DM and Glucagon
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DM and Glucagon

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    DM and Glucagon DM and Glucagon Presentation Transcript

    • APPLIED ASPECT OF INSULIN & GLUCAGON DR. LAXMIKANTA SAY
    • 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
    • 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
    • Liver       1. 2. 3. 4. 5. 6. Ketogenesis Protein synthesis Lipid synthesis Glucose output Glycogen synthesis Glycolysis
    • APPLIED ASPECT OF INSULIN HYPERGLYCEMIA HYPOGLYCEMIA
    • 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
    • PREDISPOSING FACTORS  Hereditary – Definite genetic susceptibility  Age  Obesity - BMI >30 - Insulin resistance - ability of insulin to move glucose into fat & muscle
    • 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
    • Clinical Features        1. Hyperglycemia 2. Glycosuria 3. Polyuria 4. Dehydration 5. Polydipsia 6. Polyphagia 7. Weight Loss
    • 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 +
    • 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)
    • Fat Metabolism Lipogenesis Mobilization depot fats HYPERTRIGLYCERIDAEMIA Fatty Liver Decreased Oxidation FFA Acetly Co-A Ketogenesis Ketonaemia Ketonuria Natriuresis
    • 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
    • Diagnosis  Urine glucose  Fasting plasma glucose and insulin  GTT
    • GTT
    • 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
    • HYPOGLYCEMIA  1. Iatrogenic - insulin overdose -Overdose of oral hypoglycemic agents  2. β – cell adenoma  3. Functional - delayed secretion of insulin - severe exercise
    • 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
    • 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
    • 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
    • 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
    • Blood glucose regulation Insulin Hyperglycemia Hypoglycemia Glucagon
    • THANK YOU