regulation of blood sugar

Seminar-5
By
Dr.M.S.Bala Vidyadhar

 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

 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.

 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.”

 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.

 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 Cycle
Kreb’s Cycle
Proteins
Amino acids
Fats
Fatty acids
Carbohydrates
Glucose Pyruvate
ATP

 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.

 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.

 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.

 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.

 The pancreas detects the change in blood glucose
concentration and releases the appropriate hormone:

 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.

 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 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.

 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
Glucose
Insulin
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
Somatosta
tin 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
Pancreatic
α-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
intestine
Raises

 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.

 Glucose controls Insulin and Glucagon release

 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.

 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.

 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 Action Insulin Glucagon
Glycogen synthesis ↑ ↓
Glycolysis (energy release) ↑ ↓
Lipogenesis ↑ ↓
Protein synthesis ↑ ↓
Glycogenolysis ↓ ↑
Gluconeogenesis ↓ ↑
Lipolysis ↓ ↑
Ketogenesis ↓ ↑

 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 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

 Based on the level of blood sugar in the body, two
major types of disorders occur:
1. Hyperglycemia
2. Hypoglycemia

 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 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.

 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 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 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
pancreas
2. Destruction of β-cells by viral infection
3. Congenital disorder of β-cells
4. Destruction of β-cells during autoimmune diseases.
5. It is due to the development of antibodies against β-
cells

 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 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 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.

 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.

 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.

 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.

 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 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 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.

 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.

 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.

 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 is the increase in rate and depth of
respiration caused by severe acidosis.

 Osmotic diuresis leads to dehydration, which
causes circulatory shock. It occurs only in severe
diabetes.

 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.

 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.

 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.

 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.

 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.

 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.

 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.

 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 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.

 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

 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 treatment
 The most complication of DM occur is hypoglycemia
episode.
 Hyperglycemia
 After treatment
 Infection control
 Dietary intake
 Medications : salicylates increase insulin secretion and
sensitivity avoid aspirin.

 Initial signs : mood changes, decreased spontaneity,
hunger and weakness.
 Followed by sweating, incoherence, tachycardia.
 Consequenced in unconsiousness, hypotention,
hypothermia, seizures, coma, even death.

 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.

 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.

 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.

 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.

 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.

 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).

 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.

 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]

 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

 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,

 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.

 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.

 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)

 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=66461
8652
 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].

 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

 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

 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

 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.

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