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70 Cards in this Set
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- Back
what are the targets of glucagon
what are the targets of insulin |
liver
adipose Insulin: liver, fat, sk MM |
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what does glucagon do to urea
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increased
**glucagon stimulates brakdown of aa to from glucose |
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what does somatostatin do to glucagon
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decreased
**glucagon also inhibited by: glucose on blood, insulin, FA and ketoacids |
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what are the 3 hormones secreted by the pancrease
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1. Glucagon
2. Insulin 3. Somatostatin (also comes from hypothalamus) |
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is the secretion of the pancrease stim by the hypothalamic hypophyseal system
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nope, the secretion of inculin/glucagon by the pancreas is controlled humorally, ie by conc of substarte in the blood
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what all things release somatostatin
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hypothalamus
GI Pancreas |
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insulin is the hormone of what? while glucagon is the hormone of what
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Insulin: abundance. secreted when nutrients are in abundance, insulin helps us store this excess fuel
Glucagon: starvation, promotes mobilization of fuel stores whn nutrients are low |
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are insulin/glucagon workind in a paracrine manner
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sure thing
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are insulin/glucagon counterregulatory?
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sure thing
*antagonists, when one is secreted the other is not |
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nutrient flow through the GO stimulates the pancrease to do what
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release exocrine digestive enzymes and endocrine homromes
**hormones and digestion is released at same time |
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so hormone secretion in the pancreas is stim by nutirent flow in GI, where are nutrients released to?
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the portal vein where they meet the products of digestion
**pancrease is in a great location for this fx |
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what cell in the islet releases insulin, gluc, somatostatin, pancreatic polypeptide
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insulin: b
Glucagon: a somatostatin: delta pancreatic polypeptide: F |
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where are hormones in the pancreas made and stored
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islet of lanterhan
a: glucagon b: insulin delta: somatostatin F:pancreatic polypeptide |
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do the cell types of the islets talk
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you bet, gap junctions btwn a, b and ab
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is insulin released as a prohormone
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yep, it has C peptide that needs to be cleaved
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what is the structure of insulin
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a chain and b chain
**also has c peptide in prohormone stage |
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so insulin is a peptide hormone, what do we know about its synthesis and storage
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prepoinsulin
proinsulin Packaged and stored in granules (proinsulin, C is sttached) |
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what is in the secretory granule for insulin? what is required for granule movement?
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proinsulin, with C peptide. when released insulin and c are released in 1:1 ratio (insulin has super short half life)
**granule movemnt requires a good microtubule system |
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how can we approximate the levels of insulin in circulation despite its SUPER short 1/2 life
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measure C protein, its released 1:1 and C stays aroun dlonger
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what is the most importatn insulinogogue? waht is the mech
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metabolism of glucose
*glucose enters the B cell in the islet of langerhan and is oxidized to make ATP *ATP closes K channels *this DEPOLARIZES the b cell *depolarization opens Ca channels *Ca signals isulin granules to be released **insulinogogue stim insulin secretion. Others include: glucagon, GLP, AA, GH, Cortisol |
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what is the mech of Glucose stim insulin secretion
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glucose enters the B cells in islets of langerhan and is oxidized to form ATP
ATP closes K channels --> DEPOLARIZATION depolarization leads to Ca incerase Ca signals exocytosis of granules that contain insulin |
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what decreases the release of insulin
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blood glucose
somatostatin NE, EPI |
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what things stim insulin secretion
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glucose, AA, FA
Glucagon GLP Ach |
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how can insulin modulators increase/decrease insulin release
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cAMP to icnrease Ca and cause exocytosis
PLC to alter cAMP levels |
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so increase in glucose, FA, or AA will stim secretion of insulin. how is this a clevel cech to also stop secretion
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secretion stim insulin, insulin then decreases these things in the blood. When the decreased conc is detected insulin secretion is stopped
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is insulin secretion pulsatile, continuous, ect?
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Biphasic. Initial spike, late phase gradual increase with plateau
**at first there is a build up of insulin in granules and when blood glucose is high all of the granules are reelased, this causes a SPIKE (increase adn also a decrease) **after the spike if more insuin is needed it is made denovo and then there is a steady increase in inculin release. **second phase begins about 10 min after stim and can last for a hours and |
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we know glucose is the major stim for insulin secretion is more insulin released when glucose is oral or IV
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ORAL
when taken through GI the glucose also stim Glucose dependent insulinotropic peptice (GIP) and GLP1. Both of which independently increase insulin secretion. This gets the body ready for the glucose load that is about to come **IV GIP and GLP arent sitm |
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when glucose is seen in the GI what other hormones are secreted in order to better accomadate the coming glucose load
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GIP
GLP **both stim insulin secretion independtly. THis REALLY amps up the insulin released |
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what does the insulin receptro look like? how does it work
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a and b sunbunits
a binds insulin b is the RTK **when inculin binds to the a subinut the b subunit pi itself. and IRS (insulin receptor substrates) the IRS does its thing and then the receptor is engulfed |
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waht are IRS
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when insulin binds a subunit or receptor it causes the b subunit to pi itself and IRS
IRS are the tings that cause the physiological response to increase glucose uptake |
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so the insulin can work a few dif ways, whats the normal respone when bound? what about a fast thing? longer? **note these activities are regulated byt he IRS that was Pi by the b subunit
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Normal: insulin binds and IRS are Pi and cause Glut 4 to be inserted in the membrane
FAST: AA and electrolytes enter through channels SLow: Lipogenic effects will cause gene expression |
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what does insulin do to glucose metabolism in gthe liver, sk mm, fat
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increase glucose transport in all 3
**in the liver and sk mm only glycogen synthesis is done **no glycogen synthesis in the fat |
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what does insulin do to fat metabilism? where are these effects seen?
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recall inculin acts on the liver, fat, and sk mm
Lipogenesis in the liver and fat made VLDL and cholesterol in liver all tissues take up FFA |
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wjat does insulin do to protein metabolism?
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stim aa uptake and protein synthesis. inhibit protein breakdown ++ N balance
doen in the liver, fat, and sk mm |
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what is the N balance in the presence of insulin
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positive
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does insulin work fast? what does it immediatly, after a bit, and more delayed
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YES!!! within seconds there is in increase in the transport of glucose, aa, and K
within minutes it stim protein and glycogen synthesis and after hours it stimulates lipogenesis **the different IRS cause diff things |
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we know inculin is the major product of b cells, what else do b cells secrete
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1. amylin: decrease glucose uptake un mm and decrease food intake, delay gastric emptying. used to treat DM II
2. Pancreatistatin: autofeedback regulation of inculin release |
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what are amylin nad pancreastatin
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they are the other products of the b cell (insulin is main)
Amylin: decreases glucose uptake in mm, decrease food intake, delay gastric emptying Pancreastatin: autofeedback regulation of insulin release |
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does insulin stim the release of FFA
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nope
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summary: what 3 tissues doe insulin work on? what stim, inhibits
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sk mm, liver, fat
Stim by glucose, FFA, AA in blood. inhibited by a decrease in these things int he blood |
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other than metabolism, what else does insulin affect?
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1. heart: increase CO (+ inotropic effect)
2. thermogensis, get hot after you eat lots 3. increase E expenditure 4. decreases neuropeptide Y to supress appetite 5. increase K reabe |
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what does insulin do to appetite
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supress it by decreaseing neuropeptide Y
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what does insulin do to K
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increase reabs of K and PO4
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is glycogen a prohormone? is insulin
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BOTH are
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where is the proglucoagon hormone made
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a cells of pancreas
also in intestine |
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what does glucagon do? when is it secreted
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secreted when blood glucose is low to increase blood sugar levels
**total opposite of insulin, mobilizes fuels rather than storing them |
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so the main insulinogogue was glucose. what is the main glucagonogue
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hypoglycemia
**low blood sugar causes the release of glucagon which will mobalize sugars from the cells to enter the blood |
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so with insulin it was released whn glucose in blood was high and then inhibited when glucose was low. what is teh pattern for glucagon
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glucagon causes FFA, ketoacids, and glocose to enter the blood, when these increase in the blood glucagon secretion is inhibited
AA in the blood on the other hand signal to the body that proteins are being broken down adn so will release glucagon so the aa can be converted to sugar |
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aa in the blood do what to glucagon
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stimulate the release of glucagon! hmm, glucagon then stim the conversion of aa to glucose
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what does glucagon do to carb metabolism
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glycogenolysis
gluconeogenesis Seen in the liver only. glucagon does NOT affect the sk mm |
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does glucagon affect the sk mme?
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no way jose, only insulin acts on sk mm
Glucogon acts on the fat and liver |
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what does glucagon do to lipid metabolism
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lipolysis
ketogenesis, make ketone bodies to make glucose **ketogeneis only occurs in the liver, lipolysis occurs in the liver and fat |
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without insulin what state can we enter
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acidosis
ketone bodies from ketogenesis |
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what does glucagon do to protein
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increase aa uptake in the liver for gluconeogenesis
**proteolysis to free aa so they can be used to make glucose **increases N in the pee - N balance |
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+ N with what hormone
- N with what hormone |
+ inculin
- glucagon |
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summary of glucagon! wht tissue, what stim, inhibits
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the liver nad fat
A decrease in plasma glucose leads to gluconeogenesis, glycogenolysis, ketogenesis, and lipolysis to increase plasma glucose, FFA, and ketoacids adn decrease AA |
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when glucagon has been secreted what happens to aa and ketoacids in the blood
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aa decrease (used to make glucose)
ketoacids increase |
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what does it mean that insulin and glucagon are sounterregulated
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when plasma glucose increases insulin is secreted and glucagon is inhibited
**if in the other hand plasma glucsose drpos glucagon is stim and insulin is inhibited |
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an increase in what other hormones accompany an increase in glucagon
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cortisol
GH Epi **when plasma glucose drops all of thses will be released |
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so if our plasma glucose levels frop what do we need to do and what hormones do it?
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get it up!!!
Glucose is preferred fuel for brain so we use glucagon 1st to get glucose 1. EPI 2. GH 3. Cortisol **we then use thse as back up |
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waht is our back up plan if glucagon isnt working to keep glucse levels in the blood high
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1. EPI
2. GH 3. Cortisol |
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what is the mormal ration of I to G
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2
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what happens to the molar I:G ratio when exercising
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decreases!
less insuliln is there. We are using our blood sugars so glucagon is released to maintain glucose levels *aids lipolysis, gluconeogenesis, glycogenolysis |
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what happens to metabolism when the I:G ration is 1
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LOW, less insulin and more glucagon so increase lipolysis, glycogenolysis, gluconeogenesis
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what does it mean in your G"I is 10
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you just had a ton of carbs
**increased insulin secretion to promote uptake and storage of glucose and others |
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what metabolic paths are stim by insulin? glucagon
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glucose oxidation
glycogen synthesis protein synthesis lipogenesis fed state, promote storage Glucagon: lipolysis gluconeogensis glycogenolysis fasted state, promote mobilization |
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a high I:G stim what?
low? |
High: promotes storage. causes blood to decrease glucose AA FA and ketone bodies
Low: promotes mobilization. Increase Glucose AA FA and ketone bodies in the blood |
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where is somatostatin made? what does it do?
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delta cells of pancreas
hypothalamus GI tract INHIBITS: insulin glucagon GH GI hormone secreion, motility, papsin, blood flow |
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the role of somatostatin is waht?
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modulat the resposne of insulin and glucagon to the ingestion of food
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somatostatin inhibits what hormones
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insulin
glucagon GH **also inhibits GI fx and motility |