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The Endocrine Pancreas-Regulation of Carbohydrate Metabolism PowerPoint Presentation

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This medical PowerPoint presentation talks about the endocrine pancreas, a specialized part of the pancreas that secretes hormones such as insulin and glucagon. These hormones play a critical role in regulating carbohydrate metabolism in the body.

Insulin is produced by the beta cells of the pancreas and is released in response to elevated blood glucose levels. Insulin helps to lower blood glucose levels by promoting the uptake of glucose into cells, particularly muscle and adipose tissue, and by promoting the storage of glucose in the liver and muscle tissue in the form of glycogen. Insulin also inhibits the breakdown of glycogen in the liver and muscle tissue, thereby preventing the release of glucose into the bloodstream.

Glucagon is produced by the alpha cells of the pancreas and is released in response to low blood glucose levels. Glucagon acts in opposition to insulin and promotes the release of glucose from the liver into the bloodstream through the breakdown of glycogen (glycogenolysis) and the conversion of non-carbohydrate sources (such as amino acids) into glucose (gluconeogenesis).

In addition to insulin and glucagon, other hormones such as somatostatin and pancreatic polypeptide also play a role in regulating carbohydrate metabolism. Somatostatin inhibits the release of both insulin and glucagon, while pancreatic polypeptide is thought to play a role in regulating appetite and food intake.

Tags : Endocrine Pancreas, Regulation of Carbohydrate Metabolism, insulin, glucagon, somatostatin, pancreatic polypeptide, endocrinology, endocrinology PowerPoint presentation

Published on : Apr 18, 2023 | Views : 1467 | Downloads : 8

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Slide 1-

The Endocrine Pancreas Regulation of Carbohydrate Metabolism
Slide 2-

Pancreatic Anatomy Gland with both exocrine and endocrine functions 15-25 cm long 60-100 g Location: retro-peritoneum, 2nd lumbar vertebral level Extends in an oblique, transverse position Parts of pancreas: head, neck, body and tail
Slide 3-

Pancreas
Slide 4-

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 Border b/w head and neck is determined by GDA insertion SPDA and IPDA anastamose between the duodenum and the right lateral border
Slide 5-

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
Slide 6-

Body of Pancreas Elongated, long structure Anterior surface, separated from stomach by lesser sac Posterior surface, related to aorta, lt. adrenal gland, lt. renal vessels and upper 1/3rd of lt. kidney Splenic vein runs embedded in the post. Surface Inferior surface is covered by transverse mesocolon
Slide 7-

Tail of Pancreas Narrow, short segment Lies at the level of the 12th 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)
Slide 8-

Pancreatic Duct Main duct (Wirsung) runs the entire length of pancreas Joins CBD at the ampulla of Vater 2 – 4 mm in diameter, 20 secondary branches Ductal pressure is 15 – 30 mm Hg (vs. 7 – 17 in CBD) thus preventing damage to panc. duct Lesser duct (Santorini) drains superior portion of head and empties separately into 2nd portion of duodenum
Slide 9-

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  Inferior pancreaticoduodenal artery which divides into anterior and posterior branches
Slide 10-

Arterial Supply of Pancreas Anterior collateral arcade between anterosuperior and anteroinferior PDA Posterior collateral arcade between posterosuperior and posteroinferior PDA Body and tail supplied by splenic artery by about 10 branches Three biggest branches are Dorsal pancreatic artery Pancreatica Magna (midportion of body) Caudal pancreatic artery (tail)
Slide 11-

Pancreatic Arterial Supply
Slide 12-

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
Slide 13-

Venous Drainage of the Pancreas
Slide 14-

Lymphatic Drainage Rich periacinar network that drain into 5 nodal groups Superior nodes Anterior nodes Inferior nodes Posterior PD nodes Splenic nodes
Slide 15-

Innervation of Pancreas Sympathetic fibers from the splanchnic nerves Parasympathetic fibers from the vagus Both give rise to intrapancreatic periacinar plexuses Parasympathetic fibers stimulate both exocrine and endocrine secretion Sympathetic fibers have a predominantly inhibitory effect
Slide 16-

Innervation of Pancreas Peptidergic neurons that secrete amines and peptides (somatostatin, vasoactive intestinal peptide, calcitonin gene-related peptide, and galanin Rich afferent sensory fiber network Ganglionectomy or celiac ganglion blockade interrupt these somatic fibers (pancreatic pain)
Slide 17-

Pancreatic Hormones, Insulin and Glucagon, Regulate Metabolism
Slide 18-

Production of Pancreatic Hormones by Three Cell Types Alpha cells produce glucagon. Beta cells produce insulin. Delta cells produce somatostatin.
Slide 19-

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
Slide 20-

Pancreatic Hormones, Insulin and Glucagon, Regulate Metabolism Figure 22-8: Metabolism is controlled by insulin and glucagon
Slide 21-

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.
Slide 22-

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).
Slide 23-

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:
Slide 24-

Specific Targets of Insulin Action: Carbohydrates Activation of glycogen synthetase. Converts glucose to glycogen. Inhibition of phosphoenolpyruvate carboxykinase. Inhibits gluconeogenesis. Increased activity of glucose transporters. Moves glucose into cells.
Slide 25-

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.
Slide 26-

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
Slide 27-

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
Slide 28-

Insulin Action on Cells: Dominates in Fed State Metabolism
Slide 29-

Insulin: Summary and Control Reflex Loop
Slide 30-

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).
Slide 31-

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.
Slide 32-

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++)
Slide 33-

Glucagon prevents hypoglycemia by  cell production of glucose Liver is primary target to maintain blood glucose levels Glucagon Action on Cells: Dominates in Fasting State Metabolism
Slide 34-

Glucagon Action on Cells: Dominates in Fasting State Metabolism
Slide 35-

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
Slide 36-

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.
Slide 37-

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.
Slide 38-

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.
Slide 39-

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 Hormonal Regulation of Nutrients
Slide 40-

Turnover Rate Rate at which a molecule is broken down and resynthesized. Average daily turnover for carbohydrates is 250 g/day. Some glucose is reused to form glycogen. Only need about 150 g/day. Average daily turnover for protein is 150 g/day. Some protein may be reused for protein synthesis. Only need 35 g/day. 9 essential amino acids. Average daily turnover for fats is 100 g/day. Little is actually required in the diet. Fat can be produced from excess carbohydrates. Essential fatty acids: Linoleic and linolenic acids.
Slide 41-

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
Slide 42-

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.
Slide 43-

Energy Regulation of Pancreas Islets of Langerhans contain 3 distinct cell types: a cells: Secrete glucagon. b cells: Secrete insulin. D cells: Secrete somatostatin.
Slide 44-

Regulation of Insulin and Glucagon Mainly regulated by blood [glucose]. Lesser effect: blood [amino acid]. Regulated by negative feedback. Glucose enters the brain by facilitated diffusion. Normal fasting [glucose] is 65–105 mg/dl.
Slide 45-

Regulation of Insulin and Glucagon (continued) When blood [glucose] increases: Glucose binds to GLUT2 receptor protein in b cells, stimulating the production and release of insulin. Insulin: Stimulates skeletal muscle cells and adipocytes to incorporate GLUT4 (glucose facilitated diffusion carrier) into plasma membranes. Promotes anabolism.
Slide 46-

Oral Glucose Tolerance Test Measurement of the ability of b cells to secrete insulin. Ability of insulin to lower blood glucose. Normal person’s rise in blood [glucose] after drinking solution is reversed to normal in 2 hrs. Insert fig. 19.8
Slide 47-

Regulation of Insulin and Glucagon Parasympathetic nervous system: Stimulates insulin secretion. Sympathetic nervous system: Stimulates glucagon secretion. GIP: Stimulates insulin secretion. GLP-1: Stimulates insulin secretion. CCK: Stimulates insulin secretion.
Slide 48-

Regulation of Insulin and Glucagon Secretion (continued)
Slide 49-

Glucose homeostasis – Putting it all together Figure 26.8 Insulin Beta cellsof pancreas stimulatedto release insulin intothe blood Bodycellstake up moreglucose Blood glucose leveldeclines to a set point;stimulus for insulinrelease diminishes Liver takesup glucoseand stores it asglycogen High bloodglucose level STIMULUS:Rising blood glucoselevel (e.g., after eatinga carbohydrate-richmeal) Homeostasis: Normal blood glucose level(about 90 mg/100 mL) STIMULUS:Declining bloodglucose level(e.g., afterskipping a meal) Alphacells ofpancreas stimulatedto release glucagoninto the blood Glucagon Liverbreaks downglycogen and releases glucoseto the blood Blood glucose levelrises to set point;stimulus for glucagonrelease diminishes
Slide 50-

Hormonal Regulation of Metabolism Absorptive state: Absorption of energy. 4 hour period after eating. Increase in insulin secretion. Postabsorptive state: Fasting state. At least 4 hours after the meal. Increase in glucagon secretion.
Slide 51-

Absorptive State Insulin is the major hormone that promotes anabolism in the body. When blood [insulin] increases: Promotes cellular uptake of glucose. Stimulates glycogen storage in the liver and muscles. Stimulates triglyceride storage in adipose cells. Promotes cellular uptake of amino acids and synthesis of proteins.
Slide 52-

Postabsorptive State Maintains blood glucose concentration. When blood [glucagon] increased: Stimulates glycogenolysis in the liver (glucose-6-phosphatase). Stimulates gluconeogenesis. Skeletal muscle, heart, liver, and kidneys use fatty acids as major source of fuel (hormone-sensitive lipase). Stimulates lipolysis and ketogenesis.
Slide 53-

Insert fig. 19.10 Effect of Feeding and Fasting on Metabolism
Slide 54-

Diabetes Mellitus Chronic high blood [glucose]. 2 forms of diabetes mellitus: Type I: insulin dependent diabetes (IDDM). Type II: non-insulin dependent diabetes (NIDDM).
Slide 55-

Comparison of Type I and Type II Diabetes Mellitus Insert table 19.6
Slide 56-

Type I Diabetes Mellitus b cells of the islets of Langerhans are destroyed by autoimmune attack which may be provoked by environmental agent. Killer T cells target glutamate decarboxylase in the b cells. Glucose cannot enter the adipose cells. Rate of fat synthesis lags behind the rate of lipolysis. Fatty acids converted to ketone bodies, producing ketoacidosis. Increased blood [glucagon]. Stimulates glycogenolysis in liver.
Slide 57-

Consequences of Uncorrected Deficiency in Type I Diabetes Mellitus Insert fig. 19.11
Slide 58-

Type II Diabetes Mellitus Slow to develop. Genetic factors are significant. Occurs most often in people who are overweight. Decreased sensitivity to insulin or an insulin resistance. Obesity. Do not usually develop ketoacidosis. May have high blood [insulin] or normal [insulin]. Insert fig. 19.12
Slide 59-

Treatment in Diabetes Change in lifestyle: Increase exercise: Increases the amount of membrane GLUT-4 carriers in the skeletal muscle cells. Weight reduction. Increased fiber in diet. Reduce saturated fat.
Slide 60-

Hypoglycemia Over secretion of insulin. Reactive hypoglycemia: Caused by an exaggerated response to a rise in blood glucose. Occurs in people who are genetically predisposed to type II diabetes. Insert fig. 19.13
Slide 61-

Metabolic Regulation Anabolic effects of insulin are antagonized by the hormones of the adrenals, thyroid, and anterior pituitary. Insulin, T3, and GH can act synergistically to stimulate protein synthesis.