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Type 2 Diabetes Mellitus An overview

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Title: Type 2 Diabetes Mellitus An overview


1
Type 2 Diabetes Mellitus An overview
  • Dr Jayaprakash P
  • Endocrinologist Diabetologist
  • Medical Trust Hospital
  • Kochi

2
  • risk factors
  • patho-physiology
  • diagnosis
  • complications
  • prevention
  • dietary recommendations
  • management
  • recent advances in the diagnosis and management

3
  • IDDM is now Type 1 DM
  • NIDDM is now Type 2 DM

4
What is Type 2 Diabetes Mellitus (T2DM)?
  • Current ADA definition1
  • T2DM is a metabolic disease characterized by
    hyperglycemia, resulting from a combination of
    resistance to insulin action and an inadequate
    insulin secretory response
  • T2DM involves 2 primary pathogenic processes
  • Progressive decline in pancreatic islet function
    (? insulin secretion and inadequately suppressed
    glucagon secretion)2,3
  • Diminished tissue responses to insulin (insulin
    resistance)2,4

ADAAmerican Diabetes Association 1American
Diabetes Association. Diabetes Care. 2006
29(suppl 1) S43S48. 2Weyer C, et al. J Clin
Invest. 1999 104 787794. 3Müller WA, et al. N
Engl J Med. 1970 283 109115. 4Ahrén B, Pacini
G. Diabetes Obes Metab. 2005 7 28.
5
Risk Factors
  • Age gt 45 years
  • Overweight (BMI gt 25)
  • Hypertension
  • Dyslipidemia
  • PCOD
  • H/o vascular disease
  • Family history
  • Physical inactivity
  • Race/Ethnicity
  • Previous IFG/IGT
  • H/O GDM or baby weighing gt4.5 kg
  • other clinical conditions associated with insulin
    resistance (e.g., severe obesity, acanthosis
    nigricans)

6
T2DM susceptibility loci
18 regions of the genome have been linked with
influencing type 2 diabetes risk
7
Diabetes Affects 246 Million People Worldwide
Europe 2007 53 million
Africa, Eastern Mediterraneanand Middle
East 2007 35 million
The Americas 2007 45 million
SE Asia and W Pacific 2007 114 million
Nationwide Diabetes Prevalence Categories
T2DM represents 9095 of cases (Centers for
Disease Control and Prevention. National Diabetes
Fact Sheet, 2005. Atlanta, Ga US Department of
Health and Human Services 2005.) Adapted from
International Diabetes Federation. Diabetes
Atlas. 2nd ed. 2003 3rd ed. 2006.
8
Prevalence of Diabetes Asia
No. (Millions) With Diabetes in 20- to 79-Year
Age Group ( of Population)
Country
Global prevalence of diabetes, 2007
gt20
14-20
10-14
8-10
6-8
4-6
lt4
Nationwide Diabetes Prevalence Categories
T2DM represents 9095 of cases (Centers for
Disease Control and Prevention. National
Diabetes Fact Sheet, 2005.Atlanta, Ga US
Department of Health and Human Services
2005.) Adapted from International Diabetes
Federation. Diabetes Atlas. 2nd ed. 2003 3rd ed.
2006.
9
Global Prevalence of Diabetes Projected to More
Than Double Between 1995 and 2030
1995
2000
2030
130
120
110
India
100
90
UnitedStates
80
70
China
Estimated Prevalence (millions)
Turkey
60
Pakistan
50
40
Nigeria
30
20
10
0
Africa
Americas
Eastern Mediterranean
Europe
Southeast Asia
Western Pacific
T2DM represents 9095 of cases Adapted from
World Health Organization. Country and regional
data. Available at http//www.who.int/diabetes/fa
cts/world_figures/en/. Accessed April 14, 2006
King H, et al. Diabetes Care. 1998 21 14141431.
10
Is it the Globalization ?
11
Mc.. Giant Meals
  • Mc.. Big Extra with Cheese, super-sized soft
    drink fries 1805 calories and 84 grams of
    fat!!!

12
Social Impact of Modernization/ Westernization
  • Machine driven jobs
  • Higher tech, computers, tv, dvd
  • Lower quality foods
  • Loss of traditional nutritious diets
  • Loss of places for children to play
  • Population growth
  • Ageing population
  • Stress

13
Diagnostic Criteria
14
ADA Diagnostic Criteria for T2DM have been
Evolving
ADA Diagnostic Criteria
Year
19791
FPG gt140 mg/dL or2-h PG (OGTT) gt200 mg/dL
19972,3
FPG gt126 mg/dL or2-h PG (OGTT) gt200 mg/dL
20064
FPG gt126 mg/dL or 2-h PG (OGTT) gt200 mg/dL
20095
No new diagnosticcriteria mentioned
ADAAmerican Diabetes Association FPGfasting
plasma glucose HbA1chemoglobin A1c OGTToral
glucose tolerance test PGplasma
glucoseT2DMtype 2 diabetes mellitus ADA
asserted that the group treatment goal is lt7.0,
but individual treatment goal should be as close
to normal (lt6.0) as possible without inducing
significanthypoglycemia (Diabetes Care. 2006
29 S4S42). 1National Diabetes Data Group.
Diabetes. 1979 28 10391057. 2American Diabetes
Association. Diabetes Care.1997 20 11831197.
3American Diabetes Association. Diabetes Care.
1997 20(suppl 1) S5S13. 4American Diabetes
Association. Diabetes Care. 200629(suppl 1)
S43S48 5 Nathan DM, et al. Diabetes Care. 2009
32193203.
15
WHO Diagnostic Criteria
IFGimpaired fasting glucose IGTimpaired
glucose tolerance T2DMtype 2 diabetes mellitus
WHOWorld Health Organization In asymptomatic
patients, 2 abnormal fasting values are required
for diagnosis Adapted from World Health
Organization. Definition, Diagnosis and
Classification of Diabetes Mellitus and Its
Complications. Geneva WHO1999.
16
ADA Diagnostic Cut Points for IFG, IGT, and
Diabetes
IFG IGT
Normal Glucose
ADAAmerican Diabetes Association IFGimpaired
fasting glucose IGTimpaired glucose
tolerance Adapted from American Diabetes
Association. Diabetes Care. 2006 29 (Suppl 1)
S43S48.
17
CLINICAL FEATURES
18
CLINICAL FEATURES
  • Polyuria
  • Polydipsia
  • Polyphagia
  • Weight loss
  • Blurred vision
  • Poor wound healing
  • Increase in infections
  • Candidal vaginitis/balanitis
  • UTI
  • Malignant Otitis Externa

19
Hyperglycemia
  • Drowsy
  • Flushed
  • Thirsty

20
Screening Recommendations for DM in presumably
healthy individuals
  • All persons at age ? 45 yrs
  • High Risk
  • BMI ? 27 kg/m2
  • First degree relative with T2DM
  • GDM or baby gt 9Ib
  • Hypertension (? 140/90mm Hg)
  • TG ? 250 mg/dl, HDL-ch 35 mg/dl
  • Previous IGT or IFG
  • Signs of Insulin resistance

21
Pathophysiology
22
Abnormal Pancreatic Islet Function Determines the
Development of IGT and T2DM in the Setting of
Insulin Resistance
Age, lifestyle, environmental factors
IGTimpaired glucose tolerance NGTnormal
glucose tolerance T2DMtype 2 diabetes
mellitus Adapted from Ahrén B, et al. Diabetes
Obes Metab. 2005 7 28.
23
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24
Anatomy of Pancreas
25
Islet of Langerhans
26
Inadequate ?-cell Compensation for Insulin
Resistance
95 CI
Nonprogressors (n23)
NGT
NGT
Insulin Secretion
NGT
NGT
IGT
Progressors (n11)
T2DM
Resistant
Sensitive
Insulin Resistance
CIconfidence interval IGTimpaired glucose
tolerance NGTnormal glucose tolerance
T2DMtype 2 diabetes mellitus Adapted from Weyer
C, et al. J Clin Invest. 1999 104 787794.
27
REGULATION OF BLOOD GLUCOSE
PANCREAS
INSULIN SECRETION
MUSCLE
LIVER GLUCOSE PRODUCTION
BLOOD GLUCOSE
PERIPHERAL GLUCOSE UPTAKE
INTESTINE GLUCOSE ABSORPTION
ADIPOSE
28
Normal pancreatic function
Glucose dependent insulin secretion
Insulin synthesis
Somatostatin secretion
Glucagon secretion
Pancreatic cells
?-cell
?-cell
?-cell
Ørskov et al. Endocrinology 198812320092013.
Drucker et al. Proc Natl Acad Sci USA
19878434343438.
29
Roles of Insulin and Glucagon in Normal Glucose
Homeostasis
Glucose (plasma concentration)
Insulin and glucagon secretion are also
influenced by other nutrients, hormones, and
neural input Adapted from Berne RM, Levy MN,
eds. Physiology. St. Louis, Mo Mosby, Inc 1998
822847.
30
Pancreatic Islet Dysfunction Leads to
Hyperglycemia in T2DM
? Glucose
HGOhepatic glucose output Adapted from Ohneda A,
et al. J Clin Endocrinol Metab. 1978 46
504510 Gomis R, et al. Diabetes Res Clin Pract.
1989 6 191198.
31
ß-cell Function Continues to Decline Regardless
of Intervention in T2DM
Progressive Loss of ß-cell Function Occurs prior
to Diagnosis
Sulfonylurea (n511)
100
Diet (n110)
Metformin (n159)
80
60
ß-cell Function ()
40
20
0
5
4
3
2
1
0
1
2
3
4
5
6
Years since Diagnosis
T2DMtype 2 diabetes mellitus ß-cell function
measured by homeostasis model assessment
(HOMA) Adapted from UKPDS Group. Diabetes. 1995
44 12491258.
32
Loss of Postprandial Glycemic Control Precedes
Stepwise Deterioration of Fasting with Worsening
Diabetes
HbA1chemoglobin A1c T2DMtype 2 diabetes
mellitusMonnier L, et al. Diabetes Care. 2007
30 263269.
33
Compensatory Increase in ß-cell Insulin Secretion
Fails During Progression of T2DM
N149
25 20 - 15 - 10 - 5 - 0 -
Fasting Plasma Insulin (µU/mL)

0
60 100 140 180 220 260 300
Fasting Plasma Glucose (mg/dL)
T2DMtype 2 diabetes mellitus Protocol
3H-3-glucose administered for 2 hours in control
group (n72) and 3 hours in diabetic group
(n77) Adapted from DeFronzo RA, et al.
Metabolism. 1989 38 387395.
34
Complications
35
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36
Tissue Damage in Many Organ Systems Leads to
Serious Long-term Complications in T2DM
Brain and Cerebral Circulation (stroke, TIA)
Eyes (retinopathy, glaucoma, cataracts)
Heart and Coronary Circulation (angina, MI, CHF)
Kidneys (nephropathy, ESRD)
Peripheral Nervous System (peripheral neuropathy)
Peripheral Vascular Tree (peripheral vascular
disease, gangrene, amputation)
CHFcongestive heart failure ESRDend-stage
renal disease MImyocardial infarction
TIAtransient ischemic attack T2DMtype 2
diabetes mellitus Adapted from International
Diabetes Federation. Complications. Available at
http//www.eatlas.idf.org/complications. Accessed
April 14, 2006.
37
Complications at Diagnosis of T2DM
  • Retinopathy (gt1 microaneurysm) 21
  • Abnormal ECG 18
  • Absent foot pulses 14
  • Impaired reflexes /vibration sense 7
  • Angina pectoris 3
  • Intermittent claudication 3
  • Myocardial infarction 2
  • UKPDS VIII, 1991

38
Cardiovascular Complications
  • Leading cause of death in diabetic patients
  • 2-4 times greater risk of ischemic heart disease
    or stroke
  • Prone to silent heart attacks or atypical
    presentation
  • Increased risk of cardiomegaly and CHF
  • High incidence of peripheral vascular disease

39
Ophthalmologic Complications
  • Diabetic Retinopathy is the leading cause of
    blindness in patients 25-74
  • Increased risk of glaucoma and cataracts
  • 97 of DM patients taking insulin have some form
    of retinopathy
  • Intensive glucose control lowers risk of
    proliferative retinopathy by 75
  • Red and/or painful eye or simple headache
    warrants intraocular pressure measurement
  • Fundus exam cotton wool spots, microaneurysms,
    vascular proliferation

40
Diabetic Nephropathy
  • Leading cause of end stage renal disease
  • Accounts for 43 of all cases of new onset renal
    failure per year
  • Renal hypertension results in protein deposition
    and sclerosis of glomerulus
  • Microalbuminuria clinical marker for presence and
    degree nephropathy
  • Add ACEI and avoid nephrotoxic drugs, yearly 24
    hour urine protein level

41
Normal glomerulus Hyaline Deposition
42
Foot and Lower Extremity Ulcers
  • Affects 15 of diabetic patients, 20 of diabetic
    admissions
  • Pathologic triad neuropathy, atherosclerotic
    vascular disease, impaired immunity
  • Risk factors High HBA1C, older age, duration of
    disease, tight fitting shoes, smoking
  • Classification
  • Non-limb-threatening lt2cm ulceration and no
    inflammation
  • Limb-threatening gt2cm ulceration or
    inflammation, ascending lymphangitis, bone
    involvement, nonpalpable pulses
  • Life-threatening signs of sepsis, metabolic
    derangements (DKA, HHNKS)

43
Glycemic Control and Treatment Options
44
The Triad of Treatment
45
Standard Approach to the Management of T2DM
Treatment Intensification
Adapted from Riddle MC. Endocrinol Metab Clin
North Am. 2005 34 7798.
46
Lifestyle measures
47
Primary prevention in high risk population
  • structured programs that emphasize lifestyle
    changes
  • moderate weight loss (7 body weight)
  • regular physical activity (150 min/week)
  • dietary strategies including reduced calories and
    reduced intake of dietary fat
  • dietary fiber (14 g fiber/1,000 kcal) and foods
    containing whole grains (one-half of grain
    intake)

48
Controlling diabetes (secondary prevention)
  • carbohydrate from fruits, vegetables, whole
    grains, legumes and low-fat milk is encouraged
  • Monitoring carbohydrate intake
  • Limit saturated fat to 7 of total calories.
  • Intake of trans fat should be minimized
  • lower dietary cholesterol to 200 mg/day
  • Two or more servings of fish per week (with the
    exception of fried fish)
  • protein intake (1520 of energy)
  • Alcohol one drink per day or less for women and
    two drinks per day or less for men

49
Alcohol equivalents
  • 1 Drink
  • 12 oz (360ml) beer
  • 5 oz (60ml) wine
  • 1.5 oz (18ml) distilled spirits
  • small peg 30 ml
  • large peg 60 ml

50
Antidiabetic Drugs
51
Antidiabetic Drugs
  • Insulin Secretagogues
  • Sulfonylureas. Meglitinides
  • Sensitizers
  • Biguanides, Thiazolidinediones
  • Alpha-glucosidase inhibitors
  • Acarbose, Voglibose
  • Peptide analogs
  • Incretin mimetics - Glucagon-like peptide (GLP)
    analogs and agonists
  • DPP-4 inhibitors
  • Sitagliptin, Vildagliptin
  • Amylin analogues
  • Pramlitinide

52
Pharmacologic Targets of Current Drugs Used
inthe Treatment of T2DM
Biguanides Increase glucose uptake and decreases
hepatic glucose production
53
Major Adverse Events
Metformin1
SUs1
Meglitinides1
TZDs1-3
a-glucosidase inhibitors1
Incretin mimetics4-8
CHFcongestive heart failure GIgastrointestinal
SUsulfonylurea T2DMtype 2 diabetes mellitus
TZDthiazolidinedione aRole uncertain 1Inzucchi
SE. JAMA. 2002 287 360372 2Avandia US
Prescribing Information 3Dormandy JA, et al.
Lancet. 2005 366 12791289 4Buse JB, et al.
Diabetes Care. 2004 27 26282635 5DeFronzo RA,
et al. Diabetes Care. 2005 28 10921100
6Kendall DM, et al. Diabetes Care. 2005 28
10831091 7Kolterman OG, et al. Am J Health-Syst
Pharm. 2005 62 173181 8Byetta US Prescribing
Information.
54
Contraindications and Precautions
Contraindicated in renal dysfunction, avoid in
liver disease, monitor renal function
Metformin
Use with caution in elderly, and in renal and
hepatic impairment, watch for hypoglycemia
SUs
Use with caution in elderly, and in renal and
hepatic impairment
Meglitinides
Contraindicated in severe liver disease,
congestive heart failure,
monitor liver enzymes
TZDs
a-glucosidase inhibitors
Not recommended in severe renal impairment,
check serum liver enzymes
Exenatide injectable
Use caution in severe renal or severe GI disease
GIgastrointestinal SUsulfonylurea T2DMtype 2
diabetes mellitus TZDthiazolidinedione From
Glucophage package insert. Princeton, NJ
Bristol-Myers Squibb Company, 2004 Starlix
package insert. East Andover, NJ Novartis
Pharmaceuticals Corporation, 2004 Avandia
package insert. Research Triangle Park, NC
GlaxoSmithKline, 2006 Byetta package insert.
San Diego, CA Amylin Pharmaceuticals, Inc, 2006.
55
ADA Diagnostic Criteria and Treatment Goals for
T2DM have been Evolving
ADA Treatment Goal
ADA Diagnostic Criteria
Year
19791
FPG gt140 mg/dL or2-h PG (OGTT) gt200 mg/dL
FPG lt140 mg/dL
19972,3
FPG gt126 mg/dL or2-h PG (OGTT) gt200 mg/dL
HbA1c lt7.0
HbA1c lt7.0 (general goal) HbA1c lt6.0
(individual goal)
20064
FPG gt126 mg/dL or 2-h PG (OGTT) gt200 mg/dL
HbA1c 7.0 is call for actionto initiate or
change therapy
20095
No new diagnosticcriteria mentioned
HbA1c lt7.0
ADAAmerican Diabetes Association FPGfasting
plasma glucose HbA1chemoglobin A1c OGTToral
glucose tolerance test PGplasma
glucoseT2DMtype 2 diabetes mellitus ADA
asserted that the group treatment goal is lt7.0,
but individual treatment goal should be as close
to normal (lt6.0) as possible without inducing
significanthypoglycemia (Diabetes Care. 2006
29 S4S42). 1National Diabetes Data Group.
Diabetes. 1979 28 10391057. 2American Diabetes
Association. Diabetes Care.1997 20 11831197.
3American Diabetes Association. Diabetes Care.
1997 20(suppl 1) S5S13. 4American Diabetes
Association. Diabetes Care. 200629(suppl 1)
S43S48 5 Nathan DM, et al. Diabetes Care. 2009
32193203.
56
Current Treatment Goals for Glycemic Control
ACEAmerican College of Endocrinology
ADAAmerican Diabetes Association
HbA1chemoglobin A1c IDFInternational Diabetes
Federation Adapted from 1ADA / EASD consensus
statement Nathan DM, et al. Diabetes Care.
32193203 2American Association of Clinical
Endocrinologists, American College of
Endocrinology. Endocr Pract. 2002 8 (Suppl 1)
511 3International Diabetes Federation. Global
Guideline for Type 2 Diabetes. Brussels
International Diabetes Federation 2005.
57
ADA and EASD algorithm for the management of
type 2 diabetes
Tier 1
Well validated therapies
Lifestyle and met intensive insulin
Atdiagnosis Lifestylemetformin
Lifestyle andmet basal insulin
Lifestyle and met SUa
Step 1
Step 2
Step 3
Tier 2
Less well validated therapies
Lifestyle and met pio
Lifestyle and met pio SUa
No hypoglycaemia Oedema/CHF Bone loss
Lifestyle and met GLP-1 agonistb
Lifestyle andmet basal insulin
No hypoglycaemia Weight loss Nausea/vomiting
Reinforce lifestyle interventions every visit and
check HbA1C every 3 months until HbA1C is lt7
and then at least every 6 months. The
interventions should be changed if HbA1C is 7
aSUs other than glybenclamide (glyburide) or
chlorpropamide. bInsufficient clinical use to be
confident regarding safety. Metmetformin
Piopioglitazone SUsulfonylurea
Nathan et al., Diabetes Care 2008 Epub
58
American Association of Clinical
Endocrinologists algorithm for patients with T2DM
Initiate monotherapyMetformin, TZD,
secretagogues, DPP-4 inhibitors, a-glucosidase
inhibitors
Drug-naïve patientsHbA1c 67
HbA1c 78
Initiate combination therapySecretagogue
metformin, TZD, or a-glucosidase inhibitor TZD
metforminDPP-4 metformin or TZDSecretagogue
metformin TZD Fixed-dose combinationsInsulin
Lifestyle Changes
Intensify combination therapyTo address fasting
and postprandial glucose levels
HbA1c 810
HbA1c gt10
Initiate / intensify insulin therapy
As aboveExenatide may be combined with oral
therapies in patients not achieving goals
Patients currently pharmacologically treated
DPP-4dipeptidyl peptidase-4 T2DMtype 2
diabetes mellitus TZDthiazolidinedioneAACE
Diabetes Mellitus Clinical Practice Guidelines
Task Force. Endocr Pract. 2007 13 (Suppl 1)
1634.
59
UKPDS 35 Significant Risk Reduction for T2DM
Complications with Each 1 Reduction in Mean HbA1c
Risk Reduction with 1 Decline in Updated HbA1c
N3642
P lt0.0001
P lt0.0001
P0.035
P0.021
P lt0.0001
0 15 30 45
14
12
16
19
21
37
43
CHFcongestive heart failure HbA1chemoglobin
A1c PVDperipheral vascular disease
MImyocardial infarction Adapted from Stratton
IM, et al. BMJ. 2000 321 405412.
60
UKPDS Glycemic Control Worsens over Time
9
8
Median HbA1c ()
7
ADA goal (7.0)
Upper limit of normal range (6.2)
6
0
0
2
4
6
8
10
Time from Randomization (y)
ADAAmerican Diabetes Association
HbA1chemoglobin A1c Adapted from UK Prospective
Diabetes Study (UKPDS) Group. Lancet. 1998 352
854865.
61
Progression of Hyperglycemia in T2DM
(Retrospective Analysis)
Riedel AA, et al. Diabetes. 2006 55 (Suppl 1)
A132.
62
ADOPT Study Progression of Hyperglycemia in T2DM
Treatment difference (95 CI)Rosiglitazone vs
metformin, ?0.13 (?0.22 to ?0.05)
P0.002 Rosiglitazone vs glyburide, ?0.42 (?0.50
to ?0.33) P lt0.001
8.0
7.6
7.2
HbA1c ()
6.8
Annualized slope (95 CI)
6.4
Rosiglitazone, 0.07 (0.06 to 0.09) Metformin,
0.14 (0.13 to 0.16) Glyburide, 0.24 (0.23 to
0.26)
6.0
0
0
1
2
3
4
5
Time (y)
No. of Patients 4012 3308 2991 2583 2197 822
Significant difference rosiglitazone vs other
treatment groups with Hochberg adjustment Kahn
SE, et al. N Engl J Med. 2006 355 24272443.
63
OHAs Sulfonylureas
64
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65
SU Mode of action
  • Binding to SUR protein
  • Closure of KATP channels, membrane depolarization
    activation of voltage dependent Ca2 channels
  • Ca2 flux to increase cytoplasmic Ca2 ,
    contraction of microtubular system exocytosis
    of ISG

66
Insulin Preparations
67
LATEST ADDITION GLP1 Agonists DPP4 Inhibitors
68
Latest Drugs
Biguanides Increase glucose uptake and decreases
hepatic glucose production
DDP-4dipeptidyl peptidase-4 GLP-1glucagon-like
peptide-1 T2DMtype 2 diabetes mellitusAdapted
from Cheng AY, Fantus IG. CMAJ. 2005 172
213226.Ahrén B, Foley JE. Int J Clin Pract
2008 62 8-14.
69
monitoring
70
Urine Glucose Testing - Is It Still Useful?
71
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72
SMBG with glucometers
73
SMBG
74
HbA1c and average glucose
75
Trends of Diabetes in India
  • Increasing prevalence in urban population
  • Occurs at younger age
  • 54 had diabetes before the age of 50 yrs.
  • Prevalence of IGT is higher than DM (14 vs
    12.1)
  • Undiagnosed DM is more than known DM (CURES 9.1
    vs 6.1)
  • Majority of patients are non-obese but centrally
    obese

76
SUMMARY
  • T2DM is already an epidemic of dangerous
    proportions
  • The epidemic is still growing
  • India is at the epicenter of this epidemic
  • Early diagnosis with routine screening should be
    mandatory
  • Early and sustained glycemic control can prevent
    or minimise future complications

77
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