This is presentation for chapter II of HAL Diabetes Club O Here Its explained about causes of Diabetes and what and how it happens in T2 DM.

1. Educator
Dr. Raj Thorat
HAL DIABETES CLUB

2. CHAPTER II
Etiology & Pathogenesis
(हेतुविज्ञान तथा विकृ तत विज्ञान)

3. PART I – DIABETES EDUCATION
. Energy & Metabolism
. Insulin and Pancreas
• Pathogenesis of Diabetes
• Etiology of Diabetes

4. ENERGY AND METABOLISM
ऊर्ाा तथा चयापचय

5. ENERGY AND METABOLISM
• All living organisms must obtain and use energy to live.
“energy cannot be created or destroyed, but only changed from
one form into another or transferred from one object to another.”
- Julius Robert Mayer

6. ENERGY AND METABOLISM
• All living organisms must obtain and use energy to live.
• Energy is derived in the form of Calories/ATP by Metabolism
of Food we eat

7. ENERGY AND METABOLISM
• All living organisms must obtain and use energy to live.
• Energy is derived by Metabolism of Food we eat in the form of
Calories/ATP
• Metabolism = the chemical processes that occur within a living
organism in order to maintain life

8. FOOD NUTRIENT GROUPS
• Carbohydrates कर्बोदके (Dairy,grains,fruits)
• Proteins प्रथिने (seafood,eggs,milk)
• Fats वसा/चरर्बी (Oils,butter)

11. WHAT IS ROLE OF INSULIN

16. CHECK THIS VIDEO TO SIMPLIFY IT

20. WHAT IS INSULIN

22. ( अग्न्याशय / स्िादुवपंड )

24. WHAT HAPPENS IN TYPE 2 DM
Pathogenesis of Type 2 DM

25. WHAT IS DIABETES?

26. WHAT IS DIABETES?
 The term Diabetes mellitus (DM) describes a metabolic disorder of
multiple aetiology characterized by chronic hyperglycaemia (high
levels of blood glucose) with disturbances of carbohydrate, fat
and protein metabolism resulting from defects in insulin
production/secretion, insulin action, or both.

27.  Was previously called non-insulin-dependent diabetes
mellitus (NIDDM) or adult-onset diabetes.
TYPE 2 DIABETES

28.  Was previously called non-insulin-dependent diabetes
mellitus (NIDDM) or adult-onset diabetes.
 Type 2 diabetes may account for about 90% to 95% of all
diagnosed cases of diabetes.
TYPE 2 DIABETES

29.  Was previously called non-insulin-dependent diabetes
mellitus (NIDDM) or adult-onset diabetes.
 Type 2 diabetes may account for about 90% to 95% of all
diagnosed cases of diabetes.
 It usually begins as insulin resistance, a disorder in which the
cells do not use insulin properly. As the need for insulin rises,
the pancreas gradually loses its ability to produce insulin.
TYPE 2 DIABETES

30.  Was previously called non-insulin-dependent diabetes
mellitus (NIDDM) or adult-onset diabetes.
 Type 2 diabetes may account for about 90% to 95% of all
diagnosed cases of diabetes.
 It usually begins as insulin resistance, a disorder in which the
cells do not use insulin properly. As the need for insulin rises,
the pancreas gradually loses its ability to produce insulin.
 Type 2 diabetes is associated with older age, obesity, family
history of diabetes, history of gestational diabetes, impaired
glucose metabolism, physical inactivity, and race/ethnicity.
TYPE 2 DIABETES

31.  Was previously called non-insulin-dependent diabetes
mellitus (NIDDM) or adult-onset diabetes.
 Type 2 diabetes may account for about 90% to 95% of all
diagnosed cases of diabetes.
 It usually begins as insulin resistance, a disorder in which the
cells do not use insulin properly. As the need for insulin rises,
the pancreas gradually loses its ability to produce insulin.
 Type 2 diabetes is associated with older age, obesity, family
history of diabetes, history of gestational diabetes, impaired
glucose metabolism, physical inactivity, and race/ethnicity.
 Type 2 diabetes is increasingly being diagnosed in children
and adolescents.
TYPE 2 DIABETES

32. 32
• Type 2 DM is characterized by the presence of both Insulin
Resistance (tissue insensitivity) and some degree of Insulin
Deficiency or b- cell dysfunction
• Type 2 DM occurs when a diabetogenic lifestyle (excessive
calories, inadequate caloric expenditure and obesity) is
superimposed upon a susceptible genotype
TYPE 2 DM

33. PATHOGENESIS OF TYPE 2 DM

34. INSULIN RESISTANCE AND b-CELL DYSFUNCTION
ARE CORE DEFECTS OF TYPE 2 DIABETES
Insulin
resistance
Genetic
susceptibility,
Obesity,
Western lifestyle
Type 2 diabetes
IR
b-cell
dysfunction
b
Rhodes CJ & White MF. Eur J Clin Invest 2002; 32 (Suppl. 3):3–13.

35. • Major defect in individuals with type 2 diabetes
• Reduced biological response to insulin
• Strong predictor of type 2 diabetes
• Closely associated with obesity
What is insulin resistance?
IR
1American Diabetes Association. Diabetes Care 1998; 21:310–314.
2Beck-Nielsen H & Groop LC. J Clin Invest 1994; 94:1714–1721. 3Bloomgarden ZT. Clin Ther 1998; 20:216–231.
4Haffner SM, et al. Circulation 2000; 101:975–980. 5Boden G. Diabetes 1997; 46:3–10.

37. WHAT IS b-CELL DYSFUNCTION?
• Major defect in individuals with type 2 diabetes
• Reduced ability of b-cells to secrete insulin in response to hyperglycemia
b
b
b
b
DeFronzo RA, et al. Diabetes Care 1992; 15:318–354.

38. LOSS OF b-CELL FUNCTION OCCURS
BEFORE DIAGNOSIS
Time from diagnosis (years)
Up to
50%
loss
100
80
60
40
b-cellfunction(%)
20
0
Diagnosis
-10 -9 -8 -7 -6 -5 -4 -3 -2 -1 1 2 3 4 5 6
Holman RR. Diabetes Res Clin Prac 1998; 40 (Suppl.):S21–S25.

39. 39
How Insulin Decrease
Plasma Glucose Level?

43. HOW DO INSULIN RESISTANCE & b-CELL DYSFUNCTION
COMBINE TO CAUSE TYPE 2 DIABETES?
Abnormal
glucose tolerance
Hyperinsulinemia,
then b-cell failure
Normal IGT* Type 2 diabetes
Post-
prandial
glucose
Insulin
resistance
Increased insulin
resistance
Fasting
glucose
Hyperglycemia
Insulin
secretion
*IGT = impaired glucose tolerance

44. MORE THAN 80% OF PATIENTS PROGRESSING
TO TYPE 2 DIABETES ARE INSULIN RESISTANT
Insulin resistant;
low insulin secretion
(54%)
Insulin resistant;
good insulin secretion
(29%)
Insulin sensitive;
good insulin
secretion (1%)
Insulin sensitive;
low insulin secretion
(16%)
83%
Haffner SM, et al. Circulation 2000; 101:975–980.

48. INSULIN RESISTANCE/BETA CELL DYSFUNCTION
ETIOLOGY OF T2DM
• Genetic
• Diabetogenic Lifestyle
• Comorbid Conditions
• Secondary Diabetes

49. ETIOLOGY OF T2DM
Genetic
A) Maturity Onset Diabetes of Young (MODY)
- Diabetes runs in generations ( ≥ 3 generations)
- Early development of DM (2nd - 3rd Decades of Life)
- Usually Non-Obese
- Defects in Beta Cell Function (Genetic defect)
B) TCF7L2 gene

50. ETIOLOGY OF T2DM
Diabetogenic Lifestyle
A) Obesity
B) Inactivity
C) Dietary Habits

51. ETIOLOGY OF T2DM
Diabetogenic Lifestyle
A) Obesity
- Body weight greater than 120% of Desirable body
weight
- Abodminal Obesity
- Body Mass Index (BMI ≥ 25)

52. International Diabetes Federation Definition:
Abdominal obesity plus two other components: elevated BP, low HDL,
elevated TG, or impaired fasting glucose

53. ~90% OF PEOPLE WITH
TYPE 2 DIABETES ARE
OVERWEIGHT OR OBESE
World Health Organization, 2005. http://www.who.int/dietphysicalactivity/publications/facts/obesity

55. ETIOLOGY OF T2DM
Diabetogenic Lifestyle
B) Inactivity
- Sedentary Lifestyle
- Lack of Exercise

56. INACTIVITY – DIABETES RISK FACTOR

57. ETIOLOGY OF T2DM
Diabetogenic Lifestyle
C) Dietary Habits
- High calorie Diet (Junk Food)

58. HIGH CALORIE DIET – RISK FACTOR FOR DIABETES

59. ETIOLOGY OF T2DM
Diabetogenic Lifestyle
A) Obesity
- BMI ≥ 25
- Abdominal Obesity
B) Inactivity
- Sedentary Lifestyle
- Lack of Exercise
C) Dietary Habits
- High calorie Diet (Junk Food)

60. ETIOLOGY OF T2DM
Comorbid Conditions
A) Hypertension (High Blood Pressure)
B) Dyslipidaemia (High Cholesterol)
C) Previous Pre-DM (IGT/IFBSL)
D) Gestational DM (Diabetes in Pregnancy)
C) Polycystic Ovarian Syndrome

61. ETIOLOGY OF T2DM
Secondary Diabetes
A) Drugs
- Steroids
- Diuretics,Beta Blockers (BP lowering medicines)
- Statins (Cholesterol lowering medicines)
- Others
B) Infections
C) Pancreas Abnormality
D) Hormonal Abnormality
E) Others

64. मधुमेह होण्यासाठीच्या र्ोखमीचे कारक आहेत…
• अत्यथिक शारीररक वजन (ववशेषतः कमरेभोवती)
• मिुमेहाचा पाररवाररक इततहास
• शारीररक गततववथििंचा अभाव
• अतत पोषण
• तणाव

66. Type 2
• Older age
• Overweight
• Hypertension
• Abnormal lipid levels
• Genetics
• Race/ethnicity
• History of gestational diabetes
• History of vascular disease
• Inactivity
Type 1
• Under 30
• Genetics
• Autoimmune
• Environment
• Viral infection
• Idiopathic
COMPARISON OF RISK FACTORS FOR DIABETES

67. END OF PART I
----------------------
Short Break = 15 minutes

69. PART II – GENERAL EDUCATION
• Word of Meet
• Myth & Fact
• Nutrition Tip
• Did you Know
• Medical Tip
• Thought of the Day
• Role Model
• Achievers
• Take Home message
• Food for Thought
• Question & Answer – Discussion

70. WORD OF MEET

71. HYPERTENSION
WORD OF MEET

72. HYPERTENSION
• Shortform – HTN
• abnormally high blood pressure
WORD OF MEET

73. HYPERTENSION
• Shortform – HTN
• Abnormally high blood pressure
Normal blood pressure is
below 120/80 mm Hg and above 90/60 mm
WORD OF MEET

74. MYTH & FACT

75. Myth - All medicines must be taken after eating food
MYTH & FACT

76. Myth - All Medicines must be taken after eating food
Fact – Not all medicines are required to take after meals
- Consult Doctor for medicine timing & its regard to meals
MYTH & FACT

77. NUTRITION TIP

78. • Whenever possible while
working / Idle at Home / Workplace,
prefer standing to sitting
NUTRITION TIP

79. NUTRITION TIP

80. NUTRITION TIP

81. DID YOU KNOW

82. DID YOU KNOW

83. MEDICAL TIP

84. Make sure your doctor knows about
any allergies and adverse reactions
you have had to medicines.
MEDICAL TIP

85. THOUGHT OF THE DAY

87. SMILE
THOUGHT OF THE DAY

88. December 2012
- 39yrs/Male
- Obese (Body weight 82.20 kgs)
- Blood Pressure – 170/100 mm Hg
- Blood Sugar – F = 160 , PP = 203 , HBA1C = 6.38%
ROLE MODEL

89. A candidate with very high risk of future complications and
indicated for starting multiple medicines
- Patient was given a choice of Lifestyle Modification,Exercise
- He was a motivated and a determined person
- Took everything seriously and started Exercise, Diet and
Lifestyle Modification.
- No Medicine started for High Blood Sugar
ROLE MODEL

90. December 2015
- Body weight 72 kgs ( Reduced 10 kgs)
- Blood Pressure – 140/90 mm Hg
- Blood Sugar – F = 74 , PP = 104
November 2017
- Body weight 65 kgs ( Reduced total 17 kgs)
- Blood Pressure – 138/88 mm Hg
- Blood Sugar – F = 73 , PP = 98, HBA1C = 5.8%
ROLE MODEL

91. ROLE MODEL
Month/Year Weight
(Kgs)
Blood
Pressure
(mm Hg)
Fasting BSL
(mg%)
PP BSL
(mg%)
HBA1C (%)
Dec 2012 82.20 170/100 160 203 6.38
Dec 2015 72 140/90 74 104
Nov 2017 65 138/88 73 88 5.8

92. A BIG ROUND OF APPLAUSE FOR OUR
ROLE MODEL

93. A BIG ROUND OF APPLAUSE FOR OUR
ROLE MODEL
Mr Ajit Bhandarkar

94. Mrs Jaronia Xavier
Hba1c 7
ACHIEVER

95. TAKE HOME MESSAGE

96.  The term Diabetes mellitus (DM) describes a metabolic
disorder of multiple aetiology characterized by chronic
hyperglycaemia (high levels of blood glucose) with
disturbances of carbohydrate, fat and protein metabolism
resulting from defects in insulin production/secretion, insulin
action, or both.
TAKE HOME MESSAGE

97.  The term Diabetes mellitus (DM) describes a metabolic
disorder of multiple aetiology characterized by chronic
hyperglycaemia (high levels of blood glucose) with
disturbances of carbohydrate, fat and protein metabolism
resulting from defects in insulin production/secretion, insulin
action, or both.
 Type 2 DM is characterized by the presence of both
Insulin Resistance (tissue insensitivity) and some degree
of Insulin Deficiency or b- cell dysfunction
TAKE HOME MESSAGE

98.  The term Diabetes mellitus (DM) describes a metabolic disorder of
multiple aetiology characterized by chronic hyperglycaemia (high
levels of blood glucose) with disturbances of carbohydrate, fat
and protein metabolism resulting from defects in insulin
production/secretion, insulin action, or both.
 Type 2 DM is characterized by the presence of both Insulin
Resistance (tissue insensitivity) and some degree of Insulin
Deficiency or b- cell dysfunction
 Type 2 DM occurs when a diabetogenic lifestyle (excessive
calories, inadequate caloric expenditure and obesity) is
superimposed upon a susceptible genotype
TAKE HOME MESSAGE

99. FOOD FOR THOUGHT

100. FOOD FOR THOUGHT
• Polyuria
• Polydypsia
• Polyphagia

104. NEXT CLUB MEETING
Club O - Sunday 8th April 2018