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How Does Insulin Signal The Cell To Take In Glucose?

Nutrient Intake And Hormonal Control Of Insulin Action

Nutrient Intake And Hormonal Control Of Insulin Action

Insulin and Metabolism Insulin is a major metabolism regulating hormone secreted by β-cells of the islets of Langerhans of the pancreas. The major function of insulin is to counter the concerted actions of a number of hyperglycemia-generating hormones and to maintain low blood glucose levels. In addition to its role in regulating glucose metabolism, insulin stimulates lipogenesis, diminishes lipolysis, and increases amino acid transport into cells. Because there are numerous hyperglycemic hormones, untreated disorders associated with insulin generally lead to severe hyperglycemia and shortened life span. Insulin as Growth Factor Insulin also exerts activities typically associated with growth factors. Insulin is a member of a family of structurally and functionally similar molecules that includes the insulin-like growth factors (IGF-1 and IGF-2), and relaxin. The tertiary structure of all four molecules is similar, and all have growth-promoting activities. Insulin modulates transcription and stimulates protein translocation, cell growth, DNA synthesis, and cell replication, effects that it holds in common with the insulin-like growth factors and relaxin. back to the top Insulin is synthesized, from the INS gene, as a preprohormone in the β-cells of the islets of Langerhans. The INS gene is located on chromosome 11p15.5 and is composed of 3 exons that generate four alternatively spliced mRNAs, all of which encode the same 110 amino acid preproprotein. The signal peptide of preproinsulin is removed in the cisternae of the endoplasmic reticulum. The insulin proprotein is packaged into secretory vesicles in the Golgi, folded into its native structure, and locked in this conformation by the formation of two disulfide bonds. Specific protease activity cleaves the center thir Continue reading >>

Insulin And Student Response Sheet

Insulin And Student Response Sheet

1. In the space below, properly document each of the three sources you found that show how insulin signals a cell to take in glucose from the blood. Under each documented source, write an explanation of why it is a legitimate and reliable source of information about insulin and its effects on cells. R, Bowen. (2009, August). Physiological Effect of Insulin. Colostate. Retrieved from This source is legitimate because the information is up to date until 2009 and has an author. Also there are very few ads and the sponsor is popular for their knowledge. There is also a contact information, if you have any comments or anything to correct. Insulin and Glucose Regulation (n.d.). In bcs.whfreeman. from This source is legitimate because the sponsor is popular for their tutorials. The site is knowledgeable and has no errors, a lot of info, and there’s also a quiz to see if you learned what you read. Jagoda, Robin. (2011, March). How Does Insulin Signal a Cell to Take in Glucose From the Blood?. Livestrong Foundation. Retrieved from This source is legitimate because it has an author and also citations on where they got the information from. Very few ads, but no errors and there’s also a comment box, where you can comment the mistakes they made if there was any. 2. Take notes on the relationship between insulin and glucose. Draw sketches or diagrams if necessary. Glucose is the main source of energy and insulin is the key to body cells. Both work together to give energy to the body cells. The insulin opens the door of the body cells for the glucose to enter the body. If the body does not produce insulin then the body cells won’t be able to get any glucose and it means that they have type 1 diabetes. If the insulin cannot unlock the body cells door then that means that they ha Continue reading >>

How Fat Cells Work

How Fat Cells Work

In the last section, we learned how fat in the body is broken down and rebuilt into chylomicrons, which enter the bloodstream by way of the lymphatic system. Chylomicrons do not last long in the bloodstream -- only about eight minutes -- because enzymes called lipoprotein lipases break the fats into fatty acids. Lipoprotein lipases are found in the walls of blood vessels in fat tissue, muscle tissue and heart muscle. Insulin When you eat a candy bar or a meal, the presence of glucose, amino acids or fatty acids in the intestine stimulates the pancreas to secrete a hormone called insulin. Insulin acts on many cells in your body, especially those in the liver, muscle and fat tissue. Insulin tells the cells to do the following: The activity of lipoprotein lipases depends upon the levels of insulin in the body. If insulin is high, then the lipases are highly active; if insulin is low, the lipases are inactive. The fatty acids are then absorbed from the blood into fat cells, muscle cells and liver cells. In these cells, under stimulation by insulin, fatty acids are made into fat molecules and stored as fat droplets. It is also possible for fat cells to take up glucose and amino acids, which have been absorbed into the bloodstream after a meal, and convert those into fat molecules. The conversion of carbohydrates or protein into fat is 10 times less efficient than simply storing fat in a fat cell, but the body can do it. If you have 100 extra calories in fat (about 11 grams) floating in your bloodstream, fat cells can store it using only 2.5 calories of energy. On the other hand, if you have 100 extra calories in glucose (about 25 grams) floating in your bloodstream, it takes 23 calories of energy to convert the glucose into fat and then store it. Given a choice, a fat cell w Continue reading >>

What Is Insulin?

What Is Insulin?

Insulin is a hormone; a chemical messenger produced in one part of the body to have an action on another. It is a protein responsible for regulating blood glucose levels as part of metabolism.1 The body manufactures insulin in the pancreas, and the hormone is secreted by its beta cells, primarily in response to glucose.1 The beta cells of the pancreas are perfectly designed "fuel sensors" stimulated by glucose.2 As glucose levels rise in the plasma of the blood, uptake and metabolism by the pancreas beta cells are enhanced, leading to insulin secretion.1 Insulin has two modes of action on the body - an excitatory one and an inhibitory one:3 Insulin stimulates glucose uptake and lipid synthesis It inhibits the breakdown of lipids, proteins and glycogen, and inhibits the glucose pathway (gluconeogenesis) and production of ketone bodies (ketogenesis). What is the pancreas? The pancreas is the organ responsible for controlling sugar levels. It is part of the digestive system and located in the abdomen, behind the stomach and next to the duodenum - the first part of the small intestine.4 The pancreas has two main functional components:4,5 Exocrine cells - cells that release digestive enzymes into the gut via the pancreatic duct The endocrine pancreas - islands of cells known as the islets of Langerhans within the "sea" of exocrine tissue; islets release hormones such as insulin and glucagon into the blood to control blood sugar levels. Islets are highly vascularized (supplied by blood vessels) and specialized to monitor nutrients in the blood.2 The alpha cells of the islets secrete glucagon while the beta cells - the most abundant of the islet cells - release insulin.5 The release of insulin in response to elevated glucose has two phases - a first around 5-10 minutes after g Continue reading >>

Diabetes: What’s Insulin Resistance Got To Do With It?

Diabetes: What’s Insulin Resistance Got To Do With It?

Invisible changes in the body begin long before a person is diagnosed with type 2 diabetes. That’s both bad news (no symptoms mean you won’t know you have it) and good news (you can prevent or delay it if you’re at risk). One of the most important unseen changes? Insulin resistance. Insulin in a Nutshell Insulin is a key player in developing type 2 diabetes. This vital hormone—you can’t survive without it—regulates blood sugar (glucose) in the body, a very complicated process. Here are the high points: The food you eat is broken down into glucose. Glucose enters your bloodstream, which signals the pancreas to release insulin. Insulin helps glucose enter the body’s cells so it can be used for energy. Insulin also signals the liver to store glucose for later use. Glucose enters cells, and glucose levels in the bloodstream decrease, signaling insulin to decrease too. Lower insulin levels alert the liver to release stored glucose so energy is always available, even if you haven’t eaten for a while. That’s when everything works smoothly. But this finely tuned system can quickly get out of whack, as follows: A lot of glucose enters the bloodstream. The pancreas pumps out more insulin to get glucose into cells. Over time, cells stop responding to all that insulin—they’ve become insulin resistant. The pancreas keeps making more insulin to try to make cells respond. Eventually, the pancreas can’t keep up, and glucose keeps rising. Now What? Lots of glucose in the bloodstream is very damaging to the body and needs to be moved into cells as soon as possible. There’s lots of insulin, too, telling the liver and muscles to store glucose. When they’re full, the liver sends the excess glucose to fat cells to be stored as body fat. Yep, weight gain. And what Continue reading >>

Insulin Signaling And The Regulation Of Glucose Transport

Insulin Signaling And The Regulation Of Glucose Transport

Go to: GLUT4 TRANSLOCATION OCCURS IN MULTIPLE STAGES In the absence of insulin, Glut4 slowly recycles between the plasma membrane and vesicular compartments within the cell, where most of the Glut4 resides. Insulin stimulates the translocation of a pool of Glut4 to the plasma membrane, through a process of targeted exocytosis (4,5) (Figure 1). At the same time, Glut4 endocytosis is attenuated (6,7). Thus, the rate of glucose transport into fat and muscle cells is governed by the concentration of Glut4 at the cell surface and the duration for which the protein is maintained at this site. There is substantial evidence that Glut4 exists in specialized vesicles sequestered within the cell, but the precise intracellular location and trafficking pathways of these vesicles are unclear. Following internalization, Glut4 is localized into tubulovesicular and vesicular structures that are biochemically distinct from but possibly interacting with the recycling endosomal network (8). In adipocytes, these vesicles are retained in a perinuclear region in the cell via an unknown mechanism that might involve a tethering protein (9) or continuous futile recycling (10). The Glut4 compartment is enriched in the v-SNARE (soluble N-ethylmaleimide sensitive factor attachment protein) protein VAMP2 (vesicle-associated membrane protein 2) but not the related VAMP3/cellubrevin isoform that is present in recycling endosome (11). Consistent with these data, ablation of transferrin receptor containing endosomes does not impair insulin-stimulated Glut4 translocation (12). The microtubule network and actin cytoskeleton play a role in Glut4 trafficking, either by linking signaling components or by directing movement of vesicles from the perinuclear region to the plasma membrane in response to insulin. Continue reading >>

Glucose Transporters, Insulin, And Diabetes

Glucose Transporters, Insulin, And Diabetes

Sort Describe how insulin-dependent GLUT-4 transporters function (8 steps)? 1) insulin binds to insulin receptors 2) cytoplasmic side of the receptor phosphorylates itself 3) signal transduction pathway is activated 4) GLUT-4 transporters are lying in wait in cytoplasmic vesicles 5) signal transduction pathway leads to rapid fusion of GLUT-4 containing vesicles with the membrane 6) more GLUT-4 receptors allow glucose to be taken in more rapidly 7) glucose level drops in the bloodstream and interstitial fluid 8) Glut-4 transporters are brought back in to cell via endocytosis What is hyperglycemia and what are some of the major symptoms? Abnormally high blood glucose Symptoms: *excessive thirst *excessive urination *retina and kidney damage *capillaries get destroyed *nerve damage *diabetic shock, coma and death What is hypoglycemia and what are some of the major symptoms? abnormally low blood glucose *normally from insulin overdoes in type 2 diabetes *dizziness *disorientation *nausea *faintness *loss of consciousness *death Continue reading >>

How Does Insulin Signal Cells To Take In Glucose

How Does Insulin Signal Cells To Take In Glucose

Transcript of How does insulin signal cells to take in glucose By Olivia Devina and Bryanna When you eat, and after it is digested the glucose enters the blood. Then is signals the pancreas to make insulin After the Pancreas receives signals that glucose is in the blood it then sends insulin receptors. Then the insulin binds to the insulin receptors. The membrane (door) only stays open to glucose so long, as their is insulin bound to the receptors on the cell. The insulin is released and the glucose transporters close. How insulin takes in glucose Then this signals the glucose transporters. glucose flows through the glucose transporters. The glucose is then made into energy for the cells to function properly Bibliography Jagoda, R. (2011, May 07). How does insulin signal a cell to take in glueose from the blood. Retrieved from nobel media. (Febr, 2009). Nobel prize organization. Retrieved from . Retrieved from Uploaded by davejaymanriquez on Jan 21, 2009 Full transcript Continue reading >>

Can Fat 'feel' Fat? Size-sensing Protein Controls Glucose Uptake And Storage In Fat Cells

Can Fat 'feel' Fat? Size-sensing Protein Controls Glucose Uptake And Storage In Fat Cells

"Although we have created a mouse that is resistant to weight gain by removing the SWELL1 protein, the mouse is not healthy; it has insulin resistance and glucose intolerance," says Rajan Sah, MD, PhD, assistant professor of internal medicine at the University of Iowa Carver College of Medicine and senior author of the study. Type 2 diabetes is one of the more serious health problems associated with obesity. The disease makes cells less sensitive to insulin and causes blood sugar levels to become abnormally high. It is healthier for the body to store excess glucose as fat rather than have it circulating in the blood where it can damage blood vessels and nerves. In healthy people, insulin released in response to high glucose levels acts on many different tissues to coordinate use or storage of the glucose. It triggers fat cells to take up excess glucose and store it as fat. Sah's study, which was published recently in Nature Cell Biology, found that removing SWELL1 from fat cells in mice disrupts this insulin signaling pathway and prevents fat cells from taking up glucose. Sah and his team homed in on SWELL1 because of several pieces of converging evidence. Fat cells have a tremendous capacity to expand - up to 30 times their normal volume in the context of obesity. It's also long been known that changes in fat cell size alters fat cell signaling. Through exploratory experiments investigating cell swelling in fat cells from lean and obese mice as well as fat cells obtained from bariatric surgery patients, Sah and his team serendipitously identified SWELL1 protein as an essential component of fat cells' volume-sensing mechanism. From unrelated work by other researchers, they also knew that this protein was involved in a signaling pathway common to all cells. In fat cells Continue reading >>

An Overview

An Overview

Nearly 400 million people worldwide are living with diabetes, and that number is expected to jump to almost 600 million by 2035, according to the International Diabetes Federation. For many people, diabetes can be controlled with diet, exercise and, often, insulin or other drugs. However, complications from diabetes can be serious and include kidney failure, nerve damage, vision loss, heart disease and a host of other health issues. In this section: What is diabetes? How is diabetes treated? How are we using stem cells to understand diabetes? What is the potential for stem cells to treat diabetes? At its most basic, diabetes is a condition in which the body cannot regulate or properly use sugar (called glucose) in the blood. The pancreas, which helps the small intestine digest food, has hundreds of thousands of cell clusters called islets of Langerhans where beta cells live. Beta cells produce insulin, which is released into the bloodstream when blood sugar levels reach a certain threshold. The insulin signals other cells in the body to take up sugar, the primary energy source for all the body’s cells. Type 1, also known as juvenile diabetes. In type 1 diabetes, the body’s immune system attacks the beta cells in the pancreas. When the beta cells are damaged, they don’t produce insulin, or at least not enough insulin. Other cells never get the signal to take up sugar, so they don’t get the energy they need to function properly, and high sugar levels in the blood end up causing damage to the kidneys, eyes, nervous system and other organs. Type 2 diabetes, also called adult-onset diabetes. In type 2 diabetes, cells in the body become resistant to insulin. They don’t respond to the signals insulin sends out, so they don’t take up sugar from the blood. The beta c Continue reading >>

How Insulin And Glucagon Work

How Insulin And Glucagon Work

Insulin and glucagon are hormones that help regulate the levels of blood glucose, or sugar, in your body. Glucose, which comes from the food you eat, moves through your bloodstream to help fuel your body. Insulin and glucagon work together to balance your blood sugar levels, keeping them in the narrow range that your body requires. These hormones are like the yin and yang of blood glucose maintenance. Read on to learn more about how they function and what can happen when they don’t work well. Insulin and glucagon work in what’s called a negative feedback loop. During this process, one event triggers another, which triggers another, and so on, to keep your blood sugar levels balanced. How insulin works During digestion, foods that contain carbohydrates are converted into glucose. Most of this glucose is sent into your bloodstream, causing a rise in blood glucose levels. This increase in blood glucose signals your pancreas to produce insulin. The insulin tells cells throughout your body to take in glucose from your bloodstream. As the glucose moves into your cells, your blood glucose levels go down. Some cells use the glucose as energy. Other cells, such as in your liver and muscles, store any excess glucose as a substance called glycogen. Your body uses glycogen for fuel between meals. Read more: Simple vs. complex carbs » How glucagon works Glucagon works to counterbalance the actions of insulin. About four to six hours after you eat, the glucose levels in your blood decrease, triggering your pancreas to produce glucagon. This hormone signals your liver and muscle cells to change the stored glycogen back into glucose. These cells then release the glucose into your bloodstream so your other cells can use it for energy. This whole feedback loop with insulin and gluca Continue reading >>

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Save Time And Improve Your Marks With Cite This For Me

10,587 students joined last month! ✔ Save your bibliographies for longer ✔ Super fast and accurate citation program ✔ Save time when referencing ✔ Make your student life easy and fun ✔ Pay only once with our Forever plan ✔ Use our extensive Premium features (Plagiarism checks, Word Add On...) ✔ Create and edit multiple bibliographies Continue reading >>

Overview Of Insulin Signaling Pathways

Overview Of Insulin Signaling Pathways

​Introduction Insulin is a hormone released by pancreatic beta cells in response to elevated levels of nutrients in the blood. Insulin triggers the uptake of glucose, fatty acids and amino acids into liver, adipose tissue and muscle and promotes the storage of these nutrients in the form of glycogen, lipids and protein respectively. Failure to uptake and store nutrients results in diabetes. Type-1 diabetes is characterized by the inability to synthesize insulin, whereas in type-2 diabetes the body becomes resistant to the effects of insulin, presumably because of defects in the insulin signaling pathway. A. Glucose storage and uptake ​​​The insulin receptor is composed of two extracellular α subunits and two transmembrane β subunits linked together by disulphide bonds (Figure 1). Binding of insulin to the α subunit induces a conformational change resulting in the autophosphorylation of a number of tyrosine residues present in the β subunit (Van Obberghen et al., 2001). These residues are recognized by phosphotyrosine-binding (PTB) domains of adaptor proteins such as members of the insulin receptor substrate family (IRS) (Saltiel and Kahn 2001; Lizcano and Alessi 2002). Receptor activation leads to the phosphorylation of key tyrosine residues on IRS proteins, some of which are recognized by the Src homology 2 (SH2) domain of the p85 regulatory subunit of PI3-kinase (a lipid kinase). The catalytic subunit of PI3-kinase, p110, then phosphorylatesphosphatidylinositol (4,5) bisphosphate [PtdIns(4,5)P2​] leading to the formation of Ptd(3,4,5)P3. A key downstream effector of Ptd(3,4,5)P3 is AKT, which is recruited to the plasma membrane. Activation of AKT also requires the protein kinase 3-phosphoinositide dependent protein kinase-1 (PDK1), which in combination w Continue reading >>

Physiologic Effects Of Insulin

Physiologic Effects Of Insulin

Stand on a streetcorner and ask people if they know what insulin is, and many will reply, "Doesn't it have something to do with blood sugar?" Indeed, that is correct, but such a response is a bit like saying "Mozart? Wasn't he some kind of a musician?" Insulin is a key player in the control of intermediary metabolism, and the big picture is that it organizes the use of fuels for either storage or oxidation. Through these activities, insulin has profound effects on both carbohydrate and lipid metabolism, and significant influences on protein and mineral metabolism. Consequently, derangements in insulin signalling have widespread and devastating effects on many organs and tissues. The Insulin Receptor and Mechanism of Action Like the receptors for other protein hormones, the receptor for insulin is embedded in the plasma membrane. The insulin receptor is composed of two alpha subunits and two beta subunits linked by disulfide bonds. The alpha chains are entirely extracellular and house insulin binding domains, while the linked beta chains penetrate through the plasma membrane. The insulin receptor is a tyrosine kinase. In other words, it functions as an enzyme that transfers phosphate groups from ATP to tyrosine residues on intracellular target proteins. Binding of insulin to the alpha subunits causes the beta subunits to phosphorylate themselves (autophosphorylation), thus activating the catalytic activity of the receptor. The activated receptor then phosphorylates a number of intracellular proteins, which in turn alters their activity, thereby generating a biological response. Several intracellular proteins have been identified as phosphorylation substrates for the insulin receptor, the best-studied of which is insulin receptor substrate 1 or IRS-1. When IRS-1 is activa Continue reading >>

Ch 105 - Chemistry And Disease

Ch 105 - Chemistry And Disease

Diabetes The following is from the WebMD Health "In general, people with diabetes either have a total lack of insulin (type 1 diabetes) or they have too little insulin or cannot use insulin effectively (type 2 diabetes). Type 1 diabetes (formerly called juvenile-onset or insulin-dependent diabetes), accounts for 5% to 10% of all people with diabetes. In type 1 diabetes, the body's immune system destroys the cells that release insulin, eventually eliminating insulin production altogether from the body. Without insulin, cells cannot absorb sugar (glucose), which they need to produce energy. Type 2 diabetes (formerly called mature-onset or non�insulin-dependent diabetes) can develop at any age, but most commonly becomes apparent during adulthood. However, the incidence of type 2 diabetes in children is rising. Type 2 diabetes accounts for the vast majority of people with diabetes�more than 90%. In contrast to type 1 diabetes, type 2 diabetes is characterized by insulin resistance. Insulin resistance refers to the inability of the body tissues to respond properly to insulin. Insulin resistance develops because of multiple factors, including genetics, obesity, increasing age, and having high blood sugar over long periods of time. How are these diseases different? Type 1 diabetes Type 2 diabetes Symptoms usually start in childhood or young adulthood. People often seek medical help because they are seriously ill from sudden symptoms of high blood sugar. May not have symptoms before diagnosis. Usually the disease is discovered in adulthood; however, there is an increasing number of children being diagnosed with the disease. Episodes of low blood sugar level (hypoglycemia) common No episodes of low blood sugar level, unless taking insulin or certain oral diabetes medic Continue reading >>

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