1. Centro para el Manejo de Datos
Centro de Diabetes para Puerto Rico
Estado Libre Asociado
de Puerto Rico
Centro para el Manejo de Datos
Centro de Diabetes para Puerto Rico
Estado Libre Asociado
de Puerto Rico

2. over the past few decades, diabetes has emerged as an important medical problem in developing regions of the world
In a more recent report on global diabetes estimates and projections for the years 2000–2030,Wild et al. showed that the worldwide prevalence of diabetes for all age groups would increase from 2.8% in 2000 to 4.4% in 2030, with a corresponding 114% increase in the numbers, from 171 million to 366 million. The greatest relative increases will occur in developing regions, namely India and the Middle Eastern Crescent

3. Important contributors include an increase in the urban population in developing countries and an increase in the proportion of people >65 years of age across the world

4. Diabetes mellitus (DM) is a common syndrome and caused by lack or decreased effectiveness of endogenous insulin
The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels.

5. Classification of primary diabetes
Type 1 (insulin-dependent (IDDM), juvenile onset):
Only 5–10% of those with diabetes
May occur at any age but more common in patients <30y.
results from a cellular-mediated autoimmune destruction of the β-cells of the pancreas

6. Some patients, particularly children and adolescents, may present with ketoacidosis as the first manifestation of the disease.
These patients are also prone to other autoimmune disorders such as Hashimoto’s thyroiditis, vitiligo, autoimmune hepatitis and pernicious anemia.

7. Type 2 (non-insulin dependent (NIDDM), maturity onset):
90–95% of those with diabetes
the cause is a combination of resistance to insulin action and an inadequate compensatory insulin secretory response
a degree of hyperglycemia sufficient to cause pathologic and functional changes in various target tissues, but without clinical symptoms, may be present for a long period of time before diabetes is detect

8. The Normal Pancreatic Islet
“An understanding of the normal physiology of the pancreas is important for any discussion of type 2 diabetes. The pancreas is an organ that has both exocrine and endocrine functions. The endocrine tissue makes up only 1% to 5% of the total pancreatic mass in adults. It is randomly distributed throughout the exocrine pancreas, with a greater concentration in the head of the pancreas.1 The endocrine cells are arranged into units called islets of Langerhans. Each islet of Langerhans contains several types of cells, namely, alpha-, beta-, gamma-, and delta-cells. Beta-cells predominate and tend to be located in the center of the islet. Beta-cells make up approximately 70% to 80% of the islet mass. Gamma- and delta-cells constitute less than 10% of the islets. The alpha- and beta-cells both play important roles in glucose homeostasis.2 Beta- cells produce insulin and amylin, and alpha-cells produce glucagon. Both insulin and glucagon are essential for glucose homeostasis. When blood glucose is elevated after meals, beta-cells release insulin into the bloodstream. Alternatively, when blood glucose levels fall, alpha-cells release glucagon. These responses help maintain a normal glycemic state.”3,4
Gamma- and delta-cells also produce important substances. Gamma-cells produce pancreatic polypeptide (PP) and delta-cells produce somatostatin.2 In studies, exogenous administration of pancreatic polypeptide reduced gastric acid secretion mediated by cholecystokinin and increased transit times in the intestine. Somatostatin’s actions are inhibitory. In the pituitary, it inhibits the secretion of growth hormone and thyrotropin, and in the pancreas, it inhibits insulin, glucagon, and pancreatic polypeptide. Somatostatin also inhibits several gut peptides and gastric acid secretion. Pancreatic exocrine secretion is also affected by both pancreatic polypeptide and somatostatin.5
References:
1. Foulis AK, Clark A. Pathology of the pancreas in diabetes mellitus. In: Kahn CR, Weir GC, eds. Joslin’s Diabetes Mellitus. 13th ed. Philadelphia, Pa: Lea & Febiger; 1994:265–281.
2. Cleaver O, Melton DA. Development of the endocrine pancreas. In: Kahn CR, Weir GC, King GL, Jacobson AM, Moses AC, Smith RJ, eds. Joslin’s Diabetes Mellitus. 14th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2005: 21–39.
3. Porte D Jr, Kahn SE. The key role of islet dysfunction in type II diabetes mellitus. Clin Invest Med. 1995;18:247–254.
4. Ward WK, Beard JC, Halter JB, Pfeifer MA, Porte D Jr. Pathophysiology of insulin secretion in non-insulin-dependent diabetes mellitus. Diabetes Care. 1984;7:491–502.
5. Boushey RP, Drucker DJ. Gastrointestinal hormones and gut endocrine tumors. In: Larsen PR, Kronenberg HM, Melmed S, Polonsky KS, eds. Williams Textbook of Endocrinology. 10th ed. Philadelphia, Pa: Saunders; 2003:1777–1796.

9. Islet Cell Dysfunction and Abnormal Glucose
Homeostasis in Type 2 Diabetes
Structural Changes in Islets With Type 2 Diabetes
In the normal pancreas, the exocrine cells make up the majority of the organ. The endocrine cells in the islets of Langerhans constitute about 1% to 5% of the pancreatic mass.1 There are between 300,000 and 1.5 million islets in the adult pancreas. Beta-cells, the insulin-producing cells, constitute approximately 70% to 80% of the islet mass.2 Beta-cell mass is determined by the balance between the production of beta-cells and the disappearance of beta-cells. The production of beta-cells is determined by the rates of neogenesis and replication. The disappearance of beta-cells is determined by the rate of cell death by necrosis or apoptosis.5
In type 2 diabetes, there are structural changes in the islets of the pancreas. Up to 90% of patients with type 2 diabetes develop amyloid deposits between the capillaries and the islets. These deposits form cords that compress the islets.3 Amylin, also referred to as islet amyloid polypeptide, is the peptide constituting the deposits and is normally produced by beta-cells. Where amyloid deposits are found, reduction in beta-cell mass of the islet is also observed. However, it is not known whether amyloid deposits cause a reduction in the number of beta-cells. The role of amylin is still being investigated.4 Beta-cell mass may be affected by impaired neogenesis and proliferation of beta-cells. In patients with type 2 diabetes there is an increased frequency of beta-cell apoptosis, also known as programmed cell death.5,6 This process leads to a reduction in insulin production. This illustrates structural changes in islets with type 2 diabetes.
References:
1. Foulis AK, Clark A. Pathology of the pancreas in diabetes mellitus. In: Kahn CR, Weir GC, eds. Joslin’s Diabetes Mellitus. 13th ed. Philadelphia, Pa: Lea & Febiger; 1994:265–270.
2. Cleaver O, Melton DA. Development of the endocrine pancreas. In: Kahn CR, Weir OC, King GL, Jacobson AM, Moses AC, Smith RJ, eds. Joslin’s Diabetes Mellitus. 14th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2005:21–39.
3. Roth J, Komminoth P, Klöppel G, Heitz PU. Diabetes and endocrine pancreas. In: Damjanov I, Linder J, eds. Anderson’s Pathology. 10th ed. St. Louis, Mo: Mosby-Year Book Inc. 1996:2042–2070.
4. Leahy JL. β-cell dysfunction in type 2 diabetes mellitus. In: Kahn CR, Weir GC, eds. Joslin’s Textbook of Diabetes. 14th ed. Philadelphia, Pa: Lea & Febiger; 2005:449–461.
5. Butler AE, Janson J, Bonner-Weir S, Ritzel R, Rizza RA, Butler PC. β-cell deficit and increased β-cell apoptosis in humans with type 2 diabetes. Diabetes. 2003;52:102–110.
6. Marchetti P, Del Guerra S, Marselli L, et al. Pancreatic islets from type 2 diabetic patients have functional defects and increased apoptosis that are ameliorated by metformin. J Clin Endocrinol Metab. 2004;89:5535–5541.

10. Most patients with this form of diabetes are obese, obesity itself causes some degree of insulin resistance
Insulin resistance may improve with weight reduction and/or pharmacological treatment of hyperglycemia but is seldom restored to normal

11. The risk of developing this form of diabetes increases with:
age,
obesity,
and lack of physical activity.
In women with prior GDM
Individuals with hypertension or dyslipidemia

13. Type 1 DM Younger More lean Insulin-deficient Low triglycerides
Older
Overweight
Insulin-resistant
High TG’s/Low HDL-C

14. Gestational diabetes mellitus (GDM)
GDM is defined as any degree of glucose intolerance with onset or first recognition during pregnancy.
GDM complicates 4% of all pregnancies in the U.S., resulting in 135,000 cases annually

15. Presentation of DM Acute: Ketoacidosis
Sub-acute: Weight loss, polydipsia, polyuria, lethargy, irritability, infections (candidiasis, skin infection, recurrent infections slow to clear), genital itching, blurred vision, tingling in hands/feet.

16. With complications: Presentation with skin changes, peripheral neuropathy with risk of foot ulcers, amputations, nephropathy, eye disease
Asymptomatic: DM may be detected on routine screening during well man/woman checks .

17. Natural History of DM 2 Years from diagnosis Onset Diagnosis
-10 -5 5 10 15
Onset
Diagnosis
Insulin secretion
Insulin resistance
Postprandial glucose
Fasting glucose
Microvascular complications
Macrovascular complications
Pre-diabetes
Type 2 diabetes
Adapted from Ramlo-Halsted BA, Edelman SV. Prim Care. 1999;26: ;
Nathan DM. N Engl J Med ;347:

18. Impact of Diabetes Mellitus
The leading cause of nontraumatic lower extremity amputations
Diabetes is a dangerous disease, not just because of the disease itself, but it is associated with high rates of LEA, Renal Disease, CHD and blindness (Supercourse)
The leading cause of new cases of end stage renal disease
A 2- to 4- fold increase in cardio- vascular mortality
The leading cause of new cases of blindness in working- aged adults

19. Criteria for the Diagnosis of Diabetes

20. Global Prevalence of Diabetes

21. Estimated global prevalence of type 1 and type 2 diabetes
Type 2 diabetes has now reached epidemic proportions in many developing and most developed nations. Not only have we already witnessed a dramatic increase, but the epidemic of Type 2 diabetes will continue to escalate around the world in the coming decades. The epidemic is clearly on. It is estimated that the global number of persons with diabetes will rise from 151 million in the year 2000, to 221 million by the year 2010 (13), and to 300 million by 2025 (15). This rise is predicted to occur in virtually every country in the world, with the greatest increases expected in developing countries.

22. Global Prevalence Estimates, 2000 and 2030
4.4 %
2.8 %
Reference: Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes. Diabetes Care. 2004; 27(5):
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23. Year 2000 Diabetes in the World millions 31.7 20.8 17.7 8.4 6.8 China
India
31.7
Year 2000
China
20.8
USA
17.7
Japan
6.8
Indonesia
8.4
millions
Reference: Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes. Diabetes Care. 2004; 27(5):
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24. Year 2010 Diabetes in the World millions 79.4 42.3 30.3 21.3 8.9 China
India
79.4
Year 2010
China
42.3
USA
30.3
Japan
8.9
Indonesia
21.3
millions
Reference: Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes. Diabetes Care. 2004; 27(5):
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25. Prevalence of Diabetes by Country
* > 18 years only. Centers for Disease Control and Prevention. Behavioral Risk Factor Surveillance System Atlanta, GA: United States, Department of Health and Human Services.
** Dunstan DW, Zimmet PZ, Welborn TA, Courten MP, Cameron AJ, Sicree RA, et al. The raising prevalence of diabetes and impaired glucose tolerance. Diabetes Care. 2002; 25(5):
*** Warsy AS, el-Hazmi MA. Diabetes mellitus, hypertension and obesity-common multifactorial disorders in Saudis. Eastern Mediterranean Health Journal. 1999; 5(6):
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26. Prevalence of Diabetes in Adults United States, BRFSS* 1998 - 2003
* BRFSS = “Behavioral Risk Factor Surveillance System” (>18 years). Centers for Disease Control and Prevention. Behavioral Risk Factor Surveillance System Atlanta, GA: United States, Department of Health and Human Services.
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27. Global Incidence of IDDM
The overall results demonstrate that China has the lowest incidence in the world

30. National Diabetes Statistics

31. RISK FACTORS OF DM

32. GENETIC RISK
There is ample evidence that type 2 diabetes has a strong genetic component.
Type 2 diabetes clusters in families.
The lifetime risk of developing type 2 diabetes is about 40% in offspring of one parent with type 2 diabetes ; the risk approaches 70% if both parents have diabetes.

33. Intriguingly, the risk in the offspring seems to be greater if the mother rather than the father has type 2 diabetes
a first-degree relative of a patient with type 2 diabetes has a threefold increased risk of developing the disease

34. ADULT OBESITY
Obesity and weight gain are major risk factors for type 2 diabetes, and they have been blamed for or implicated in the rising prevalence of diabetes worldwide.
A community-based survey in Saudi Arabia in 1995–2000 of people aged 30–70 years found that 36.9% were overweight and 35.5% were obese.
Men were more likely to be overweight and women were more likely to be obese

35. CHILDHOOD OBESITY
The sharp increase in the prevalence of overweight and obesity worldwide is not only limited to adults, but also extends to adolescents and children and even to preschool children. This increase in weight led to an increase in the incidence of type 2 diabetes in childhood, to a point that it is becoming more common than type 1 diabetes in a few countries, such as in Japan and Taiwan

36. Dietary risk factors
Studies utilizing a variety of epidemiological approaches have implicated a range of lifestyle-related environmental factors in the etiology of type 2 diabetes

37. CARBOHYDRATE AND DIETARY FIBER
refined carbohydrates, and sugars in particular, might be involved in the etiology of type 2 diabetes
Over 40 studies have examined the role of sugars in the etiology of type 2 diabetes, with about half suggesting a positive association and a comparable number suggesting no association

38. On the other hand, there is rather more support for the suggestion that foods rich in slowly digested or resistant starch or high in dietary fiber (nonstarch polysaccharide) might be protective In controlled experiments, diets high in soluble fiber-rich foods [20] or foods with a low glycemic index are associated with improved diurnal blood glucose profiles and long-term overall improvement in glycemic control, as evidenced by reduced levels of glycated hemoglobin

39. Some other studies provide indirect support for this hypothesis
Some other studies provide indirect support for this hypothesis. Diabetes risk appears to be lower in Seventh-Day Adventists who are vegetarians than in those who are not strict vegetarians [22].
The diet of vegetarians is characterized by a high intake of dietary fiber, but differs in other ways from that of nonvegetarians. In addition to not eating meat and animal products, vegetarians also have less saturated fat,more polyunsaturated fat and a diet which differs in micronutrient composition when compared with nonvegetarians.

40. DIETARY FATS
More than 60 years ago, Himsworth [23] suggested that high intakes of fat increased the risk of diabetes in populations and individuals.
In the San Luis Valley Diabetes Study, a high fat intake was associated with an increased risk of type 2 diabetes and impaired glucose tolerance (IGT) [25];

41. in a follow-up, 1 to 3 years later, fat consumption predicted progression to type 2 diabetes in those with IGT

42. On the other hand, no association was found between fat intake and risk of type 2 diabetes in a 12-year follow-up of women in Gothenburg, Sweden
The type of dietary fat may also be relevant. Saturated fatty acids were positively related to fasting and postprandial glucose levels in normoglycemic Dutch men, the effect being independent of energy intake and obesity.

43. In a recent Italian study, intake of butter (rich in palmitic and myristic acids) was positively associated with fasting glucose levels, and the use of olive oil (high in oleic acid) was inversely associated with fasting glucose Levels
The ratio of polyunsaturated to saturated fatty acids in serum phospholipids has been shown to be inversely associated with insulin secretion and positively associated with insulin action

44. PROTEIN There are no firm epidemiological data concerning
the role of protein intake in the etiology of
type 2 diabetes,
though the fact that meat-eating
Seventh-Day Adventists have higher rates than
those who do not eat meat has been taken to
suggest a possible deleterious effect of animal
protein

45. The strong positive associations
between animal protein and saturated fatty acids
and vegetable protein and dietary fiber mean that
it is almost impossible to disentangle separate
effects in epidemiological studies.
High intakes of proteins, especially animal
protein, appear to be associated with an increased
risk of nephropathy in type 1 diabetes [44], so
restriction of protein may help to delay progression
of microalbuminuria to clinical nephropathy

46. OTHER DIETARY FACTORS Several micronutrients, most notably chromium,
zinc, magnesium and vitamin E, have been implicated
in the pathogenesis of type 2 diabetes
and/or been shown to be associated with improved
glycemic control.
However, no epidemiological
studies have provided convincing support for the
role of any of these nutrients in the etiology of the
disease. There is, perhaps, rather more support for
the suggestion vitamin D deficiency may be important

47. Vitamin D deficiency impairs insulin release,
followed, if prolonged, by impairment of insulin
secretion and reduction of glucose tolerance which
progresses to irreversible diabetes.

48. smooking The role of smoking
as a risk factor for type 2 diabetes has received
relatively little attention. Smoking induces insulin
resistance [51], and cigarette smokers have
been shown to be relatively glucose intolerant and
Dyslipidemic
Thus, smokers might be expected to be at
considerably increased risk of type 2 diabetes.

49. PHYSICAL INACTIVITY In cross-sectional epidemiological
studies, type 2 diabetes rates have been shown
to be lower amongst physically active individuals
than amongst those not having regular physical
activity

50. The protective effect of physical
activity against type 2 diabetes has been confirmed
in several prospective studi

51. Prevalence of Factors Associated with Diabetes, Puerto Rico BRFSS* 2003
* BRFSS = “Behavioral Risk Factor Surveillance System” (>18 years). Centers for Disease Control and Prevention. Behavioral Risk Factor Surveillance System Atlanta, GA: United States, Department of Health and Human Services.
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53. Stages in the Evolution of Major Diabetes Surveillance Indicators
Primary Prevention
Physical activity
IFG / IGT
Diet/nutrition
Body composition
Preventive Care Practices
Foot exam
HbA1c testing
Dilated eye examination
Diabetes education
Prediabetes
Death
Normal
Diabetes
Complications
The future:
Continued evolution of all domains.
New generation quality of care
Community or system level
County and state level
Health service measures for PP
Indicators of Burden:
DM prevalence and incidence
Acute complications
Amputation
ESRD
CVD
Death
Risk Factors for Complications
Uncontrolled blood pressure
Inadequate glycemic control
Hyperlipidemia
Smoking
Sedentary behavior
Examination of the natural history of diabetes reveals different indicators at different stages of the disease (Supercourse)
Desai et al J Public Health Management Practice, 2003 (suppl). S44-51

54. Treatment
In some individuals with diabetes, adequate glycemic control can be achieved with weight reduction, exercise, and/or oral glucoselowering agents.
Individuals with extensive -cell destruction and therefore no residual insulin secretion require insulin for survival.

55. NutritionalManagement of D M
Diets rich in monounsaturated fat reduce total and low-density lipoprotein cholesterol without adverse effects on high- density lipoprotein cholesterol or triglyceride levels

56. a range of carbohydrate (45–60%) and fat (25–35%) intakes is compatible with good diabetes control provided that low glycaemic index carbohydrates and foods high in monounsaturated fat are promoted.
monounsaturated fatty acids should provide between 10 and 20% total energy

57. Glycemic index of certain food items
Low GI: Pasta, Basmati rice, wholegrain products, porridge, oat-based cereal bars, lentils and pulses including baked beans, and kidney beans
High GI: Corn Flakes, Rice Krispies, sugared cereals, white bread, rice (other than Basmati), potatoes, fruit juice, bananas, honey sandwich

58. for those people with Type 1 diabetes, especially
in those with hypertension, intakes of protein should not exceed 10–20% total energy because of the increased risk of nephropathy
It is recommended that a diet rich in foods which naturally contain significant quantities of antioxidants, especially fruit and vegetables, is followed

59. The normal protein requirements are:
. 2 g/kg per day in early infancy
. 1 g/kg per day for a 10-year-old
. 0.8 g/kg in later adolescence towards adulthood

60. Nutritional recommendations for childhood and adolescent Type 1 diabetes
Total daily energy intake should be distributed as follows:
(i) Carbohydrate >50%
mainly as complex higher fibre carbohydrate
moderate sucrose intake
(ii) Fat 30–35%
Mainly monounsaturated fat
(iii) Protein 10–15% (decreasing with age)
Fruit and vegetables (recommend five portions per day)