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Pancrease

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  • 1. Dr. Zeenat Hussain Foundation “The ultimate value of life depends upon awareness and the power of contemplation rather than upon mere survival.” Aristotle Dr. Zeenat Hussain Foundation is working to create awareness against the diseases among the common people of Pakistan. This lecture is also a part of this campaign. Your cooperation and feed back shall be highly appreciated.
  • 2. The Endocrine Pancreas Regulation of Carbohydrate Metabolism Presented By: Nasir Nazeer
  • 3. Pancreas- Brief History Herophilus, Greek surgeon first described pancreas.  Wirsung discovered the pancreatic duct in 1642.  Pancreas as a secretory gland was investigated by Graaf in 1671.  R. Fitz established pancreatitis as a disease in 1889.  Whipple performed the first pancreaticoduodenectomy in 1935 Duct of  Santorini Duct of Wirsung
  • 4. Pancreatic Anatomy  Gland with both exocrine and endocrine functions  15-25 cm long in length  60-100 grams in weight  Location: retro-peritoneum, 2nd lumbar vertebral level  Extends in an oblique, transverse position  Parts of pancreas: head, neck, body and tail
  • 5. Pancreas
  • 6. Head of Pancreas  Includes uncinate process  Flattened structure, 2 – 3 cm thick  Attached to the 2nd and 3rd portions of duodenum on the right  Emerges into neck on the left
  • 7. Neck of Pancreas  2.5 cm in length  Straddles SMV and PV  Antero-superior surface supports the pylorus  Superior mesenteric vessels emerge from the inferior border  Posteriorly, SMV and splenic vein confluence to form portal vein  Posteriorly, mostly no branches to pancreas
  • 8. Body of Pancreas  Elongated, long structure  Anterior surface, separated from stomach by lesser sac  Posterior surface, related to aorta, adrenal gland, renal vessels and upper 1/3 rd of kidney  Splenic vein runs embedded in the post. Surface  Inferior surface is covered by transverse mesocolon
  • 9. Tail of Pancreas  Narrow, short segment  Lies at the level of the 12 th thoracic vertebra  Ends within the splenic hilum  Lies in the splenophrenic ligament  Anteriorly, related to splenic flexure of colon  May be injured during splenectomy (fistula)
  • 10. Pancreatic Duct  Main duct (Wirsung) runs the entire length of pancreas  2 – 4 mm in diameter, 20 secondary branches  Ductal pressure is 15 – 30 mm Hg thus preventing damage to pancreatic duct  Lesser duct (Santorini) drains superior portion of head and empties separately into 2nd portion of duodenum
  • 11. Arterial Supply of Pancreas  Variety of major arterial sources (celiac, SMA and splenic)  Celiac  Common Hepatic Artery  Gastroduodenal Artery  Superior pancreaticoduodenal artery which divides into anterior and posterior branches  SMA (Superior mesentric artery)  Inferior pancreaticoduodenal artery which divides into anterior and posterior branches
  • 12. Pancreatic Arterial Supply
  • 13. Venous Drainage of Pancreas  Follows arterial supply  Anterior and posterior arcades drain head and the body  Splenic vein drains the body and tail  Major drainage areas are  Suprapancreatic PV  Retropancreatic PV  Splenic vein  Infrapancreatic SMV  Ultimately, into portal vein
  • 14. Venous Drainage of the Pancreas
  • 15. Lymphatic Drainage  Rich periacinar network that drain into 5 nodal groups Superior nodes Anterior nodes Inferior nodes Posterior nodes Splenic nodes
  • 16. Pancreatic Hormones, Insulin and Glucagon, Regulate Metabolism
  • 17. Production of Pancreatic Hormones by Three Cell Types Alpha cells produce glucagon. Beta cells produce insulin. Delta cells produce somatostatin.
  • 18. Islet of Langerhans Cross-section    Three cell types are present, A (glucagon secretion), B (Insulin secretion) and D (Somatostatin secretion) A and D cells are located around the perimeter while B cells are located in the interior Venous return containing insulin flows by the A cells on its way out of the islets
  • 19. Pancreatic Hormones, Insulin and Glucagon, Regulate Metabolism Figure 22-8: Metabolism is controlled by insulin and glucagon
  • 20. Structure of Insulin  Insulin is a polypeptide hormone, composed of two chains (A and B)  BOTH chains are derived from proinsulin, a prohormone.  The two chains are joined by disulfide bonds.
  • 21. Roles of Insulin Acts on tissues (especially liver, skeletal muscle, adipose) to increase uptake of glucose and amino acids. - without insulin, most tissues do not take in glucose and amino acids well (except brain). Increases glycogen production (glucose storage) in the liver and muscle. Stimulates lipid synthesis from free fatty acids and triglycerides in adipose tissue. Also stimulates potassium uptake by cells (role in potassium homeostasis).
  • 22. The Insulin Receptor  The insulin receptor is composed of two subunits, and has intrinsic tyrosine kinase activity.  Activation of the receptor results in a cascade of phosphorylation events: phosphorylation of insulin responsive substrates (IRS) RAS RAF-1 MAP-K MAP-KK Final actions
  • 23. Specific Targets of Insulin Action: Carbohydrates Increased activity of glucose transporters. Moves glucose into cells. Activation of glycogen synthetase. Converts glucose to glycogen. Inhibition of phosphoenolpyruvate carboxykinase. Inhibits gluconeogenesis.
  • 24. Specific Targets of Insulin Action: Lipids Activation of acetyl CoA carboxylase. Stimulates production of free fatty acids from acetyl CoA. Activation of lipoprotein lipase (increases breakdown of triacylglycerol in the circulation). Fatty acids are then taken up by adipocytes, and triacylglycerol is made and stored in the cell.
  • 25. Regulation of Insulin Release  Major stimulus: increased blood glucose levels - after a meal, blood glucose increases - in response to increased glucose, insulin is released - insulin causes uptake of glucose into tissues, so blood glucose levels decrease. - insulin levels decline as blood glucose declines
  • 26. Insulin Action on Cells: Dominates in Fed State Metabolism  ↑ glucose uptake in most cells (not active muscle)  ↑ glucose use and storage  ↑ protein synthesis  ↑ fat synthesis
  • 27. Insulin Action on Cells: Dominates in Fed State Metabolism
  • 28. Insulin: Summary and Control Reflex Loop
  • 29. Other Factors Regulating Insulin Release  Amino acids stimulate insulin release (increased uptake into cells, increased protein synthesis).  Keto acids stimulate insulin release (increased glucose uptake to prevent lipid and protein utilization).  Insulin release is inhibited by stress-induced increase in adrenal epinephrine - epinephrine binds to alpha adrenergic receptors on beta cells - maintains blood glucose levels  Glucagon stimulates insulin secretion (glucagon has opposite actions).
  • 30. Structure and Actions of Glucagon Peptide hormone, 29 amino acids Acts on the liver to cause breakdown of glycogen (glycogenolysis), releasing glucose into the bloodstream. Inhibits glycolysis Increases production of glucose from amino acids (gluconeogenesis). Also increases lipolysis, to free fatty acids for metabolism. Result: maintenance of blood glucose levels during fasting.
  • 31. Mechanism of Action of Glucagon  Main target tissues: liver, muscle, and adipose tissue  Binds to a Gs-coupled receptor, resulting in increased cyclic AMP and increased PKA activity.  Also activates IP3 pathway (increasing Ca++)
  • 32. Glucagon Action on Cells: Dominates in Fasting State Metabolism  Glucagon prevents hypoglycemia by ↑ cell production of glucose  Liver is primary target to maintain blood glucose levels
  • 33. Glucagon Action on Cells: Dominates in Fasting State Metabolism
  • 34. Targets of Glucagon Action  Activates a phosphorylase, which cleaves off a glucose 1-phosphate molecule off of glycogen.  Inactivates glycogen synthase by phosphorylation (less glycogen synthesis).  Increases phosphoenolpyruvate carboxykinase, stimulating gluconeogenesis  Activates lipases, breaking down triglycerides.  Inhibits acetyl CoA carboxylase, decreasing free fatty acid formation from acetyl CoA  Result: more production of glucose and substrates for metabolism
  • 35. Regulation of Glucagon Release  Increased blood glucose levels inhibit glucagon release.  Amino acids stimulate glucagon release (high protein, low carbohydrate meal).  Stress: epinephrine acts on beta-adrenergic receptors on alpha cells, increasing glucagon release (increases availability of glucose for energy).  Insulin inhibits glucagon secretion.
  • 36. Other Factors Regulating Glucose Homeostasis  Glucocorticoids (cortisol): stimulate gluconeogenesis and lipolysis, and increase breakdown of proteins.  Epinephrine/norepinephrine : stimulates glycogenolysis and lipolysis.  Growth hormone: stimulates glycogenolysis and lipolysis.  Note that these factors would complement the effects of glucagon, increasing blood glucose levels.
  • 37. Hormonal Regulation of Nutrients Right after a meal (resting): - blood glucose elevated - glucagon, cortisol, GH, epinephrine low - insulin increases (due to increased glucose) - Cells uptake glucose, amino acids. - Glucose converted to glycogen, amino acids into protein, lipids stored as triacylglycerol. - Blood glucose maintained at moderate levels.
  • 38. Hormonal Regulation of Nutrients A few hours after a meal (active): - blood glucose levels decrease - insulin secretion decreases - increased secretion of glucagon, cortisol, GH, epinephrine - glucose is released from glycogen stores (glycogenolysis) - increased lipolysis (beta oxidation) - glucose production from amino acids increases (oxidative deamination; gluconeogenesis) - decreased uptake of glucose by tissues - blood glucose levels maintained
  • 39. Regulation of Energy Metabolism  Energy reserves:   Molecules that can be oxidized for energy are derived from storage molecules (glycogen, protein, and fat). Circulating substrates:  Molecules absorbed through small intestine and carried to the cell for use in cell respiration. Insert fig. 19.2
  • 40. Pancreatic Islets (Islets of Langerhans)  Alpha cells secrete glucagon. Stimulus is decrease in blood [glucose].  Stimulates glycogenolysis and lipolysis.  Stimulates conversion of fatty acids to ketones.   Beta cells secrete insulin. Stimulus is increase in blood [glucose].  Promotes entry of glucose into cells.  Converts glucose to glycogen and fat.  Aids entry of amino acids into cells. 
  • 41.  Glucose homeostasis – Putting it all together Insulin Beta cells of pancreas stimulated to release insulin into the blood High blood glucose level STIMULUS: Rising blood glucose level (e.g., after eating a carbohydrate-rich meal) Body cells take up more glucose Liver takes up glucose and stores it as glycogen Homeostasis: Normal blood glucose level (about 90 mg/100 mL) Blood glucose level rises to set point; stimulus for glucagon release diminishes Figure 26.8 Blood glucose level declines to a set point; stimulus for insulin release diminishes STIMULUS: Declining blood glucose level (e.g., after skipping a meal) Alpha cells of pancreas stimulated to release glucagon into the blood Liver breaks down glycogen and releases glucose to the blood Glucagon

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