in the 20--‐79 years age group.

According to the International Diabetic Federation (IDF), this

number is expected to grow to 380 million by 2025.

The IDF published findings revealing that in 2007, the country with

the largest numbers of people with diabetes is India (40.9 million),

followed by China (39.8 million), the United States (19.2 million),

Russia (9.6 million) and Germany (7.4 million).

INTERNATIONAL DIABETES FEDERATION

The International Diabetes Federation (IDF) is an umbrella

organisation of over 200 national diabetes associations in

over 160 countries.

It represents the interests of the growing number of people

with diabetes and those at risk.

The Federation has been leading the global diabetes

community since 1950.

IDF’s mission is to promote diabetes care, prevention and a

cure worldwide.

DIABETES CONTROL IN INDIA India is home to forty million people with diabetes—nearly 15

percent of the global diabetes burden and projections show

that this will increase to seventy million by 2025.

Diabetes disproportionately affects people of working ages

and accounts for US$2.2 billion in annual health care costs in

India alone.

Ref: National programme on prevention and control of diabetes in India: Need to

focus. Ramesh Verma, Pardeep Khanna, Bharti. Australasian Medical Journal

[AMJ 2012, 5, 6, 310--‐315]

RECENT ADVANCES

The “National Diabetes control program” was launched on a

pilot basis during the VIIth Five Year Plan in some districts of

Tamil Nadu, Karnataka and Jammu & Kashmir.

Due to paucity of funds in subsequent years this programme

could not be expanded further in remaining states.

However, during 1995--‐96, a sum of 12 lakh rupees was

allocated for the programme and subsequently in 1997--‐98

an allocation of one core was made.

National diabetes prevalence is 4.3 percent in India.

Prevalence is higher among people living in cities compared to

rural areas, those in the South compared to the North, and those

of high socioeconomic status (SES) compared to low SES.

During 1971–2000, urban diabetes prevalence rose from 1.2

percent to 12.1 percent.

However, studies show that diabetes has risen rapidly in rural

areas, with a threefold increase (from 2.4 percent to 6.4 percent)

in rural southern India over a fourteen-year period. Ref: Finding A Policy Solution To India’s Diabetes Epidemic.

by Karen Siegel, K.M. Venkat Narayan, and Sanjay Kinra

CURRENT POLICIES AND PRACTICES

The Ministry of Health spearheaded a national consultation in

2005 to “identify action pathways and partnerships for

implementing the Global Strategy in the context of India.”

The pilot phase of the National Program on Diabetes, CVD,

and Stroke (NPCDS) was launched in seven states in January

2008.

No national awareness survey has been performed, but a recent

study in Chennai found that awareness of diabetes as a public

health priority and knowledge of diabetes prevention is poor,

especially among women and people with little education.

Although India accounts for approximately 15 percent of the

global burden of diabetes, it contributes 1 percent of the

world’s diabetes research.

There are few data on the quality of diabetes care, no national

monitoring system for processes and outcomes of care, and no

translational research to turn knowledge into action.

Only two national diabetes surveys have been conducted since

1975.

The Integrated Disease Surveillance (IDS) program,

launched in 2004, analyzes population wide chronic disease

risk factors, but it needs improvement.

More recently National Heart, Lung, and Blood Institute

(NHLBI) Chronic Disease Initiative and the International

Diabetes Federation (IDF) BRIDGES Initiative provide

potential for Indian researchers to work with policymakers and

uncover practical, country-specific solutions.

Ref: Ministry of Health and FamilyWelfare, “Pilot Phase of the National

Programme for Prevention and Control of Diabetes, Cardio-Vascular Diseases,

and Stroke Launched,” Press Release, 4 January 2008,

MUMBAI, INDIA – SEPTEMBER 30, 2013 Sanofi, IDF and PHFI partner to fight diabetes among children in

India:

Sanofi (EURONEXT: SAN and NYSE: SNY), the International

Diabetes Federation (IDF) and Public Health Foundation of India

(PHFI) announced their first joint public health initiative in India,

KiDS (Kids and Diabetes in Schools).

For children with Type 1 diabetes, the project aims to encourage a safe

and supportive school environment to manage their diabetes and avoid

discrimination.

In addition, the program will raise awareness on diabetes (Type 1 and

Type 2) and benefits of healthy nutrition and exercise habits among

school children.

RECOGNITION PROGRAMS

The Consultative Section on Diabetes Education (DECS) of

the International Diabetes Federation (IDF) was established

in 1994.

One of DECS’ functions is to conduct and/or stimulate the

development of programmes and activities relevant to

diabetes education worldwide.

PROGRAMMES THAT ARE CURRENTLY RECOGNIZED BY IDF:

2015-2017:

Certificate Course on Diabetology (CCD) by the Diabetic

Association of Bangladesh - DAB (Bangladesh)

Certificate Course in Gestational Diabetes Mellitus (CCGDM) by

the Public Health Foundation of India - PHFI (India)

Certified Diabetes Educator-India (CDEI) by the Manav Seva

Foundation Inc. Not for Profit Corporation 501©3, USA (India)

Diabetic Foot Workshop for Nurses by the Endocrinology &

Metabolism Research Institute of Tehran University of Medical

Sciences (Iran)

Comprehensive Course in Diabetes Management by the

Endocrinology & Metabolism Research Institute of Tehran

University of Medical Sciences (Iran).

Intensive Training Course for Diabetes Educators by

the Philippine Center for Diabetes Education Foundation, Inc.

(Philippines)

MSc, Postgraduate Diploma and Postgraduate Certificate in

Diabetes by the University of Leicester (UK)

Masters (MSc) in Diabetes by the University of South Wales

(UK)

Postgraduate Diabetes Diploma by the Cardiff University (UK)

CONCLUSION

REFERENCES: Essentials of medical physiology by Y.Sembuligam.(6th edition)

Glucose Homeostasis-Counter Regulation by Dr.Sarma.R.V.S.N

M.D., Consultant Physician and Chest Specialist

https://en.wikipedia.org/wiki/Blood_sugar_regulation?oldid=664618652

Understanding the processes behind the regulation of blood

glucose by Pat James, PhD; Roger McFadden, MSc. 20th April

2004 Vol 100 No 16 www.nursingtimes.net.

National programme on prevention and control of diabetes in

India: Need to focus. Ramesh Verma, Pardeep Khanna, Bharti.

Australasian Medical Journal [AMJ 2012, 5, 6, 310--‐315].

REFERENCES CONTD Ministry of Health and FamilyWelfare, “Pilot Phase of the

National Programme for Prevention and Control of

Diabetes, Cardio-Vascular Diseases, and Stroke Launched,”

Press Release, 4 January 2008.

Finding A Policy Solution To India’s Diabetes Epidemic. by

Karen Siegel, K.M. Venkat Narayan, and Sanjay Kinra

http://content.healthaffairs.org/content/27/4/1077.full.html

Sanofi, IDF and PHFI partner to fight diabetes among

children in India :

http://www.idf.org/diabetesatlas/5e/Update2012

REFERENCES CONTD National Program for Prevention and Control of Diabetes,

CVD and Stroke in India: Dr Sudhir Gupta Chief Medical

Officer (Non Communicable Diseases), Directorate General

of Health Services, Ministry of Health & Family Welfare, New

Delhi, India.

Recent developments in diabetes control and prevention in

India by H.T.Pandve, P.S.Chawla, K.Fernandez, S.A.Singru:

Int J Diab Dev Ctries, July-September 2010,Vol.30, Issue 3

Normal Regulation of Blood Glucose The Important Roles of

Insulin and Glucagon: Diabetes and Hypoglycemia by

James Norman M D, FACS, FACE

REFERENCES CONTD

Ref: Type 1 1/2 diabetes: myth or reality? Juneja

r, palmer jp. Autoimmunity. 1999;29(1):65-83.

Ref: Estimation of Blood Glucose levels from GCF in

patients with or without Diabetes Mellitus Tajinder

Bansal, Ruchika Bansal, Deepa Jatti, Jithender Reddy

Kubbi, Irfana Khursheed J Adv Med Dent Scie Res

2014;2(3):4-9.

www.wikipedia.com

www.google.com

PREVIOUS YEAR QUESTIONS Endocrine action on blood sugar level in DM- RGUHS

(May-2010). 20 mks.

Regulation of Blood Sugar-RGUHS (Sept.2005).20 mks

Diabetes Mellitus – RGUHS (2002).20 mks.

Homeostasis – RGUHS (1995). 10mks.

Auto- Immune diseases-RGUHS (2013) (7 mks)

Diabetes Mellitus- Manipal University (2011-April).20

mks.

THANK YOU