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Insulin Secretion Quizlet

Chapter 16- Endocrine

Chapter 16- Endocrine

Sort Aldosterone * reduces Na+ excretion by kidneys by reabsorption in tubules * "Where salt goes, water follows" * decreases urine production * same effect as ADH but goes about it differently * Increases blood pressure * Activates Renin Angiotension Aldosterone mechanism in kidneys NET EFFECT: reduces water loss and maintains blood pressure by maintaining blood volume Continue reading >>

Insulin Secretion, Action And Counter Regulatory Hormones

Insulin Secretion, Action And Counter Regulatory Hormones

What do the Epsilon cells in IoLs produce? Which animal's insulin is similar to humans? What is insulin primarily synthesised as and where? 5-10 mins after preproinsulin assembly in endoplasmic reticulum, it is processed into proinsulin (change from 110 AA to 86) How is proinsulin converted into active insulin? Maturation by cellular endopeptidases in the Golgi apparatus. Endopeptidases cleave off C peptide from insulin by breaking the bonds between lysin 64 and arginine 65, and between arg 31 and 32 (86 AA to 21 + 30 AA (insulin) and 35 AA (C-peptide)) At which points is the endogenous production of insulin regulated? The synthesis and secretion of insulin is linked T/F Describe the mechanism of insulin secretion Glucokinase acts as the glucose sensor for insulin secretion. Pyruvate -> ATP (via krebs and ETC) which raises ATP:ADP ratio K+ATP channels close, depolarise membrane and voltage gated Calcium channels open. What level does glucose have to exceed to initiate insulin secretion? What are the two phases of insulin release from beta cells? 1. Rapidly triggered in response to increased blood glucose levels 2. Sustained slow release of newly formed vesicles What are some other signals that trigger and amplify insulin release? - Parasymp acetylcholine release via phospholipase C How do leucine and arginine amplify insulin secretion? -Intracellular catabolism increased ATP/ADP ratio -Leucine acts through allosteric activation of glutamate dehydrogenase (GDH) and can also be transaminated to alpha ketoisocaproate (KIC) that is converted to acetyl coA -Arginine can directly depolarise the plasma membrane How does GLP-1 amplify insulin secretion? Through g-protein coupled receptor GLP-1R How do Free Fatty Acids amplify insulin secretion? Activation of Free Fatty Acid Re Continue reading >>

Anatomy Ch 18 Regulation Of Glucagon And Insulin Secretion

Anatomy Ch 18 Regulation Of Glucagon And Insulin Secretion

first step in the regulation of glucagon and insulin secretion low blood glucose level (hypoglycemia) stimulates secretion of glucagon from alpha cells second step in the regulation of glucagon and insulin secretion glucagon acts on hepatocytes (liver cells) to convert glycogen into glucose (gylcogenolysis) and forms glucose from lactic acid and certain amino acids (gluconeogenesis) third step in the regulation of glucagon and insulin secretion glucose released by hepatocytes raises blood glucose level to normal fourth step in the regulation of glucagon and insulin secretion if blood glucose continues to rise, hyperglycemia inhibits release of glucagon fifth step in the regulation of glucagon and insulin secretion high blood glucose (hyperglycemia) stimulates beta cells to secrete insulin sixth step in the regulation of glucagon and insulin secretion insulin accelerates facilitated diffusion of glucose into cells, speeds up conversion of glucose into glycogen (glycogenesis), and speeds up synthesis of fatty acids (lipogenesis) seventh step in the regulation of glucagon and insulin secretion Continue reading >>

Insulin & Glucagon

Insulin & Glucagon

Sort What biological actions INCREASE due to glucagon? INCREASE IN: - Glycogenolysis - Gluconeogensis* - Fatty acid oxidation - Ketogenesis - uptake of AA (*Glucagon STIMULATES gluconeogenesis by increase gene expression of PEPCK. Does so by binding to CREB-P-a leucine zipper binding domain) Continue reading >>

Insulin Flashcards | Quizlet

Insulin Flashcards | Quizlet

once nutrients have been absorbed, you shift into the "what or what" state? Concentrations of what 2 things fall in the plasma? You shift into a state of BLANK preventing concentrations of what molecules from falling to far? This keeps what from going too low or high? once nutrients have been absorbed, you shift into the "postabsorptive" or "fasted" state. Concentrations of glucose and amino acids fall in the plasma. You shift into a state of Catabolism preventing concentrations of small molecules from falling to far. This keeps plasma glucose from going too low. glucose concentrations should vary from (#s) glucose concentrations should vary from 80-120 mg/dL plasma. limits fluctuations so glucose doesnt go too high or too low This switch between anabolism and catabolism is mediated by hormones secreted by what place in the body, what 2 things are secreted? This switch between anabolism and catabolism is mediated by hormones secreted by the pancreas, insulin and glucagon (stimulates an increase in blood sugar levels, thus opposing the action of insulin). endocrine secretes hormones directly into blood insulin is BLANK. causes what molecule to go to what 3 things? anabolic (causes glucose -> glycogen & amino acid -> protein) beta cells interact with what to secrete what? beta cells interact with glucose to secrete insulin hormones are secreted by "what" of which cells in where? hormones are secreted by "islets" (endocrine) of endocrine cells in the pancreas soon after eating, blood glucose decreases or increases?, acts directly on which cells and causes what secretion? soon after eathing, blood glucose increases, acts directly on beta cells and causes insulin secretion binding activates what? The receptor does what to itself? and also does this to various what? binding Continue reading >>

Insulin Secretion And Action

Insulin Secretion And Action

In healthy human what are the blood glucose levels normally Why is the brain highly dependent on extracellular glucose concentration Metabolise other substrates other than glucose Extract enough glucose from extracellular fluid at low concentrations because entry is not facilitated by insulin It is made in pancreatic beta cells in the islet of langerhans Form of 2 chains joined by disulphide bonds. Insulin is initially synthesised as preproinsulin in pancreatic beta cells. Afterwards in the endoplasmic reticulum it is processed to produce pro-insulin Proinsulin is matured in the Golgi apparatus through the action of cellular enteropeptidases within the Golgi apparatus. Enteropeptidases cleave off C peptide from insulin by breaking the bonds between lysine 64 and arginine 65 and between arginine 31 and 32 It is produced and stored as a hexamer, while the active form is the monomer. The hexamer is inactive with more long term stability and acts to keep the highly reactive insulin protected. The insulin is stored in the vesicles ready for release Insulin secretion is triggered by increase in cytoplasmic calcium concentration. This is a result in the opening of voltage gated calcium channels in the plasma membrane. Opening of these channels is controlled by membrane potential which is determined by ATP sensitive potassium channels Glucose enters the beta cells through the glucose transporter GLUT-2. Glucokinase converts glucose to glucose-6-phosphate. Glucose undergoes glycolysis where lots of ATP is made. This leads to a rise in ATP:ADP ratio in the cell. Normally at low levels of glucose the ATP sensitive potassium channels are open allowing the efflux of potassium. So resting membrane potential is hyperpolarised at -70mV. The increased ATP:ADP ratio causes the ATP sensi Continue reading >>

Sc17 L3 Beta Cell Biology And Insulin Secretion

Sc17 L3 Beta Cell Biology And Insulin Secretion

What is the percentage of total pancreatic mass that is the Islets of Langerhans? How many islets do the adult human pancreas contain? What percentage of these cells are beta-cells? What percentage of these cells are either alpha or delta cells? Where do you find the insulin secreting beta cells within the islet? Where do you find the glucagon secreting alpha cells within the islet? Which, out of insulin, glucagon and somatostatin, are inhibitory and which are stimulatory? What occurs first when there is an increase in blood glucose levels? What transporter does the glucose enter the B cell through? What happens to the glucose once it is inside the cell? What happens when there is an increase in intracellular ATP? What happens when the K+ ATP sensitive channel closes? There is a build up of positive charge within the B cell Opening of the Voltage Dependent Calcium Channels What does the opening of the VDCC channels caused? 100-200 nano molar of calcium within the cell What does this increase in intracellular Ca2+ lead to? Translocation of the insulin secreting granules Which fuse with the membrane > release insulin What drug targets the K+ ATP sensitive channels? Therefore increases intracellular positive charge Therefore depolarisation of the cell membrane Therefore translocation of the insulin secreting granules By how much does the basal insulin concentration increase when glucose levels increase? In what form does secreted insulin travel in the circulation? What is the half life of circulating insulin? Hormones secreted by adipocytes make the cells less sensitive to insulin > insulin resistance develops Due to the decreased sensitivity of the cells to insulin what do the B cells do to respond? B cells secrete more insulin to compensate for resistance Continue reading >>

Unit 3- Insulin And Glucagon

Unit 3- Insulin And Glucagon

Sort steps of biosynthesis of insulin in beta-cells 1. insulin gene expressed in nucleus of B-cells (insulin mRNA) 2. translation in cytosol, synthesis of N-terminal signal sequence directs complex to RER 3. signal sequence hydrophobic and directs to lumen of RER; preproinsulin is formed 4. in RER, preproinsulin is cleaved-->proinsulin and signal sequence; disulfide bridges between A and B chains are correctly aligned with help of PDI (protein disulfide isomerase) and a molecular chaperone protein 5. properly folded proinsulin -->cis-Golgi apparatus; cleaved into C-peptide and insulin 6. C-peptide and insulin stored in vesicles ready for secretion 7. upon arrival of signal, equimolar amounts of active insulin and C-peptide are released how beta cells detect blood glucose variations 1. glucose enters B-cells via GLUT-2 (insulin INDEPENDENT glucose transporter) *glucose transport exceeds rate of glucose utilization and is not limiting 2. glucose trapped in beta cells through phosphorylation to glucose-6-P catalyzed by glucokinase 3. G6P->glycolysis->TCA cycle->ETC to produce ATP *ATP/ADP ratio increases in cell with glucose concentration 4. elevated ratio inhibits ATP-sensitive potassium channel 5. accumulation of K+ in cytosol of B-cells = membrane depolarization 6. opening of a voltage-gated calcium channel = influx of calcium 7. increase in cytosolic calcium triggers regulated exocytosis of insulin in secretory vessels minor regulators of glucagon secretion -certain amino acids stimulate secretion *note: amino acids can stimulate both glucagon and insulin -Insulin and incretins (GLP-1) inhibit secretion Neural factors: -epinephrine- stimulates release of glucagon (regardless of glucose concentration) -neural input from CNS can stimulate secretion -cortisol and growth h Continue reading >>

Insulin And Glucagon Secretion

Insulin And Glucagon Secretion

islets of langerhans, secretin insulin and glucagon, somatostatin, and pancreatic polypeptide secretes digestive enzymes and bicarbonate into duodenum body's energy reserves: short term supply insulin actions promoting energy reserve preservation antilipolytic and antiketogenic, antigluconeogenic glycogenic and lipogenic, amino acid uptake and protein production Na-K ATPase, drives cellular K+ influx and Na+ efflux in patients with renal failure: can rapidly and temporarily relieve hyperkalemia shift of K+ out of cells with concomitant shift of H+ into cells--associated with normal anion gap (hyperchloremic) high anion gap acute metabolic acidosis is not associated with shift of K+ out of cells and shift of H+ into cells Rough ER: leader sequence directs entry to ER remainder forms B,C, and A peptide domains N-terminal cleavage removes 24 aa leader sequence folding forms S-S bonds that stabilize tertiary structure central C peptide region cleavage from proinsulin begins in Golgi maturate and keep converting proinsulin to insulin, driving crystal formation two monomers dimerize and associate with zinc and associate with each other, 2 Zn hexamers for compact intragranular storage alkalinization destabilizes crystalline form and hexamers degrade into dimers an monomers supplies 30% of liver's blood, oxygen-rich and nutrient-poor supplies 70% of liver's blood, oxygen-poor but nutrient rich promotes proper folding within ER to promote/stabilize disulfide bond formation between A and B peptides may play role in minimizing neurological and microvascular diabetes-related damage most numerous cells in islets of langerhans predominantly central localization within islets proinsulin--5% level of insulin, weak insulin action amylin--causes plaque formation may cause diabetes ACh s Continue reading >>

Endocrine Pancreas: Insulin And Glucagon

Endocrine Pancreas: Insulin And Glucagon

Sort 5 steps of insulin release (explain/draw) 1. GLUT2 transporters bring glucose inside B cells. glucose floats down concentration gradient. passive facilitated diffusion. 2. glucose metabolized to produce ATP 3. when ATP is present it binds to K channels, and closes them. this results in more K staying inside cell. K is positive, so the inside of cell gets more positive, causing B cell to depolarize 4. calcium channels respond to depolarization. when B cell is at resting potential, the channel is closed. when it depolarizes in response to glucose, the channel opens---calcium influx. 5. calcium influx triggers exocytosis of vesicles with insulin inside GPCR signaling cascade 1. GPCR binds to a signal; G-protein binds to GTP and is activated, initiating a signaling cascade. 2. G-protein activates adenylyl cyclase (an amplifier enzyme that takes a signal and amplifies it in the cell) 3. this changes ATP to cAMP 4. G-protein can either be stimulatory or inhibitoyr. Continue reading >>

Endocrine Pancreas- Glucagon & Insulin

Endocrine Pancreas- Glucagon & Insulin

Sort Describe what happens in diabetic ketoacidosis No insulin = Not enough receptors Cells can't take in glucose Starved for fuel Lipolysis releases FFAs FFAs make Ketones Ketones are acid= Metabolic Acidosis Hyperventilation to compensate Acidosis causes hyperkalemia No insulin: K+ can't get into cell High glucose spills into urine causes volume loss DKA: Acid and K+ effect - cells starved for glucose -lypolysis to increase free fatty acids for energy - FFAS lead to lipid trash called ketones - ketones are acid - transcellular acid shift -blood potassium up - potassium spills into urine - blood level up of potassium; body level down Dipeptidyl Dipeptidase 4 inhibitors Sitagliptin Saxagliptin Linagliptin - Prevent breakdown of Glucose-dependent insulintropic peptide and Glucagon like peptide - Increase insulin release - Decrease Glucagon - Slow stomach motility Describe glucagon - produced by alpha cells (10-20% of islet cells) - liver hormone - raises glucose - raises FFAs - uses amino acids to make glucose instead of protein - increases gluconeogenesis - breaks down glycogen (glycogenolysis) - inhibits glycogen formation - increases lipolysis - decreases lipogenesis - increases FFAs - increases ketones Continue reading >>

Insulin, Pancreas

Insulin, Pancreas

Sort Explain the steps of regulation of insulin 1. Glucose enters the beta cells via GLUT2 receptor 2. Cellular respiration > ATP production 3. ATP sensitive K+ channel pump inhibits K+ from leaving the cell and the cell becomes depolarized 4. Voltage gated Ca2+ channels open due to depolarization and Ca2+ enters the cell 5. Ca2+ stimulates exocytosis of vesicles containing insulin 6. Insulin enters the blood stream via that exocytosis How are target cells activated by insulin? tyrosine kinase Insulin receptor is activated by insulin and autophosphorylates when bound. A primary effect:Translocation of glucose transporter 4 (GLUT4) to the target cell membrane. GLUT4 is found in striated muscle & adipose GLUTs transport glucose into cells via facilitated diffusion What are the major effects of glucagon on target cells? Glucose utilized by muscle cells Liver cells release glucose into bloodstream Through the breakdown of triglycerides By conversion of amino acids from bloodstream Glucose is released into bloodstream What are some treatments for DM-1? Which insulins are short acting and which are long? Humulin™ (insulin isophane & insulin regular) -short Humalog™ (lispro) -short Lantus™ (glargine) -long Levemir™ (detemir) -long Continue reading >>

Insulin Secretion And Replacement

Insulin Secretion And Replacement

T/F? insulin resistance alone is enough to cause hyperglycemia/DM2 False - DM2 requires both insulin resistance and progressive destruction of beta cells (decreasing production of insulin) order of insulin biosynthesis in pancreatic beta cells preproinsulin --> proinsulin --> insulin + C-peptide what activates beta cells to secrete insulin? glucose - it enters beta cell, makes ATP, closes K channel, causes influx of Ca, secretory granules with insulin, proinsulin and C-peptide are released this hormone is co-released from beta cells with insulin. slows the rate of gastric emptying --> controls how much glucose is absorbed at a time so blood glucose level is maintained what are two incretin hormones that can activate beta cells to secrete insulin? glucose dependent insulinotropic hormone (GIP) incretins increase insulin levels more when glucose is administered orally rather than through IV when glucose is given IV, two phases of insulin release can be seen. first phase - release of beta cell secretory granules closest to the beta cell membrane what are MODY mutations and how do they cause hyperglycemia? MODY - maturity onset-diabetes of the young Continue reading >>

1) Insulin Secretion

1) Insulin Secretion

Between meals, pancreatic beta cells produce and store insulin in intracellular vesicles called insulin granules. Insulin granules are membrane bound vesicles in which beta cells store insulin. Found in pancreatic beta cells. The hormone insulin is composed of two polypeptide chains: chain A and chain B. They are connected by two disulfide bonds. Both chains come from the same precursor protein: preproinsulin. The posttranslational processing and folding for preproinsulin into mature active insulin involves the formation of disulfide bonds and its cleavage (cleavage of signal sequence and chain C). => preproinsulin lacks disulfide bonds and cleavage => proinsulin has disulfide bonds but lacks cleavage => insulin has disulfide bonds and is product of cleavage After a meal, glucose concentration in the blood increases. Beta cells in the pancreas senses this increase in blood glucose levels and releases insulin into the blood stream. Glucose cannot penetrate the cell membrane. It needs a transporter protein, GLUT4. Insulin's job is to signal to target cells that the blood glucose levels are high and that now is a good time to deploy GLUT4 transporter to bring glucose into the cells. Thus, the function of insulin is to promote the uptake of glucose by muscle cells that use it for energy and by fat cells that store it as triglycerides, or fats, and by liver cells. It does this by upregulating GLUT4 in muscle, fat, and liver cells. How is stored insulin released from the pancreatic beta cells into the blood stream? **Insulin secretion is regulated by glucose 1) when glucose levels are high, GLUT2 transporter allows glucose to enter beta cells. ***In pancreatic beta cells, it is GLUT2 and they are always present. In muscle and fat cells, it is GLUT4. 2) The increased concentr Continue reading >>

Insulin And Glucagon

Insulin And Glucagon

Sort symptoms of hypoglycemia adrenergic symptoms: - from a sudden drop in glucose - anxiety, palpitations, tremor, sweating - from epinephrine release regulated by hypothalamus, and adrenals in response to hypoglycemia neuroglycopenia - gradual decrease - not sudden - not enough to trigger adrenergic response <40 mg/dl - if severe and prolonged causes impaired brain function headache, confusion, seizures, coma, death hypoglycemia and alcohol intoxication - massive incr in cytosolic NADH = pyruvate -> lactate = lactic acidosis = OAA -> malate - these rxns decrease gluconeogenesis and can cause hypoglycemia in patients without glycogen - decreased OAA and increased acetyl CoA = alcoholic ketoacidosis - alcohol = increase TAG because decrease FFA ox = fatty liver - if continued = alcoholic hepatitis or alcoholic cirrhosis Continue reading >>

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