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DM and Glucagon
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DM and Glucagon

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  • 1. APPLIED ASPECT OF INSULIN & GLUCAGON DR. LAXMIKANTA SAY
  • 2. Actions of Insulin on Adipose Tissue       1. 2. 3. 4. 5. 6. Glucose entry Fatty acid synthesis Glycerol phosphate synthesis Triglyceride deposition Activation of Lipoprotein lipase K+ uptake
  • 3. Muscle         1. 2. 3. 4. 5. 6. 7. 8. Glucose entry Glycogen synthesis Aminoacid uptake Protein synthesis Protein catabolism release of Gluconeogenic AA Ketone uptake K+ uptake
  • 4. Liver       1. 2. 3. 4. 5. 6. Ketogenesis Protein synthesis Lipid synthesis Glucose output Glycogen synthesis Glycolysis
  • 5. APPLIED ASPECT OF INSULIN HYPERGLYCEMIA HYPOGLYCEMIA
  • 6. DIABETES MELLITUS  It is a syndrome of impaired carbohydrate , fat and protein metabolism caused by either due to lack of insulin secretion or decrease sensitivity of tissues to insulin. Type I Type II
  • 7. PREDISPOSING FACTORS  Hereditary – Definite genetic susceptibility  Age  Obesity - BMI >30 - Insulin resistance - ability of insulin to move glucose into fat & muscle
  • 8. Clinical Types  1. Pre – diabetic or Potential Diabetic - Strong genetic predisposition  2. Latent Diabetic - Stress, Obesity  3. Clinical Diabetes  4. Overt diabetes mellitus - Juvenile & MODY  5. Secondary DM - diseases associated - Pancreatitis (destruction of B- cells), Acromegaly, Cushing’s syndrome
  • 9. Clinical Features        1. Hyperglycemia 2. Glycosuria 3. Polyuria 4. Dehydration 5. Polydipsia 6. Polyphagia 7. Weight Loss
  • 10. Pathophysiology of DM Protein Catabolism Aminoacidaemia Gluconoegenesis NH2 of AA converted to Urea & Excretion Urinary N2 excretion (Negative N2 balance) CELLULAR DEHYDRATION Loss of Cellular K+ to ECF Urinary excretion of K +
  • 11. Carbohydrate metabolism HYPERGLYCEMIA Glycosuria Polyuria (Osmotic Diuresis) Wate & electolyte loss DEHYDRATION Haemoconcentration, Blood Volume Peripheral Circulatory Failure Tissue Hypoxia Decreased B.P Cerebral Blood Flow , Renal Flow Anuria Renal Failure COMA & DEATH (metabolic acidosis, renal failure, cerebral ischemia, dehydration)
  • 12. Fat Metabolism Lipogenesis Mobilization depot fats HYPERTRIGLYCERIDAEMIA Fatty Liver Decreased Oxidation FFA Acetly Co-A Ketogenesis Ketonaemia Ketonuria Natriuresis
  • 13. COMPLICATIONS OF DM  1. Microvascular abnormality - diabetic retinopathy, - diabetic nephropathy  2. Macrovascular abnormality - accelerated atheroscelerosis - stroke, MI  3. Neuropathic abnormality - diabetic neuropathy - atherosclerotic insufficiency - reduced resistance to infection - chronic ulceration & gangrene
  • 14. Diagnosis  Urine glucose  Fasting plasma glucose and insulin  GTT
  • 15. GTT
  • 16. CLINICAL COMPARISION FEATURE TYPE I TYPE II Age at onset < 40 yrs >40 yrs Body mass Low to normal Obese Ketosis & Acidosis High Incidence Rare Plasma insulin Low or absent Normal to high Plasma glucagon High , can be suppressed High , resistant to suppression Plasma glucose High High Insulin sensitivity Normal Reduced Therapy Insulin Wt. loss , drugs , insulin
  • 17. HYPOGLYCEMIA  1. Iatrogenic - insulin overdose -Overdose of oral hypoglycemic agents  2. β – cell adenoma  3. Functional - delayed secretion of insulin - severe exercise
  • 18. HYPOGLYCEMIA Plasma glucose in mg/dl 90 Inhibition of insulin secretion 75 60 45 Glucagon , GH , Epinephrine secretion Cortisol secretion , Cognitive dysfunction Lethargy 30 Coma , Convulsion 15 0 Permanent brain damage , Death
  • 19. GLUCAGON  Linear polypeptide, Mol. Wt. 3485  Produced by A – cells of Pancreatic islets & upper GI  29 AA  Human Preproglucagon found in Pancreas, GI & Brain  Product of single mRNA
  • 20. ACTION OF GLUCAGON Liver - Glycogenolysis - Gluconeogenesis - Inhibit storage of TG - Ketogenic Adipose tissue - Lipolysis +ve ionotropic action Increase blood flow to kidney Bile secretion Inhibits gastric acid secretion
  • 21. REGULATION OF SECRETION Stimulators  Low glucose  Amino acids  CCK , Gastrin  Cortisol  Exercise  Infections & stress  β adr. stimulation  Acetylcholine Inhibitors  High glucose  Somatostatin  Secretin  FFA  Ketones  Insulin  α adrenergic stimulation  GABA
  • 22. Blood glucose regulation Insulin Hyperglycemia Hypoglycemia Glucagon
  • 23. THANK YOU

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