Diabetes Update:

2010

Dr. Dany Irawan. Sp. PD

RS. SANTO VINCENTIUS A PAULO.
SURABAYA
1. What is DM
2. How to regulate Blood Sugar?
3. What is Insulin Resistace
4. How is Diabetes Diagnosed ?
5. Who Should You Screen ?
6. What is HbA1c ?
7. How to Prevent ?
8. How to Manage?
9. What is the Complication ?
What is DM ?
 Do you know
what diabetes is?

Do you think more

people are affected
by diabetes What factors do you
nowadays? think contribute to
diabetes?

Do you know that

diabetes can cause
complications in other
organs? Can diabetes be
prevented?

Mohan D et al. J Assoc Physicians India 2005; 53:283287.

DIABETES MELLITUS

Definition: a metabolic disorder in

which
there is deficiency of insulin production
or
resistance of organs to the effect of
insulin
Diabetes Mellitus :
a group of diseases characterised
by high levels of blood glucose
resulting from defects in insulin
production, insulin action, or both
Definition

genetically influenced metabolic disorder of

carbohydrate, fat, and protein metabolism
characterized by abnormally high blood glucose
levels due to inadequate or absent insulin
production and or impaired insulin action
(Millonig & Miller,1999)
In other wordsdefects in insulin secretion,
metabolism, or both
What is Diabetes

It is a disease where blood sugar levels in

the blood are too high.
Definition of Diabetes

Definition
A chronic disease with abnormalities in:

Metabolism of carbohydrate, protein, fat and

insulin (resulting in hyperglycemia).

Structure and function of blood vessels and

nerves (resulting in complications).
CLASSIFICATION

Type I Diabetes
Type II Diabetes
Prediabetes
Gestational Diabetes
Others-genetic defects,cystic fibrosis,drug
induced or chemical induced
 Why Diabetes?

18 million diagnosed
Estimated that 6 million are undiagnosed
Third leading cause of death in the U.S.
Leading cause of blindness
*Patient education is the cornerstone of diabetic
treatment and management*
*Complications can be prevented or delayed
through intensive treatment*
How to regulate Blood Sugar?
 PANCREAS:
Produces and secretes insulin, which
stimulates the transport of glucose
across the plasma membranes of
muscles, fat and liver cells
Produces and secretes glucagon
(stimulates liver to release glucose
that is stored in adipose tissue)
Regulation of Blood
Glucose Concentration
Beta cells secrete insulin
Alpha cells produce hormone glucagon
Delta cells inhibit release of both insulin
and glucagon
Insulin and glucagon regulate blood sugar
concentrations
When working properly the following
occurs:
Regulation of High
Blood Glucose
We all just ate our beta cells should be
responding to the rising blood sugar levels
by now.
Insulin signals other tissues muscle and
adipose to take in glucose
If the glucose is not used for energy it is
stored in adipose tissue.
Result lowered blood sugars
Regulation of Low Blood Sugars
Now if you had missed supper :

If blood sugars are low alpha cells in the

pancreas are stimulated to release glucagon
from the pancreas which stimulates the liver to
release glucose for energy. Homeostasis is
maintained.
Regulation of Blood Glucose
DIABETES MELLITUS
Diabetes is a disorder of metabolism--the way
our bodies use digested food for growth and
energy.
Most of the food we eat is broken down into
glucose, the form of sugar in the blood.
Glucose is the main source of fuel for the
body.
<http://diabetes.niddk.nih.gov/dm/pubs/overview/index.htm#what>
DIABETES MELLITUS
After digestion, glucose passes into the
bloodstream, where it is used by cells for growth
and energy.
For glucose to get into cells, insulin must be
present.
Insulin is a hormone produced by the pancreas,
a large gland behind the stomach.

<http://diabetes.niddk.nih.gov/dm/pubs/overview/index.htm#what>
DIABETES MELLITUS
NORMAL: When non-diabetic people eat,
the pancreas automatically produces the
right amount of insulin to move glucose
from blood into our cells.

<http://diabetes.niddk.nih.gov/dm/pubs/overview/index.htm#what>
DIABETES MELLITUS
DIABETES: In people with diabetes, when they
eat, the pancreas either produces little or no
insulin, or the cells do not respond appropriately
to the insulin that is produced (or both) =>
glucose builds up in the blood, overflows into the
urine, and passes out of the body in urine =>
body loses its main source of fuel even though
blood contains large amounts of glucose.
<http://diabetes.niddk.nih.gov/dm/pubs/overview/index.htm#what>
What is Insulin Resistace
What is insulin resistance?
Major defect in individuals with type 2
diabetes1
Reduced biological response to insulin13
Strong predictor of type 2 diabetes4
Closely associated with obesity5
IR

1American Diabetes Association. Diabetes Care 1998; 21:310314.

2Beck-Nielsen H & Groop LC. J Clin Invest 1994; 94:17141721. 3Bloomgarden ZT. Clin Ther 1998; 20:216231.
4Haffner SM, et al. Circulation 2000; 101:975980. 5Boden G. Diabetes 1997; 46:310.
 What is -cell dysfunction?
Major defect in individuals with type 2
diabetes
Reduced ability of -cells to secrete

insulin in response to hyperglycemia

DeFronzo RA, et al. Diabetes Care 1992; 15:318354.

Insulin resistance and -cell
dysfunction are core defects of
type 2 diabetes
Genetic susceptibility,
obesity, Western
lifestyle

-cell
Insulin
resistance IR dysfunction

Type 2 diabetes
Rhodes CJ & White MF. Eur J Clin Invest 2002; 32 (Suppl. 3):313.
How do insulin resistance and -cell
dysfunction combine to cause type 2
diabetes?
Normal IGT* Type 2 diabetes

Insulin Increased insulin

resistance resistance

Insulin Hyperinsulinemia,
secretion then -cell failure

Post-
prandial Abnormal
glucose glucose tolerance

Fasting
Hyperglycemia
glucose

*IGT = impaired glucose tolerance

Insulin resistance reduced
response to circulating insulin
Insulin
resistance IR

Liver Muscle Adipose

tissue

Glucose output Glucose uptake Glucose uptake

Hyperglycemia
 Overall, 75% of patients with
type 2 diabetes die from
cardiovascular disease

Gray RP & Yudkin JS. Cardiovascular disease in diabetes mellitus. In Textbook of Diabetes 2nd Edition, 1997. Blackwell Sciences.
Insulin resistance is as strong a
risk factor for cardiovascular
disease as smoking
1.8

1.6

1.4

1.2

1.0

0.8

0.6
Age Smoking Total cholesterol: Insulin
HDL cholesterol resistance

Bonora E, et al. Diabetes Care 2002; 25:11351141.

 Insulin resistance is closely
linked to cardiovascular disease
Present in > 80% of
people with type 2 diabetes1

Insulin Approximately doubles

resistance IR the risk of a cardiac event2

Implicated in almost half of

CHD events in individuals
with type 2 diabetes2

1Haffner SM, et al. Circulation 2000; 101:975980.

2Strutton D, et al. Am J Man Care 2001; 7:765773.
~90% of people with type 2
diabetes are overweight or
obese

World Health Organization, 2005. http://www.who.int/dietphysicalactivity/publications/facts/obesity

 How is -cell function
measured?
-cell function is difficult to measure and
most methods are impractical for large-
scale use1
Homeostasis model assessment (HOMA)
provides a simple estimate
of -cell function2
Proinsulin:insulin ratio is sometimes used
as a marker of -cell
dysfunction1
1Matthews DR, et al. Diabetologia 1985; 28:412419.
2Bergman RN, et al. Eur J Clin Invest 2002; 32 (Suppl. 3):3545.
 Why does the -cell fail?
Oversecretion of
insulin to compensate
for insulin resistance1,2

Glucotoxicity2 Lipotoxicity3

Chronic Pancreas High circulating

hyperglycemia free fatty acids

-cell
dysfunction
1Boden G & Shulman GI. Eur J Clin Invest 2002; 32:1423.
2Kaiser N, et al. J Pediatr Endocrinol Metab 2003; 16:522.
3Finegood DT & Topp B. Diabetes Obes Metab 2001; 3 (Suppl. 1):S20S27.
Glycemic control declines over
time Diet
Sulfonylurea or insulin
9
Median HbA1c (%)

6.2% upper limit of normal range

6
0
0 3 6 9 12 15
Years from randomization

UK Prospective Diabetes Study (UKPDS) Group. Lancet 1998; 352:837853.

Loss of -cell function occurs
before diagnosis
100
Up to
80 Diagnosis 50%
-cell function (%)

loss
60

40

20

0
-10 -9 -8 -7 -6 -5 -4 -3 -2 -1 1 2 3 4 5 6
Time from diagnosis (years)

Holman RR. Diabetes Res Clin Prac 1998; 40 (Suppl.):S21S25.

How is Diabetes Diagnosed ?
How is Diabetes Diagnosed?

Fasting Plasma Glucose 2 hour OGTT (mg/dl)

Normal <100 <140

Impaired Fasting >100 to 125 -

Glucose
Impaired Glucose - >140 and <200
Tolerance
Diabetes >126 2 times on >200 random
different days
*ADA: American Diabetes Assn
** AACE: American Association of
Clinical Endocrinologists
Causes of Hyperglycemia
Loss of 1st phase insulin release

Peripheral tissue insulin resistance

Hepatic glucose overproduction

Relative lack of insulin

Increased gastric emptying time

Increased glucagon production after meals

Over time the inner linings of the blood vessels are affected thus affecting
many organs.
Blood Glucose Goals
ADA*Goals AACE**
(mg/dl) (mg/dl)

Pre-meal 70 to 130 <110

Post-meal <180 <140

A1C <7% <6.5%

Pre-Diabetes

Pre-diabetes refers to a state between

normal and diabetes = fasting
plasma glucose 100-125mg/dL (higher
than normal but not high enough for
diagnosis of diabetes)

Affects about 41 million people in USA

(previously referred to as either impaired fasting glucose or impaired glucose
tolerance)
Who should you Screen ?
Screening
Who should you screen?
Adults who are overweight (BMI>25) or
obese(BMI >30) and have 1 or more
additional risk factors
Routine testing for others not meeting
criteria should begin at age 45
If normal repeat every 3 years or more
frequently if risk status changes
 Risk Factors
Physical inactivity
1st degree relative with diabetes
High risk ethnic groups(African-
Amer,Latino,Asian-Amer,Pacific Islanders)
Women who delivered a baby >9lbs +GDM
Hypertension
HDL<35 or Trigs >250
Women with PCOS
IGT or IFG on previous testing
Hx CVD
Severe obesity or acanthosis nigricans
Risk factors

Family history of diabetes

Older than 30 years of age
Lack of physical activity
Sedentarism ( person with little or no
physical activity)
Poor diet
Excessive weight
Acanthosis Nigricans
What is HbA1c ?
Glucose Contributions to HbA1c

HbA1c =

Fasting Glucose, Postprandial Glucose,

Influenced by: Influenced by:
Hepaticglucose
production
+ Preprandial glucose
Glucose load from meal

Hepatic sensitivity to Insulin secretion

insulin Insulin
sensitivity in peripheral
tissues and liver
Postprandial glucose
Most of the day may be postprandial
HbA1c = FPG + PPG
Postprandial from the time glucose starts
to rise until it comes down again
Time period up to 2.5 h after a meal
normal individuals 1.5 h
Testing of PPG recommended 2h after the
start of a meal
Glycosylated proteins
Caused by non-enzymatic glycosylation
Glycosylated hemoglobin
HbA1c - LGI ref range 4.6-6.5 %
indicates previous 2-3 months glycaemic exposure
n.b. affetced by altered red cell survival
Fructosamine
mirrors glycosylation of all serum proteins
indicates previous 2-3 weeks glycaemic exposure
used pregnancy/children in some sites
Glycosylated albumin
indicates previous several days glycaemic exposure
not commonly used
Hemoglobin A1c
HbA1c is stable glycosylated
hemoglobin
Its percentage concentration
indicates cumulative glucose
exposure
Hemoglobin A1c
A good indicator of blood glucose control.
Gives a % that indicates control over the
preceding 2-3 months.
Performed 2 times a year.
A hemoglobin of 6% indicates good
control and level >8% indicates action is
needed.
Lowering HbA1C Reduces Risk of Complications
 Diagnosing Diabetes Using A1C
Diabetes diagnosed when A1C 6.5%
Confirm with a repeat A1C test
Not necessary to confirm in symptomatic persons with
PG >200 mg/dL
If A1C testing not possible, use previous tests
Can not be used during pregnancy because of
changes in red cell turnover
A1C 6.0% should receive preventive
interventions (pre-diabetes)
A1C: reliable measure of chronic glucose levels;
values vary less than FPG and testing more
convenient for patients (can be done any time of
day)
July 2009, International Committee, American Diabetes Association & International Diabetes Federation
 Correlation of A1C with Average Glucose
Mean plasma glucose
A1C (%) mg/dl mmol/l
6 126 7.0
7 154 8.6
8 183 10.2
9 212 11.8
10 240 13.4
11 269 14.9
12 298 16.5

Diabetes Care 32(Suppl 1):S19, 2009

Why to Treat DM
 Why to treat diabetes mellitus?

stroke

blindness

myocardial
infraction

kidney failure
haemodialysis gangrene
amputation
nerve damage
In type I acute complication and death
You cant see or fell the symptoms
-untill something really bad
happens
How to Manage Diabetes
MAJOR TARGETED SITES
OF DRUG CLASSES
Pancreas Beta-cell dysfunction

Sulfonylureas
Meglitinides Muscle & fat
Liver
DPP-4 inhibitor
Hepatic glucose
overproduction Insulin
Glucose level resistance

Biguanides Gut Thiazolidinediones

Thiazolidinediones Biguanides

DPP-4 inhibitors Reduced Insulin

glucose -glucosidase
absorption
GLP1 analogue inhibitors

Insulin
TREATMENT OPTIONS
FOOD BETA CELL FUNCTION
EXERCISE GLUCAGON
ORAL SUPPRESSION
PARENTERAL INSULIN RESISTANCE
TREATMENT OPTIONS
ORAL
SECRETAGOGUES
SULFONYLUREAS
NONSULFONYLUREAS
INSULIN RESISTANCE
THIAZOLIDINEDIONES (TZD)
METFORMIN
GLUCAGON SUPPRESSION
INCRETINS (INtestinal SECRETION of Insulin)
JANUVIA
STARCH BLOCKERS
ACARBOSE
TREATMENT OPTIONS

PARENTERAL
SUBCUTANEOUS
INCRETIN MIMETICS
INSULIN

TRANSPULMONARY
TREATMENT OPTIONS
ORAL
SECRETAGOGUES
SULFONYLUREAS
NONSULFONYLUREAS
INSULIN RESISTANCE
THIAZOLIDINEDIONES (TZD)
METFORMIN
GLUCAGON SUPPRESSION
INCRETINS (INtestinal SECRETION of Insulin)
JANUVIA
STARCH BLOCKERS
ACARBOSE
TREATMENT OPTIONS ORAL

ORAL
SECRETAGOGUES
SULFONYLUREAS
GLYBURIDE
GLIPIZIDE
GLIMEPIRIDE (LONG ACTING)
NONSULFONYLUREAS
NATEGLINIDE (STARLIX)
REPAGLINIDE (PRANDIN)
TREATMENT OPTIONS ORAL

ORAL
INSULIN RESISTANCE
THIAZOLIDINEDIONES (TZD)
PIOGLITAZONE (ACTOS)
ROSIGLITAZONE (AVANDIA)
METFORMIN
Type 2 Diabetes Medications
Class Route Example Action A1c

Insulin Increasing:
Sulfonylureas Oral Glyburide, Insulin 1-2%
glipizide,
glimepiride
Non-sulfonylurea Oral Repaglinide, Insulin 1-1.5%
secretagogues nateglinide
Insulin Injection Insulin
GLP-1 Injection Exenatide Insulin 1%
agonists Glucagon
Gastric emptying
Satiety
DDP-4 Oral Sitagliptin Insulin .6-.8%
inhibitors Glucagon
Vildagliptin
GLP = glucagon-like peptide
DPP = dipeptidyl peptidase
Type 2 Diabetes Medications cont.
Class Route Example Action A1C
Other Target Actions:
Biguanides Oral Metformin Hepatic 1-2%
glucose
output;
Insulin
resistance
Alpha- Oral Acarbose, CHO .5-1%
glucosidase miglitol absorption
inhibitors
Thiazolidine- Oral Pioglitazone, Insulin 1-1.5%
diones rosiglitazone resistance
Inzucchi, 2009
Current Treatment Paradigm
Pathophysiology-Oriented Approach
Intensify
Lifestyle Early Combinations Combinations Add
Changes of Glucose- Of Glucose- Insulin
+- Lowering Lowering Agents
Metformin Agents Consider Insulin

Combination therapy from the outset

Treatment designed to address the underlying
pathophysiology
Vigorous effort to meet glycemic targets
Simultaneous rather than sequential therapy
Early stepwise titrations to meet glycemic targets
American Diabetes Association and the European Association for the Study of Diabetes.
Diabetes Care 2009;32:193
ADA and EASD: Treatment for Type 2
Diabetes
Type 2 Diabetes: A Progressive
Disease

Lifestyle
Medical Nutrition Therapy Medical Nutrition Therapy
Lifestyle Alone
Interventions Medications
or Insulin
with Medications

Meds
TREATMENT OPTIONS ORAL

ORAL 150
NGT
T2DM

GLUCAGON

Insulin (mU/ml)
100

SUPPRESSION 50

INCRETINS (GLP-1)
SECRETED BY THE L-
0
-60 0 60 120 180 240

CELLS OF THE Time (min)

DISTAL ILEUM 160

NGT

CIRCULATES TO THE 140

T2DM

PANCREAS

Glucagon (pg/ml)
STIMULATES INSULIN 120

SECRETION 100

INHIBITS GLUCAGON 80

SECRETION -60 0 60 120

Time (min)
180 240
TREATMENT OPTIONS ORAL

GLUCAGON SUPPRESSION
INCRETINS (GLP-1)---GLIP-ONE
THERE ARE NO ORAL INCRETINS
BUT THERE IS AN ORAL WAY TO HELP
NATURALLY OCCURRING INCRETINS
GLIPTINS (DPP-4 INHIBITORS)
SITAGLIPTIN (JANUVIA)
VILDAGLIPTIN (GALVUS )
Synthesis, Secretion, and Metabolism
of GLP-1 and GIP
DPP-4 Degrades GLP-1
TREATMENT OPTIONS
PARENTERAL
INCRETIN MIMETICS
DIRECT STIMULATION OF INSULIN
DIRECT INHIBITION OF GLUCAGON
Exenatide (BYETTA)
Amylin (SYMLIN)

NOT DEGRADED BY DPP-4

LONG-ACTING
TREATMENT OPTIONS

PARENTERAL
SUBCUTANEOUS
INCRETIN MIMETICS
INSULIN

TRANSPULMONARY
INSULIN
INSULIN THERAPY

LONG ACTING ANALOGUES

LANTUS
LEVEMIR

RAPID ACTING ANALOGUES

HUMALOG
NOVORAPID
APIDRA
INSULIN THERAPY

MIXTURES
75/25 HUMALOG MIX
70/30 NOVOLOG MIX
INSULIN THERAPY

IS INSULIN INEVITABLE ?
b-Cell Function Declines Regardless
of Intervention in Type 2 Diabetes
 Normal Insulin Secretion

Meal Meal Meal

Serum insulin (mU/L)

50
Bolus insulin needs
40

30

20

10 Basal Insulin Needs

0
0 2 4 6 8 10 12 14 16 18 20 22 24
Hours
Kendall DM. N Engl J Med 322:898, 1990
Copyright 2000 International Diabetes Center, Minneapolis, MN, USA
 Insulin Therapy
Type of Insulin Onset of Peak Action Monitor the
Action Effect in:

Bolus Insulin
Lispro (Humalog) <15 min 0.5-1.5 h 2h
Aspart (Novorapid) <15 min 0.5-1.5 h 2h
Glulisine (Apidra) <15 min 0.5-1.5 h 2h
Regular 30-60 min 2-3 h 4 h (next meal)
Basal Insulin
Glargine (Lantus) ~1 h peakless 10-12 h
Determir (Levemir) 1-2 g peakless 10-12 h
NPH 2-4 h 6-10 h 8-12 h
Mixtures
70/25 NPL/Lispro <15 min Dual
50/50 NPL/Lispro <15 min Dual
70/30 NPA/Aspart <15 min Dual
70/30 NPH/Regular 0.5-1 h Dual
 Insulin Time Action Curves

Rapid (Lispro, Aspart, Apidra)

Relative Insulin Effect

Short (Regular)
Intermediate (NPH)

Long (Glargine, Levemir)

0 2 4 6 8 10 12 14 16 18 20
Time (Hours)
 Basic Insulin Therapy
Split Mixed Insulin (R/N)
R/N R/N
Serum insulin (U/mL)

50

40

30 Reg Reg

20

10 NPH NPH

0
0 2 4 6 8 10 12 14 16 18 20 22 24

Time of Day
International Diabetes Center
Park Nicollet
 Flexible Insulin Regimen:
RA - RA - RA LA

RA RA RA Long-Acting
Serum insulin (mU/L)

50

40

30
RA RA
20 RA

10
Glargine
0
0 2 4 6 8 10 12 14 16 18 20 22 24

Hours
ABCs of Diabetes Management
Glycemic Control
A1c <7.0%
Preprandial plasma 70-130 mg/dL
glucose
Postprandial plasma <180 mg/dL
glucose
Blood pressure <130/80 mmHg
Lipids
LDL-Cholesterol <100 mg/dL (<70 mg/dL)
Triglycerides <150 mg/dL
HDL Men:>40 mg/dL;
Women: >50 mg/dL
Aspirin therapy Adults, age of 3040 y
Smoking cessation Universal

Diabetes Care 2009;29:S10

How to Prevent
 United Nations. Resolution on Diabetes.
http://www.unitefordiabetes.org/assets/files/UN_Resolution.pdf.
 Simple steps
to prevent diabetes
Small Steps, Big Rewards
US National Diabetes Education
Program
Diabetes can be prevented or
delayed:Small steps, Big rewards
Diabetes can be prevented through small steps:
Lose a modest amount of weight (57%)
by building up to 30 mins of physical
activity/day
and following a low-calorie, low-fat
eating plan

For big rewards:

Healthier and longer life
Avoid serious complications such as heart disease,
stroke, blindness, kidney failure and amputations
Peace of mind

Campaign run by the US National Diabetes Education

Programme

National Diabetes Education Program. Small steps. Big Rewards. Prevent Type 2 Diabetes.
http://ndep.nih.gov/campaigns/SmallSteps/SmallSteps_index.htm.
Regular physical activity can
make a huge difference
Magnitude of the Problem

300 The number of

people with
250
diabetes will nearly
200 double within the
150
1995 first quarter of this
2000
millennium.
100 2025

50 World Health Report, 1997;

Geneva: WHO.
0
millions
Developed Vs Developing

Region 2000 2025

Developed 6.2% 7.6%

countries 54.8 million 72.2 million
Developing 3.5% 4.9%
countries 99.6 million 227.7 million

King et al, Diabetes Care 1998; 21: 1414-31

Why is the prevalence of
Type 2 diabetes increasing?
Aging of the population.
Increased incidence due to
urbanization especially in the
developing countries.
More sedentary lifestyle.
Food consumption patterns, more
foods with high fat content and more
refined carbohydrates.
Factors associated with
Type 2 diabetes
Non Modifiable Modifiable
1- Genetic 1- Behavioral and
factors. lifestyle-related:
such as obesity and
2- Demographic
physical inactivity.
determinants:
such as age and 2- Metabolic and
ethnicity. intermediate risk
categories: such as
IGT, IFG and GDM.
Why should we prevent
diabetes?

To reduce human suffering.

To alleviate the economic burden.

To prevent morbidity and mortality

from diabetes-related CVD.
Levels of prevention in
Type 2 diabetes

Primary: Includes activities aimed

at preventing diabetes from
occurring in susceptible populations
or individuals.
Secondary: Early diagnosis and effective control
of diabetes in order to avoid or at least delay
the progress of the disease.
Tertiary: Includes measures taken to prevent
complications and disabilities due to diabetes.
 Why the primary prevention?

There is an urgent need to take the

prevention of cardiovascular disease
more seriously. The only sensible
strategy is the population approach to
primary prevention.
Beaglehole, the Lancet 2001; 358: 661-3
Metabolic syndrome
prevention

The main components of the

metabolic syndrome are: glucose
intolerance (diabetes or IGT),
obesity, hypertension and
dyslipidemia.
All of those components are risk
factors for CVD and can be
targeted in life style interventions
to prevent Type 2 diabetes.
Primary prevention
Most of the results on prevention come
from studies on high risk groups rather
than populations.
Studies have shown that people with IGT
has a 2-7 fold higher risk of progression to
Type 2 diabetes than persons with normal
glucose tolerance.
Among the factors that predicted
progression were obesity, elevated fasting
and 2-h blood glucose and fasting insulin
concentrations.
Types of interventions

Behavioral interventions: including

changing diet and increasing
physical activity.
And/or
Pharmacological interventions:
utilizing pharmaceutical agents to
improve glucose tolerance and
insulin sensitivity.
 Behavioral interventions

Several studies has shown that diet and

physical activity reduced the incidence of
Type 2 diabetes.
Example: The Swedish Malmo study
showed that diet and exercise for 5
years in men with IGT reduced the
incidence of Type 2 diabetes by 50%.
Eriksson et al, Diabetologia 1991; 34: 891-8
Examples

The DaQing Chinese study showed that

over 6 years there were significant and
similar reductions in the incidence of
diabetes in subjects with IGT who were
randomized to diet, exercise, or
combined diet-exercise treatment
groups.
Pan et al, Diabetes Care, 1997; 20: 537-44
Cumulative incidence of diabetes
at 6 years
70
60

50
40

30

20
10
0
Control Diet Exercise D&E
Data from: Pan et al, Diabetes Care, 1997; 20: 537-44
 Examples- Cont

The Finnish Diabetes Prevention Study

showed that Type 2 diabetes can be
prevented by changes in the lifestyles of high-
risk subjects (middle-aged, overweight
subjects with IGT). The risk of diabetes was
reduced by 58% in the intervention group.
The cumulative incidence was 11% in the
intervention group compared to 23% in the
control group.
Tuomilehto et al. NEJM, 2001; 344: 1343-50
 Pharmacological interventions

Several studies examined the effects

of various therapeutics in the
prevention of diabetes.

The evidence for the ability of

pharmacological interventions to
prevent Type 2 diabetes awaits
confirmation.
 Examples

The Diabetes Prevention Program

(DPP) funded by the NIH-USA to
perform a major IGT intervention to
examine the potential for prevention of
Type 2 diabetes. It includes both
lifestyle and pharmacological
interventions.
Diabetes Prevention Program, Diabetes Care 1999; 22: 623-4
 Population-based prevention

Solid data on the ability of community

wide programs encouraging healthy
diet and exercise to reduce the
incidence of Type 2 diabetes are not
yet available.
However, some studies has shown the
ability of such programs in reducing
the risk factors for diabetes among
other non-communicable diseases.
Secondary prevention

The purpose of secondary

prevention activities such as
screening is to identify
asymptomatic people with diabetes.

Is there an effective intervention

that may retard the progression of
disease or the severity of its
complications?
 Screening approaches

Population screening

Selective screening

Opportunistic screening
Tertiary prevention

Includes actions taken to prevent and

delay the development of acute or
chronic complications.
Acute complications: such as
hypoglycemia, severe hyperglycemia
and infections.
Chronic complications: such as
atherosclerosis, retinopathy,
nephropathy, neuropathy and foot
problems.
Effective interventions

Strict metabolic control, education

and effective treatment.

Screening for complications in

their early stages when
intervention is more effective.
Obstacles and barriers for
prevention

Economic problems: unavailability

of needed resources.

Socio-cultural problems.

Lack of data, knowledge and skills.

Examples of socio-cultural
barriers:

Obesity is not considered

negatively.
No value given to physical
exercise.
Changing diet is very difficult.
No time is granted to do physical
exercise at work.
Fatalism.
What is the Complication of DM