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82 Cards in this Set
- Front
- Back
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5 hormones secreted by the pancreas:
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-Insulin
-Glucagon -Amylin -Somatostatin -Pancreatic Polypeptide |
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What are the 2 major tissue types of the pancreas?
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-Acini
-Islets of Langerhans |
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Acini secrete _______
Islets secrete _______ |
Acini = digestive enzymes
Islets = digestive hormones |
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Where do the hormones secreted from islet cells go?
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Into capillaries around which the islets are organized.
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3 major cell types in islets of langerhans; what % is each?
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-Beta = 60%
-Alpha = 25% -Delta = 10% |
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What is secreted by each cell?
Alpha Beta Delta PP |
Alpha = glucagon
Beta = insulin + amylin Delta = Somatostatin PP = pancreatic polypeptide |
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What does Insulin inhibit?
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Glucagon secretion
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What does Amylin inhibit?
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Insulin secretion
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What does Somatostatin inhibit?
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Secretion of both insulin and glucagon
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Where else is SST made and released?
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In the hypothalamus - it's the same polypeptide, just made in 2 different places.
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What is the main stimulus for insulin secretion?
What does insulin secretion result in when there is carbohydrate excess? |
Stimulus = Energy abundance - especially excess carbohydrates.
Result: storage of glycogen in liver and muscles. |
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What happens to additional excess carbs when no more glycogen can be stored?
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They get stored in fat tissue.
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What are the 3 effects of Insulin on protein metabolism during energy abundance?
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-Promotes amino acid uptake
-Promotes AA conversion to protein -Prevents protein breakdown |
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What is the initial form of insulin when synthesized?
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Proinsulin
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What does proinsulin consist of?
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-A chain
-C peptide -B chain -2 disulfide bonds |
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What is C-peptide?
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The peptide that connects the Bchain to the Achain
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What creates Insulin?
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Post-translational processing in which enzymes cleave the C-peptide.
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So what gets released when one mole of insulin is secreted from the pancreas?
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1 mol of C-peptide
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So for a person that is producing no endogenous insulin, such as a person w/ Type I Diabetes, how could you tell?
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There would be no c-peptide in the blood, because the exogenous therapeutic form of insulin doesn't have c-peptide.
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What type of receptor is the Insulin receptor?
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An enzyme-linked receptor
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What is the insulin receptor made up of?
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2 alpha subunits - extracellular
2 beta subunits - transmembrane |
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What happens when Insulin binds the extracellular alpha subunits of its receptor?
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It causes autophosphorylation of the transmembrane B-subunit.
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What does autophosphorylation of the beta subunit result in?
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Tyrosine Kinase activity
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What does receptor tyrosine kinase activity result in?
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The activation of a phosphorylation cascade that activates or inhibits enzymes for metabolism.
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What are the enzymes that are effected by insulin binding its tyrosine kinase receptor called?
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Insulin receptor substrates (IRS)
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What are 6 things affected by Insulin receptor activation?
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-Glucose transport (Glut4)
-Protein synthesis -Fat synthesis -Glucose synthesis -Growth/gene expression -Brain control of hunger |
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Where does glucose uptake NOT increase when insulin is high?
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In the brain - glucose transport is not controlled by insulin in the brain!!
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What do muscle cells use for energy during most of the day when you're not eating?
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Fatty acids
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What causes muscles to use glucose after you eat?
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Insulin which increases their permeability to glucose.
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Is insulin the only thing that will allow the muscle cells to use large amounts of glucose?
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No; exercising and the actual contraction of muscle increases its permeability to glucose too.
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If you used one word for insulin what would it be? Why?
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ANABOLIC
Because it induces storage of glucose, protein/fat synthesis, and glucose synthesis. |
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Does insulin secretion depend on what type of food you eat?
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Nope; If you eat protein you want to store it. If you eat fat you want to store it. If you eat sugar you want to store it.
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So what are the 3 main target tissues for insulin?
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-Muscle
-Fat -Liver |
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2 Anabolic effects of insulin on the Liver:
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1. Glycogen storage
2. Glycolysis |
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2 Anticatabolic effects of insulin on the liver:
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-Inhibits glycogenolysis
-Inhibits ketogenesis -Inhibits gluconeogenesis |
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What are the 2 main things insulin does to muscle in general?
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1. Promotes protein synthesis
2. Promotes glycogen synthesis |
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How does insulin promote protein synthesis in muscle? (2 ways)
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1. Increases AA uptake
2. Stimulates protein synthesis via ribosomes |
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How does insulin promote glycogen synthesis in muscle? (3 ways)
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1. Increases glucose transport
2. Enhances activity of glycogen synthetase 3. Inhibits activity of glycogen phosphorylase |
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Is muscle capable of take the phosphate off glucose-6-phosphate?
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No; so it's NOT source of free glucose for gluconeogenesis.
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How does insulin stimulate increased glucose uptake by muscle?
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By increasing the concentration of glut4 transporters in the cells.
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What does Insulin do to fat?
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Promotes triglyceride storage
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What are the 3 ways by which insulin promotes triglyceride storage in fat?
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1. Induces lipoprotein lipase to make FA's available for absorption into fat cells
2. Increases glucose uptake 3. Inhibits lipolysis |
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So what happens when you have TOO MUCH insulin?
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You get fat
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What are the 4 stimulators of insulin secretion? Which is most important?
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1. Glucose (most important)
2. Amino acids 3. Fatty acids 4. GH/Cortisol |
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How do GH and Cortisol stimulate Insulin?
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Indirectly; when you're starving, cortisol is released and prevents glucose uptake in muscle so the blood glucose goes up. Islet cells respond appropriately to release insulin.
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Is there a difference in giving oral glucose versus IV infusion?
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YES!! Oral glucose goes through the GI tract and stimulates GI hormones that increase the GAIN of the islet cells so for every unit of glucose you get more insulin.
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What do we call the GI hormones that increase the response of insulin to a sugar intake?
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Amplifiers
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What inhibits insulin secretion?
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Somatostatin
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What is the effect of SST on insulin secretion?
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It DAMPENs the release; it buffers against wild insulin swings.
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So what type of glucose transporter is found on islet beta cells?
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Glut2
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Is glut2 insulin sensitive?
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ABSOLUTELY NOT - that would be like putting the cart before the horse.
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What is the response of the beta cell to an increase in blood glucose?
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1. Glu -> Glu6P via glucokinase
2. Gets burned to increase ATP 3. ATP close K channel, depolarizes cell, opens Ca channel 4. Ca influx allows insulin granules to dock/secretion occurs. |
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What do the alpha cells of the islets produce?
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Glucagon
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What are the target tissues of Glucagon?
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-Liver
-Fat |
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What is the main role of Glucagon?
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To increase gluconeogenesis
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So why doesn't Glucagon effect muscle?
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Because muscle doesn't DO gluconeogenesis.
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In the liver what does Glucagon stimulate?
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-Glycogenolysis
-Amino acid uptake -FFa uptake -Ketoacid synthesis |
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Why does Glucagon stimulate AA and FFA uptake in the liver?
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Because you need them to make glucose
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What does Glucagon inhibit in the liver?
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Glycolysis
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So during the fasting state when Insulin is LOW and Glucagon is HIGH what will be happening?
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Insulin is preventing glucose uptake by muscles
Glucagon is preventing hypoglycemia by increasing blood glucose |
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What are 4 inhibitors of Glucagon release by alpha cells?
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FIGS
-Free fatty acids -Insulin -Glucose -Somatostatin |
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What is the type of inhibition of SST on glucagon?
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The same as for insulin - it DAMPENS the secretion to prevent wild swings in hormone levels.
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What do Amino acids do to glucagon?
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STIMULATE THE RELEASE OF GLUCAGON
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Why do amino acids stimulate the release of glucagon?
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Because if you were a hyena living in Africa and you ate a HUGE meal of ONLY PROTEIN, if you didn't have glucagon you would become hypoglycemic because your blood sugar wouldn't increase, but insulin is still stimulated by AAs.
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So amino acids stimulate:
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-Insulin
AND -Glucagon |
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What are Glucagon-like peptides?
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GI hormones that are secreted from the gut in response to eating a meal
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What is the acute effect of GLPs?
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Increased gain of the islet beta cells so that when glucose comes along, more insulin is released.
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When after feeding does GLP get released?
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When food hits the stomach - long before glucose is absorbed.
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What does GLP do in the chronic term?
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Increases beta cell mass.
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What is a good use of the chronic effect of GLPs to increase beta cell mass?
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It helps type II diabetics overcome insulin resistance.
Also nauseates them so they don't eat so freaking much. |
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What flucutates more during a normal 24-hour period; glucagon or insulin? Why?
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Insulin - because glucagon responds to starving states, and the average person doesn't starve if they eat 3 meals a day.
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After you eat a meal, what is the insulin response like?
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GLPs cause a big increase in insulin; then, while glucose is STILL high, insulin drops in response to SST and the waning of GLPs
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Why is it SO IMPORTANT that insulin drops despite blood sugar still being high after a meal?
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Because it prevents your blood sugar from going TOO low and making you become hypoglycemic.
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So the 2 things that cause insulin to decrease after a meal:
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1. Waning of GLPs
2. Increase in SST from the pancreas Delta cells to dampen the system |
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What is the process that occurs in the FED state?
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1. Insulin goes up
2. Glucose uptake goes up in muscle fat and liver 3. Counterreg hormones are inhibited (Glucocorticoids and GH) |
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What is the process that occurs in the FASTED (starving) STATE?
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1. Insulin is LOW
2. Counterreg hormones are HIGH 3. Glucose is produced by the liver |
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So what happens if there is no insulin?
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There is no storage of glucose; it all spills into the urine and causes osmotic diuresis of very sweet pee.
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So what happens when you give a normal person a blood glucose tolerance test?
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Blood glucose goes up
CCK/GlP stimulates insulin Glucose uptake occurs Blood glucose returns to control. |
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What is the definition of hypoglycemia? Neuroglycopenia?
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Hypo = <70
Neuro = <40-50 |
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What happens to an abnormal person (diabetic) in a glucose tolerance test?
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GI hormones still go up
Big HUUUUGE increase in blood sugar (no uptake in fat/muscle) Takes forever to go back to control. |
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Why does the diabetic's blood sugar even go back down to ctrl?
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Because it gets peed in the urine via osmotic diuresis.
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What is Diabetes mellitus?
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Too much sweet urine
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