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Insulin And Glucagon Are Hormones Released By The Quizlet

Insulin And Glucagon:hormonal Regulation Of Glucose Metabolism

Insulin And Glucagon:hormonal Regulation Of Glucose Metabolism

is a carrier for passive glucose movement across the membrane. Principal transporter for glucose transfer from blood to intestine, liver and pancreas, and for renal glucose reabsorption. has high transport capacity, but low affinity (high Km, ca. 15-20 mM) is localized to the cytoplasmic vesicles Redistributed to the cytoplasmic membrane in response to insulin when insulin is stimulated, Glut4 moves out of the (intracellular vesicles) inside the cell to the cell surface leads to up to 10 fold increase in glucose absorption by adipose and muscle tissues. In what organelle does Glut2 act like Glut4 ? Glut2 is regulated in a similar way in the small intestine. Glucose transporters1& 3 (Low capacity,high affinity) Normal Glucose level in blood:slow entry into all cells Elevated Glucose level in blood:slow entry into all cells Glucose transporter4 (GLUT4) Insulin stimulated Normal Glucose level in blood:Relatively small role Elevated Glucose level in blood:Fast entry into fat and muscle depots Glucose transporter2 (GLUT2) High capacity, low affinity) Normal Glucose level in blood:Relatively small role Elevated Glucose level in blood:Fast entry into hepatocytes (liver),intestine, pancreatic beta and alpha cells, and kidney Insulin indicates a period of high blood sugar and activates glycogen synthesis and glucose uptake ___ in _____ tissues Glucagon signals low blood sugar, activates glycogen breakdown and initiates gluconeogenesis in Epinephrine leads to the breakdown of glucose through two pathways to trigger the release of free glucose into the blood: occurs In the In the pancreas, insulin is released in response to high glucose At physiological conditions, hexokinases I-III are saturated. Efficiency of glucose phosphorylation by glucokinase (Hexokinase IV) varies with gl Continue reading >>

Insulin And Glucagon

Insulin And Glucagon

organ responsible for both digestion and glucose homeostasis represents most of the pancreas and is formed by acinar cells involved in the secretion of digestive enzymes into the duodenum tubular network connecting acinar cells (secretory) with the gut tube formed by islets of Langerhans, responsible for hormonal secretion, it is just 1-2% of pancreatic mass islet of Langerhans cells that are responsible for glucagon synthesis and secretion and make up 15-20% of the islets islet of Langerhans cells that are responsible for insulin synthesis and secretion and are the most abundant cell type located mostly in the middle of the pancreatic islets of Langerhans (60-80%) islet of Langerhans cells responsible for somatostatin synthesis and secretion (5-10%) islet of Langerhans cells responsible for pancreatic polypeptide synthesis and secretion (15-20%) a group of gastrointestinal hormones released in response to carbohydrate-containing meals (released in response to glucose); it is also an agent that stimulates a signal to secrete insulin incretin that has low levels during fasting; it is secreted from L-cells of the intestine and is released within minutes of eating a glucose-containing meal; it prepares the pancreas for the nutrient load to enter the blood; it also stimulates insulin secretion and inhibits glucagon release; it is degraded in circulation by DPP-4 w/in 1-2 minutes Continue reading >>

Pancreatic Hormones: Insulin, Glucagon, And Somatostatin

Pancreatic Hormones: Insulin, Glucagon, And Somatostatin

1-2 mil/pancreas, in clusters between ducts carry secretions into portal vein, then gen circulation 51 aa, 3 disulfide bridges, syn as one long protein, cleaved into final form, half life is 6 mins binds to cell surface, alters internal kinase, initiates phosphorylation cascade, glucose transporter (GLUT4) move to cell surface, glucose uptake within seconds alteration of intracellular link between insulin and binding and the insert of GLUT into membrane increase in speed of internal degradation of insulin-receptor complex increases glucose uptake into muscles and adipose tissue, unused glucose is stored as glycogen (nervous system doesn't require insulin for glucose transport) inhibits gluconeogenesis in liver, excess glucose is converted to fatty acids increases glucose uptake into adipose tissue (convert glycerol for triglycerides), FFA absorption into adipose tissue, triglyceride syn in liver, reduces lipase action in adipose tissue How does insulin deficiency affect fat metabolism? adipose tissue lipase is activated (FFA levels increase) excess FFA increases cholesterol and triglyceride syn in liver excess FFA are broken down into acetoacetic acid (leads to acidosis and convert to ketones) How does insulin affect protein metabolism? increases transport of glucose and aa into muscle cells, action of ribosomes in protein syn decreases catabolism of proteins by lysosomes, gluconeogenesis by liver How does insulin deficiency affect protein synthesis? it stops, catabolism of protein increases, plasma aa levels increase excess aa are burned for energy or used for gluconeogenesis, urea levels increase in urine, muscle wasting, weakness, organ dsyfunction increased plasma glucose, increased plasma aa, CCK, glucagon, incretins, beta-AD and cholinergic stim decreased plasma Continue reading >>

Nutrition Chapters 4 Study Questions

Nutrition Chapters 4 Study Questions

are a category of single sugar molecules that are absorbed easily in the small intestine. consist of two molecules of sugar joined together. is the most abundant sugar molecule, and the preferred source of energy for the brain. are a category of nutrient compounds consisting of long chains of sugar molecules. is a type of simple carbohydrate composed of a glucose molecule and a fructose molecule. Plants store glucose as polysaccharides in this form. The storage form of glucose in humans and animals. What are the enzymes that are responsible for the break down of starches? What enzymes are responsible for breakdown of disaccharides? These are absorbed by the small intestine and enter the bloodstream. Insulin is produced and released from the? In response to insulin or glucagon, either glycogenesis or gluconeogenesis, respectively will take place in the ? The body can either use ________ for energy, convert to glycogen, or store it as fat. what occurs when blood glucose levels drop below 70 mg/dl? As part of the response to increased blood glucose after a meal, Insulin triggers the of _____________________ on the cell membrane in the body to be increased. What is a key hormone produced by the pancreas that plays a key role in regulating blood glucose levels after a meal? What is the storage form of glucose in the liver and muscles of humans and animals? What is glucose converted to for storage in fat tissue? What is the key hormone produced by the pancreas that plays an important role in regulating blood glucose levels during times of fasting? hormones that have no effect on blood glucose levels? Continue reading >>

Biochemistry: Insulin And Glucagon

Biochemistry: Insulin And Glucagon

Sort Which of these processes are increased with insulin vs. glucagon? 1. Glycogenolysis 2. Glycogen synthesis 3. Triglyceride synthesis 4. Gluconeogenesis 5. Lipolysis 6. Fatty acid synthesis 7. Liver glycolysis Insulin increases 1. Glycogen synthesis 2. Fatty acid synthesis 3. Triglyceride synthesis 4. Liver glycolysis Glucagon increases: 1. Glycogenolysis 2. Gluconeogenesis 3. Lipolysis What is the effect of glucagon on: 1.Blood Glucose 2. Liver glycogen 3. Adipose triglycerides 4. Muscle Protein 5. Liver glucose metabolism 6. Second messenger system 1.Blood Glucose: ↑ (glucose released to blood) 2. Liver glycogen: Promotes breakdown 3. Adipose triglycerides: Lack of Insulin Promotes TG breakdown and release of FA to blood. 4. Muscle Protein: no effect 5. Liver glucose metabolism: Promotes gluconeogenesis 6. Second messenger system: Heptahelical - Trimeric G ↑ cAMP --> PKA (ser/thr kinase) Consequences of not maintaining glucose and lipid levels. Excess glucose, lipid and amino acids must be removed from blood. 1. Excess sugar and amino acids would cause a ___________ state. 2. Excess glucose can cause ___________ of proteins 3. Excess lipid can cause _________________ 1. Excess sugar and amino acids would cause a hyper-osmotic state. 2. Excess glucose can cause non-enzymatic glycosolation of proteins 3. Excess lipid can cause atherosclerosis 1. Hyperglycemia - high blood glucose -Can cause hyper-osmotic coma by pulling water out of cells (particularly brain cells) 2. Polyuria - urge to urinate frequently 3. Polydipsia - increased thirst 4. Weight loss - despite good appetite 5. Increased reliance on lipid metabolism 6. Non-enzymatic glycosylation of proteins -easily detected on hemoglobin -retinopathy, nephropathy, neuropathy, vascular Dx? Diabetes Mellitus Gluc Continue reading >>

Insulin And Glucagon

Insulin And Glucagon

Sort end effects of insulin stimulation (1) the membranes of about 80% of the body's cells markedly increase their uptake of glucose (2) the cell membrane becomes more permeable to many of the amino acids, potassium ions, and phosphate ions (3) There are more delayed effects of insulin (10-15 minutes) that result form changes in the activity of intracellular enzymes (4) even slower effects continue to occur form hours and even several days. They result from changes in protein synthesis that are induced by insulin mechanism by which liver releases glucose back into the BS (1) decrease in BS causes the pancreas to decrease its secretion of insulin (2) lack of insulin then reverses all the effects in the mechanism that caused glucose storage in the liver, eventually stopping further synthesis of glycogen by the liver and preventing further uptake of glucose by liver cells (3) lack of insulin activates the enzyme phosphorylase (4) enzyme glucose phosphatase not becomes activated by the lack of insulin and causes the phosphate radical to split away from the glucose; this allows free glucose to diffuse back into the blood Different factors that lead to increased FA synthesis in the liver (1) After liver glycogen concentration is at its max (5-6% of mass), glycogen synthesis is inhibited and the excess glucose is split into pyruvate in the glycolytic pathway, and is then converted to Acetyl-CoA (2) Citrate and isocitrate ions then help to activate Acetyl-CoA carboxylase to form malonyl-CoA (3) FAs synthesized in the liver are made into triglycerides and packaged into VLDL to travel to adipose tissues where lipoprotein lipase splits them up into FA's again to be absorbed into the adipose cells Summary of the mechanisms for the control of BG (1) liver functions as an important B Continue reading >>

Hormones

Hormones

Sort What's the deal with glucose uptake by cells? When blood glucose drops below the normal range, the release of glucagon promotes the release of glucose into the blood from energy stores, such as liver glycogen, increasing the blood glucose concentration Cells will either store or burn glucose but the liver takes up glucose and makes a polymer out of it -glycogen has a similar structure to starch -most of our energy storage is in the form of fat What's the deal with glycerol and amino acids? blood glucose levels too low --> amino acids and glycerol converted int glucose (through glycogen hydrolysis) and glucose is released into the bloodstream when the blood glucose levels decreases to a level at or below the normal range, a primary effect of glucagon is to signal liver cells to increase glycogen hydrolysis, convert amino acids and glycerol to glucose, and release glucose into the bloodstream What can happen when fat becomes the main substrate for cellular respiration? -pH level increases, ion balances are imbalanced -In severe case, acidic metabolites formed during fat breakdown accumulate in the blood, threatening life by lowering blood pH and depleating sodium and potassium ions from the body -if not respiring glucose enough, then you lower your carbs so your body will break down fat -you can increase level of CO2 but that messes with the pH of blood 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, Glucagon & Glucose Homeostasis: Diabetes Mellitus

Insulin, Glucagon & Glucose Homeostasis: Diabetes Mellitus

Sort *HbA1c* In the blood stream are the red blood cells, which are made of a molecule, haemoglobin. Glucose sticks to the haemoglobin to make a 'glycosylated haemoglobin' molecule, called haemoglobin A1C or HbA1C. The more glucose in the blood, the more haemoglobin A1C or HbA1C will be present in the blood. Interaction of hormones: what happens if there are receptors for factors with opposing effects? A) Strength of cases B) Balancing act --insulin decreases blood glucose --glucagon and adrenaline increase it C) Permissive effects - i.e. estrogen on progesterone receptor Describe water soluble hormones. GI tract polypeptide hormones that facilitate insulin secretion: A) Produced in GI tract and Secreted in blood B) Can be stored in the cell in vesicles C) Can be released in response to a calcium spikes D) Doesn't really need carrier proteins (but may have) E) Will work via a cell surface receptor F) Binding will initiate internalization and degradation of that factor G) Initiates some cell signaling event Examples: Insulin Endorphins - polypeptides in CNS and other sites --Opiate like actions --Produce a large amount If you are in extreme pain *What is the role of Cyclic AMP (cAMP)?* Critical for regulating secretion in secretory cells --Elevating cAMP increases secretion of insulin (fasting state) --Decreasing cAMP lowers secretion (fasting state) Often linked to g-protein coupled cells: Gs, Gi, and Gq (see slide 13 for the adenylyl cyclase system) Describe the secretion of Calcium. A) Movement of vesicles inside secretory cells B) Hormones that stimulate release of other hormones C) Control of flux from calcium outside of cell, or release of stored calcium (hormonal - endoplasmic reticulum. Mitochondria stores ca but not under hormonal control) *Identify active short Continue reading >>

Regulation Of Glucose Through The Hormones Insulin And Glucagon

Regulation Of Glucose Through The Hormones Insulin And Glucagon

Sort Hyperglycemia High blood glucose. High blood glucose happens when the body has too little insulin or when the body can't use insulin properly.Term used to describe hormones such as glucagon that elevate blood glucose levels. If you have type 1, you may not have given yourself enough insulin. If you have type 2, your body may have enough insulin, but it is not as effective as it should be. You ate more than planned or exercised less than planned. You have stress from an illness, such as a cold or flu. Youve just attended a football game with your friend sharon who is diabetic. While sharon drank only one beer during the game she is having trouble walking straight her speech is slurred and she is not making sense. what does it mean when we say sharon is diabetic? what is the most likely explanation for sharons current behavior? how could you help her? when we say sharon is diabetic this means that she has insufficient insulin action in her body. the most likely explanation for sharons behavior is that she has taken too much insulin and is experiencing hypoglycemia. You could help her by making sure she gets a sugary snack. Continue reading >>

Insulin And Glucagon From The Pancreas

Insulin And Glucagon From The Pancreas

Sort Insulin and Glucagon from the Pancreas Endocrine function: Secretes hormones that enter the blood Islets of Langerhans 2-3% of the pancreas by weight Islets are vascularized, innervated; have four basic cell types: A cells B cells D cells F cells Insulin and Glucagon from the Pancreas: different cell types A cells: Make Glucagon Are about 20% of Islet cells Surround -cells B cells: = -cells Make Insulin 60-75% of Islet cells D cells: Make Somatostatin Are 3-5% of Islet cells F cells: Make Pancreatic Polypeptide Are found in one end lobe of the pancreas where they are the predominant cell type in the Islets Insulin - the first protein sequenced: Sanger, F., 1945 The free amino groups of insulin. Biochem. J. 39: 507-515 Sanger, F., 1949 The terminal peptides of insulin. Biochem. J. 45: 563-574 Sanger, F., and H. Tuppy, 1951a The amino-acid sequence in the phenylalanyl chain of insulin. 1. The identification of lower peptides from partial hydrolysates. Biochem. J. 49: 463-481 Sanger, F., and H. Tuppy, 1951b The amino-acid sequence in the phenylalanyl chain of insulin. 2. The investigation of peptides from enzymic hydrolysates. Biochem. J. 49: 481-490 Sanger, F., and E. O. P. Thompson, 1953a The amino-acid sequence in the glycyl chain of insulin. 1. The investigation of lower peptides from partial hydrolysates. Biochem. J. 53: 353-366 Sanger, F., and E. O. P. Thompson, 1953b The amino-acid sequence in the glycyl chain of insulin. 2. The investigation of peptides from enzymic hydrolysates. Biochem. J. 53: 366-374 Ryle, A. P., F. Sanger, L. F. Smith and R. Kitai, 1955 The disulphide bonds of insulin. Biochem. J. 60: 542-556 "It has frequently been suggested that proteins may not be pure chemical entities but may consist of mixtures of closely related substances with no a 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, Glucagon, And Diabetes Mellitus

Insulin, Glucagon, And Diabetes Mellitus

Sort Pancreas is composed of two types of tissue 1) the acini - secrete digestive juices into the duodenum 2) islets of Langerhans - secrete insulin and glucagon directly into the blood -contain 3 major types of cells (alpha, beta, and delta): -beta cells - 60% of islets; lie mainly in the middle of each islet and secrete INSULIN and AMYLIN -alpha cells - 25% of islets; secrete GLUCAGON -delta cells - 10% of islets; secrete SOMATOSTATIN **at least one other type of cell, the PP CELL, is present in small numbers in the islets and secretes PANCREATIC PEPTIDE (uncertain function) Insulin Structure -composed of two amino acid chains, connected to each other by disulfide linkages **When the two amino acid chains are split, it loses functional activity -preprosinsulin ---cleaved in the ER--> proinsulin (3 chains of peptides, A, B, and C) ---further cleaved in the Golgi apparatus--> INSULIN (composed of the A and B chain connected by disulfide linkages) + the C chain peptide, called CONNECTING PEPTIDE (C peptide) **Both are packaged in the secretory granules and secreted in equimolar amounts. ~5-10% are still on proinsulin form Insulin receptor -combo of 4 subunits held together by disulfide linkages -2 alpha subunits - lie entirely outside the cell membrane -2 beta subunits - penetrate through the membrane, protruding into the cell cytoplasm **the insulin binds with the alpha subunits on the outside of the cell, but because of the linkages with the beta subunits, the portions of the beta subunits protruding into the cell become autophosphorylated --> activates TYROSINE KINASE, which in turn causes phosphorylation of multiple other intracellular enzymes including a group called INSULIN-RECEPTOR SUBSTRATES (IRS) -different types of IRS (IRS-1, IRS-2, IRS-3) are expressed i diff Continue reading >>

Pancreatic Hormones: Insulin And Glucagon

Pancreatic Hormones: Insulin And Glucagon

-produce four hormones: insulin, glucagon, somatostatin, and pancreatic polypeptide -role of pancreatic polypeptide not well described (structurally similar to neuropeptide Y) -first isolated from hypothalamic extracts and shown to inhibit pituitary release of pancreatic hormones -inhibits gastric acid and pepsin secretion -approx. 1 million found in adult pancreas -hormones produced by discrete islet cells -B-cells make up the bulk of the islets (70%) and secrete insulin -a-cells secrete glucagon and represent 20-25% of the islets -delta cells secrete somatostatin and represent 6% of cell mass -only a few cells release pancreatic polypeptide -well vascularized (10-15% of pancreatic blood flow) -direction of blood flow from the center of the islet to the periphery -postulated that this arrangement is important b/c it transports insulin from the central region to the periphery -innervated by adrenergic and cholinergic fibers of the autonomic nervous system -neural inputs to the islets can influence both insulin and glucagon secretion and therefore are involved in glucose homeostasis -pancreas veins drain into the portal venous system so all hormones released by the pancreas must first pass through the liver -the liver is a major target tissue for both hormones and a major site of hormone degradation -a large part of secreted insulin is thought to be removed by the liver in what is termed the 'first pass' -polypeptide consisting of two chains, a and b, linked by two disulfide bridges -synthesized in B-cells as a single chain 86-AA precursor preproinsulin -preproinsulin contains signal peptide necessary for the translocation of the peptide from the rough ER into its internal compartments -signal sequence is then cleaved leaving proinsulin -proinsulin required for the prop 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 >>

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