Pancreatic Hormones Part II

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Pancreatic Hormones Part II


Lecture number:
15
Pages:
6
Type:
Lecture Note
School:
University of Southern California
Course:
Bisc 307l - General Physiology
Edition:
1
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BISC 307L 1st Edition Lecture 15 Current Lecture  Control of Insulin Secretion in Pancreatic B cells o o Insulin the first endocrine hormone that was well studied o Small protein o The rectangle is beta cell o How does the cell know when its time to secrete insulin?  Main mechanism is exerted by glucose itself and amino acids in the plasma  Blood glucose and blood plasma  Glucose enters through GLUT 2 which results in increase in ATP which binds to a ATP sensitive K+ channel which is usually open when there are low levels of ATP so when there is high level of ATP this channel is blocked. This blocking of the formally open K+ channels depolarizes the membraneopens Ca2+ channelstrigger for exocytosis of vesicles containing insulin o Two methods that stimulate insulin release:  1. Parasympathetic activity  2. Secretion of Incretins (small intestinal hormones)  1. GLP1 Glucagon like peptide 1  2. GIP Gastric inhibitory peptide (now called glucose dependent insulinotropic peptide)  stimulates secretion of insulin due to glucose  *Both are part of a feed forward system that anticipate a rise in blood nutrient before the meal is taken in. They prime the beta cell so that they are more sensitive to the rise in blood glucose when it actually happens* o Main mechanism of inhibiting of insulin secretion  Sympathetic activity  Slide 5- Insulin Stimulates Glucose uptake in resting skeletal muscle and adipocytes o Three cell types  1. Skeletal muscle cells  this slide- resting  when insulin binds to receptor this stimulates the insertion of preformed GLUT4 into membrane of resting skeletal muscle- were previously in the membrane but in the absence of insulin binding to receptor these GLUT 4 receptors are internalized and stored in vesicles just under the membrane  When insulin binds, the GLUT 4 receptors emerge and become activeas a result plasma glucose is lowered (leaves ECF into cells)  Active skeletal muscle is not described, will result in insertion of GLUT 4 transporters INDEPENDENT of insulin receptors (why diabetic patients urged to exercise because don’t need insulin in active skeletal muscle)  2. Fat cells in adipose tissue  this slide- same mechanism  3. Liver cells (next slide)



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