Evolving Health: Why Can't We Convert Fat To Glucose?
As evident by many sugar-laden soda pop "potbellies" of North America, lipogenesis can obviously occur from drinking and eating too much sugar (1). Wouldnt it be just grand to reverse the process and be able to lose all that fat via gluconeogenesis? Unfortunately mammals do not have the ability to synthesize glucose from fats (1). The fact is that once glucose is converted to acetyl coA there is no method of getting back to glucose. The pyruvate dehydrogenase reaction that converts pyruvate to acetyl CoA is not reversible (1p252). Because lipid metabolism produces acetyl CoA via beta-oxidation, there can be no conversion to pyruvate or oxaloacetate that may have been used for gluconeogenesis (1p252). Further, the two carbons in the acetyl CoA molecule are lost upon entering the citric acid cycle (1p252). Thus, the acetyl CoA is used for energy (1p252). There are some fatty acids that have an odd number of carbon atoms that can be converted to glucose, but these are not common in the diet (1p253). Maybe they should be made more common. Do they taste good? 1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009. Continue reading >>
Gluconeogenesis
Not to be confused with Glycogenesis or Glyceroneogenesis. Simplified Gluconeogenesis Pathway Gluconeogenesis (GNG) is a metabolic pathway that results in the generation of glucose from certain non-carbohydrate carbon substrates. From breakdown of proteins, these substrates include glucogenic amino acids (although not ketogenic amino acids); from breakdown of lipids (such as triglycerides), they include glycerol (although not fatty acids); and from other steps in metabolism they include pyruvate and lactate. Gluconeogenesis is one of several main mechanisms used by humans and many other animals to maintain blood glucose levels, avoiding low levels (hypoglycemia). Other means include the degradation of glycogen (glycogenolysis)[1] and fatty acid catabolism. Gluconeogenesis is a ubiquitous process, present in plants, animals, fungi, bacteria, and other microorganisms.[2] In vertebrates, gluconeogenesis takes place mainly in the liver and, to a lesser extent, in the cortex of the kidneys. In ruminants, this tends to be a continuous process.[3] In many other animals, the process occurs during periods of fasting, starvation, low-carbohydrate diets, or intense exercise. The process is highly endergonic until it is coupled to the hydrolysis of ATP or GTP, effectively making the process exergonic. For example, the pathway leading from pyruvate to glucose-6-phosphate requires 4 molecules of ATP and 2 molecules of GTP to proceed spontaneously. Gluconeogenesis is often associated with ketosis. Gluconeogenesis is also a target of therapy for type 2 diabetes, such as the antidiabetic drug, metformin, which inhibits glucose formation and stimulates glucose uptake by cells.[4] In ruminants, because dietary carbohydrates tend to be metabolized by rumen organisms, gluconeogenesis occurs Continue reading >>
Lipid Metabolism
on on Fats (or triglycerides) within the body are ingested as food or synthesized by adipocytes or hepatocytes from carbohydrate precursors ([link]). Lipid metabolism entails the oxidation of fatty acids to either generate energy or synthesize new lipids from smaller constituent molecules. Lipid metabolism is associated with carbohydrate metabolism, as products of glucose (such as acetyl CoA) can be converted into lipids. Lipid metabolism begins in the intestine where ingested triglycerides are broken down into smaller chain fatty acids and subsequently into monoglyceride molecules (see [link]b) by pancreatic lipases, enzymes that break down fats after they are emulsified by bile salts. When food reaches the small intestine in the form of chyme, a digestive hormone called cholecystokinin (CCK) is released by intestinal cells in the intestinal mucosa. CCK stimulates the release of pancreatic lipase from the pancreas and stimulates the contraction of the gallbladder to release stored bile salts into the intestine. CCK also travels to the brain, where it can act as a hunger suppressant. Together, the pancreatic lipases and bile salts break down triglycerides into free fatty acids. These fatty acids can be transported across the intestinal membrane. However, once they cross the membrane, they are recombined to again form triglyceride molecules. Within the intestinal cells, these triglycerides are packaged along with cholesterol molecules in phospholipid vesicles called chylomicrons ([link]). The chylomicrons enable fats and cholesterol to move within the aqueous environment of your lymphatic and circulatory systems. Chylomicrons leave the enterocytes by exocytosis and enter the lymphatic system via lacteals in the villi of the intestine. From the lymphatic system, the chylo Continue reading >>
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- Exercise and Glucose Metabolism in Persons with Diabetes Mellitus: Perspectives on the Role for Continuous Glucose Monitoring
Gluconeogenesis - Kansas State Hn 400 Human Nutrition
Gluconeogenesis: The opposite of glycolysis, using other products like amino acids to make glucose. Amino acid uptake go from the amino acids through the amino acid transporters into the hepatocyte. The anabolic pathway of amino acids leads to protein synthesis. The catabolic pathway of amino acids can lead to gluconeogenesis that assist the formation of glucose. As shown below gluconeogenesis is like glycolysis in reverse with an oxaloacetate workaround. Oxaloacetate is a TCA cycle intermediate that is formed instead of directly converting pyruvate to phosphoenolpyruvate, which would be glycolysis exactly in reverse. Oxaloacetate then is just what is formed as an intermediate between the two steps. This gluconeogenesis animation does a good job of illustrating and explaining gluconeogenesis. We can use amino acids in gluconeogenesis to make glucose, but we cannot use ALL amino acids. Fatty acids cannot be used to form glucose because it makes Acetyl-CoA. The transition reaction that forms acetyl CoA from pyruvate is a one way reaction. This means that Acetyl-CoA can't be used to form pyruvate. In othe words, we can not go back from Acetyl-CoA to pyruvate. This occurs in the liver & kidney to some extent. Glucose is exported to tissues. Pyruvate is decarboxylated - the carboxyl group (-COOH) is split forming carbon dioxide. It is dehydrogenated - elimination of hydrogren It is added to CoA to form Acetyl CoA - remember CoA is Coenzyme A, responsible for oxidizing pyruvate in the Citric Acid/Kreb's cycle Why can't Acetyl CoA be used to from glucose through the Kreb's cycle? Because the Acetyl CoA carbons are given off as CO2, there is no carbon skeleton left to be used for gluconeogenesis. Glycerol can be used, but it makes very little glucose. Shows where all the amino Continue reading >>
Gluconeogenesis - Encyclopedia Article - Citizendium
Many 3- and 4- carbon substrates can enter the gluconeogenesis pathway. Lactate from anaerobic respiration in skeletal muscle is easily converted to pyruvate in the liver cells; this happens as part of the Cori cycle . However, the first designated substrate in the gluconeogenic pathway is pyruvate . Oxaloacetate (an intermediate in the citric acid cycle ) can also be used for gluconeogenesis. Many amino acids , upon amino group removal, yield intermediates of the citric acid cycle and can therefore be used for net synthesis of oxaloacetate (and thereafter glucose) . Even-chain fatty acids are oxidized into the two-carbon acetyl CoA , which is further oxidized to CO2 in the citric acid cycle . Acetyl CoA cannot be used for gluconeogenesis in animals because it cannot be converted in oxaloacetate (or other gluconeogenic subtrates). However, plants and some microorganisms can convert acetylCoA into oxaloacetate through the glyoxylate cycle . The last round of beta-oxidation of odd-chain fatty acids yields propionyl CoA , a precursor for the citric acid cycle intermediate succinyl CoA . These fatty acids may therefore be used for gluconeogenesis. Glycerol , which is a part of all triacylglycerols , can also be used in gluconeogenesis, after conversion into dihydroxyacetone phosphate. Gluconeogenesis begins with the formation of oxaloacetate through carboxylation of pyruvate at the expense of one molecule of ATP , but is inhibited in the presence of high levels of ADP. This reaction is catalyzed by pyruvate carboxylase . Oxaloacetate is then decarboxylated and simultaneously phosphorylated by phosphoenolpyruvate carboxykinase to produce phosphoenolpyruvate . One molecule of GTP is hydrolyzed to GDP in the course of this reaction. Both reactions take place in mitochondria . Continue reading >>
Gluconeogenesis Flashcards | Quizlet
What is the definition of gluconeogensis? the synthesis of glucose from noncarbohydrate precursors how many days do the direct glucose reserves sufficient for the needs of the body? how many grams of glucose does the brain need daily? how many grams of glucose does the entire body need daily? how many grams of glucose are in body fluids to use for the body? how mans grams of readily mobilized glucose are there in glycogen stores? What is the major site of gluconeogenesis? mostly by the liver, and a smaller amount in the kidney 1. decreased insulin/glucagon ratio as in an overnight fast 3. high protein-low carb diet (need minimum of 50 g carb for insulin secretion) 4. stress; due to the hormones cortisol and epinephrine which are elevated under these conditions What are the 4 major non-carbohydrate presursors used as substrates for gluconeogenesis? 2. amino acids (muscle protein degradation in skeletal muscle) 3. glycerol (triglyceride breakdown in adipose tissue) what is lactate's role in the gluconeogenic pathway? 1. during vigorous exercise, lactate buildup and NADH 2. NADH can be reoxidized during the reduction of pyruvate to lactate 3. lactate is then returned to the liver, where it can be reoxidized to pyruvate by liver LDH the liver provides glucose to muscle for exercise and then reprocesses lactate into new glucose in the liver, what is the reaction when lactate enters from the blood? Lactate + LDH -> pyruvate + 6 phosphoryl groups -> glucose to the muscle what compound does muscle protein degradation give to gluconeogenesis? what is the process of alanine for conversion to glucose? alanine + alanine aminotransferase -> pyruvate what compound does triglyceride breakdown in adipose tissue give to gluconeogenesis? what is the process of glycerol for conversion to Continue reading >>
Gluconeogenesis: Endogenous Glucose Synthesis
Reactions of Gluconeogenesis: Gluconeogenesis from two moles of pyruvate to two moles of 1,3-bisphosphoglycerate consumes six moles of ATP. This makes the process of gluconeogenesis very costly from an energy standpoint considering that glucose oxidation to two moles of pyruvate yields two moles of ATP. The major hepatic substrates for gluconeogenesis (glycerol, lactate, alanine, and pyruvate) are enclosed in red boxes for highlighting. The reactions that take place in the mitochondria are pyruvate to OAA and OAA to malate. Pyruvate from the cytosol is transported across the inner mitochondrial membrane by the pyruvate transporter. Transport of pyruvate across the plasma membrane is catalyzed by the SLC16A1 protein (also called the monocarboxylic acid transporter 1, MCT1) and transport across the outer mitochondrial membrane involves a voltage-dependent porin transporter. Transport across the inner mitochondrial membrane requires a heterotetrameric transport complex (mitochondrial pyruvate carrier) consisting of the MPC1 gene and MPC2 gene encoded proteins. Following reduction of OAA to malate the malate is transported to the cytosol by the malate transporter (SLC25A11). In the cytosol the malate is oxidized to OAA and the OOA then feeds into the gluconeogenic pathway via conversion to PEP via PEPCK. The PEPCK reaction is another site for consumption of an ATP equivalent (GTP is utilized in the PEPCK reaction). The reversal of the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) reaction requires a supply of NADH. When lactate is the gluconeogenic substrate the NADH is supplied by the lactate dehydrogenase (LDH) reaction (indicated by the dashes lines), and it is supplied by the malate dehydrogenase reaction when pyruvate and alanine are the substrates. Secondly, one mo Continue reading >>
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Why Can't Fat Produce Glucose?
Tousief Irshad Ahmed Sirwal Author has 77 answers and 106.2k answer views Acetyl CoA is NOT a substrate for gluconeogenesis in animals 1. Pyruvate dehydrogenase reaction is irreversible. So, acetyl CoA cannot be converted back to pyruvate. 2. 2C Acetyl CoA enters the TCA cycle by condensing with 4C oxaloacetate. 2 molecules of CO2 are released & the oxaloacetate is regenerated. There is no NET production of oxaloacetate. Animals cannot convert fat into glucose with minimal exceptions 1. Propionyl CoA derived from odd chain fatty acids are converted to Succinyl CoA Glucogenic 2. Glycerol derived from triglycerides are glucogenic. Answered Mar 26, 2017 Author has 942 answers and 259.1k answer views Yijia Xiong pointed out that the glycerol portion of triglycerides (fats) can indeed be converted to glucose. It is not so energy-inefficient that it is avoided by our bodies. If nutritionally, we are in a gluconeogenesis mode (building up glucose stores rather than consuming them), glycerol would be a perfectly acceptable precursor. However, I think the original question had more to do with the vast bulk of the triglycerides that are not glycerol, but are fatty acids. And it is true that we cant produce glucose from fatty acids. The reason is that the catabolic reactions of fatty acids break off two carbon atoms at a time as Acetyl-CoA. But our metabolic suite of pathways has no way to convert a two-carbon fragment to glucose. The end product of glycolysis is pyruvate, a three-carbon compound. Pyruvate can be back-synthesized into glucose. But the committing reaction for the Krebs cycle is the pyruvate dehydrogenase step, forming acetyl-CoA. That reaction is not reversible. Once pyruvate loses a carbon atom, it cant go back. The three main macronutrients are carbohydrates, pr Continue reading >>
Glucose Can Be Synthesized From Noncarbohydrate Precursors - Biochemistry - Ncbi Bookshelf
Glucose is formed by hydrolysis of glucose 6-phosphate in a reaction catalyzed by glucose 6-phosphatase. We will examine each of these steps in turn. 16.3.2. The Conversion of Pyruvate into Phosphoenolpyruvate Begins with the Formation of Oxaloacetate The first step in gluconeogenesis is the carboxylation of pyruvate to form oxaloacetate at the expense of a molecule of ATP . Then, oxaloacetate is decarboxylated and phosphorylated to yield phosphoenolpyruvate, at the expense of the high phosphoryl-transfer potential of GTP . Both of these reactions take place inside the mitochondria. The first reaction is catalyzed by pyruvate carboxylase and the second by phosphoenolpyruvate carboxykinase. The sum of these reactions is: Pyruvate carboxylase is of special interest because of its structural, catalytic, and allosteric properties. The N-terminal 300 to 350 amino acids form an ATP -grasp domain ( Figure 16.25 ), which is a widely used ATP-activating domain to be discussed in more detail when we investigate nucleotide biosynthesis ( Section 25.1.1 ). The C -terminal 80 amino acids constitute a biotin-binding domain ( Figure 16.26 ) that we will see again in fatty acid synthesis ( Section 22.4.1 ). Biotin is a covalently attached prosthetic group, which serves as a carrier of activated CO2. The carboxylate group of biotin is linked to the -amino group of a specific lysine residue by an amide bond ( Figure 16.27 ). Note that biotin is attached to pyruvate carboxylase by a long, flexible chain. The carboxylation of pyruvate takes place in three stages: Recall that, in aqueous solutions, CO2 exists as HCO3- with the aid of carbonic anhydrase (Section 9.2). The HCO3- is activated to carboxyphosphate. This activated CO2 is subsequently bonded to the N-1 atom of the biotin ring to Continue reading >>
Why Can Fatty Acids Not Be Converted Into Glucose? : Mcat
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How Does The Body Adapt To Starvation?
- [Instructor] In this video, I want to explore the question of how does our body adapt to periods of prolonged starvation. So in order to answer this question, I actually think it's helpful to remind ourselves first of a golden rule of homeostasis inside of our body. So in order to survive, remember that our body must be able to maintain proper blood glucose levels. I'm gonna go ahead and write we must be able to maintain glucose levels in our blood, and this is important even in periods of prolonged starvation, because it turns out that we need to maintain glucose levels above a certain concentration in order to survive, even if that concentration is lower than normal. And this of course brings up the question, well, how does our body maintain blood glucose levels? So let's go ahead and answer this question by starting off small. Let's say we have a mini case of starvation, let's say three or four hours after a meal. Your blood glucose levels begin to drop, and so what does your body do to resolve that? Well, at this point, it has a quick and easy solution. It turns to its glycogen stores in the liver. Remember that our body stores up these strings of glucose inside of our body so that we can easily pump it back into the blood when we're not eating. But unfortunately humans only have enough glycogen stores to last us about a day, so after a day of starvation, our body's pretty much reliant exclusively on the metabolic pathways involved in gluconeogenesis, which if you remember is the pathway by which we produce new or neo glucose. And we produce this glucose from non-carbohydrate precursor molecules. So let's think about what else we have in our body. Remember that our other two major storage fuels are fats, and we usually think about fatty acids containing most of th Continue reading >>
Principles Of Biochemistry/gluconeogenesis And Glycogenesis
Gluconeogenesis (abbreviated GNG) is a metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates such as lactate, glycerol, and glucogenic amino acids. It is one of the two main mechanisms humans and many other animals use to keep blood glucose levels from dropping too low (hypoglycemia). The other means of maintaining blood glucose levels is through the degradation of glycogen (glycogenolysis). Gluconeogenesis is a ubiquitous process, present in plants, animals, fungi, bacteria, and other microorganisms. In animals, gluconeogenesis takes place mainly in the liver and, to a lesser extent, in the cortex of kidneys. This process occurs during periods of fasting, starvation, low-carbohydrate diets, or intense exercise and is highly endergonic. For example, the pathway leading from phosphoenolpyruvate to glucose-6-phosphate requires 6 molecules of ATP. Gluconeogenesis is often associated with ketosis. Gluconeogenesis is also a target of therapy for type II diabetes, such as metformin, which inhibits glucose formation and stimulates glucose uptake by cells. Lactate is transported back to the liver where it is converted into pyruvate by the Cori cycle using the enzyme lactate dehydrogenase. Pyruvate, the first designated substrate of the gluconeogenic pathway, can then be used to generate glucose. All citric acid cycle intermediates, through conversion to oxaloacetate, amino acids other than lysine or leucine, and glycerol can also function as substrates for gluconeogenesis.Transamination or deamination of amino acids facilitates entering of their carbon skeleton into the cycle directly (as pyruvate or oxaloacetate), or indirectly via the citric acid cycle. Whether fatty acids can be converted into glucose in animals has been a longst Continue reading >>
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Gluconeogenesis: Endogenous Glucose Synthesis
Reactions of Gluconeogenesis: Gluconeogenesis from two moles of pyruvate to two moles of 1,3-bisphosphoglycerate consumes six moles of ATP. This makes the process of gluconeogenesis very costly from an energy standpoint considering that glucose oxidation to two moles of pyruvate yields two moles of ATP. The major hepatic substrates for gluconeogenesis (glycerol, lactate, alanine, and pyruvate) are enclosed in red boxes for highlighting. The reactions that take place in the mitochondria are pyruvate to OAA and OAA to malate. Pyruvate from the cytosol is transported across the inner mitochondrial membrane by the pyruvate transporter. Transport of pyruvate across the plasma membrane is catalyzed by the SLC16A1 protein (also called the monocarboxylic acid transporter 1, MCT1) and transport across the outer mitochondrial membrane involves a voltage-dependent porin transporter. Transport across the inner mitochondrial membrane requires a heterotetrameric transport complex (mitochondrial pyruvate carrier) consisting of the MPC1 gene and MPC2 gene encoded proteins. Following reduction of OAA to malate the malate is transported to the cytosol by the malate transporter (SLC25A11). In the cytosol the malate is oxidized to OAA and the OOA then feeds into the gluconeogenic pathway via conversion to PEP via PEPCK. The PEPCK reaction is another site for consumption of an ATP equivalent (GTP is utilized in the PEPCK reaction). The reversal of the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) reaction requires a supply of NADH. When lactate is the gluconeogenic substrate the NADH is supplied by the lactate dehydrogenase (LDH) reaction (indicated by the dashes lines), and it is supplied by the malate dehydrogenase reaction when pyruvate and alanine are the substrates. Secondly, one mo Continue reading >>
- Exercise and Glucose Metabolism in Persons with Diabetes Mellitus: Perspectives on the Role for Continuous Glucose Monitoring
- Postprandial Blood Glucose Is a Stronger Predictor of Cardiovascular Events Than Fasting Blood Glucose in Type 2 Diabetes Mellitus, Particularly in Women: Lessons from the San Luigi Gonzaga Diabetes Study
- Exercise and Blood Glucose Levels
Can Sugars Be Produced From Fatty Acids? A Test Case For Pathway Analysis Tools
Can sugars be produced from fatty acids? A test case for pathway analysis tools Department of Bioinformatics, 2Bio Systems Analysis Group, Friedrich-Schiller-Universitt Jena, Ernst-Abbe-Platz 2, 07743 Jena, Germany and 3School of Life Sciences, Oxford Brookes University, Headington, Oxford, OX3 0BP, UK *To whom correspondence should be addressed. Search for other works by this author on: Department of Bioinformatics, 2Bio Systems Analysis Group, Friedrich-Schiller-Universitt Jena, Ernst-Abbe-Platz 2, 07743 Jena, Germany and 3School of Life Sciences, Oxford Brookes University, Headington, Oxford, OX3 0BP, UK *To whom correspondence should be addressed. Search for other works by this author on: Department of Bioinformatics, 2Bio Systems Analysis Group, Friedrich-Schiller-Universitt Jena, Ernst-Abbe-Platz 2, 07743 Jena, Germany and 3School of Life Sciences, Oxford Brookes University, Headington, Oxford, OX3 0BP, UK Search for other works by this author on: Department of Bioinformatics, 2Bio Systems Analysis Group, Friedrich-Schiller-Universitt Jena, Ernst-Abbe-Platz 2, 07743 Jena, Germany and 3School of Life Sciences, Oxford Brookes University, Headington, Oxford, OX3 0BP, UK Search for other works by this author on: Bioinformatics, Volume 25, Issue 1, 1 January 2009, Pages 152158, Luis F. de Figueiredo, Stefan Schuster, Christoph Kaleta, David A. Fell; Can sugars be produced from fatty acids? A test case for pathway analysis tools, Bioinformatics, Volume 25, Issue 1, 1 January 2009, Pages 152158, Motivation: In recent years, several methods have been proposed for determining metabolic pathways in an automated way based on network topology. The aim of this work is to analyse these methods by tackling a concrete example relevant in biochemistry. It concerns the question wh Continue reading >>
Lecture Outline
Chapter 22Gluconeogenesis, Glycogen, Pentose Phosphate OK, so now we know how sugars are broken down andoxidized. We also know how sugars canbe made in plants and other photosynthetic organisms by using light energy toeffectively reverse the oxidation of sugars.But there are a few loose ends that we have not dealt with in themetabolism of sugars. One of thesecenters on the fact that glucose is the soluble form of energy that runs aroundin the blood stream. However, what doyou do if your source of food is mostly protein instead of sugar (a carnivorousdiet, for example)? If you have nosugar, then our mechanism for getting energy around to the different parts ofthe body is, at least in part, defeated.We need to be able to convert other molecules into glucose. For this we use a process calledgluconeogenesis. There may also becircumstances where we have ample glucose and want to store some of it in aform that could be rapidly converted for use later on. We can do this by generating a glucosepolymer called glycogen (similar to starch in plants). This material is stored and can be rapidlybroken down and released as glucose into the bloodstream. Finally, we are going to need a way ofgenerating the reductive power (mostly NADPH) needed for anabolism. We do not have photosynthesis to rely on, sowe use a process called the pentose phosphate pathway. Thebasic starting material used in gluconeogenesis is pyruvate. Lots of different compounds can be convertedto pyruvate including: Lactateproduced in the muscles during vigorous anaerobic exercise Essentiallyall the TCA components Notethat lactate produced in the muscle is transferred back to the liver forprocessing to form glucose. Whatcannot be converted to pyruvate is acetyl CoA (except through TCAintermediates, but these results i Continue reading >>
