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Metabolism FOOD proteins sugars fats amino acids fatty acids simple sugars (glucose) muscle proteins liver glycogen fat lipids glucose
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Mammalian Pancreas Gall bladder duodenum liver Bile Duct Pancreas Pancreatic duct -Exocrine Pancreas: secretes digestive enzymes, alkaline pancreatic fluid -Endocrine Pancreas: secretes hormones that regulate carbohydrate, lipid, and protein metabolism
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Endocrine Pancreas Islets of Langerhans: 4 cell types – cells: secrete glucagon – cells: secrete insulin – cells: secrete somatostatin –F cells: secrete pancreatic polypeptide Islets of Langerhans Exocrine cells capillaries
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Pancreatic Hormones Insulin Glucagon Somatostatin
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INSULIN Regulation of Secretion –Hyperglycemia stimulates release Glucose sensors in cells –Gastric Inhibitory Peptide Released from cells of the small intestine Potent stimulator of insulin secretion –Somatostatin: inhibits insulin release (paracrine) –Autonomic nervous system Parasympathetic activation increases insulin release Sympathetic activation blocks insulin release Epinephrine (from adrenal) blocks insulin release
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INSULIN Action at Target Tissues –Activation of insulin receptor: Increases transport of glucose, amino acids, and fatty acids into cells Glucose transporter:
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INSULIN Action at Target Tissues –Activation of insulin receptor: Increases transport of glucose (glucose transporter), amino acids, and fatty acids into cells –Enhancement of anabolic pathways, decrease in catabolic pathways –Increases enzymes that activate: Glycogen formation (liver) Lipogenesis (fat) Protein Synthesis (muscle)
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Pancreatic Hormones Insulin –Hypoglycemic, glycogenic, lipogenic, anabolic Glucagon Somatostatin
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Glucagon Hyperglycemic (increases plasma glucose) –(one of many in the body) Actions at target cells –Liver Promotes glycogenolysis Promotes gluconeogenesis –Fat Tissue Promotes lipolysis
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Pancreatic Hormones Insulin –Hypoglycemic, glycogenic, lipogenic, anabolic Glucagon –Hyperglycemic, lipolytic Somatostatin –Paracrine agent –Believed to inhibit insulin and glucagon release –May regulate uptake of nutrients from the gut
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Glucose Regulation Insulin: decreases blood glucose levels Glucagon: increases blood glucose levels Somatostatin: regulates insulin and glucagon levels (paracrine) and nutrient uptake at the gut
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DIABETES MELLITUS Type I—juvenile onset—insulin dependent –IDDM –Underproduction of insulin Type II—adult onset—non-insulin dependent –NIDDM –Insulin receptor resistance –Post-receptor mechanism problem
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Insulin Dependent: IDDM Possibly results from autoimmune reaction –The body’s immune system attacks the cells Pancreatic markedly reduced –Symptoms only appear after ~80% loss of cells No insulin……physiological repercussions? Treatment –Insulin injections –Recent methods
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Islet Transplantation Inside the patient Separate islets from exocrine pancreas Encapsulate islets (immune protection) Inject into abdomen
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Non-Insulin Dependent: NIDDM Usually occurs in overweight individuals over 40 years of age –Associated with abdominal fat in women Target cells become resistant to insulin –insulin receptor Fewer receptors Receptors have lower affinity Receptor blocked (possibly by antibody) –Post-receptor mechanisms
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Diabetes Prevelence in US %
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