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Effect Of Insulin On Fat Metabolism

The Science Behind Fat Metabolism

The Science Behind Fat Metabolism

Per the usual disclaimer, always consult with your doctor before experimenting with your diet (seriously, go see a doctor, get data from blood tests, etc.). Please feel free to comment below if you’re aware of anything that should be updated; I’d appreciate knowing and I’ll update the content quickly. My goal here is to help a scientifically curious audience know the basic story and where to dive in for further study. If I’m successful, the pros will say “duh”, and everyone else will be better informed about how this all works. [UPDATE: based on a ton a helpful feedback and questions on the content below, I’ve written up a separate article summarizing the science behind ketogenic (low-carb) diets. Check it out. Also, the below content has been updated and is still very much applicable to fat metabolism on various kinds of diets. Thanks, everyone!] tl;dr The concentration of glucose in your blood is the critical upstream switch that places your body into a “fat-storing” or “fat-burning” state. The metabolic efficiency of either state — and the time it takes to get into one from the other — depends on a large variety of factors such as food and drink volume and composition, vitamin and mineral balances, stress, hydration, liver and pancreas function, insulin sensitivity, exercise, mental health, and sleep. Carbohydrates you eat, with the exception of indigestible forms like most fibers, eventually become glucose in your blood. Assuming your metabolism is functioning normally, if the switch is on you will store fat. If the switch is off, you will burn fat. Therefore, all things being equal, “diets” are just ways of hacking your body into a sufficiently low-glycemic state to trigger the release of a variety of hormones that, in turn, result in Continue reading >>

Insulin Effects In Muscle And Adipose Tissue.

Insulin Effects In Muscle And Adipose Tissue.

Abstract The major effects of insulin on muscle and adipose tissue are: (1) Carbohydrate metabolism: (a) it increases the rate of glucose transport across the cell membrane, (b) it increases the rate of glycolysis by increasing hexokinase and 6-phosphofructokinase activity, (c) it stimulates the rate of glycogen synthesis and decreases the rate of glycogen breakdown. (2) Lipid metabolism: (a) it decreases the rate of lipolysis in adipose tissue and hence lowers the plasma fatty acid level, (b) it stimulates fatty acid and triacylglycerol synthesis in tissues, (c) it increases the uptake of triglycerides from the blood into adipose tissue and muscle, (d) it decreases the rate of fatty acid oxidation in muscle and liver. (3) Protein metabolism: (a) it increases the rate of transport of some amino acids into tissues, (b) it increases the rate of protein synthesis in muscle, adipose tissue, liver, and other tissues, (c) it decreases the rate of protein degradation in muscle (and perhaps other tissues). These insulin effects serve to encourage the synthesis of carbohydrate, fat and protein, therefore, insulin can be considered to be an anabolic hormone. Continue reading >>

Insulin And Fat Storage

Insulin And Fat Storage

We left off last week with the question, “What prevents fat from leaving the fat cell?” If you missed out on it, you may want to read The Futility of Low-Calorie Diets. To quickly recap, we talked about the fact that your body has two main fuels: glucose (sugar) or fat. The preferred source of fuel is fat, but under certain circumstances, we can shift the body to using more sugar rather than fat. At times, such as being chased by a rabid dog, this is a good thing. However, it’s not a good thing if sugar remains the main fuel for most of the day. Relying on sugar means you’re not burning fat. Many people make lifestyle choices and nutrition decisions that have basically locked up their extra stored fat in their fat cells, making it useless for energy. The only way you can lose fat is if you use fat. You’ll be unsuccessful at losing fat if you don’t burn fat, even if you eat fewer calories and burn more through exercise. You can lose weight, but most of the loss will come from lean body mass, or muscle tissue, not fat. Fat Storage and Insulin The most significant factor in fat storage is the level of insulin in the blood. Insulin has many effects on the body. With respect to fat storage, insulin increases the storage of fat in fat cells and prevents fat cells from releasing fat for energy. This is such a key point for people to understand that I’ll repeat it: Insulin increases the storage of fat in fat cells and prevents the cells from releasing it for energy. Eight hormones stimulate fat utilization: epinephrine, norepinephrine, adrenocorticotrophic hormone (ACTH), glucagon, thyroid-stimulating hormone, melanocyte-stimulating hormone, vasopressin and growth hormone. One hormone prevents fat utilization: insulin. The pancreas releases insulin when blood suga Continue reading >>

Insulin

Insulin

This article is about the insulin protein. For uses of insulin in treating diabetes, see insulin (medication). Not to be confused with Inulin. Insulin (from Latin insula, island) is a peptide hormone produced by beta cells of the pancreatic islets, and it is considered to be the main anabolic hormone of the body.[5] It regulates the metabolism of carbohydrates, fats and protein by promoting the absorption of, especially, glucose from the blood into fat, liver and skeletal muscle cells.[6] In these tissues the absorbed glucose is converted into either glycogen via glycogenesis or fats (triglycerides) via lipogenesis, or, in the case of the liver, into both.[6] Glucose production and secretion by the liver is strongly inhibited by high concentrations of insulin in the blood.[7] Circulating insulin also affects the synthesis of proteins in a wide variety of tissues. It is therefore an anabolic hormone, promoting the conversion of small molecules in the blood into large molecules inside the cells. Low insulin levels in the blood have the opposite effect by promoting widespread catabolism, especially of reserve body fat. Beta cells are sensitive to glucose concentrations, also known as blood sugar levels. When the glucose level is high, the beta cells secrete insulin into the blood; when glucose levels are low, secretion of insulin is inhibited.[8] Their neighboring alpha cells, by taking their cues from the beta cells,[8] secrete glucagon into the blood in the opposite manner: increased secretion when blood glucose is low, and decreased secretion when glucose concentrations are high.[6][8] Glucagon, through stimulating the liver to release glucose by glycogenolysis and gluconeogenesis, has the opposite effect of insulin.[6][8] The secretion of insulin and glucagon into the Continue reading >>

Metabolic Effects Of Insulin

Metabolic Effects Of Insulin

1. Metabolic Effects of Insulin on Cellular Uptake of Glucose Supachai A. Basit, RMT, PhD 2. Overview • Four major organs play a dominant role in fuel metabolism • Integration of energy metabolism is controlled primarily by the actions of insulin and glucagon 3. Insulin • Polypeptide hormone produce by the beta cells of the islet of Langerhans of the pancreas • Most important hormone coordinating the use of fuels by tissues • Metabolic effects  anabolic – Favoring the synthesis of glycogen, triacylglycerols and protein 4. Structure of Insulin • 51 amino acids • Polypeptide A and B, linked together by a disulfide bridges • Intramolecular disulfide bridge between amino acid residues of the A chain 5. Synthesis of Insulin • Two inactive precursors  cleaved to form the active hormone plus the C-peptide • C-peptide  essential for proper insulin folding 6. Stimulation of Insulin Secretion • Insulin and glucagon secretion is closely coordinated at the islet of Langerhans • Secretion is regulated so that the rate of hepatic glucose production is kept equal to the use of glucose by peripheral tissues 7. Stimulation of Insulin Secretion is Increased by: Glucose • ß cells contain Glut-2 transporters and have glucokinase activity and thus can phosphorylate glucose in amounts proportional to its actual concentration in blood • Ingestion of CHO rich meal leads to a rise in blood glucose, which is a signal for insulin secretion and decrease glucagon synthesis and release 8. Stimulation of Insulin Secretion is Increased by: Amino Acids • Ingestion of protein causes a transient rise in plasma amino acids level, which in turn induces the secretion of insulin • Elevated plasma arginine stimulates insulin secretion 9. Stimulation of Insulin Secre Continue reading >>

Hyperinsulinemia, Hyperproinsulinemia And Insulin Resistance In The Metabolic Syndrome

Hyperinsulinemia, Hyperproinsulinemia And Insulin Resistance In The Metabolic Syndrome

, Volume 52, Issue5 , pp 426432 | Cite as Hyperinsulinemia, hyperproinsulinemia and insulin resistance in the metabolic syndrome For better comprehension of the metabolic syndrome, it is necessary to differentiate the effect of insulin on glucose metabolism on the one hand, and on other metabolic activities on the other hand. Whereas glucose utilization is affected by insulin resistance, the effect of insulin on lipid metabolism, ion and aminoacid transport does not seem to be diminished. Lipid metabolism, however, seems to play a crucial role in the induction of the vicious cycle. Increased energy and fat ingestion may be due to an increased number of galanin secreting cells in the hypothalamus. The excessive fat intake results in an increased rate of release of insulin and increased influx of triglycerides into the blood. From these triglycerides an excess of free fatty acids is released by the action of lipoprotein lipase. The increased plasma free fatty acid level then results in insulin resistance affecting glucose metabolism. Also, these free fatty acids may impair the secretion of insulin. Induction of insulin resistance results in higher glucose levels, which may cause hyperinsulinemia. Hyperinsulinemia maintains the elevation of triglycerides. When diabetes becomes overt and elevated glucose levels prevail, the hyperinsulinism acts on the metabolic pathways which are still sensitive to insulin, namely lipid metabolism, aminoacid transport and ion transport. Insulinproinsulininsulin resistancemetabolic syndrometriglyceridesfree fatty acidsfat intakegalanin This is a preview of subscription content, log in to check access. Unable to display preview. Download preview PDF. Boden, G., Chen, X., Ruiz, J., White, J. V., and Rossetti, L., Mechanisms of fatty acid-indu Continue reading >>

Insulin Vs. Fat Metabolism Ftw

Insulin Vs. Fat Metabolism Ftw

Insulin is there to grow fat tissue for the obesity epidemic, not replenish glycogen after yoga. Teaser: insulin-induce hypoglycemia can get deadly quite fast, and there is no equivalent for the effects of insulin on fat. However, the effects of insulin on fat are 100 times more powerful. Background: Hormone sensitive lipase (HSL) responds to insulin by inhibiting lipolysis. It halts fat burning. It got its name because its THEE most hormone-sensitivelipase in the body. The hormone about which we are speaking is of course insulin. And the enzyme, or at least one of the enzymes as it were, is HSL. To be clear, it takes very little insulin to inhibit HSL. Just a dollop, in fact. Effect of very small concentrations of insulin on forearm metabolism. Persistence of its action on potassium and free fatty acids without its effect on glucose. (Zierler and Rabinowitz, 1964) Expt 1. Since were all about jabbing people with insulin lately, lets get at it again. Jab someone with about 100 uU (/min*kg), and muscle and fat vacuum glucose out of the blood. Same goes for potassium; and adipose gets all stingy too it stops releasing and starts storing fat. This is healthy, and its part of why people say insulin, and by extension carbohydrate, causes lean people grow fat tissue. What do you think would happen in an insulin resistant obese crowd. Less glucose vacuuming, but scrooge adipose will still responds with gravitas, by saving more and spending less? Likely. HSL is like the little piggys straw house. The strong young wolf can blow it down. The COPD emphysema wolf can blow it down because its made of straw. Thus, insulin causes lean people to grow fat tissue, and it causes obese people to grow more fat tissue. In other words, with regard to common obesity, being resistant to insuli Continue reading >>

The Role Of Insulin In The Body

The Role Of Insulin In The Body

Tweet Insulin is a hormone which plays a key role in the regulation of blood glucose levels. A lack of insulin, or an inability to adequately respond to insulin, can each lead to the development of the symptoms of diabetes. In addition to its role in controlling blood sugar levels, insulin is also involved in the storage of fat. Insulin is a hormone which plays a number of roles in the body’s metabolism. Insulin regulates how the body uses and stores glucose and fat. Many of the body’s cells rely on insulin to take glucose from the blood for energy. Insulin and blood glucose levels Insulin helps control blood glucose levels by signaling the liver and muscle and fat cells to take in glucose from the blood. Insulin therefore helps cells to take in glucose to be used for energy. If the body has sufficient energy, insulin signals the liver to take up glucose and store it as glycogen. The liver can store up to around 5% of its mass as glycogen. Some cells in the body can take glucose from the blood without insulin, but most cells do require insulin to be present. Insulin and type 1 diabetes In type 1 diabetes, the body produces insufficient insulin to regulate blood glucose levels. Without the presence of insulin, many of the body’s cells cannot take glucose from the blood and therefore the body uses other sources of energy. Ketones are produced by the liver as an alternative source of energy, however, high levels of the ketones can lead to a dangerous condition called ketoacidosis. People with type 1 diabetes will need to inject insulin to compensate for their body’s lack of insulin. Insulin and type 2 diabetes Type 2 diabetes is characterised by the body not responding effectively to insulin. This is termed insulin resistance. As a result the body is less able to t Continue reading >>

Fatty Acid Metabolism, Energy Expenditure And Insulin Resistance In Muscle

Fatty Acid Metabolism, Energy Expenditure And Insulin Resistance In Muscle

Abstract Fatty acids (FAs) are essential elements of all cells and have significant roles as energy substrates, components of cellular structure and signalling molecules. The storage of excess energy intake as fat in adipose tissue is an evolutionary advantage aimed at protecting against starvation, but in much of today's world, humans are faced with an unlimited availability of food, and the excessive accumulation of fat is now a major risk for human health, especially the development of type 2 diabetes (T2D). Since the first recognition of the association between fat accumulation, reduced insulin action and increased risk of T2D, several mechanisms have been proposed to link excess FA availability to reduced insulin action, with some of them being competing or contradictory. This review summarises the evidence for these mechanisms in the context of excess dietary FAs generating insulin resistance in muscle, the major tissue involved in insulin-stimulated disposal of blood glucose. It also outlines potential problems with models and measurements that may hinder as well as help improve our understanding of the links between FAs and insulin action. Overview Fatty acids (FAs) are organic acids largely defined by the length and saturation of the aliphatic side chain attached to a carboxylic acid. In animals, these side chains normally contain an even number of carbon atoms and FAs are grouped into short chain (2–6 carbon atoms), medium chain (8–12 carbon atoms), long chain (14–18 carbon atoms) and very long chain (20–26 carbon atoms). The major types of FAs in the circulation and in the tissues of mammals are the long-chain and very-long-chain FAs with varying degrees of saturation. These include palmitic acid (C16:0), palmitoleic acid (C16:1), stearic acid (C:18:0 Continue reading >>

The Science Of Insulin

The Science Of Insulin

Insulin is perhaps the most well known of all hormones and in the halls of health, fitness, and fat loss. It is mostly maligned and drastically misunderstood. As with many things in health and fitness there is more to the simple story told about insulin. Insulin basics Insulin functions very much like your hands when you are eating. Just as it would be extremely difficult to eat without hands, insulin feeds the tissue of the body in the same way. Insulin is required to facilitate nutrient uptake in the cells. Without insulin, your cells would literally starve and die. Insulin is made in the beta cells of the pancreas and is released into the blood stream in response to food. It assures these nutrients get into the cell. Insulin’s primary job is to make sure the cells have enough glucose, and therefore it has a strong impact on blood sugar levels. In fact, glucose is the primary stimulator of insulin release. In response to food and/or stress, blood glucose levels will rise. Insulin is used to lower blood sugar and balance things back out. Insulin Resistance Insulin works by increasing the amount of glucose receptors on the membranes of cells. So, when insulin interacts with cellular physiology it results in an increased ability for the cell to take in glucose. When insulin is repeatedly secreted in large quantities, over time the cells become less sensitive to its message. This is analogous to walking into a room with a strong smell. When you first enter, you are acutely aware of the odor and may cover your nose in response. After several minutes however, the smell becomes diminished and you no longer smell it. This is what happens to the cells when they become insulin resistant. They no longer respond to insulin the same way. This has consequences for cellular energy Continue reading >>

Effects Of Insulin, Glucose And Glycerol On Fat Metabolism In Alloxan-diabetic Sheep

Effects Of Insulin, Glucose And Glycerol On Fat Metabolism In Alloxan-diabetic Sheep

EFFECTS OF INSULIN, GLUCOSE AND GLYCEROL ON FAT METABOLISM IN ALLOXAN-DIABETIC SHEEP The effects of insulin, glucose injection and oral glycerol on blood or plasma levels of glucose, free fatty acids (FFA), acetic acid and ketone bodies have been studied in alloxan-diabetic sheep. Insulin (05 i.u./kg.) lowered glucose levels only slightly, but induced a prompt and marked fall in FFA and acetate levels; ketones declined steadily after the first hour. The rate of utilization of injected glucose was considerably slower in diabetic than in non-diabetic sheep. FFA levels did not decline after glucose injection, while acetate levels declined slowly. Ketone levels were not affected significantly. Glycerol (180 ml.) per os reduced acetate and ketone levels, while tending to increase FFA values. Blood glucose also increased considerably. These data are consistent with present knowledge of the metabolic lesions in severe diabetes. However, it is concluded that there is impairment of acetate and, probably, ketone oxidation in severe diabetic ketosis. Finally, the metabolic changes recorded are compared with those which occur after insulin, glucose or glycerol administration to ewes showing clinical signs of ovine pregnancy toxaemia following severe and prolonged undernourishment in late pregnancy. Continue reading >>

How Insulin Really Works: It Causes Fat Storage…but Doesn’t Make You Fat

How Insulin Really Works: It Causes Fat Storage…but Doesn’t Make You Fat

Many people believe that insulin is to blame for the obesity epidemic. When you understand how it actually works, you’ll know why this is a lie. Insulin has been taking quite a beating these days. If we’re to listen to some “experts,” it’s an evil hormone whose sole goal is making us fat, type 2 diabetics. Furthermore, we’re told that carbohydrates also are in on the conspiracy. By eating carbs, we open the insulin floodgates and wreak havoc in our bodies. How true are these claims, though? Does it really make sense that our bodies would come with an insidious mechanism to punish carbohydrate intake? Let’s find out. What is Insulin, Anyway? Insulin is a hormone, which means it’s a substance the body produces to affect the functions of organs or tissues, and it’s made and released into the blood by the pancreas. Insulin’s job is a very important one: when you eat food, it’s broken down into basic nutrients (protein breaks down into amino acids; dietary fats into fatty acids; and carbohydrates into glucose), which make their way into the bloodstream. These nutrients must then be moved from the blood into muscle and fat cells for use or storage, and that’s where insulin comes into play: it helps shuttle the nutrients into cells by “telling” the cells to open up and absorb them. So, whenever you eat food, your pancreas releases insulin into the blood. As the nutrients are slowly absorbed into cells, insulin levels drop, until finally all the nutrients are absorbed, and insulin levels then remain steady at a low, “baseline” level. This cycle occurs every time you eat food: amino acids, fatty acids, and/or glucose find their way into your blood, and they’re joined by additional insulin, which ushers them into cells. Once the job is done, insu Continue reading >>

Studies On The Metabolism Of Adipose Tissue. Xii. The Effects Of Insulin And Epinephrine On Free Fatty Acid And Glycerol Production In The Presence And Absence Of Glucose*

Studies On The Metabolism Of Adipose Tissue. Xii. The Effects Of Insulin And Epinephrine On Free Fatty Acid And Glycerol Production In The Presence And Absence Of Glucose*

Studies on the Metabolism of Adipose Tissue. XII. The Effects of Insulin and Epinephrine on Free Fatty Acid and Glycerol Production in the Presence and Absence of Glucose* Cite this: Biochemistry 1963, 2, 2, 383-388 Article Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days. Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts. The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Note: In lieu of an abstract, this is the article's first page. This article is cited by 272 publications. Nicolas J. Pillon, Roxane E. Vella, Laurent Soulre, Michel Becchi, Michel Lagarde, and Christophe O. Soulage . Structural and Functional Changes in Human Insulin Induced by the Lipid Peroxidation Byproducts 4-Hydroxy-2-nonenal and 4-Hydroxy-2-hexenal. Chemical Research in Toxicology 2011, 24 (5) , 752-762. DOI: 10.1021/tx200084d. William B. Benjamin, Irwin Singer, and Susan T. Fish. Actions of insulin, epinephrine, and dibutyryl adenosine cyclic 5'-monophosphate on fat cell protein phosphorylations. Adenosine cyclic 5'-monophosphate dependent and independent mechanisms. Biochemistry 1975, 14 (15) , 3301-3309. DOI: 10.1021/bi00686a003. Robert L. Jungas. Fatty acid synthesis in adipose tissue incubated in t Continue reading >>

Insulin And Glucagon

Insulin And Glucagon

Acrobat PDF file can be downloaded here. The islets of Langerhans The pancreatic Islets of Langerhans are the sites of production of insulin, glucagon and somatostatin. The figure below shows an immunofluorescence image in which antibodies specific for these hormones have been coupled to differing fluorescence markers. We can therefore identify those cells that produce each of these three peptide hormones. You can see that most of the tissue, around 80 %, is comprised of the insulin-secreting red-colored beta cells (ß-cells). The green cells are the α-cells (alpha cells) which produce glucagon. We see also some blue cells; these are the somatostatin secreting γ-cells (gamma cells). Note that all of these differing cells are in close proximity with one another. While they primarily produce hormones to be circulated in blood (endocrine effects), they also have marked paracrine effects. That is, the secretion products of each cell type exert actions on adjacent cells within the Islet. An Introduction to secretion of insulin and glucagon The nutrient-regulated control of the release of these hormones manages tissue metabolism and the blood levels of glucose, fatty acids, triglycerides and amino acids. They are responsible for homeostasis; the minute-to-minute regulation of the body's integrated metabolism and, thereby, stabilize our inner milieu. The mechanisms involved are extremely complex. Modern medical treatment of diabetes (rapidly becoming "public enemy number one") is based on insight into these mechanisms, some of which are not completely understood. I will attempt to give an introduction to this complicated biological picture in the following section. Somewhat deeper insight will come later. The Basics: secretion Let us begin with two extremely simplified figur Continue reading >>

Insulin

Insulin

Insulin is a hormone secreted by the beta cells of pancreas, and is important in the regulation of carbohydrate and fat metabolism in the body. Marie Boran Discovery: The discovery of Insulin by Banting and Best in 1922 was a major breakthrough in endocrinology. Chemistry: Insulin is made up of 2 polypeptide chains linked by disulphide linkages. Synthesis: Insulin is synthesized as preprohormone having molecular weight of 11500. It is converted into proinsulin in endoplasmic reticulum with molecular weight of 9000, and finally into insulin in Golgi apparatus having molecular weight of 5808. Metabolism Insulin has a plasma half life of 6 minutes before being broken down catalyzed by the enzyme Insulinase. Insulin receptor Insulin receptor is made up of 4 subunits which are linked through disulphide linkages. There are 2 alpha and 2 beta subunits. The 2 alpha subunits are located outside cell membrane and have the insulin binding site. The 2 beta subunits penetrate cell membrane. Mechanism of Action of Insulin Mechanism of action can be well understood considering the following points: 1. Binding of insulin with alpha subunit 2. Autophosphorylation of alpha subunit 3. Activation of tyrosine kinase 4. Phosphorylation of intracellular enzymes Metabolic effects The metabolic effects of insulin include: 1. Glucose uptake (glucose transport proteins) 2. Amino acid, potassium & phosphate uptake 3. Phosphorylation of enzymes (10-15 min) 4. DNA transcription & RNA translation (hours-days) Effects of Insulin: Insulin affects the following: 1. Carbohydrate metabolism Insulin has profound effects on the following: a. Skeletal muscles: Insulin promotes glucose uptake and metabolism by the skeletal muscles. The muscles use fats in the resting state of the body as the membranes are imp Continue reading >>

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