Diabetes mellitus type 2


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Diabetes mellitus type 2

  1. 2. <ul><li>Diabetes mellitus is a chronic disease characterized by derangement in carbohydrates, fat and protein metabolism </li></ul>
  2. 3. <ul><li>Type 2 diabetes mellitus comprises an array of dysfunctions resulting from: </li></ul><ul><li>the combination of resistance to insulin action </li></ul><ul><li>inadequate insulin secretion. </li></ul><ul><li>It is disorders are characterized by hyperglycemia and associated with microvascular (ie, retinal, renal, possibly neuropathic), macrovascular (ie, coronary, peripheral vascular), and neuropathic (ie, autonomic, peripheral) complications. </li></ul>
  3. 4. <ul><li>Type 2 </li></ul><ul><li>diabetes </li></ul>Insulin resistance  -cell dysfunction
  4. 5. <ul><li>Obesity </li></ul><ul><li>Insulin resistance </li></ul><ul><li>Abnormal insulin secretion </li></ul><ul><li>Excess glucose production </li></ul><ul><li>Beta-cell failure </li></ul>
  5. 7. <ul><li>Insulin resistance is a condition in which the body produces insulin but does not use it properly. </li></ul>
  6. 8. <ul><li>The circulating free fatty acids associated with obesity also responsible for insulin resistance of the muscle and liver. </li></ul>
  7. 9. <ul><li>Decreased glucose uptake by skeletal muscle and adipose tissue. </li></ul><ul><li>Increased glucose output by Liver-Gluconeogenesis. </li></ul><ul><li>In the early stages of obesity the pancreas compensates for the IR by overproducing insulin so that glucose homeostasis is maintained. </li></ul><ul><li>This leads to HYPERGLYCEMIA & HYPER INSULINEMIA </li></ul>
  8. 10. Chronic hyperglycemia Glucotoxicity 2 Lipotoxicity 3 Oversecretion of insulin to compensate for insulin resistance 1,2  -cell dysfunction
  9. 11. <ul><li>The elevated levels of free fatty acids and or cytokines lead to gradual loss of the ability of the pancreas to overproduce insulin , a process called decompensation- Lipotoxity </li></ul><ul><li>Glucose, the main regulator of insulin secretion and production, exerts negative effects on beta-cell function when present in excessive amounts over a prolonged period- glucotoxicity . </li></ul>
  10. 12. IR Insulin resistance Liver Muscle Adipose tissue  Glucose output  Glucose uptake  Glucose uptake Hyperglycemia
  11. 13. <ul><li>It rarely develops in DM-II </li></ul><ul><li>Insulin present in DM-II is enough to prevent uncontrollable release of fatty acids from adipocytes and fattyacids reaching the liver or synthesized de novo are directed to triacyglycerol. </li></ul>
  12. 14. <ul><li>If it is develops: </li></ul><ul><li>Insulin Deficiency </li></ul><ul><ul><li>Increased Glycogenolysis </li></ul></ul><ul><ul><li>Increased Gluconeogenesis </li></ul></ul><ul><ul><li>Increased Hepatic glucose output </li></ul></ul><ul><ul><li>Decreased Peripheral glucose uptake </li></ul></ul><ul><ul><li>Elevates blood glucose </li></ul></ul><ul><ul><li>Increased Lipolysis </li></ul></ul><ul><ul><li>Increased Release of FFA in liver </li></ul></ul><ul><ul><li>Increased VLDL & ketones </li></ul></ul><ul><ul><li>Ketonemia and hyperTG </li></ul></ul><ul><ul><li>Acidosis & Diuresis </li></ul></ul>
  13. 15. <ul><li>It is a characteristics of DM-II </li></ul><ul><li>Results from an increase in VLDL without hyperchylomicronemia. </li></ul><ul><li>This happens by hepatic synthesis of fatty acids and diversion of free fatty acids reaching the liver in to triacylglycerol and VLDL. </li></ul>
  14. 16. <ul><li>Normal </li></ul>Normal TG Type 2 diabetes High TG Low HDL cholesterol Small dense LDL (diabetic dyslipidaemia) Normal insulin level Impaired insulin action to inhibit VLDL production Increased liver fat Insulin deficiency exacerbates hypertriglyceridaemia
  15. 17. <ul><li>Chronic complications – </li></ul><ul><li> Microvascular- retinopathy , nephropathy, </li></ul><ul><li> neuropathy. </li></ul><ul><li> Macrovascular - cardiovascular, </li></ul><ul><li> cerebrovascular, </li></ul><ul><li> peripheral vascular </li></ul><ul><li> diseases. </li></ul><ul><li> Acute complications – diabetic ketoacidosis, </li></ul><ul><li> hyperosmalor coma. </li></ul>
  16. 18. <ul><li>Hyperglycaemia in insulin independent tissues (nerve, lens, retina) gives rise to polyol formation. </li></ul><ul><li>The enzyme aldose reductase catalyses the reduction of glucose to sorbitol, which is converted to fructose. </li></ul><ul><li>Sorbitol does not easily easily cross cell membranes and its accumulation may cause damage by osmotic effect (e.g. in the lens). </li></ul><ul><li>Sorbitol trapped in retinal cells, the cells of the lens, and the Schwann cells that myelinate peripheral nerves can damage these cells, leading to retinopathy, cataracts and peripheral neuropathy. </li></ul>
  17. 20. Carbohydrate Glucose(G)-I (I)-Insulin Carbohydrate Acarbose Reduces absorption Sulphonylurea Repaglinide Stimulates pancreas Metformin Reduces hepatic glucose output (??muscle/fat effects) Thiazolidinediones Reduce Insulin Resistance