Physical activity, type II diabetes, and metabolic syndrome: prevention and intervention

1. Physical activity, type II diabetes, and metabolic syndrome:prevention and intervention

2. 糖尿病定義我國衛生署, WHO, ADA • 糖尿病 • 空腹至少8 小時靜脈血漿糖值≧126 mg/dl • 75 公克口服葡萄糖耐量試驗(oral glucose tolerance test, OGTT)，2 小時的靜脈血漿糖值≧200 mg/dl • 前期糖尿病(prediabetes) • 空腹血糖異常(impaired fasting glucose, IFG): 空腹血漿糖值110-126 mg/dl • 葡萄糖耐量異常(impaired glucose tolerance, IGT): OGTT2小時靜脈血漿糖值140-200 mg/dl

3. Key defects in onset of hyperglycemia in Type II DM • ↑Hepatic glucose production • ↓insulin secretion • ↓insulin action • Insulin resistance: suppressed or delayed response to insulin • Usually due to defect in cells that respond to insulin, rather than insulin production • Pivotal pathophysiological defects: Insulin resistance in muscle and liver, beta-cell failure Teixeira-Lemos, 2011

4. Exercise/insulin activate GLUT-4 (glucose transporter-4) translocation

5. 葉曉文, 2011

6. 葉曉文, 2011

7. 葉曉文, 2011

8. 葉曉文, 2011

9. Definition of metabolic Syndrome • National Cholesterol Education Program’s Adult Treatment Panel III report (ATP III) • if 3 out of the following 5 criteria • Central obesity 腰圍 • Europe/US: ≥ 94 cm (male) or ≥ 80 cm (female) • Taiwan: ≥ 90 cm (male) or ≥ 80 cm (female) • HDL < 40 mg/dl (male) or < 50 mg/dl (female) • Triglycerides > 150 mg/dl • fasting glucose > 100 mg/dl • blood pressure > 130/85 mmHg

10. Worldwide prevalence of metabolic syndrome Desroches, 2007

11. Definition of metabolic syndrome in children: International Diabetes Federation

12. Lakka, 2007

13. Physical activity in etiology of MetS Lakka, 2007

14. Obesity and diabetes37,878 women, 6.9 years follow-up Weinstein, 2004

15. PA and diabetes Weinstein, 2004

16. Energy expenditure and diabetes Weinstein, 2004

17. Walking and diabetes Weinstein, 2004

18. PA, obesity and diabetes Weinstein, 2004

19. PA, obesity and diabetes Weinstein, 2004

20. PA, obesity and diabetesneed to combine PA and weight loss Weinstein, 2004

21. PA, obesity, and risk for DM Hu, 2007

22. PA, fasting glucose, and risk for DM Hu, 2007

23. PA, fasting glucose, obesity, and risk for DM Hu, 2007

24. Bassuk, 2005

25. Bassuk, 2005

26. ProActive TrialPhysical activity measured by accelerometry30-50 yr, low PA, follow-up 1 year Simmons, 2008

27. Moderate PA reduce fasting insulinPhysical activity measured by accelerometry Ekelund, 2009

28. Vigorous PA and MetS Lakka, 2007

29. PA intensity and type II diabetesInsulin Resistance Atherosclerosis Study, n=1625, 1992-94 Vigorous:  6 METs Mayer-Davis EJ, 1998

30. PA intensity and type II diabetesInsulin Resistance Atherosclerosis Study, n=1625, 1992-94 Vigorous:  6 METs Mayer-Davis EJ, 1998

31. 2-wk interval training in obese men • 4-6 30s Wingate/session, 6 sessions Whyte, 2010

32. 2-wk interval training in obese men Whyte, 2010

33. Change in PA and Type II DM Lakka, 2007

34. Increase PA, decrease DM risk Hu, 2007

35. Finnish Diabetes Prevention Program:3234 at-risk, 2.8 years follow-up Church, 2011

36. Lifestyle (exercise) prevent MS Orchard, 2005

37. Lifestyle (exercise) prevent MS Orchard, 2005

38. Exercise training and insulin resistance Church, 2011

39. MONET study137 overweight/obese postmenopausal women MONET: Montreal–Ottawa New Emerging Team Karelis, 2008

40. MONET study137 overweight/obese postmenopausal women Karelis, 2008

41. MONET study6 mo. caloric restriction/resistance exercise

42. MONET study6 mo. caloric restriction/resistance exercise Drapeau, 2011

43. The HERITAGE Family Study • investigate the contribution of regular exercise to changes in risk factors for cardiovascular disease and Type 2 diabetes • genetics of cardiovascular, metabolic, and hormonal responses to exercise training • ages of 17 and 65 yr • healthy but sedentary • 20-wk aerobic exercise training program

44. PA decrease risk factors in those already having MetS Katzmarzyk, 2003

45. PA decrease number of risk factor in those already having MetS Katzmarzyk, 2003

46. PA decrease number of risk factor in high-risk subjects Katzmarzyk, 2003

47. Type II DM and reactive oxygen species (ROS) • oxidative stress secondary to hyperglycaemia and hyperlipidaemia occurs before the appearance of clinical manifestations of late diabetes complications • suggesting a key role in the pathogenesis of the disease. • Insulin resistance and pancreatic b-cell dysfunctionare modulated by ROS • ROS disrupt insulin-induced cellular redistribution of insulin receptor substrate-1 (IRS-1) and phosphatidylinositol 3-kinase (PI3K), impairing insulin-induced glucose transporter type 4 (GLUT4) translocation in 3T3-L1 adipocytes Teixeira-Lemos, 2011

48. Type II DM and inflammation • dyslipidaemic phenotype of diabetes: ↑TG, ↑ oxidized LDL, ↓HDL • lipotoxicity profile of diabetes • Lack of exercise leads to accumulation of visceral or deep subcutaneous adipose stores, leads to large adipocytes that are resistant to insulin-evoked lipolysis suppression, resulting in ↑release of FFA and glycerol • fat cells produce adipocytokines (adipokines) • go to muscle, liver and arterial tissue, where exert deleterious effects on metabolism and vascular function • Adipose tissue of obese and type 2 diabetic individuals is infiltrated by mononuclear cells and is in a state of chronic inflammation Teixeira-Lemos, 2011

49. Type II DM and inflammation • The adipocytes and infiltrated macrophages secrete pro-inflammatory/pro-thrombotic cytokines • TNF-a, IL-6, resistin, adipsin, acylation-stimulating protein (ASP), plasminogen activator inhibitor 1 (PAI-1) and angiotensinogen • promote atherogenesis and cause insulin resistance • Low adiponectin in type II DM • a potent insulin-sensitizing and anti-atherogenic adipokine Teixeira-Lemos, 2011

50. Exercise prevent Type II DMantioxidant and anti-inflammation Teixeira-Lemos, 2011