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DIGESTION: GI Tract • Four Functions: A. B. C. D. • Motility: Movement of substances Secretion: Enzymes / digestive juices Digestion: Physical catabolism of food Absorption: nutrients into circulation Innervation of the GI: 1. Parasympathetic 2. Sympathetic One muscular tube: smooth vs. skeletal muscle • - Peristalsis segmentation DIGESTION: Catabolism • • Start of digestion: Mouth- Salivary amylase Absorption: 1. Sm. Intestine: vitamins and minerals 2. Lg. Intestine: water and salts • Carbohydrates Salivary Amylase Mouth long sugars Pancreatic amylase Sm. Intestine Other enzymes Sm. Intestine • double sugars long sugars double sugars double sugars simple sugars Proteins Pepsinogen/Pepsin Trypsinogen/Trypsin Other Enzymes Stomach Sm. Intestine Sm. Intestine Proteins AA chains Proteins AA chains AA chains single AAs 1 DIGESTION: Catabolism • Fats Bile Salts Lipases Sm. Intestine(liver) Sm. Intestine(pancreas) Emulsification(droplets) TGs Fatty acid + Monoglycerides • Enhanced absorption in Small intestine by Villi HORMONES • Chemical released by one cell to travel to another cell to exert an effect - 1,25(OH)2VitD3, PTH, Oxytocin, EPO, Insulin • Insulin: -Islet cells, stimulated by high levels of blood glucose, purpose is to lower blood glucose levels Insulin levels -Islet cells Muscle cells Fat Cells Plasma levels of Blood glucose Liver -Islet cells 2 DIABETES MELLITUS • ‘Open loop’ disease of glucose regulation 1) IDDM: no insulin production- Injections required 2) NIDDM: Functional insulin produced, effector tissue problematic • Effector tissues: 1. Muscle/Fat: Insulin receptor = Tyrosine Kinase Signaling induces GLUT4 exocytosis, Glucose flux into cell. 2. Liver: Insulin binding activates glycogenic enzymes Liver does not have GLUT4, only GLUT2 (signaling independent) -cell glucose/insulin feedback • 1. 2. 3. 4. 5. 6. GLUT2-K(ATP)-V Gated Ca2+ Channels Glucose flux into cell via GLUT2 Increase in [ATP]in Decrease in GK(ATP) Voltage increase Opening of V-Gated Ca2+ channel, Ca2+ flux in Release of vesicles containing insulin PM GLUT4 Plasma Glucose Plasma Insulin Glycogenesis Net flux of glucose into cells Plasma Glucose 3 GLUCAGON • Protein secreted by -islet cells of the pancreas • • • • Release stimulated by low plasma glucose Glucagon receptor on liver: GPCR cAMP release Glucagon release leads to glycogen breakdown sensor & comparator: -islet cells • Actuating signals: glucagon levels Plasma Glucose Plasma Glucagon Conversion of glycogen to glucose Flux of glucose out of liver Plasma Glucose PITUITARY • • • • • Pituitary is closely associated with hypothalamus Pituitary stalk connects pituitary to hypothalamus Posterior pituitary hormones: vasopressin and oxytocin Hypothalamus secretes ‘Releasing Hormones’ RHs travel through capillaries to the anterior pituitary, binding receptors to cause release of a hormone into blood stream 4 RELEASING HORMONES & HORMONES Hypothalamus TRH Anterior Pituitary TSH Peripheral effects release of thyroid hormones (thyroxin) GHRH GH Stimulate cell growth (GHRs) GnRH LH, FSH stimulate production of sex hormones in the gonads (Test., Est., Progest.) HORMONE SPECIFICS Two broad categories: 1. Lipid Soluble: Intracellular receptors 2. Non-lipid soluble: Plasma membrane receptors Corresponding receptors 1. GPCR cAMP flux: V2, Glucagon, RH 2. Ionotropic 3. Intracellular activity: Insulin Tyrosine Kinase GLUT4 exocytosis 5 BODY TEMPERATURE • Mammals have a T > external and internal set point • Sensors for body temp are central thermoreceptor neurons in hypothalamus and peripheral thermoreceptor neurons in skin • Comparator uses input from both sets of sensors and sends actuating signals: – Body too hot: Increase sweat, increase flushing* – Body too cool: decrease sweat, decrease flushing, shivering. • Long term: release of hormones to raise body metabolism • Fever: higher set point • *Flushing = flow of blood near skin in capillary beds 6