Diabetes Mellitus

Definition

“Diabetes is a group of metabolic disorders

or a clinical syndrome, characterized by
hyperglycemia due to relative or absolute
lack of insulin”
CLASSIFICATION

Type 1 Diabetes Mellitus or IDDM-Insulin Dependent

Diabetes Mellitus (absolute deficiency of insulin)

Type 2 Diabetes Mellitus or NIDDM-Non- Insulin

Dependent Diabetes Mellitus (Relative deficiency of
insulin)

Gestational Diabetes Mellitus (GDM)

Type 1 Diabetes Mellitus or IDDM
Type 1 Diabetes Mellitus results from autoimmune
destruction of beta cells of pancreas

It usually occurs in children and adolescents and

typically present with Ketoacidosis

It is acute in onset
When insulin deficiency is severe the signs
and symptoms like
dehydration,
nausea,
vomiting and
progression of acidosis are
observed

The patient breath may have fruity odour

suggesting ketoacidosis
Type 2 Diabetes Mellitus or NIDDM
Type 2 Diabetes Mellitus is characterized by

Relative lack of insulin secretion,

Resistance to insulin action by the peripheral
tissues
Increased hepatic glucose production

It usually develops after the age of 40 years

Signs and symptoms includes,
glycosuria,
Increased thrust,
hyperosmality,
blurred vision,
proteinuria and
foot ulceration or gangrene.
Gestational Diabetes Mellitus (GDM)
GDM is defined as

“Glucose intolerance which usually develops due to

stress during pregnancy and it complicates

approximately in 7% of pregnancies”
Complications of Diabetes Mellitus
Acute complications

It include Ketoacidosis,

lactic acidosis,

hyperglycemia and

hyperosmolar non-ketotic coma

 Long term complications

Micro vascular Macro vascular

complications complications

Neuropathy – Foot Stroke,

ulcers, mouth ulcers etc
MI,
Retinopathy – blurred
vision
Dyslipidaemias and
Nephropathy – kidney
failure CVS disorders
Epidemiology
Type 1 Diabetes Mellitus

Accounts for up to 10% of all cases of Diabetes Mellitus

Rare in Japan and pacific Asia

Sweden, Sardinia and Finland have highest prevalence of

beta cell destruction (30-45%) and associated with higher
incidence of Diabetes Mellitus (22 to 35 per 100,000)
Type 2 Diabetes Mellitus
 Accounts 70-90% of all cases of Diabetes Mellitus

Prevalence of Type 2 Diabetes Mellitus in US is about 8.7% in

persons age 20 or more and in UK about 1.4 millions people
are affected with Type 2 Diabetes Mellitus

Prevalence of Type 2 Diabetes Mellitus increases with age and

is high among Indians and South Africans (30%)

There is a 20 times more chances of developing Type 2

Diabetes Mellitus in well fed population than in lean
population of the same race
Prevalence of diabetes in India

Diabetes in India is in rising

 The latest prevalence statistics suggest that

one in every five Indians is a diabetic
Etiology and risk factors
Type 1 Diabetes Mellitus

It mainly develops due to autoimmunity or idiopathic

 In 90% individuals with Diabetes Mellitus found to have

islet cell antibodies, antibodies to glutamic acid

decarboxylase and antibodies to insulin

Type 2 Diabetes Mellitus

Type 2 Diabetes Mellitus have stronger relationship

with genetic factor than type 1 Diabetes Mellitus

Identical twins have higher chances of developing

Type 2 Diabetes Mellitus as much as 100%

If parents have Type 2 Diabetes Mellitus the risk of

the child eventually developing Type 2 Diabetes
Mellitus is 5-10% where as 1-2% in Type 1 Diabetes
Mellitus
 Type 2 Diabetes Mellitus

Multiple risk factors like,

Obesity,
Family history,
Sedentary life style,
Race and ethnicity,
Hypertension,
Dyslipidaemias,
History of gestational Diabetes Mellitus
Diagnosis of diabetes mellitus
The lab data used in the diagnosis of Diabetes Mellitus are
as follows,

Random Capillary Blood Glucose (RBG)

Fasting Capillary Blood Glucose (FCBG)

Glucose Tolerance Test (GTT)

Postprandial Blood Sugar (PPBS)

HbA1C (Glycosylated hemoglobin)

Random capillary blood glucose (RBG)

Capillary blood glucose level when blood is withdrawn

randomly

Normal: 140-159mg/dL

Impaired: 160-199mg/dL

Diabetes Mellitus: ≥200mg/dL

Fasting capillary blood glucose (FCBG)

It is usually done in the morning before breakfast with

overnight fasting

Normal: 80 - 100mg/dL

Impaired: 100-125mg/dL

Diabetes Mellitus: ≥126mg/dL

Glucose tolerance test (GTT)
GTT is carried out by giving 75grams of glucose load orally
and after two hour of glucose load plasma glucose levels
are measured

Normal: <140mg/dL

Impaired: 140-199mg/dL

Diabetes Mellitus: ≥200mg/dL

Post-prandial blood sugar (PPBS)

Measurement of capillary blood glucose level after two

hours of a meal

Normal: <120mg/dL

Impaired: 121-160mg/dL

Diabetes Mellitus: >160mg/dL

HbA1C (Glycosylated heamoglobin)

It is the amount or % of glucose bound to hemoglobin

Normal: <5.8%

Impaired: 5.8-6.9%

Diabetes Mellitus: ≥7%

Criteria for diagnosis of Diabetes Mellitus
Symptoms of Diabetes Mellitus (i.e. poly urea, polydypsia
and unexplained weight loss)
Plus
Random Blood Glucose level ≥200mg/dL
Or
FCBG ≥126mg/dL
Or
GTT ≥200mg/dL
Pathophysiology
Type 1 Diabetes Mellitus

There is absolute deficiency of insulin due to immune

mediated destruction of beta cells of pancreas or due to
idiopathic causes

Generally beta cells destruction is mediated by T-

lymphocytes
Type 1 Diabetes Mellitus
It characterized by mainly 4 features,

Presence of immune markers just prior to beta cell

destruction

Hyperglycemia when 80-90% cells are destroyed

Transient remission period

Established disease with associated complications and

death
Type 2 Diabetes Mellitus
It is characterized by,

Defects in insulin secretion

Insulin resistance (in liver and in

peripheral tissues)
Impaired insulin secretion

Secretion of insulin is impaired due to relative

destruction of pancreatic beta cells, to the extent of 50%

Hence in type 2 Diabetes Mellitus there is still production

of insulin by remaining cells and hence it is also called as
Non Insulin Dependent Diabetes Mellitus
Insulin resistance- In liver
When plasma glucose level is low liver produces glucose
from non-carbohydrate sources through gluconeogenesis

When plasma glucose level is high insulin secretion

increases and it is carried to the liver through portal vein,
where it acts on liver cells and inhibit the production of
glucose

But in Diabetes Mellitus the liver cells are resistance to

insulin action and there by production of glucose
continues leading to marked hyperglycemia
Insulin resistance- Peripheral (muscle)

Muscle is the major site for glucose uptake and about

80% of body glucose uptake occurs in the skeletal muscles

There is a direct relationship between the glucose uptake

and insulin levels i.e. increase in insulin level increases
the glucose uptake

In type2 Diabetes Mellitus the glucose uptake decreases

by 50% due to resistance to insulin action by the muscle
cells, this ultimately leads to hyperglycemia
Insulin resistance- Peripheral (adipocytes)
In diabetic and non-diabetic humans, FFAs (Free Fatty
Acids) are stored in the adipocytes as triglycerides and
serves as energy source during conditions of fasting

 The release of FFA is regulated by the insulin level, as

insulin is a potent inhibitor of lipolysis

 In Diabetes Mellitus there is resistance to insulin action

that lead to release of more FFAs and this will cause more
production of glucose by liver using FFA and hence there
is an ultimate increase in blood glucose level
Management

-Non pharmacological methods

 Goals
The primary goal of the treatment is

 To reduce the risk of micro vascular and macro vascular

complications

To ameliorate the signs and symptoms

To reduce the morbidity and mortality

To improve the quality of life

 General approach

ABC control

Adapting non-pharmacological methods

Use of pharmacological therapy

 ABC control

A – HbA1C

B – Blood pressure control

C – Cholesterol and other lipoid control

Treatment Goals for the ABCs of Diabetes
HbA1C < 7 %
Pre prandial plasma glucose 90–130 mg/dl
Peak postprandial plasma glucose < 180 mg/dl
(usually 1 to 2 hours after the start of a meal)

Blood pressure
In case of diabetic patients, the goal blood pressure should be
130/80 mmHg

Cholesterol – Lipid Profile (mg/dl)

LDL Cholesterol < 100 mG/dL
HDL Cholesterol Men > 40 Women > 50 mG/dL
Triglycerides < 150 mG/dL
 Impact of ABC control
Studies have found that,
Strict blood pressure control reduces risk of,

Retinopathy progression (34%)

vision loss (47%)
Diabetes related deaths (32%)
Micro vascular disease (37%)
Heart failure (56%)
Stroke (44%)
Diet
While planning diabetes diet the following important
factors may be considered,

Fiber should be at least 40 gm / day

Instead of 3 heavy meals, it is ideal to go with 4-5

small mid intervals

Replace bakery products and fast foods by simple

whole cooked cereals, and don't eat

carbohydrates 2 hours before bedtime
Consume fresh fruit and vegetables 3- 5 times a

day
Carbohydrates
It is recommended that 60% of the calories should be
obtained from carbohydrates

This can be divided in to 4-5 equal parts

One-third (33%) of the diet is served during lunch

another one-third during dinner (33%)

Of the remaining one-third 25% is served during

breakfast and the rest (9%) during evening tea or at
bedtime
 Proteins
It is recommended that 15-20% of the total
calories be derived from proteins

Meat and meat products, milk, pulses

legumes and nuts are all rich in proteins
 Fats

It is recommended that 15-25 % of the calories are

derived from fat

 People with diabetes, should consume less of

saturated fats (ghee, butter, vanaspati etc.), as
compared to PUFA –poly-unsaturated oils (sunflower,
safflower oils) and MUFA- mono-unsaturated oils
(palm oil, olive oil etc.)
 Vitamins and Minerals

These are protective factors which in small

amounts are essential for the body

They are available in green leafy vegetables,
fresh fruits, milk, cereals, nuts etc.
 Dietary Fiber
It is an important part of diabetes diet and is present in
all cereals, legumes, fruits and vegetables

 Intake of 25 g of fiber per 1000 calories is considered to

be optimum for a diabetic

Long-term consumption of insoluble fiber (present in

cereals) also improves glucose control
Counseling points about diabetic diet
Eat food at fixed hours
Do not overeat
Do not eat immediately after a workout
Make sure you have three proper meals & light snacks in
between
Eat about the same amounts of food each day
Eat your meals and snacks at about the same times each day
Make sure the gaps between your meals are short
Do not eat fast; Masticate and munch your food well before
you swallow
Drink a lot of water that will help flush the toxins off your
system
Avoid fried foods and sweetmeats
 Counseling points about diabetic diet . . .
Include fresh vegetable salad in every meal
Include sprouts in the diet
Take your medicines at the same times each day
Exercise at the same time each day
Avoid smoking. Smoking leads to heart disease and poor
circulation
Check your feet for cuts, blisters, and swelling which are likely to
result from diabetes-related nerve damage
Take good sleep daily
Check your blood sugar level regularly
Try to stick up to the plan made up for sugar control
Check the other tests such as kidney function, liver function, heart
function, ketone level etc
Check your weight periodically and maintain ideal body weight
Exercise
 Exercise plan

Flexibility- such as stretching done before

walking

Strengthening- Such as lifting light

weights to build calorie-burning muscle mass

Aerobic activity- Such as walking, dancing,

swimming or biking to burn calories and
reduce heart risk.
 Counseling points
Check with your doctor before beginning to exercise
Start slowly five or ten minutes a day is a good beginning
if you have been very inactive
Wear comfortable, supportive shoes and cotton socks.
Check your feet after exercise for any signs of poor fit or
injury
Carry a diabetes identification card
Check your blood sugar before and after exercise, this is
especially important for anyone who takes insulin, a
sulfonylurea or a meglitinide as these medicines may
create risk for low blood sugar.
 Counseling points . . .
Carry something to eat that contains glucose. Use it to
prevent or treat low blood sugar if needed
Stretch and warm up at the beginning of your activity.
This helps prevent injuries
Drink more liquids that contain no calories, like water,
when exercising
If you have leg or chest pains during exercise, stop
exercising and call your doctor
Avoid exercising if your fasting blood sugar is above 300
mg/dL (16.7 mol/L) or less than 70 mg/dL(3.9 mmol/L)
Management of diabetes
Pharmacological therapy
Treatment options:
The regimens used to treat diabetes are classified as
1. Insulins

2. Oral hypoglycemic agents

Insulins
Insulin is an anabolic and anti-catabolic hormone and plays an
important role in protein, carbohydrate and fat metabolism

In non-diabetic humans 1 IU of insulin is secreted every hour

and it increases to 5-10 times when glucose is ingested

Approximately 40 IU of insulin is secreted by pancreatic

cells every day

Types 1 diabetes mellitus patient have absolute deficiency of

insulin and hence these patients needs insulin exogenously
Insulin types

Rapid acting Insulins

Short acting Insulins

Intermediate acting Insulins

Long acting Insulins

Pre – mixed Insulins

Type of Insulin & Brand Role in Blood Glucose
Onset Peak Duration
Names Management
Rapid-Acting
Humalog or lispro 15-30 min. 30-90 min 3-5 hours Rapid-acting insulin
covers insulin needs for
Novolog or aspart 10-20 min. 40-50 min. 3-5 hours
meals eaten at the same
time as the injection.
This type of insulin is
Apidra or glulisine 20-30 min. 30-90 min. 1-2½ hours
used with longer-acting
insulin.
Short-Acting
Regular (R) humulin or Short-acting insulin
30 min. -1 hour 2-5 hours 5-8 hours
novolin covers insulin needs for
Velosulin (for use in the meals eaten within 30-60
30 min.-1 hour 2-3 hours 2-3 hours minutes
insulin pump)
Intermediate-Acting
NPH (N) 1-2 hours 4-12 hours 18-24 hours Intermediate-acting
insulin covers insulin
needs for about half the
day or overnight. This
Lente (L) 1-2½ hours 3-10 hours 18-24 hours type of insulin is often
combined with rapid- or
short-acting insulin.
Long-Acting
Ultralente (U) 30 min.-3 hours 10-20 hours 20-36 hours Long-acting insulin
No peak time; insulin is covers insulin needs for
Lantus 1-1½ hour 20-24 hours about 1 full day. This
delivered at a steady level
type of insulin is often
Levemir or detemir(FDA combined, when needed,
1-2 hours 6-8 hours Up to 24 hours with rapid- or short-
approved June 2005)
acting insulin.
Pre-Mixed*
Humulin 70/30 30 min. 2-4 hours 14-24 hrs
Novolin 70/30 30 min. 2-12 hours Up to 24 hours
These products are
Novolog 70/30 10-20 min. 1-4 hours Up to 24 hours generally taken twice a
Humulin 50/50 30 min. 2-5 hours 18-24 hrs day before mealtime.
Humalog mix 75/25 15 min. 30 min.-2½ hours 16-20 hours
Oral hypoglycemic agents
5 – classes of oral agents for the treatment of type 2 Diabetes Mellitus are available,
under three different headings,

 α – Glucosidase inhibitors

 Eg: Acarbose

 Insulin sensitizers

 1. Biguanides- Metformin

 2. Thiazolidinediones (Glitazones) – Pioglitazone, Rosiglitazone

 Insulin secretogogues

1. Sulfonylurea – Tolbutamide, Glibenclamide (Gliburide), Gliclazide,

Glimepiride, Glipizide.

2. Meglitinides – Rapaglinide, Nateglinide

α – GLUCOSIDASE INHIBITORS
α – Glucosidase inhibitors competitively inhibit enzymes
maltase,
isomaltase,
sucrase and
glucomaltase in the small
intestine,

delaying the break down of sucrose and complex

carbohydrates
DRUG PREPARATIONS MAXIMUM BRAND NAME3
DOSE

Acarbose Tab 25mg, 50mg Initially 25-50mg/day Diabose, Glubose,

Increase to 50mg tid 600mg/day K-Carb, Gludase,
After 6-8 weeks Glucar.
100mg tid

Miglitol Tab 25mg,50mg Initially 25-50mg/day Diamig, Elitox,

Increase to 50mg tid 600mg/day Euglitol, Miglit,
After 6-8 weeks Mignar, Misobit.
100mg tid

Voglibose Tab 0.2mg,.03mg Initially 200-300mcg Vocarb, Voglitor

tid Volix, Volibo
Before meals

Both miglitol and acarbose should be taken with first bite of the meal
so that drug may be present to inhibit enzyme activity.
 Contraindication

 Patients with short bowel syndrome or inflammatory bowel disease

 Patients with serum creatinine > 2mg/dL

 Adverse effects

 Gastrointestinal effects: Flatulence, diarrhoea and abdominal pain are very common.

 Hepatic effects: Above 100mg three times a day causes elevated transaminase (i.e.
ALT and ALT) levels.

 Anaemia: Anaemia may be due to decreased iron absorption from gut (incidence
<1%).

 Dermatological effects: Rash and erythema multiforme occurs rarely.

INSULIN SENSITISERS-BIGUANIDE / METFORMIN
 Metformin
 Decreases intestinal absorption of glucose
 Increases uptake of glucose from the blood into the tissues
(e.g. skeletal muscle and fat)
 Decreases glucose production in the liver (gluconeogenesis)
and
 Decreases insulin requirements for glucose disposal.

 Metformin has no effect on pancreatic insulin secretion and is

not effective in the absence of insulin.

 It enhances the sensitivity of both hepatic and, to a lesser

extant, peripheral tissues to insulin
DRUG PREPARATIO MAXIMUM BRAND NAME3
NS DOSE
Metformi Tab 250mg, Initially Exermet, Formin,
n 500mg, 500mg 1- 3000mg/ Forminal,
750mg, 3times daily. day Gluconorm SR,
850mg, Increase upto Glyciphage
1000mg 850mg 2-
3times daily
Contraindications

Due to risk of lactic acidosis, Metformin is contraindicated in following settings,

• Impaired renal function (Crcl <50ml/ml)

• Severe hepatic disease
• Acute congestive heart failure
• Pancreatitis
• Severe dehydration
• Septicaemia
• Patient receiving iodinated radiograph contrast media
• Geriatrics(>85 yrs)
• Presence of acute or chronic metabolic acidosis
Adverse effects

 Gastrointestinal effects: Diarrhaea, nausea, abdominal pain,

anorexia and metallic taste up to 30% Decreased Vit B 12 seen in
10-30%

 Lactic acidosis : <1% caused by altered normal production&

clearance of lactate.

 Hypoglycaemia: Uncommon with Metformin monotherapy;

Common when used along with sulfonylurea, repaglinide or
insulin.

 Rash: erythema, photosensitivity, hypersensitivity are reported.

INSULIN SENSITISERS- THIAZOLIDINEDIONES
 They increases the response to insulin in adipose tissue, skeletal muscle and
the liver, without stimulating insulin secretion

 The insulin sensitizing effect of thiazolidinedione agents is from binding with

and activating the peroxisome proliferator activated receptor gamma (PPAR-γ)

 PPAR-γ is found in insulin dependent glucose requiring tissues and is

involved in the regulation of genes controlling glucose homeostasis and
lipid metabolism

 Thiazolidinedione acts by enhancing insulin action and promoting glucose

utilisation in peripheral tissues are possibly by stimulating non-oxidative
glucose metabolism in muscle and suppressing gluconeogenesis in the liver.
 DRUG PREPARATIO DOSE RANGE MAXIMUM BRAND
NS DOSE NAME3
Rosiglitazo Tab 1mg, 2mg, Initially 4mg/day Enselin,
ne 4mg, 8mg 8mg Rozinorm
Increase to
Reglit,
8mg/day
Rosicon,
Pioglitazon Tab 1mg, Initially Diavista, P-
e 2mg, 15mg, 15mg/30mg 45mg Glitz, Pioglar,
30mg, 45mg Piozone
Increase to
45mg/day

Contraindication

Thiazolidinedione is contraindicated in patients having,

• Known hypersensitivity to the drug
• Heart failure
• Moderate to severe liver impairment (ALT >2.5)

Caution

Thiazolidinediones should not be used in patients with heart

failure due to risk of fluid retention.
INSULIN SENSITISERS-THIAZOLIDINEDIONES . . .
Adverse effects
 Weight gain: dose dependent increase in body weight seen with
• Rosiglitazone – 0.7-3.5 kg
• Pioglitazone – 0.5-2.8 kg
 Oedema: oedema seen in the patient population of 3-5%, using glitazones.

 Decreased Haemoglobin and haematocrit with rosiglitazone the following decreased levels are
observed
 Haemoglobin ≤ 1.0 gm/dL
 Haematocrit ≤ 3.3%

 Hepatic effects: ALT elevation seen with

 Troglitazone ≥ 1.9%
 Rosiglitazone ≥ 0.25%
 Pioglitazone ≥ 0.26%

 Hypoglycaemia: Infrequent with monotherapy, when used with sulfonylureas, repaglinide or

insulin hypoglycaemia may occur.
INSULIN SECRETOGOGUE- SULFONYLUREAS
These agents act by binding to receptors on the β-cells
in the pancreas

Insulin release from these agents resulted by,

Closing of adenosine triphosphate (ATP) dependent

potassium channels (KATP), which causes voltage
changes, the influx of calcium ions. For this action
presence of glucose is not required
INSULIN SECRETOGOGUE- SULFONYLUREAS . . .
DRUG PREPARATIO DOSE RANGE MAXIMU BRAND
NS M DOSE NAME3

Glibenclam Tab 1.25mg, Initially Daonil,

ide 2.5mg, 5mg 2.5mg/day 15-20mg Glinil,
Glybovin,
Glibet
Gliclazide T. 30mg, Initially 40mg Dianorm,
40mg, daily. 320mg Reclide
60mg,80mg Zuker, Glyloc
Glimepirid T. 1mg, 2mg, Initially 1mg Glimipid,
e 3mg, 4mg, daily. 4mg Glimulin,Gli
15mg mkap
Glipizide T. 2.5mg, Initially 5mg 40mg Diacon,
5mg, 7.5mg, daily Diaglip,
10mg Glucolip,
Dibizide
Tolbutamid Tab 500mg Initially 3gm Rastinone
e 500mg-1gm
INSULIN SECRETOGOGUES- SULFONYLUREAS . . .

Contraindications

In severe hepatic impairment

Hypersensitivity to sulfonylureas

Severe renal impairment

Glibenclamide should generally avoided in the elderly due to

its greater risk of hypoglycaemia compared to other
sulfonylureas
INSULIN SECRETOGOGUES- SULFONYLUREAS . . .
Adverse effects
Hypoglycaemia: Symptoms of hypoglycaemia include, tachycardia, sweating, palpitation,
tremor, headache, confusion, visual disturbances, irritability, personality changes, seizures
or coma, are more common with Glibenclamide, probably because of its longer half life
 When sever it can lead to permanent neurologic damage or death.

Weight gain

Gastrointestinal effects: Nausea, diarrhoea, heartburn, anorexia are seen in 1-3% of

patients receiving sulfonylureas

Dermatological effects: Erythema multiforme, exfoliative dermatitis and photosensitivity

are rare

 Haematological effects: Agrnulocytosis, aplastic anaemia and haemolytic anaemia are

rarely reported with sulfonylureas
INSULIN SECRETOGOGUES- MEGLITINIDES
Meglitinides stimulate insulin from pancreatic β cells by closing
the adenosine triphosphate (ATP) dependent potassium
channels

This is mediated through a different binding site to

sulfonylureas on the β cell.

These are taken with every meal and leads to a rapid but brief
release of insulin to reduce post-prandial plasma glucose levels.

Insulin release only occurs in the presence of glucose.

INSULIN SECRETOGOGUES- MEGLITINIDES . . .
DRUG PREPARATIONS DOSE RANGE MAXIMUM BRAND NAME3
DOSE
Nateglinide Tab 60mg, 120mg Initially 60mg tid 180mg Glinate, Natilide,
Natiz, NDS
30min before meals
Repaglinide Tab 0.5mg, 1mg, Initially 0.5mg tid 16mg Eurepa, Raplin,
2mg immediately before meals, Regan, Repa
increase every 1-2weeks
upto 4mg tid

Contraindication

• Age below 12 years

• Pregnancy and lactation

• Known hypersensitivity to Meglitinides

INSULIN SECRETOGOGUE- MEGLITINIDES . . .

Adverse effects

Hypoglycaemia: occurs, if a dose is taken and a

meal is delayed or missed.

Weight gain: Body weight has increased by about

3%

Gastrointestinal effects: Nausea, vomiting,

abdominal pain, diarrhoea and constipation are
common adverse effects with Meglitinides.
NEWER HYPOGLYCAEMIC AGENTS
- EXENATIDE
Exenatide (FDA approved) is used as adjuvant therapy to

improve glycaemic control in patients with type 2 diabetes

receiving Metformin, a sulfonylurea or a combination of

these agents but who have not achieved adequate control

NEWER HYPOGLYCAEMIC AGENTS- EXENATIDE . .

Exenatide is a synthetic analogue of the 39-amino acid

peptide amide derived from salivary secretion of the

lizard Helloderma suspectum and is functional

analogue

of human glucagon like peptide – 1 (GLP-1)

NEWER HYPOGLYCAEMIC AGENTS- EXENATIDE . . .

Various mechanism of Exenatide include, secretion of

glucose dependent insulin, suppression of inappropriately

high glucagon levels found in patients with type 2 diabetes,

delay of gastric emptying and reduction of food intake

NEWER HYPOGLYCAEMIC AGENTS- EXENATIDE . . .
Dosing
 Initially 5mcg SC as an adjunct twice daily. Maintenance, 10 mcg SC twice daily after 1 month
of therapy.

Contraindications
 Known hypersensitivity to exenatide or any product component

Precautions
 Antibody development; high titers of anti-exanatide antibodies resulting in poor glycemic
control may occur
 End-stage renal disease, dialysis, or severe renal impairment (creatinine clearance less than
30 mL/min); increased risk of gastrointestinal adverse effects
 Gastrointestinal disease, severe, including gastroparesis; increased risk of gastrointestinal
adverse effects

Adverse effects
 Nausea, hypoglycaemia, dizziness, vomiting, diarrhoea and headache are more common
adverse events with Exenatide.
Insulin Administration Technique
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