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Diabetes mellitus type 2
 

Diabetes mellitus type 2

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my biochem presentation

my biochem presentation

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    Diabetes mellitus type 2 Diabetes mellitus type 2 Presentation Transcript

    •  
      • Diabetes mellitus is a chronic disease characterized by derangement in carbohydrates, fat and protein metabolism
      • Type 2 diabetes mellitus comprises an array of dysfunctions resulting from:
      • the combination of resistance to insulin action
      • inadequate insulin secretion.
      • 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.
      • Type 2
      • diabetes
      Insulin resistance  -cell dysfunction
      • Obesity
      • Insulin resistance
      • Abnormal insulin secretion
      • Excess glucose production
      • Beta-cell failure
    •  
      • Insulin resistance is a condition in which the body produces insulin but does not use it properly.
      • The circulating free fatty acids associated with obesity also responsible for insulin resistance of the muscle and liver.
      • Decreased glucose uptake by skeletal muscle and adipose tissue.
      • Increased glucose output by Liver-Gluconeogenesis.
      • In the early stages of obesity the pancreas compensates for the IR by overproducing insulin so that glucose homeostasis is maintained.
      • This leads to HYPERGLYCEMIA & HYPER INSULINEMIA
    • Chronic hyperglycemia Glucotoxicity 2 Lipotoxicity 3 Oversecretion of insulin to compensate for insulin resistance 1,2  -cell dysfunction
      • 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
      • 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 .
    • IR Insulin resistance Liver Muscle Adipose tissue  Glucose output  Glucose uptake  Glucose uptake Hyperglycemia
      • It rarely develops in DM-II
      • 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.
      • If it is develops:
      • Insulin Deficiency
        • Increased Glycogenolysis
        • Increased Gluconeogenesis
        • Increased Hepatic glucose output
        • Decreased Peripheral glucose uptake
        • Elevates blood glucose
        • Increased Lipolysis
        • Increased Release of FFA in liver
        • Increased VLDL & ketones
        • Ketonemia and hyperTG
        • Acidosis & Diuresis
      • It is a characteristics of DM-II
      • Results from an increase in VLDL without hyperchylomicronemia.
      • This happens by hepatic synthesis of fatty acids and diversion of free fatty acids reaching the liver in to triacylglycerol and VLDL.
      • Normal
      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
      • Chronic complications –
      •  Microvascular- retinopathy , nephropathy,
      • neuropathy.
      •  Macrovascular - cardiovascular,
      • cerebrovascular,
      • peripheral vascular
      • diseases.
      •  Acute complications – diabetic ketoacidosis,
      • hyperosmalor coma.
      • Hyperglycaemia in insulin independent tissues (nerve, lens, retina) gives rise to polyol formation.
      • The enzyme aldose reductase catalyses the reduction of glucose to sorbitol, which is converted to fructose.
      • Sorbitol does not easily easily cross cell membranes and its accumulation may cause damage by osmotic effect (e.g. in the lens).
      • 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.
    •  
    • 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
    •  
    •