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67 Cards in this Set
- Front
- Back
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what 3 sources of energy stimulate release of insulin
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carbs stimulate the most (glucose)
protein stimulates 2nd most fats stimulate the least |
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what is our ultimate storage hormone
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insulin
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what does insulin stimulate
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glucose uptake in most tissues
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what is unused glucose stored as
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glycogen in muscle
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how does the brain use glucose
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brain takes up glucose
independent of insulin liver and pancreas do as well |
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what are the transporters that transport glucose
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hexotransporters
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where are the islets of langerhorns located
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pancreas, they contain alpha, beta, delta cells
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how is insulin released in Beta cells
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glucose is taken up by GLUT2
glucose gets phosphorylated by glucokinase glucose 6 phosphate gets undergoes oxidation (glycolysis) increase in intracellular ATP which causes ATP K channel to close and no more K is being pumped out of the cell membrane depolarization due to increase +ve charge voltage gated Ca channels open increase in intracellular Ca migration of vesicles to cell membrane due to increase in intracellular Ca insulin released from vesicles |
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what does insulin release in insulin independent cells depend on
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intracellular Ca
glucose being taken up by GLUT2 deactivation of K channel |
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where is insulin made
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pancreatic Beta cells
made as a single polypeptide chain that gets cleaved in the vesicle results in 2 chains held together by disulfide bonds and a C peptide |
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other than measuring someone's insulin levels what is another way you can measure the amount of insulin someone has
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measure amount of C peptides
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how is insulin stored
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in granules w/in Beta cells and it is complexed w/ zine
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how does insulin circulate
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unbound to protein
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what does the insulin receptor look like
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IGF-1 receptor
internal and external domain tyrosine kinase |
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how does the insulin receptor cause the uptake of glucose
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insulin binds to receptor
activates tyrosine kinase tyrosine kinase phosphorylates insulin receptor substrate (IRS) IRS serves as a platform and recruits the other kinase (signalining molecules) one of which will phosphorylate GLUT4 once GLUT4 gets phosphorylated it is transported to the membrane |
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where is the majority of our glucose stored
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in the muscle
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where is the GLUT4 transporter normally
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inside the cell NOT ON THE CELL MEMBRANE
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what is also secreted w/ insulin from the Beta cells
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amylin
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what does Amylin do
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suppresses secretion of additional insulin
suppresses glucagon secretion delays gastric emptying acts in the brain as a satiety factor (makes you feel full) net effect: better control of insulin release, better control of absorption of glucose, better control of appetite |
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what happens if your Beta cells are destroyed
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you lose amylin and insulin and have TYPE 1 DIABETES
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where are incretins made
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GI tract
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why does an oral dose of glucose make more insulin than an IV dose
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b/c incretins are stimulated in the GI tract by oral glucose and will increase the amount of insulin the make
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what do incretins basically do
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stimulate insulin secretion
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what are the types of incretins
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GLP1
GIP1 |
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what does Glucagon like peptide 1 do
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stimulates insulin secretion (when glucose is present)
suppresses glucagon secretion slows gastric emptying increases satiety helps improve Beta cell mass promotes insulin sensitivity |
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what are properties of Glucagon like peptide 1
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made by intestinal L cells
pre propeptide ALSO SECRETED IN RESPONSE TO EXERCISE AS WELL AS FOOD (GLUCOSE) |
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what does slowing gastric emptying do
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gives us better control over glucose absorption
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what does Glucose depepndet insulinotropic peptide-1 do
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stimulates insulin secretion (in presence of glucose)
minimal effect on gastric emptying NO EFFECT OF GLUCAGON SECRETION NOT A SATIETY FACTOR preserves Beta cell mass |
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what cells make somatostatin
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delta cells
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what regulates incretins
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dipeptidyl peptidase 4 (DPP4)
DPP4 is found in circulation and rapidly degrades incretins |
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when we can no longer store glucose as glycogen what happens
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glucose is converted to FFA and stored in adipose tissue as triglycerides
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what does insulin inhibit
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glycolysis, gluconeogenesis, ketogenesis, proteolysis, lipolysis, glycogenolysis
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right after a meal what is up
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insulin is up
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between meals what is up
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glucagon to maintain glucose levels for CNS function
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what does glucagon stimulate
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gluconeogenesis, ketogenesis, lipolysis, glycolysis, glycogenolysis
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why doesn't insulin direct glucose uptake to the liver
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b/c we need to be able to release glucose from liver when we need it
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in between meals what occurs
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liver releases glucose into blood stream
break down of fats in adipose tissue (FFA > glucose or FFA > keton bodies for fuel) |
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right after a meal what occurs
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glucose is stored as glycogen in muscles, liver
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what is common to both types of diabetes
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polydypsia
polyuria |
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what is diabetes insipidus caused
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dysfunction of antidiuretic hormone
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what is Type 1 Diabetes
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decrease or no insulin (decrease due to as the disease developes your ability to produce insulin decreases until you can't produce insulin at all)
no real cause (autoimmune, pacreatectomy) |
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when is fasting blood glucose measure
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no meal w/in 12 hrs
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when is post perandial glucose (PPG) measured
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right after a meal
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what occurs in the metabolism of someone with type 1 diabetes
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no glucose uptake in muscles or adipose tissue due to lack of insulin
liver uptakes glucose and once it can no longer be stored as glycogen it is converted to FFA and sent to the liver to be stored as TG in adipose tissue |
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what is seen in people with Type 1 diabetes
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incerease in blood lipids (due to lipolysis of fats in adipose tissue)
high blood sugar due to increase in amount of glucose in blood (due to increase in gluconeogenesis and glycogenolysis) increase in ketogenesis (make more keton bodies) |
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what are other signs and symptoms of Type 1 diabetes
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polyuria/polydypsia
glucosuria proteinuria ketoacidosis hyperglycemia muscle wasting |
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what causes proteinuria
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due to damage to glomerulus caused by glucose
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what causes ketoacidosis
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due to elevated levels of keton bodies
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what causes muscle wasting
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due to protein breakdown (proteolysis)
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WHAT OCCURS IN POLYURIA
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urine becomes hyperosmotic
water is no longer reabsorbed therefore lose water in urine glucose exits blood stream w/ filtrate |
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what is the honey moon effect
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occurs to patients who are getting insulin and after the pancreas is allowed to rest from insulin production it seems to heal a little
these patients will need a little or no insulin at all to maintain normal glucose levels may last, weeks, months, or a year EVENTUALLY FULL DEPENDENCE ON INSULIN WILL OCCUR |
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what is the main goal in treating type 1 diabetes mellitus
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maintain blood glucose levels to prevent organ damage
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what causes Type 2 diabetes mellitus
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insulin secretion defects (secreting too much or too little insulin depending on stage of diabetes)
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what occurs in Type 2 diabetes
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tissues are insulin resistant/insensitive and don't respond to it resulting in us not taking up glucose when we should (if you have high glucose and tissues are insulin resistance eventhough you are making insulin the tissues won't respond to it and since glucose stimulates insulin secretion we have high insulin)
defect in hepatic glucose management (make glucose when we shouldn't) |
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what are the subclassification of Type 2 diabetes
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non obese type 2
obsese type 2 |
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what occurs in non obese type 2?
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onset: youth or adult, MODY
strong heritable component manage by diet/exercise/oral Rx ocassionally need low dose of insulin |
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what occurs in obese type 2
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polyuria, polydypsia, fatigue, weight gain (b/c make so much insulin and store a lot of fat)
CAN'T STORE GLUCOSE treat w/ diet, exercise, oral rx, insulin sometimes |
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what are the sequelae of type 1 and 2
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retinopathy
nephropathy neuropathy |
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what is retinopathy
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small hemorrhages lead to scaring then blindness
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what occurs in nephropathy
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damage due to excess glucose and free radicals results in damage and thickening of capillary basement membrane material will damage glomerulous and you see proteinuria
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what occurs if neuropathy
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nerve damage due to free radicals
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what occurs when hyperglycemia inside the cell
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increased intracellular glucose reacts with reactive O2 species
*there is usually reducing agents to neutrolize the reactive oxygen species but due to the high amount of glucose the reducing agents are tied up metabolizing glucose reactive carbonyls on sugars (reactive carbonyls will react with anything it comes in contact with) |
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what happens to a protein when it reacts w/ a reactive carbonyl on a sugar
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the protein undergoes glyoxidation
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what happens to a lipid when it reacts w/ a reactive carbonyl on a sugar
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the lipid undergoes lipoxidation (this makes the lipid toxic)
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what can occur to proteins and lipids that are reacted w/ reactive carbonyl on sugar
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they form AGES > cell death
they undergo oxidative stress > cell death |
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what occurs in oxidative stress
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free radicals damage the DNA causing cell to undergo apoptosis
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what are AGES
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products of proteins, carbonyls, lipids
macrophages have a receptor for AGES and these cells undergo immune attack |
