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Fat To Glucose Metabolism

Relationship Of Dietary Fat To Glucose Metabolism.

Relationship Of Dietary Fat To Glucose Metabolism.

Relationship of dietary fat to glucose metabolism. Lipid Metabolism Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington St., 02111, Boston, MA, USA. [email protected] The relationship between dietary fat and glucose metabolism has been recognized for at least 60 years. In experimental animals, high fat diets result in impaired glucose tolerance. This impairment is associated with decreased basal and insulin-stimulated glucose metabolism. Impaired insulin binding and/or glucose transporters has been related to changes in the fatty acid composition of the membrane induced by dietary fat modification. In humans, high-fat diets, independent of fatty acid profile, have been reported to result in decreased insulin sensitivity. Saturated fat, relative to monounsaturated and polyunsaturated fat, appears to be more deleterious with respect to fat-induced insulin insensitivity. Some of the adverse effects induced by fat feeding can be ameliorated with omega-3 fatty acid. Epidemiological data in humans suggest that subjects with higher intakes of fat are more prone to develop disturbances in glucose metabolism, type 2 diabetes or impaired glucose tolerance, than subjects with lower intakes of fat. Inconsistencies in the data may be attributable to clustering of high intakes of dietary fat (especially animal fat) with obesity and inactivity. Metabolic studies suggest that higher-fat diets containing a higher proportion of unsaturated fat result in better measures of glucose metabolism than high-carbohydrate diet. Clearly, the area of dietary fat and glucose metabolism has yet to be fully elucidated. Continue reading >>

Why Does Fat Increase Blood Glucose?

Why Does Fat Increase Blood Glucose?

Has this ever happened to you? — You eat a meal such as fettuccine alfredo with garlic bread and tiramisu for dessert. — You take either the appropriate amount of insulin for the carbohydrate in the meal or your oral medications. — You check 2 to 3 hours after eating and see a blood glucose reading that is in range. So far, so good, right? —Then you wake up the next morning with a very high number? Ever wondered what causes this? There are two reasons. First, Fettuccine Alfredo, garlic bread and tiramisu are, for the most part, a mixture of carbohydrate and fat. But it’s the fat in the meal that is contributing to the elevated readings. Although carbohydrate is the nutrient that has the most immediate affect on blood glucose levels, fat is not glucose neutral. But only a small portion of the triglyceride (fat) molecule, called the glycerol backbone, can be used as glucose. This very small addition to the glucose pool can’t be the source of your high blood glucose readings. So if fat doesn’t directly raise blood glucose, what is it doing? For many years scientists thought that fat was a metabolically inert substance. Fat on the body was considered dead weight, just extra blubber people carted around. Well it turns out that fat has been masquerading as the quiet shy guy in the back row, all the while packing a considerable metabolic punch. A high fat meal can increase the amount of free fatty acids (FFAs) in the blood. Both repeatedly elevated levels of FFAs as found in chronic intake of high fat (especially high saturated fat) meals and obesity are associated with both skeletal muscle and liver insulin resistance. That resistance means that it will take more insulin—either made by your pancreas or from an injection—to move the glucose in the blood strea Continue reading >>

Can Fats Be Turned Into Glycogen For Muscle?

Can Fats Be Turned Into Glycogen For Muscle?

The amount of fat in the average diet and the amount of stored fat in the average body make the notion of converting that fat into usable energy appealing. Glycogen, a form of energy stored in muscles for quick use, is what the body draws on first to perform movements, and higher glycogen levels result in higher usable energy. It is not possible for fats to be converted directly into glycogen because they are not made up glucose, but it is possible for fats to be indirectly broken down into glucose, which can be used to create glycogen. Relationship Between Fats and Glycogen Fats are a nutrient found in food and a compound used for long-term energy storage in the body, while glycogen is a chain of glucose molecules created by the body from glucose for short-term energy storage and utilization. Dietary fats are used for a number of functions in the body, including maintaining cell membranes, but they are not used primarily as a source of fast energy. Instead, for energy the body relies mostly on carbohydrates, which are converted into glucose that is then used to form glycogen. Turning Fats Into Glucose Excess glucose in the body is converted into stored fat under certain conditions, so it seems logical that glucose could be derived from fats. This process is called gluconeogenesis, and there are multiple pathways the body can use to achieve this conversion. Gluconeogenesis generally occurs only when the body cannot produce sufficient glucose from carbohydrates, such as during starvation or on a low-carbohydrate diet. This is less efficient than producing glucose through the metabolizing of carbohydrates, but it is possible under the right conditions. Turning Glucose Into Glycogen Once glucose has been obtained from fats, your body easily converts it into glycogen. In gl Continue reading >>

Glucose Metabolism In Fat Cells Stimulated By Insulin And Dependent On Sodium

Glucose Metabolism In Fat Cells Stimulated By Insulin And Dependent On Sodium

SPECIFIC transport of organic and inorganic substances through biological membranes has been well established1. Transport of organic substances, such as amino-acids and sugars, may be active and is, as a rule, linked to the transport of cations2, most frequently those of sodium and potassium3. Other transport mechanisms may agree rather with the definition of facilitated diffusion which seems to be independent of cations4. It is usually thought that in insulin tissues such as muscle and adipose tissue which respond to insulin, this hormone somehow favours the facilitated diffusion of glucose and of certain other sugars5,6. Insulin also facilitates, however, the entry of some substrates which pass through by active transport7, and, furthermore, it has been shown to increase the resting electrical potential of muscle8 and of adipose tissue9, while stimulating decreasing retention of potassium and sodium ions respectively in these tissues10,11. While Hagen12 has reported that insulin has less effect on glucose metabolism by adipose tissue in the absence of sodium or potassium ions, Rodbell13 has observed normal responsiveness to insulin of isolated fat cells in the absence of sodium ions. These conflicting views have encouraged us to investigate the effects of changing the concentration of cations in the medium glucose transport and metabolism by isolated fat cells, both in the presence and absence of insulin. A marked sodium dependency of insulin-stimulated glucose metabolism in fat cells on sodium has been found. Continue reading >>

Dietary Fat Content Alters Insulin-mediated Glucose Metabolism In Healthy Men

Dietary Fat Content Alters Insulin-mediated Glucose Metabolism In Healthy Men

Dietary fat content alters insulin-mediated glucose metabolism in healthy men From the Departments of Endocrinology and Metabolism, Clinical Chemistry Laboratory of Endocrinology, and Biochemistry, Academic Medical Center, University of Amsterdam; the Center for Liver, Digestive and Metabolic Diseases, Academic Hospital Groningen, Groningen, Netherlands; and the Departments of Internal Medicine and Endocrinology, Leiden University Medical Center, Leiden, Netherlands. Address reprint requests to PHLT Bisschop, Department of Endocrinology and Metabolism (F5), Academic Medical Center, University of Amsterdam, PO Box 22700, 1100 DE Amsterdam, Netherlands. E-mail: [email protected] . Search for other works by this author on: From the Departments of Endocrinology and Metabolism, Clinical Chemistry Laboratory of Endocrinology, and Biochemistry, Academic Medical Center, University of Amsterdam; the Center for Liver, Digestive and Metabolic Diseases, Academic Hospital Groningen, Groningen, Netherlands; and the Departments of Internal Medicine and Endocrinology, Leiden University Medical Center, Leiden, Netherlands. Search for other works by this author on: From the Departments of Endocrinology and Metabolism, Clinical Chemistry Laboratory of Endocrinology, and Biochemistry, Academic Medical Center, University of Amsterdam; the Center for Liver, Digestive and Metabolic Diseases, Academic Hospital Groningen, Groningen, Netherlands; and the Departments of Internal Medicine and Endocrinology, Leiden University Medical Center, Leiden, Netherlands. Search for other works by this author on: From the Departments of Endocrinology and Metabolism, Clinical Chemistry Laboratory of Endocrinology, and Biochemistry, Academic Medical Center, University of Amsterdam; the Center for Liver, Continue reading >>

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 >>

We Really Can Make Glucose From Fatty Acids After All! O Textbook, How Thy Biochemistry Hast Deceived Me!

We Really Can Make Glucose From Fatty Acids After All! O Textbook, How Thy Biochemistry Hast Deceived Me!

Biochemistry textbooks generally tell us that we can’t turn fatty acids into glucose. For example, on page 634 of the 2006 and 2008 editions of Biochemistry by Berg, Tymoczko, and Stryer, we find the following: Animals Cannot Convert Fatty Acids to Glucose It is important to note that animals are unable to effect the net synthesis of glucose from fatty acids. Specficially, acetyl CoA cannot be converted into pyruvate or oxaloacetate in animals. In fact this is so important that it should be written in italics and have its own bold heading! But it’s not quite right. Making glucose from fatty acids is low-paying work. It’s not the type of alchemy that would allow us to build imperial palaces out of sugar cubes or offer hourly sweet sacrifices upon the altar of the glorious god of glucose (God forbid!). But it can be done, and it’ll help pay the bills when times are tight. All Aboard the Acetyl CoA! When we’re running primarily on fatty acids, our livers break the bulk of these fatty acids down into two-carbon units called acetate. When acetate hangs out all by its lonesome like it does in a bottle of vinegar, it’s called acetic acid and it gives vinegar its characteristic smell. Our livers aren’t bottles of vinegar, however, and they do things a bit differently. They have a little shuttle called coenzyme A, or “CoA” for short, that carries acetate wherever it needs to go. When the acetate passenger is loaded onto the CoA shuttle, we refer to the whole shebang as acetyl CoA. As acetyl CoA moves its caboose along the biochemical railway, it eventually reaches a crossroads where it has to decide whether to enter the Land of Ketogenesis or traverse the TCA cycle. The Land of Ketogenesis is a quite magical place to which we’ll return in a few moments, but n Continue reading >>

Fat For Fuel: Why Dietary Fat, Not Glucose, Is The Preferred Body Fuel

Fat For Fuel: Why Dietary Fat, Not Glucose, Is The Preferred Body Fuel

Contrary to popular belief, glucose is NOT the preferred fuel of human metabolism; the fact is that burning dietary fat for fuel may actually be the key to optimal health Carbohydrate intake is the primary factor that determines your body's fat ratio, and processed grains and sugars (particularly fructose) are the primary culprits behind our skyrocketing obesity and diabetes rates According to experts, carbs should make up only 20 percent of your diet, while 50-70 percent of your diet should be healthy fats. Fat is far more satiating than carbs, so if you have cut down on carbs and feel ravenous, this is a sign that you need more healthy fat to burn for fuel By Dr. Mercola While we may consider ourselves to be at the pinnacle of human development, our modern food manufacturing processes have utterly failed at improving health and increasing longevity. During the Paleolithic period, many thousands of years ago, our ancestors ate primarily vegetables, fruit, nuts, roots and meat—and a wide variety of it. This diet was high in fats and protein, and low in grain- and sugar-derived carbohydrates. The average person's diet today, on the other hand, is the complete opposite, and the average person's health is a testament of what happens when you adhere to a faulty diet. Humans today suffer more chronic and debilitating diseases than ever before. And there can be little doubt that our food choices play a major role in this development. Quite simply, you were not designed to eat large amounts of refined sugar, high fructose corn syrup, cereal, bread, potatoes and pasteurized milk products. As Mark Sisson states in the featured article:1 "If you want to live a better life and eat the best foods nature provided for health and fitness, then it's time to ditch the old paradigms an Continue reading >>

Relationship Of Dietary Fat To Glucose Metabolism

Relationship Of Dietary Fat To Glucose Metabolism

The relationship between dietary fat and glucose metabolism has been recognized for at least 60 years. In experimental animals, high fat diets result in impaired glucose tolerance. This impairment is associated with decreased basal and insulin-stimulated glucose metabolism. Impaired insulin binding and/or glucose transporters has been related to changes in the fatty acid composition of the membrane induced by dietary fat modification. In humans, high-fat diets, independent of fatty acid profile, have been reported to result in decreased insulin sensitivity. Saturated fat, relative to monounsaturated and polyunsaturated fat, appears to be more deleterious with respect to fat-induced insulin insensitivity. Some of the adverse effects induced by fat feeding can be ameliorated with omega-3 fatty acid. Epidemiological data in humans suggest that subjects with higher intakes of fat are more prone to develop disturbances in glucose metabolism, type 2 diabetes or impaired glucose tolerance, than subjects with lower intakes of fat. Inconsistencies in the data may be attributable to clustering of high intakes of dietary fat (especially animal fat) with obesity and inactivity. Metabolic studies suggest that higher-fat diets containing a higher proportion of unsaturated fat result in better measures of glucose metabolism than high-carbohydrate diet. Clearly, the area of dietary fat and glucose metabolism has yet to be fully elucidated. Do you want to read the rest of this article? ... The increase in blood glucose when feeding piglets with higher-dose fat diets or lipase supplemented diets was consistent with expectations. Fat metabolism affects glucose metabolism and insulin levels in animals ( Lichtenstein and Schwab 2000). Animals fed high-fat diet exhibited a decrease of activ Continue reading >>

Does Fat Convert To Glucose In The Body?

Does Fat Convert To Glucose In The Body?

Your body is an amazing machine that is able to extract energy from just about anything you eat. While glucose is your body's preferred energy source, you can't convert fat into glucose for energy; instead, fatty acids or ketones are used to supply your body with energy from fat. Video of the Day Fat is a concentrated source of energy, and it generally supplies about half the energy you burn daily. During digestion and metabolism, the fat in the food you eat is broken down into fatty acids and glycerol, which are emulsified and absorbed into your blood stream. While some tissues -- including your muscles -- can use fatty acids for energy, your brain can't convert fatty acids to fuel. If you eat more fat than your body needs, the extra is stored in fat cells for later use. Fat has more than twice as many calories per gram as carbs and protein, which makes it an efficient form of stored energy. It would take more than 20 pounds of glycogen -- a type of carbohydrate used for fuel -- to store the same amount of energy in just 10 pounds of fat. Your Body Makes Glucose From Carbs Almost all the glucose in your body originated from carbohydrates, which come from the fruit, vegetables, grains and milk in your diet. When you eat these carb-containing foods, your digestive system breaks them down into glucose, which is then used for energy by your cells. Any excess glucose is converted into glycogen, then stored in your muscles and liver for later use. Once you can't store any more glucose or glycogen, your body stores any leftover carbs as fat. Glucose is your brain's preferred source of energy. However, when glucose is in short supply, your brain can use ketones -- which are derived from fat -- for fuel. Since your brain accounts for approximately one-fifth of your daily calori Continue reading >>

Metabolic Functions Of The Liver

Metabolic Functions Of The Liver

Hepatocytes are metabolic overachievers in the body. They play critical roles in synthesizing molecules that are utilized elsewhere to support homeostasis, in converting molecules of one type to another, and in regulating energy balances. If you have taken a course in biochemistry, you probably spent most of that class studying metabolic pathways of the liver. At the risk of damning by faint praise, the major metabolic functions of the liver can be summarized into several major categories: Carbohydrate Metabolism It is critical for all animals to maintain concentrations of glucose in blood within a narrow, normal range. Maintainance of normal blood glucose levels over both short (hours) and long (days to weeks) periods of time is one particularly important function of the liver. Hepatocytes house many different metabolic pathways and employ dozens of enzymes that are alternatively turned on or off depending on whether blood levels of glucose are rising or falling out of the normal range. Two important examples of these abilities are: Excess glucose entering the blood after a meal is rapidly taken up by the liver and sequestered as the large polymer, glycogen (a process called glycogenesis). Later, when blood concentrations of glucose begin to decline, the liver activates other pathways which lead to depolymerization of glycogen (glycogenolysis) and export of glucose back into the blood for transport to all other tissues. When hepatic glycogen reserves become exhaused, as occurs when an animal has not eaten for several hours, do the hepatocytes give up? No! They recognize the problem and activate additional groups of enzymes that begin synthesizing glucose out of such things as amino acids and non-hexose carbohydrates (gluconeogenesis). The ability of the liver to synthe Continue reading >>

Fat Metabolism During Exercise: New Concepts

Fat Metabolism During Exercise: New Concepts

Fat Metabolism During Exercise: New Concepts Fat Metabolism During Exercise: New Concepts During intense exercise carbohydrate (not fat) can be mobilized and oxidized rapidly enough to meet the energy requirements for intense muscular contractions. Professor, Department of Kinesiology and Health Education Member, GSSI Sports Medicine Review Board 1. People store large amounts of body fat in the form of triglycerides within fat (adipose) tissue as well as within muscle fibers (intramuscular triglycerides).When compared to carbohydrate stored as muscle glycogen, these fat stores are mobilized and oxidized at relatively slow rates during exercise. 2. As exercise progresses from low to moderate intensity, e.g., 25-65% VO2max, the rate of fatty acid mobilization from adipose tissue into blood plasma declines, whereas the rate of total fat oxidation increases due to a relatively large use of intramuscular triglycerides. Intramuscular triglycerides also account for the characteristic increase in fat oxidation as a result of habitual endurance-training programs. 3. Dietary carbohydrate intake has a large influence on fat mobilization and oxidation during exercise; when dietary carbohydrate produces sufficient carbohydrate reserves in the body, carbohydrate becomes the preferred fuel during exercise. This is especially important during intense exercise because only carbohydrate(not fat) can be mobilized and oxidized rapidly enough to meet the energy requirements for intense muscular contractions. The two main sources of energy during muscular exercise are fat (triglyceride) and carbohydrate (glycogen and glucose) stored within the body, and there has been much research and practical experience over the past 30 y demonstrating the importance of muscle and liver glycogen for redu Continue reading >>

Fat Vs. Carbohydrate Metabolism During Aerobic Exercise; Fat Oxidation During Exercise

Fat Vs. Carbohydrate Metabolism During Aerobic Exercise; Fat Oxidation During Exercise

de fysiologie, anatomie en pathologie van het menselijk lichaam Carbohydrate and fat are the main substrates for the muscle used during aerobic exercise. Carbohydrates are stored in the body as muscle glycogen, liver glycogen (1) and circulating as plasma glucose (2). Fat is stored as adipose tissue and as intramuscular triglyceride (IMTG) (1). In addition, some fat is present in the circulation as plasma free fatty acids (FFA) (3) and as triglycerides (TG) incorporated in lipoproteins (2). An overview of the energy stores is provided in table 1. Based on estimates for a normal, non-obese male with a body mass of 70 kg (4). Fat provides 39 kJ g-1 and carbohydrate 17 kJ g-1. Liverglycogen is converted to glucose-6-P and dephosphorylated by glucose-6-phosphatase to form glucose (4). Glut-4 is only present in skeletal muscle and can translocate from an intracellular microsomal Glut-4 pool to the cellsurface following insulin release and/or contraction, thereby enabling a rapid increase in plasma glucose uptake (12). Glucose is converted to glucose-6-P by hexokinase (4). During muscle glycogenolysis, muscle glycogen is reduced to glucose-1-P by glycogenphosphorylase. Glucose-1-P is also converted to glucose-6-P by hexokinase (5). Intracellular glucose is metabolized in the glycolytic pathway to form pyruvate. Pyruvate is converted into lactate when the glycolytic rate exceeds the entry of pyruvate into the tricarboxylic (TCA)-cycle (5). When oxygen is present, pyruvate is converted into acetyl-CoA and oxidized within the mitochondria to form CO2 and H2O. Whereas the anaerobic metabolism of glucose yields only 2 ATP per glucose molecule the complete oxidative metabolism of glucose yields 38 ATP per glucose molecule (5). Thus the oxidative metabolism of glucose is a much mor Continue reading >>

Metabolism And Energetics

Metabolism And Energetics

Metabolism basically refers to all the chemical reactions within the body used to produce energy. This involves a complex set of processes that convert fuels into specialised compounds loaded with energy. In the body, the primary final agent to produce energy is called adenosine triphosphate (ATP) . When ATP is broken down or used by cells huge amounts of energy is released. This energy is essential for cells to grow and divide, synthesise important compounds, for muscles to contract and numerous other important functions. Metabolism therefore produces energy to perform all the functions of different tissues within the body. Metabolism works by breaking down foods in the diet or compounds in the body into their smaller components. These can then enter into special reactions to produce ATP. The left over components are recycled by the body and used to regenerate the original compounds. The body has three main types of molecules it uses for energy: Carbohydrates: These are the sugar type compounds in the body. Carbohydrates come from foods such as bread, cereal, potatoes, fruits and sugar-containing foods or bevarages. When carbohydrates are digested in the gastrointestinal system they are broken down into smaller molecules such as glucose (a simple sugar). The main storage sites for carbohydrates in the body are the liver and muscles. Lipids: This basically refers to fats (such as cholesterol) from the diet or stored in adipose tissue (in other words the body fat). Lipids are broken down into smaller components called fatty acids for energy. Therefore lipids are really just chains of fatty acids joined together. Proteins: These make up nearly three quarters of all the solid materials in the body. Proteins are thus the basic structural components in the body. They are ma Continue reading >>

Renal Amino Acid, Fat And Glucose Metabolism In Type 1 Diabetic And Non-diabetic Humans: Effects Of Acute Insulin Withdrawal

Renal Amino Acid, Fat And Glucose Metabolism In Type 1 Diabetic And Non-diabetic Humans: Effects Of Acute Insulin Withdrawal

, Volume 49, Issue8 , pp 19011908 | Cite as Renal amino acid, fat and glucose metabolism in type 1 diabetic and non-diabetic humans: effects of acute insulin withdrawal The aim of this study was to test the hypothesis that type 1 diabetes alters renal amino acid, glucose and fatty acid metabolism. We studied five C-peptide-negative, type 1 diabetic subjects during insulin replacement (glucose 5.6mmol/l) and insulin deprivation (glucose 15.5mmol/l) and compared them with six non-diabetic subjects. Leucine, phenylalanine, tyrosine, glucose and palmitate tracers were infused after an overnight fast and samples were obtained from the renal vein, femoral vein and femoral artery. Insulin deprivation significantly increased whole-body fluxes (2025%) of phenylalanine, tyrosine and leucine, and leucine oxidation (50%). Kidney contributed 510% to the whole-body leucine and phenylalanine flux. A net uptake of phenylalanine, conversion of phenylalanine to tyrosine (5mol/min) and net release of tyrosine (5mol/min) occurred across the kidney. Whole-body (three-fold) and leg (two-fold) leucine transamination increased but amino acid metabolism in the kidney did not alter with diabetes or insulin deprivation. Insulin deprivation doubled endogenous glucose production, renal glucose production was unaltered by insulin deprivation and diabetes (ranging between 100 and 140mol/min). Renal palmitate exchange was unaltered by insulin deprivation. In conclusion, kidney postabsorptively accounts for 510% of whole-body protein turnover, 1520% of leucine transamination and 1015% of endogenous glucose production, and actively converts phenylalanine to tyrosine. During insulin deprivation, leg becomes a major site for leucine transamination but insulin deprivation does not affect renal phenylalani Continue reading >>

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