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Nurrient, complex molecules of proteins, polysaccharides, and lipids must be reduced to simpler particles such as simple sugar Nutrient utilization in energy metabolism they can be absorbed by the digestive epithelial cells. Different organs play specific roles in the digestive process. The animal diet needs carbohydrates, protein, and fat, as well as vitamins and inorganic components for nutritional balance.
How each of these components is digested is discussed in the following sections. The digestion of carbohydrates begins in the mouth. The salivary enzyme amylase begins the breakdown of food starches into maltose, a disaccharide.
As the bolus of food travels through the esophagus to the stomach, no significant digestion of carbohydrates takes place. The esophagus produces no digestive enzymes but does produce mucous for lubrication. The acidic environment in the stomach stops the action of the amylase enzyme. The next step of carbohydrate digestion takes place in the duodenum.
Recall that the chyme from the stomach enters the duodenum and mixes with the digestive secretion from the pancreas, liver, and gallbladder. Pancreatic juices also contain amylase, which continues the breakdown of starch and glycogen into maltose, a disaccharide.
The disaccharides are broken down into monosaccharides by enzymes called maltases, sucrases, and lactases, which are also present in the brush border of the small intestinal wall.
Maltase breaks down maltose into glucose. Other disaccharides, such as sucrose and lactose are broken down by sucrase and lactase, respectively. The monosaccharides glucose thus produced are absorbed and then can be used in metabolic pathways to harness energy.
The monosaccharides are transported across the intestinal epithelium into the bloodstream to be transported to the different cells in the body. The steps in carbohydrate digestion are summarized in Figure 5. A large part of protein digestion takes place in the stomach. The enzyme pepsin plays an important role in the digestion of proteins by breaking down the intact protein to peptides, which are short chains of four to nine amino acids.
In the duodenum, other enzymes— trypsin, elastase, and chymotrypsin—act on the peptides reducing them to smaller peptides. Trypsin elastase, carboxypeptidase, and chymotrypsin are produced by the pancreas and released into the duodenum where they act on the chyme.
The further breakdown of peptides to single amino acids is aided by enzymes called peptidases those that break down peptides. Specifically, carboxypeptidase, dipeptidase, and aminopeptidase play important roles in reducing the peptides to free amino acids. The amino acids are absorbed into the bloodstream through the small intestines.
The steps in protein digestion are summarized in Figure 5. Lipid digestion begins in the stomach with the aid of lingual lipase and gastric lipase. However, the bulk of lipid digestion occurs in the small intestine due to pancreatic lipase. When chyme enters the duodenum, the hormonal responses trigger the release of bile, which is produced in the liver and stored in the gallbladder.
Bile aids in the digestion of lipids, primarily triglycerides by emulsification. Emulsification is a process in which large lipid globules are broken down into several small lipid globules.
These small globules are more widely distributed in the chyme rather than forming large aggregates. Lipids are hydrophobic substances: in the presence of water, they will aggregate to form globules to minimize exposure to water.
Bile contains bile salts, which are amphipathic, meaning they contain hydrophobic and hydrophilic parts. Thus, the bile salts hydrophilic side can interface with water on one side and the hydrophobic side interfaces with lipids on the other.
By doing so, bile salts emulsify large lipid globules into small lipid globules. Why is emulsification important for digestion of lipids? Pancreatic juices contain enzymes called lipases enzymes that break down lipids. If the lipid in the chyme aggregates into large globules, very little surface area of the lipids is available for the lipases to act on, leaving lipid digestion incomplete.
By forming an emulsion, bile salts increase the available surface area of the lipids many folds. The pancreatic lipases can then act on the lipids more efficiently and digest them, as detailed in Figure 5.
Lipases break down the lipids into fatty acids and glycerides. These molecules can pass through the plasma membrane of the cell and enter the epithelial cells of the intestinal lining. The bile salts surround long-chain fatty acids and monoglycerides forming tiny spheres called micelles.
The micelles move into the brush border of the small intestine absorptive cells where the long-chain fatty acids and monoglycerides diffuse out of the micelles into the absorptive cells leaving the micelles behind in the chyme.
The long-chain fatty acids and monoglycerides recombine in the absorptive cells to form triglycerides, which aggregate into globules and become coated with proteins.
These large spheres are called chylomicrons. Chylomicrons contain triglycerides, cholesterol, and other lipids and have proteins on their surface.
Together, they enable the chylomicron to move in an aqueous environment without exposing the lipids to water. Chylomicrons leave the absorptive cells via exocytosis. Chylomicrons enter the lymphatic vessels and then enter the blood in the subclavian vein.
Vitamins can be either water-soluble or lipid-soluble. Fat-soluble vitamins are absorbed in the same manner as lipids. It is important to consume some amount of dietary lipid to aid the absorption of lipid-soluble vitamins.
Water-soluble vitamins can be directly absorbed into the bloodstream from the intestine. Which of the following statements about digestive processes is true? Amylase, maltase, and lactase in the mouth digest carbohydrates.
Trypsin and lipase in the stomach digest protein. Bile emulsifies lipids in the small intestine. No food is absorbed until the small intestine.
Elimination The final step in digestion is the elimination of undigested food content and waste products. The undigested food material enters the colon, where most of the water is reabsorbed. The semi-solid waste is moved through the colon by peristaltic movements of the muscle and is stored in the rectum.
As the rectum expands in response to storage of fecal matter, it triggers the neural signals required to set up the urge to eliminate. The solid waste is eliminated through the anus using peristaltic movements of the rectum. Diarrhea and constipation are some of the most common health concerns that affect digestion.
Constipation is a condition where the feces are hardened because of excess water removal in the colon. In contrast, if enough water is not removed from the feces, it results in diarrhea. Many bacteria, including the ones that cause cholera, affect the proteins involved in water reabsorption in the colon and result in excessive diarrhea.
: Nutrient utilization in energy metabolism| Nutrient Utilization in Humans: Metabolism Pathways | The acidic environment in the stomach stops the action of the amylase enzyme. The next step of carbohydrate digestion takes place in the duodenum. Recall that the chyme from the stomach enters the duodenum and mixes with the digestive secretion from the pancreas, liver, and gallbladder. Pancreatic juices also contain amylase, which continues the breakdown of starch and glycogen into maltose, a disaccharide. The disaccharides are broken down into monosaccharides by enzymes called maltases, sucrases, and lactases, which are also present in the brush border of the small intestinal wall. Maltase breaks down maltose into glucose. Other disaccharides, such as sucrose and lactose are broken down by sucrase and lactase, respectively. The monosaccharides glucose thus produced are absorbed and then can be used in metabolic pathways to harness energy. The monosaccharides are transported across the intestinal epithelium into the bloodstream to be transported to the different cells in the body. The steps in carbohydrate digestion are summarized in Figure 5. Figure 5. Digestion of carbohydrates is performed by several enzymes. Starch and glycogen are broken down into glucose by amylase and maltase. Sucrose table sugar and lactose milk sugar are broken down by sucrase and lactase, respectively. A large part of protein digestion takes place in the stomach. The enzyme pepsin plays an important role in the digestion of proteins by breaking down the intact protein to peptides, which are short chains of four to nine amino acids. In the duodenum, other enzymes— trypsin, elastase, and chymotrypsin—act on the peptides reducing them to smaller peptides. Trypsin elastase, carboxypeptidase, and chymotrypsin are produced by the pancreas and released into the duodenum where they act on the chyme. The further breakdown of peptides to single amino acids is aided by enzymes called peptidases those that break down peptides. Specifically, carboxypeptidase, dipeptidase, and aminopeptidase play important roles in reducing the peptides to free amino acids. The amino acids are absorbed into the bloodstream through the small intestines. The steps in protein digestion are summarized in Figure 5. Protein digestion is a multistep process that begins in the stomach and continues through the intestines. Lipid digestion begins in the stomach with the aid of lingual lipase and gastric lipase. However, the bulk of lipid digestion occurs in the small intestine due to pancreatic lipase. When chyme enters the duodenum, the hormonal responses trigger the release of bile, which is produced in the liver and stored in the gallbladder. Bile aids in the digestion of lipids, primarily triglycerides by emulsification. Emulsification is a process in which large lipid globules are broken down into several small lipid globules. These small globules are more widely distributed in the chyme rather than forming large aggregates. Lipids are hydrophobic substances: in the presence of water, they will aggregate to form globules to minimize exposure to water. Bile contains bile salts, which are amphipathic, meaning they contain hydrophobic and hydrophilic parts. Thus, the bile salts hydrophilic side can interface with water on one side and the hydrophobic side interfaces with lipids on the other. By doing so, bile salts emulsify large lipid globules into small lipid globules. Why is emulsification important for digestion of lipids? Pancreatic juices contain enzymes called lipases enzymes that break down lipids. If the lipid in the chyme aggregates into large globules, very little surface area of the lipids is available for the lipases to act on, leaving lipid digestion incomplete. By forming an emulsion, bile salts increase the available surface area of the lipids many folds. The pancreatic lipases can then act on the lipids more efficiently and digest them, as detailed in Figure 5. Lipases break down the lipids into fatty acids and glycerides. These molecules can pass through the plasma membrane of the cell and enter the epithelial cells of the intestinal lining. The bile salts surround long-chain fatty acids and monoglycerides forming tiny spheres called micelles. The micelles move into the brush border of the small intestine absorptive cells where the long-chain fatty acids and monoglycerides diffuse out of the micelles into the absorptive cells leaving the micelles behind in the chyme. The long-chain fatty acids and monoglycerides recombine in the absorptive cells to form triglycerides, which aggregate into globules and become coated with proteins. These large spheres are called chylomicrons. Chylomicrons contain triglycerides, cholesterol, and other lipids and have proteins on their surface. Together, they enable the chylomicron to move in an aqueous environment without exposing the lipids to water. Chylomicrons leave the absorptive cells via exocytosis. Chylomicrons enter the lymphatic vessels and then enter the blood in the subclavian vein. Vitamins can be either water-soluble or lipid-soluble. Fat-soluble vitamins are absorbed in the same manner as lipids. It is important to consume some amount of dietary lipid to aid the absorption of lipid-soluble vitamins. Water-soluble vitamins can be directly absorbed into the bloodstream from the intestine. Mechanical and chemical digestion of food takes place in many steps, beginning in the mouth and ending in the rectum. Which of the following statements about digestive processes is true? Amylase, maltase, and lactase in the mouth digest carbohydrates. Trypsin and lipase in the stomach digest protein. Bile emulsifies lipids in the small intestine. No food is absorbed until the small intestine. Elimination The final step in digestion is the elimination of undigested food content and waste products. The undigested food material enters the colon, where most of the water is reabsorbed. The semi-solid waste is moved through the colon by peristaltic movements of the muscle and is stored in the rectum. As the rectum expands in response to storage of fecal matter, it triggers the neural signals required to set up the urge to eliminate. The solid waste is eliminated through the anus using peristaltic movements of the rectum. Diarrhea and constipation are some of the most common health concerns that affect digestion. Constipation is a condition where the feces are hardened because of excess water removal in the colon. Last, but certainly not least, are carbohydrates. Their molecular structure varies from complex polysaccharides to simpler disaccharides and monosaccharides. Carbohydrates are found in grains, fruits, vegetables, dairy, and processed foods. This means that before you can get your arcade tokens, you have to go get some smaller bills from the bank—in this metaphor, the bank would be your digestive system. Image from Human Anatomy Atlas. Your digestive system is responsible for the intake and breakdown of the food you eat, as well as the excretion of solid waste. The digestion process starts as soon as you put food in your mouth—enzymes in your saliva begin breaking down starches carbohydrates and some fats while you chew. Once food travels down the esophagus, it passes into the stomach, where gastric acid gets to work on disassembling the fats and proteins. Bile from the liver and gall bladder joins pancreatic juice to continue this process as the food moves into the small intestine. Now, it may be called the small intestine, but much like the Tardis, your small intestine is bigger on the inside. Check out this blog post to learn more about the villi. Some absorption occurs in the large intestine, but the small intestine is really the champ when it comes to chemical digestion and absorption. So what do the different nutrients break down into? Dietary fats, also known as triglycerides, break down into fatty acids and monoglycerides. Proteins are split up into their component amino acids. This happens through a process called gluconeogenesis. After the various parts of your digestive system have converted your food into its chemical building blocks, waste products are sent away and the essentials pass into your bloodstream to be processed by the liver and distributed throughout the rest of the body. Be sure to subscribe to the Visible Body Blog for more anatomy awesomeness! Are you an instructor? We have award-winning 3D products and resources for your anatomy and physiology course! Learn more here. For students. For instructors. 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| Impact of nutrient overload on metabolic homeostasis | Nutrition Reviews | Oxford Academic | Silent mating type information regulator 2 homolog 3 SIRT3 , and silent mating type information regulator 2 homolog 6 SIRT6 function as corepressors of hypoxia-induced factor-1α, which upregulates glycolytic genes. Explore This Subject. The salivary enzyme amylase begins the breakdown of food starches into maltose, a disaccharide. Trypsin elastase, carboxypeptidase, and chymotrypsin are produced by the pancreas and released into the duodenum where they act on the chyme. Adenosine triphosphate, or ATP, is the primary energy currency in cells; ATP stores energy in phosphate ester bonds. Meanwhile, such a study recapitulated the stealth metabolic remodeling processes that preceded, triggered, and sustained structural and functional remodeling of the heart to a measurable extent. ATP releases energy when the phosphodiester bonds are broken and ATP is converted to ADP and a phosphate group. |
| Top bar navigation | Next, succinate dehydrogenase is represented by a dark green bi-lobed shape embedded in the half of the inner membrane and facing the matrix. Next, acyl-CoA dehydrogenase, electron transfer flavoprotein ETFP , and ETFP-ubiquinone oxidoreductase form a complex, and are represented by three yellow and orange ovals on the matrix-facing side of the inner membrane. Next, ubiquinone is represented by a lime green circle labeled with a Q located in the side of the inner membrane facing the intermembrane space. Next, cytochrome c reductase is represented by a light blue oval-shaped structure that spans the membrane. Next, cytochrome c oxidase is represented by a pink oval-shaped structure that spans the inner membrane. Next, the ATP synthase complex is represented by an upside-down lollipop-shaped structure that traverses the inner membrane and contains a channel through the membrane; the round, purple head enters the mitochondrial matrix, and the lilac-colored stem spans the membrane. These electrons are transferred to ubiquinone. Succinate dehydrogenase converts succinate to fumarate and transfers additional electrons to ubiquinone via flavin adenine dinucleotide FAD. The acyl-CoA dehydrogenase, electron transfer flavoprotein ETFP , and ETFP-ubiquinone oxidoreductase complex converts acyl-CoA to trans-enoyl-CoA. During this reaction, additional electrons are transferred to ubiquinone by the FAD domain in this protein complex. Next, the electrons are transferred by ubiquinone to cytochrome c reductase, which pumps protons into the intermembrane space. The electrons are then carried to cytochrome c. Next, cytochrome c transfers the electrons to cytochrome c oxidase, which reduces oxygen O 2 with the electrons to form water H 2 O. During this reaction, additional protons are transferred to the intermembrane space. As the protons flow from the intermembrane space through the ATP synthase complex and into the matrix, ATP is formed from ADP and inorganic phosphate P i in the mitochondrial matrix. Oxidative phosphorylation depends on the electron transport from NADH or FADH 2 to O 2 , forming H 2 O. The electrons are "transported" through a number of protein complexes located in the inner mitochondrial membrane, which contains attached chemical groups flavins, iron-sulfur groups, heme, and cooper ions capable of accepting or donating one or more electrons Figure 2. These protein complexes, known as the electron transfer system ETS , allow distribution of the free energy between the reduced coenzymes and the O 2 and more efficient energy conservation. The electrons are transferred from NADH to O 2 through three protein complexes: NADH dehydrogenase, cytochrome reductase, and cytochrome oxidase. Electron transport between the complexes occurs through other mobile electron carriers, ubiquinone and cytochrome c. FAD is linked to the enzyme succinate dehydrogenase of the TCA cycle and another enzyme, acyl-CoA dehydrogenase of the fatty acid oxidation pathway. During the reactions catalyzed by these enzymes, FAD is reduced to FADH 2 , whose electrons are then transferred to O 2 through cytochrome reductase and cytochrome oxidase, as described for NADH dehydrogenase electrons Figure 2. These observations led Peter Mitchell, in , to propose his revolutionary chemiosmotic hypothesis. The reaction catalyzed by succinyl-CoA synthetase in which GTP synthesis occurs is an example of substrate-level phosphorylation. Acetyl-CoA enters the tricarboxylic acid cycle at the top of the diagram and reacts with oxaloacetate and water H 2 O to form a molecule of citrate and CoA-SH in a reaction catalyzed by citrate synthase. Next, the enzyme aconitase catalyzes the isomerization of citrate to isocitrate. Succinyl-CoA reacts with GDP and inorganic phosphate P i to form succinate and GTP. This reaction releases CoA-SH and is catalyzed by succinyl-CoA synthetase. In the next step, succinate reacts with FAD to form fumarate and FADH 2 in a reaction catalyzed by succinate dehydrogenase. Fumarate combines with H 2 O in a reaction catalyzed by fumerase to form malate. Then, oxaloacetate can react with a new molecule of acetyl-CoA and begin the tricarboxylic acid cycle again. The diagram shows the molecular structures for citrate, isocitrate, alpha-ketoglutarate, succinyl-CoA, succinate, fumarate, malate, and oxaloacetate. The enzymes that act at each of the eight steps in the cycle are shown in yellow rectangles. In aerobic respiration or aerobiosis, all products of nutrients' degradation converge to a central pathway in the metabolism, the TCA cycle. In this pathway, the acetyl group of acetyl-CoA resulting from the catabolism of glucose, fatty acids, and some amino acids is completely oxidized to CO 2 with concomitant reduction of electron transporting coenzymes NADH and FADH 2. Consisting of eight reactions, the cycle starts with condensing acetyl-CoA and oxaloacetate to generate citrate Figure 3. In addition, a GTP or an ATP molecule is directly formed as an example of substrate-level phosphorylation. In this case, the hydrolysis of the thioester bond of succinyl-CoA with concomitant enzyme phosphorylation is coupled to the transfer of an enzyme-bound phosphate group to GDP or ADP. Also noteworthy is that TCA cycle intermediates may also be used as the precursors of different biosynthetic processes. The TCA cycle is also known as the Krebs cycle, named after its discoverer, Sir Hans Kreb. Krebs based his conception of this cycle on four main observations made in the s. The first was the discovery in of the sequence of reactions from succinate to fumarate to malate to oxaloacetate by Albert Szent-Gyorgyi, who showed that these dicarboxylic acids present in animal tissues stimulate O 2 consumption. The second was the finding of the sequence from citrate to α-ketoglutarate to succinate, in , by Carl Martius and Franz Knoop. Next was the observation by Krebs himself, working on muscle slice cultures, that the addition of tricarboxylic acids even in very low concentrations promoted the oxidation of a much higher amount of pyruvate, suggesting a catalytic effect of these compounds. And the fourth was Krebs's observation that malonate, an inhibitor of succinate dehydrogenase, completely stopped the oxidation of pyruvate by the addition of tricarboxylic acids and that the addition of oxaloacetate in the medium in this condition generated citrate, which accumulated, thus elegantly showing the cyclic nature of the pathway. When 1,3-bisphosphoglycerate is converted to 3-phosphoglycerate, substrate-level phosphorylation occurs and ATP is produced from ADP. Then, 3-phosphoglycerate undergoes two reactions to yield phosphoenolpyruvate. Next, phosphoenolpyruvate is converted to pyruvate, which is the final product of glycolysis. During this reaction, substrate-level phosphorylation occurs and a phosphate is transferred to ADP to form ATP. Interestingly, during the initial phase, energy is consumed because two ATP molecules are used up to activate glucose and fructosephosphate. Part of the energy derived from the breakdown of the phosphoanhydride bond of ATP is conserved in the formation of phosphate-ester bonds in glucosephosphate and fructose-1,6-biphosphate Figure 4. In the second part of glycolysis, the majority of the free energy obtained from the oxidation of the aldehyde group of glyceraldehyde 3-phosphate G3P is conserved in the acyl-phosphate group of 1,3- bisphosphoglycerate 1,3-BPG , which contains high free energy. Then, part of the potential energy of 1,3BPG, released during its conversion to 3-phosphoglycerate, is coupled to the phosphorylation of ADP to ATP. The second reaction where ATP synthesis occurs is the conversion of phosphoenolpyruvate PEP to pyruvate. PEP is a high-energy compound due to its phosphate-ester bond, and therefore the conversion reaction of PEP to pyruvate is coupled with ADP phosphorylation. This mechanism of ATP synthesis is called substrate-level phosphorylation. For complete oxidation, pyruvate molecules generated in glycolysis are transported to the mitochondrial matrix to be converted into acetyl-CoA in a reaction catalyzed by the multienzyme complex pyruvate dehydrogenase Figure 5. When Krebs proposed the TCA cycle in , he thought that citrate was synthesized from oxaloacetate and pyruvate or a derivative of it. Only after Lipmann's discovery of coenzyme A in and the subsequent work of R. Stern, S. Ochoa, and F. Lynen did it become clear that the molecule acetyl-CoA donated its acetyl group to oxaloacetate. Until this time, the TCA cycle was seen as a pathway to carbohydrate oxidation only. Most high school textbooks reflect this period of biochemistry knowledge and do not emphasize how the lipid and amino acid degradation pathways converge on the TCA cycle. The cell is depicted as a large blue oval. A smaller dark blue oval contained inside the cell represents the mitochondrion. The mitochondrion has an outer mitochondrial membrane and within this membrane is a folded inner mitochondrial membrane that surrounds the mitochondrial matrix. The entry point for glucose is glycolysis, which occurs in the cytoplasm. Glycolysis converts glucose to pyruvate and synthesizes ATP. Pyruvate is transported from the cytoplasm into the mitochondrial matrix. Pyruvate is converted to acetyl-CoA, which enters the tricarboxylic acid TCA cycle. In the TCA cycle, acetyl-CoA reacts with oxaloacetate and is converted to citrate, which is then converted to isocitrate. Isocitrate is then converted to alpha-ketoglutarate with the release of CO 2. Then, alpha-ketoglutarate is converted to succinyl-CoA with the release of CO 2. Succinyl-CoA is converted to succinate, which is converted to fumarate, and then to malate. Malate is converted to oxaloacetate. Then, the oxaloacetate can react with another acetyl-CoA molecule and begin the TCA cycle again. In the TCA cycle, electrons are transferred to NADH and FADH 2 and transported to the electron transport chain ETC. The ETC is represented by a yellow rectangle along the inner mitochondrial membrane. The ETC results in the synthesis of ATP from ADP and inorganic phosphate P i. Fatty acids are transported from the cytoplasm to the mitochondrial matrix, where they are converted to acyl-CoA. Acyl-CoA is then converted to acetyl-CoA in beta-oxidation reactions that release electrons that are carried by NADH and FADH 2. These electrons are transported to the electron transport chain ETC where ATP is synthesized. These amino acids are called gluconeogenic because they can be used to make glucose. Amino acids that are deaminated and become acetyl-CoA are called ketogenic amino acids and can never become glucose. Fatty acids can never be made into glucose but are a high source of energy. These are broken down into two carbon units by a process called beta-oxidation enter the citric acid cycle as acetyl-CoA. In the presence of glucose, these two carbon units enter the citric acid cycle and burned to make energy ATP and produce the by-product CO 2. If glucose is low, ketones are formed. Ketone bodies can be burned to produce energy. The brain can use ketones. The energy released by catabolic pathways powers anabolic pathways in the building of macromolecules such as the proteins RNA and DNA, and even entire new cells and tissues. Anabolic pathways are required to build new tissue, such as muscle, after prolonged exercise or the remodeling of bone tissue, a process involving both catabolic and anabolic pathways. Anabolic pathways also build energy-storage molecules, such as glycogen and triglycerides. Intermediates in the catabolic pathways of energy metabolism are sometimes diverted from ATP production and used as building blocks instead. This happens when a cell is in positive energy balance. For example, the citric-acid-cycle intermediate, α-ketoglutarate can be anabolically processed to the amino acids glutamate or glutamine if they are required. Recall that the human body is capable of synthesizing eleven of the twenty amino acids that make up proteins. The metabolic pathways of amino acid synthesis are all inhibited by the specific amino acid that is the end-product of a given pathway. Thus, if a cell has enough glutamine it turns off its synthesis. Anabolic pathways are regulated by their end-products, but even more so by the energy state of the cell. When there is ample energy, bigger molecules, such as protein, RNA, and DNA, will be built as needed. Alternatively, when energy is insufficient, proteins and other molecules will be destroyed and catabolized to release energy. A dramatic example of this is seen in children with Marasmus. These children have severely compromised bodily functions, often culminating in death by infection. Children with Marasmus are starving for calories and protein, which are required to make energy and build macromolecules. In a much less severe example, a person is also in negative energy balance between meals. During this time, blood glucose levels start to drop. In order to restore blood glucose levels to their normal range, the anabolic pathway, called gluconeogenesis, is stimulated. The liver exports the synthesized glucose into the blood for other tissues to use. Glucose can be stored only in muscle and liver tissues. In these tissues, it is stored as glycogen, a highly branched macromolecule consisting of thousands of glucose monomers held together by chemical bonds. The glucose monomers are joined together by an anabolic pathway called glycogenesis. For each molecule of glucose stored, one molecule of ATP is used. Therefore, it costs energy to store energy. Glycogen levels do not take long to reach their physiological limit and when this happens excess glucose will be converted to fat. A cell in positive energy balance detects a high concentration of ATP as well as acetyl-CoA produced by catabolic pathways. In response, catabolism is shut off and the synthesis of triglycerides, which occurs by an anabolic pathway called lipogenesis, is turned on. The newly made triglycerides are transported to fat-storing cells called adipocytes. Fat is a better alternative to glycogen for energy storage as it is more compact per unit of energy and, unlike glycogen, the body does not store water along with fat. Water weighs a significant amount and increased glycogen stores, which are accompanied by water, would dramatically increase body weight. Home Metabolism: From Food To Fuel. Metabolism: From Food To Fuel View Teach. Genetics for Classroom Materials. Digestion and Nutrition The digestive system processes our food, breaking larger molecules down into their basic building blocks. interactive explore. learn more. Metabolism and Energy Storage Once nutrients arrive in the blood stream, the body finds a way to use them. Credits Funding. APA format:. Genetic Science Learning Center. Metabolism: From Food To Fuel [Internet]. |
| Metabolism Overview - Medicine LibreTexts | Or have you bought a product that claimed it could boost your energy level because it has added vitamins? High levels of homocysteine in the blood increases the risk for heart disease. Perturbations in myocardial energy metabolism play a causative role in cardiac pathogenesis. So where does the idea that vitamins give you energy come from? Antioxid Redox Signal. An interesting interplay between mitochondrial metabolism and mTOR complex activity has been gradually unraveled in the past decade. A red box indicates a section of the micrograph that is enlarged in the schematic diagram to the right. |
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Energy Metabolism: Carbohydrate, Protein and LipidsNutrient utilization in energy metabolism -
Coenzymes and cofactors are essential in catabolic pathways i. breaking down substances and play a role in many anabolic pathways i. building substances. Table 9. Nutrients Involved in Energy Metabolism. B Vitamins. Role in Energy Metabolism. Thiamin B 1. Assists in glucose metabolism and RNA, DNA, and ATP synthesis.
Riboflavin B 2. Assists in carbohydrate and fat metabolism. Niacin B 3. Assists in glucose, fat, and protein metabolism. Pantothenic Acid B 5. Assists in glucose, fat, and protein metabolism, cholesterol and neurotransmitter synthesis.
Assists in the breakdown of glycogen and synthesis of amino acids, neurotransmitters, and hemoglobin. Biotin B 7. Assists in amino acid synthesis and glucose, fat, and protein metabolism,. Folate B 9.
Assists in the synthesis of amino acids, RNA, DNA, and red blood cells. Protects nerve cells and assists in fat and protein catabolism, folate function, and red blood cell synthesis. Assists in metabolism, growth, development, and synthesis of thyroid hormone. Assists in carbohydrate and cholesterol metabolism, bone formation, and the synthesis of urea.
A component in sulfur-containing amino acids necessary in certain enzymes; a component in thiamin and biotin. Assists in carbohydrate, lipid, and protein metabolism, DNA and RNA synthesis. Assists in metabolism of sulfur-containing amino acids and synthesis of DNA and RNA.
Vitamins and minerals involved in energy metabolism and the role they each play. Because B vitamins play so many important roles in energy metabolism, it is common to see marketing claims that B vitamins boost energy and performance. This is a myth that is not backed by science.
As discussed, B vitamins are needed to support energy metabolism and growth, but taking in more than required does not supply you with more energy.
A great analogy of this phenomenon is the gas in your car. Does it drive faster with a half-tank of gas or a full one? It does not matter; the car drives just as fast as long as it has gas.
Similarly, depletion of B vitamins will cause problems in energy metabolism, but having more than is required to run metabolism does not speed it up.
And because B vitamins are water-soluble, they are not stored in the body and any excess will be excreted from the body, essentially flushing out the added expense of the supplements.
The B vitamins important for energy metabolism are naturally present in numerous foods, and many other foods are enriched with them; therefore, B vitamin deficiencies are rare.
Similarly, most of the minerals involved in energy metabolism and listed above are trace minerals that are not frequently deficient in the diet. However, when a deficiency of one of these vitamins or minerals does occur, symptoms can be seen throughout the body because of their relationship to energy metabolism, which happens in all cells of the body.
A lack of these vitamins and minerals typically impairs blood health and the conversion of macronutrients into usable energy i. Deficiency can also lead to an increase in susceptibility to infections, tiredness, lack of energy, and a decrease in concentration.
Because of their water-solubility, toxicities of most of these nutrients are also uncommon, as excess intake is often excreted from the body. Large quantities, particularly through supplements, can lead to adverse side effects or cause interactions with medications.
For example, too much niacin can cause flushing of the skin or dangerous drops in blood pressure, and a high intake of B 6 can lead to neuropathy. When taking vitamin or mineral supplements, always pay attention to the recommended dietary allowance and avoid exceeding the tolerable upper intake level UL.
Folate, or vitamin B 9 , is a required coenzyme for the synthesis of several amino acids and for making RNA and DNA. Therefore, rapidly dividing cells are most affected by folate deficiency.
Red blood cells, white blood cells, and platelets are continuously being synthesized in the bone marrow from dividing stem cells. When folate is deficient, cells cannot divide normally.
A consequence of folate deficiency is macrocytic anemia. Macrocytic anemia is characterized by larger and fewer red blood cells that are less efficient at carrying oxygen to cells.
It is caused by red blood cells being unable to produce DNA and RNA fast enough—cells grow but do not divide, making them large in size.
Folate is especially essential for the growth and specialization of cells of the central nervous system. Children whose mothers were folate-deficient during pregnancy have a higher risk of neural tube birth defects.
Folate deficiency is causally linked to the development of spina bifida , a neural tube defect that occurs in a developing fetus when the spine does not completely enclose the spinal cord.
Spina bifida can lead to many physical and mental disabilities Figure 9. In , the U. Food and Drug Administration FDA began requiring manufacturers to fortify enriched breads, cereals, flours, and cornmeal with folic acid a synthetic form of folate to increase the consumption of folate in the American diet and reduce the risk of neural tube defects.
Observational studies show that the prevalence of neural tube defects was decreased after the fortification of enriched cereal and grain products with folate compared to before these products were fortified.
Spina bifida left is a neural tube defect that can have serious health consequences. The prevalence of cases of spina bifida has decreased significantly with the fortification of cereal and grain products in the United States beginning in Additionally, results of clinical trials have demonstrated that neural tube defects are significantly decreased in the offspring of mothers who began taking folic acid supplements one month prior to becoming pregnant and throughout pregnancy.
In response to the scientific evidence, the Food and Nutrition Board of the Institute of Medicine IOM raised the RDA for folate to micrograms per day for pregnant women. Folate is found naturally in a wide variety of foods, including vegetables particularly dark leafy greens , fruits, nuts, beans, legumes, meat, poultry, eggs, and grains.
As mentioned previously, folic acid the synthetic form of folate is also found in enriched foods such as grains.
Dietary sources of folate. Examples of good sources pictured include spinach, black-eyed peas, fortified cereal, rice, and bread and asparagus. Source: NIH Office of Dietary Supplements.
Folate deficiency is typically due to an inadequate dietary intake; however, smoking and heavy, chronic alcohol intake can also decrease absorption, leading to a folate deficiency.
Other symptoms of folate deficiency can include mouth sores, gastrointestinal distress, and changes in the skin, hair and nails. Women with insufficient folate intakes are at increased risk of giving birth to infants with neural tube defects and low intake during pregnancy has been associated with preterm delivery, low birth weight, and fetal growth retardation.
Toxicity of folate is not typically seen due to an excess consumption from foods. However, there is concern regarding a high intake of folic acid from supplements because it could mask a deficiency in vitamin B Because folate and vitamin B 12 deficiencies are manifested by similar anemias, if a person with vitamin B 12 deficiency is taking a high dose of folic acid, the macrocytic anemia would be corrected while the underlying B 12 deficiency went undetected, which could result in significant neurological damage.
Thus, a tolerable upper intake level UL has been established for folate to prevent irreversible neurological damage due to high folic acid intake masking a B 12 deficiency. Acetyl-CoA, a two-carbon molecule common to glucose, lipid, and protein metabolism enters the second stage of energy metabolism, the citric acid cycle.
This is an irreversible process. The breakdown of fatty acids begins with the catabolic pathway, known as β-oxidation, which takes place in the mitochondria. In this catabolic pathway, four enzymatic steps sequentially remove two-carbon molecules from long chains of fatty acids, yielding acetyl-CoA molecules.
In the case of amino acids, once the nitrogen is removed deamination from the amino acid the remaining carbon skeleton can be enzymatically converted into acetyl-CoA or some other intermediate of the citric acid cycle. In the citric acid, cycle acetyl-CoA is joined to a four-carbon molecule.
In this multistep pathway, two carbons are lost as two molecules of carbon dioxide are formed. The energy obtained from the breaking of chemical bonds in the citric acid cycle is transformed into two more ATP molecules or equivalents thereof and high energy electrons that are carried by the molecules, nicotinamide adenine dinucleotide NADH and flavin adenine dinucleotide FADH 2.
NADH and FADH 2 carry the electrons hydrogen to the inner membrane of the mitochondria where the third stage of energy synthesis takes place, in what is called the electron transport chain.
In this metabolic pathway, a sequential transfer of electrons between multiple proteins occurs and ATP is synthesized. Water is also formed. The entire process of nutrient catabolism is chemically similar to burning, as carbon molecules are burnt producing carbon dioxide, water, and heat.
However, the many chemical reactions in nutrient catabolism slow the breakdown of carbon molecules so that much of the energy can be captured and not transformed into heat and light. Complete nutrient catabolism is between 30 and 40 percent efficient, and some of the energy is therefore released as heat.
Heat is a vital product of nutrient catabolism and is involved in maintaining body temperature. If cells were too efficient at transforming nutrient energy into ATP, humans would not last to the next meal, as they would die of hypothermia.
We measure energy in calories which are the amount of energy released to raise one gram of water one degree Celsius. Food calories are measured in kcal or Calories or calories. Some amino acids have the nitrogen removed then enter the citric acid cycle for energy production.
The nitrogen is incorporated into urea and then removed in the urine. The carbon skeleton is converted to pyruvate or enters the citric acid cycle directly.
These amino acids are called gluconeogenic because they can be used to make glucose. Amino acids that are deaminated and become acetyl-CoA are called ketogenic amino acids and can never become glucose.
Fatty acids can never be made into glucose but are a high source of energy. These are broken down into two carbon units by a process called beta-oxidation enter the citric acid cycle as acetyl-CoA. In the presence of glucose, these two carbon units enter the citric acid cycle and burned to make energy ATP and produce the by-product CO 2.
If glucose is low, ketones are formed. Ketone bodies can be burned to produce energy. The brain can use ketones. The energy released by catabolic pathways powers anabolic pathways in the building of macromolecules such as the proteins RNA and DNA, and even entire new cells and tissues.
Anabolic pathways are required to build new tissue, such as muscle, after prolonged exercise or the remodeling of bone tissue, a process involving both catabolic and anabolic pathways. Anabolic pathways also build energy-storage molecules, such as glycogen and triglycerides. Intermediates in the catabolic pathways of energy metabolism are sometimes diverted from ATP production and used as building blocks instead.
This happens when a cell is in positive energy balance. For example, the citric-acid-cycle intermediate, α-ketoglutarate can be anabolically processed to the amino acids glutamate or glutamine if they are required.
Recall that the human body is capable of synthesizing eleven of the twenty amino acids that make up proteins. The metabolic pathways of amino acid synthesis are all inhibited by the specific amino acid that is the end-product of a given pathway.
Thus, if a cell has enough glutamine it turns off its synthesis. Anabolic pathways are regulated by their end-products, but even more so by the energy state of the cell.
When there is ample energy, bigger molecules, such as protein, RNA, and DNA, will be built as needed. Alternatively, when energy is insufficient, proteins and other molecules will be destroyed and catabolized to release energy.
A dramatic example of this is seen in children with Marasmus. These children have severely compromised bodily functions, often culminating in death by infection. Children with Marasmus are starving for calories and protein, which are required to make energy and build macromolecules.
In a much less severe example, a person is also in negative energy balance between meals. During this time, blood glucose levels start to drop. In order to restore blood glucose levels to their normal range, the anabolic pathway, called gluconeogenesis, is stimulated.
The liver exports the synthesized glucose into the blood for other tissues to use. Glucose can be stored only in muscle and liver tissues. In these tissues, it is stored as glycogen, a highly branched macromolecule consisting of thousands of glucose monomers held together by chemical bonds.
The glucose monomers are joined together by an anabolic pathway called glycogenesis. For each molecule of glucose stored, one molecule of ATP is used.
Therefore, it costs energy to store energy. Glycogen levels do not take long to reach their physiological limit and when this happens excess glucose will be converted to fat. A cell in positive energy balance detects a high concentration of ATP as well as acetyl-CoA produced by catabolic pathways.
In response, catabolism is shut off and the synthesis of triglycerides, which occurs by an anabolic pathway called lipogenesis, is turned on. The newly made triglycerides are transported to fat-storing cells called adipocytes.
Nutrient overload occurs worldwide as a consequence of the modern ih pattern and the physical inactivity that sometimes accompanies it. Cells initiate multiple protective utilizatlon to Nutriennt to Nutrient utilization in energy metabolism intracellular metabolites DEXA scan vs traditional X-rays for bone evaluation restore metabolic homeostasis, mftabolism irreversible injury to Firming and lifting cells Nufrient occur in the meetabolism of prolonged nutrient overload. Many Potassium supplements have Nutriennt the understanding of the different detrimental effects of nutrient overload; however, few reports have made connections and given the full picture of the impact of nutrient overload on cellular metabolism. In this review, detailed changes in metabolic and energy homeostasis caused by chronic nutrient overload, as well as their associations with the development of metabolic disorders, are discussed. Overnutrition-induced changes in key organelles and sensors rewire cellular bioenergetic pathways and facilitate the shift of the metabolic state toward biosynthesis, thereby leading to the onset of various metabolic disorders, which are essentially the downstream manifestations of a misbalanced metabolic equilibrium. Based on these mechanisms, potential therapeutic targets for metabolic disorders and new research directions are proposed.
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