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Metabolic Syndrome

Metabolic Syndrome. Dr. Hasan AYDIN. Metabolic Syndrome. Clustering of cardiovascular risk factors Central obesity Diabetes Hypertension Dyslipidemia. Definition. First report.

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Metabolic Syndrome

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  1. Metabolic Syndrome Dr. Hasan AYDIN

  2. Metabolic Syndrome Clustering of cardiovascular risk factors Central obesity Diabetes Hypertension Dyslipidemia

  3. Definition

  4. Firstreport The degree of masculine differentiation to obesity: a factor determining predisposition to diabetes, atherosclerosis, gout and uric calculus disease. (Vague Am J Clin Nutr 4:20, 1956)

  5. Syndrome X Reaven 1988 Insulin resistance Glucose intolerance Raised triglycerides Low HDL cholesterol Hypertension

  6. The Metabolic SyndromeProposed Definitions ATPIII 1)Abdominal obesity 2)High triglycerides 3)Low HDL cholesterol 4)Blood pressure ≥130/85 5)High fasting glucose (three or more) WHO Main criteria Insulin resistance OR DM / IGT / IFG Other components 1)Blood pressure ≥140/90 2)Dyslipidemia 3)Central obesity 4)Microalbuminura (two or more) EGIR Main criteria Insulin resistance Other components 1)Hyperglycemia 2) Blood pressure ≥140/90 3)Dyslipidemia 4)Central obesity (two or more)

  7. NCEP ATP IIIWorking Definition of the Metabolic Syndrome ≥3 of the following

  8. Metabolic Syndrome increases with age Inter99 (n=6.784)

  9. Prevalence in Turkey METSAR Study

  10. Waist Measurements (cm) METSAR Study

  11. Waist Measurements Age Groups METSAR Study

  12. Abdominal Obesity METSAR Study

  13. What causes metabolic syndrome? Genetic predisposition Ethnicity Lifestyle and culture of inactivity and obesity Aging

  14. The Metabolic Syndrome Abdominal obesity Lipolysis FFA oxidation Physical inactivity VLDL Triglyceride HDL Insulin resistance Hypertension Endothelial dysfunction Microalbuminuria Hyperglycemia

  15. Pathogenesis of MS Type 2 Diabetes Insulin Resistance Central obesity Dyslipidemia Hypertension

  16. Environmental and genetic factors determine insulin sensitivity Insulin resistance = decreased ability of peripheral tissues to respond properly to normal circulating concentrations of insulin Variability in insulin sensitivity is accounted for by: Adiposity 25-30% Physical fitness 25-30% Genetic factors 40-50%

  17. Assessment of Insulin Sensitivity Gold Standard: Hyperinsulinemic clamp 8 Glucose Infusion Rate 120 120 Glycemia 100 6 80 80 4 60 Insulinemia 40 40 2 20 0 0 30 60 90 120 15 30 45 60 75 90 105 120

  18. Assessment of Insulin Sensitivity • Fasting insulin • Homeostasis Model Assessment (HOMA-IR) Insulin (mU/ml) x Glucose (mmol/l) / 22.5 • Quantitative Insulin Sensitivity Check Index (QUICKY) 1/[log Insulin (mU/ml) + log Glucose (mg/dl)] • Oral Glucose Tolerance Test (OGTT) • Intravenous Glucose Tolerance Test (IVGTT)

  19. Insulin sensitivity in healthylean and obese subjects 30 Obese Overweight 20 Lean SI (x10-5 min -1/pM) 10 0 30 40 15 20 25 35 45 BMI (kg/m2)

  20. Role of body fatdistribution Normal Type 2 diabetes

  21. Question Do lean insulin sensitive, lean insulin resistant, and obese insulin resistant subjects have similar abdominal fat distribution?

  22. Body Mass Index and Insulin Sensitivity **,ˆ 30 10 7.5 20 SI (x10-5 min-1/pM) ** BMI (kg/m2) 5 **,ˆ 10 2.5 0 0 LIS LIR OIR LIS LIR OIR (Cnop et al. Diabetes 51:1005, 2002)

  23. 30 20 10 0 0 100 200 300 400 Intra-abdominal fat area (cm2) Intra-abdominal fat is highly predictive ofinsulin sensitivity SI (x10-5 min -1/pM)

  24. Adipose tissue: an endocrine organ Insulin Resistance  FFA  Fat  TNFa, IL-6, Leptin, Resistin Adiponectin

  25. The Metabolic Syndrome Type 2 Diabetes Insulin Resistance Central obesity Dyslipidemia Hypertension

  26. Insulin Secretion Insulin Resistance Type 2 Diabetes Symptomatic period Asymptomatic Period Genetic Reactive Hypoglycemia Glucose Intolerance Early Clinical Diabetes Overt Diabetes Preclinical Diabetes LateClinical Period

  27. Does the metabolic syndrome predict incident diabetes?

  28. Does hyperinsulinemia predict diabetes? Percent (%) Tertile of HOMA-IR Resnick H et al. Diabetes Care 2003

  29. The Metabolic Syndrome Type 2 Diabetes Insulin Resistance Central obesity Dyslipidemia Hypertension

  30. The Metabolic Syndrome and Hypertension Intra-abdominal adiposity and insulin resistance are associated with increased: Sodium retention and sensitivity Angiotensinogen and angiotensin II levels Sympathetic activity PAI-1 levels Cortisol production in visceral fat compartment

  31. Dyslipidemia and the Metabolic Syndrome 10 5 Cholesterol (mg/dl) 0 -5 D -10 VLDL dense Insulin Resistant LDL Adiponectin IDL HDL buoyant Insulin Sensitive

  32. Does Hyperinsulinemia predict CVD?

  33. Does MS predict CVD? Percent % ATP III metabolic syndrome

  34. Does the metabolic syndrome predict CVD?

  35. How Insulin Resistance leads tocoronary disease Environmental influences Genetic influences Insulin resistance Hyperinsulinemia Increased BP Glucose intolerance Increased triglycerides Decreased HDL Increased PAI-1 Small, dense LDL Increased uric acid Coronary Artery Disease

  36. Oxidative stress NAFLD Coagulopathy Inflammation Sleep apnea syndrome Endothelial dysfunction Polycystic ovary syndrome Heart failure Obesity Hypertension Hyperglycemia Macrovascular Disease Insulin Resistance Dyslipidemia Macrovascular Disease Breast cancer

  37. Medical Evaluation ofMetabolic Syndrome Physical Exam Blood Pressure BMI Waist Circumference Atheromas Skin Tags Lab Evaluation Fasting Glucose Lipid Homocysteine hsCRP Uric Acid TSH A1c ALT Creatinine

  38. Treatment

  39. Therapy for Insulin Resistance Nonpharmacologic / Pharmacologic Exercise Weight control Diet Smoking cessation

  40. Modest Weight Loss Can Drastically Reduce Visseral Fat Before Weight Loss After 10 kg Weight Loss (95 kg, BMI 32) (85 kg, BMI 29)

  41. NCEP/ATP III GuidelinesClinical Management of the MetabolicSyndrome Management of underlying cause Weight control enhances LDL lowering and reduces all risk factors Physical activity reduces VLDL, increases HDL, and may lower LDL Management of lipid and nonlipid risk factors Treat hypertension Use of aspirin in CHD patients Treat elevated triglycerides and low HDL

  42. Dietary Interventions Reduce calories Reduce saturated fat Increase whole grains Increase fruits and vegetables Eat fish 1-2 times per week Use monounsaturated or polyunsaturated oils Olive, Canola, and Peanuts Safflower, Sunflower or Sesame seed, Corn, or Soy

  43. ExerciseInterventions Goal for Patients: 240 minutes of purposeful activity per week Write exercise prescription 10,000 steps per day

  44. Treatment: Lifestyle • Finnish Diabetes Prevention Study • STOP-NIDDM Trial • US Diabetes Prevention Program • 7% weight loss • 150 min/week exercise • Reduction of diabetes incidence by 60% • Compared to 25-30% reduction for pharmacological intervention

  45. Pharmacologic Management Aggressive Treatment of Hypertension ACE Inhibitor is the drug of choice Beta Blockers promote weight gain Thiazide diuretics increase insulin resistance Metformin 500mg BID—diabetes prevention Lipid—Statin medication or combination Aspirin for Everyone!!! Excellent Candidates for Aggressive Weight loss intervention Healthy Ways Weight Loss Meds: Sibutramine, Orlistat Aggressive Dietary Intervention: VLCD if BMI>27

  46. Treatment: Drugs • Underlying conditions (hypertension, diabetes, lipiddisorders) should be treated. • An aggressive and early treatment strategy has been proposed. • Therapeutic agents might include fibrates, statins, metformin, thiazolidinediones, and, possibly, dual PPAR-a and g agonists. • No consensus optimal treatment targets have been determined and pharmacotherapy remains at present unproven.

  47. Does Treating the MetabolicSyndrome Make a Difference? FinnishDiabetes Prevention Study

  48. Diabetes Prevention Program:Change of BMI – 1 year

  49. Diabetes Prevention Program:Goal Achievement

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