metabolic system

Define PKU and how it affects metabolism.

A birth defect that causes an amino acid called phenylalanine to build up in the body.

Explain the importance of cholesterol. .

A discussion of nutrition would be incomplete without mention of the steroid cholesterol. Although cholesterol isn't oxidized as a fuel source, it is important in many of the body's anabolic reactions. As you've read throughout this book, cholesterol is modified to produce a variety of substances, including steroid hormones, vitamin D, and bile salts. In addition, cholesterol is an important structural molecule, as it forms part of plasma membranes.

Calculate BMI. Be able to determine the obesity status given a BMI

An individual's weight in and of itself often doesn't give a clinician enough information, as it varies with several factors, particularly an individual's height. For this reason, many healthcare providers and nutritionists instead calculate a number called the body mass index (BMI), which is obtained with the following equation: BMI=Weight (kg)[Height (m)]2BMI=Weight (kg)[Height (m)]2 As you can see from the equation, BMI takes height into account, and so provides a somewhat more reliable index from which to determine relative body mass. From the BMI, a person can be classified as underweight (BMI < 18.5), normal weight (BMI = 18.5−24.9), overweight (BMI = 25.0−29.9), or obese (BMI ≥ 30.0).

Write the summary reaction for oxidative glucose metabolism.

C6H12O6+6O2→6 H2O+6 C2O+38 ATP+heatC6H12O6+6O2→6 H2O+6 C2O+38 ATP+heat

Explain how cholesterol is processed and transported

Cholesterol is found in the diet in animal-based foods such as meats and dairy products. The body generally has little to no need for dietary cholesterol, as it can be synthesized by the liver. Normally, about 15% of the body's cholesterol comes from the diet; the remaining 85% is made in the liver. Recall that cholesterol is packaged in the small intestine with other lipids as micelles, which escort these nonpolar compounds to the enterocyte membrane, where they are absorbed into the cell. In the enterocytes, cholesterol and other lipids are packaged into chylomicrons, which are then absorbed into a lacteal and eventually delivered to the liver for processing (see Chapter 22). The liver also plays a key role in distributing cholesterol throughout the body. As we noted previously, cholesterol is a steroid and so is nonpolar and hydrophobic. For this reason, it must be packaged along with other lipids onto carrier proteins called lipoproteins for safe transport through the blood. The structure of a typical lipoprotein and its lipids is shown here:

Explain the role of the liver in metabolism.

During extreme caloric restriction, carbohydrate restriction, or full starvation, the liver begins to rapidly oxidize fatty acids and produce large amounts of ketone bodies. However, the cells are able to use only so many of these ketone bodies because the lack of glucose decreases the amounts of oxaloacetate and other components of the citric acid cycle that are derived from glucose breakdown. As a result, ketone bodies accumulate in the blood, leading to a condition called ketosis (kee-TOH-sis). The body excretes many excess ketone bodies in the urine; however, if ketosis is severe, they accumulate and lower the pH of the blood, producing the dangerous condition ketoacidosis. Recall that this condition may also result from uncontrolled diabetes mellitus, in which the cells are unable to take in glucose and thus must rely on fatty acid oxidation for survival (see Chapter 16).

Define and explain the cause of hypercholesterolemia.

However, if intake exceeds about 15% of the total requirement for cholesterol, then the total blood concentration of cholesterol is likely to increase, a condition called hypercholesterolemia (hy′-per-koh-less′-ter-ah-LEE-me-uh). Individuals with hypercholesterolemia typically have high total cholesterol and LDL levels, along with a low HDL level. Another factor that can increase cholesterol is increased production by the liver. This can also be related to the diet—a high intake of saturated fats increases cholesterol production while inhibiting its excretion. Trans fats have a similar effect, increasing the production of LDLs and decreasing that of HDLs. Hypercholesterolemia can also be due to genetic defects that cause the liver to produce excess cholesterol

Explain the mechanisms that regulate feeding.

Long-term regulation of feeding is primarily hormonal. The satiety center is stimulated by the hormone leptin, which is produced by adipocytes. Leptin inhibits neurons in the hunger center while stimulating those in the satiety center to produce neurotransmitters such as pre-opiomelanocortin. These neurotransmitters have an overall anorexigenic effect, depressing the appetite. The hunger center is stimulated by a decreasing level of leptin secretion and a rising level of secretion of the hormone ghrelin (GRAY-lin) from the cells of the stomach mucosa. Ghrelin stimulates neurons in the hunger center to produce neurotransmitters such as neuropeptide Y and orexins, both of which are orexigenic, promoting hunger.

Define metabolism, catabolism and anabolism.

Metabolism: total of all the chemical reactions in a cell Metabolism is defined as the sum of the body's chemical reactions. Metabolism includes four basic processes: (1) harnessing the energy in the chemical bonds of nutrients obtained from the diet that may be used to make adenosine triphosphate, or ATP; (2) converting one type of chemical into another for the cell's synthesis reactions; (3) carrying out synthesis reactions and assembling macromolecules such as proteins, polysaccharides, nucleic acids, and lipids; and (4) breaking down macromolecules into their monomers or other smaller compounds. Catabolism: process where large, complex molecules are broken down into smaller ones releasing energy The first is a series of reactions collectively known as catabolism (kah-TAEH-bohl-izm; cata- = "down"). Recall that a catabolic reaction is one in which a substance is broken down into smaller parts (see Chapter 2). Although certain reactions in a catabolic pathway may require the input of energy, the process as a whole releases energy that the cell can harness to drive reactions such as ATP production. glucose, fatty acid and amino acids are broken down via catabolism Anabolism: Synthesis of complex macromolecules from smaller building blocks The second phase of metabolism is known as anabolism (aeh-NAEH-bohl-izm; ana- = "up"). As we discussed previously, an anabolic reaction is one in which smaller compounds are combined to make a larger compound (see Chapter 2). Via anabolism, cells build proteins, nucleic acids, carbohydrates, lipids, and all other macromolecules. Anabolic reactions require energy, and anabolism is driven by the energy liberated from catabolism.

Explain fatty acid anabolism.

The synthesis of fatty acids somewhat resembles β-oxidation in reverse; however, they are still separate pathways that require different enzymes and take place in different locations. Fatty acid synthesis occurs by a process called Lipogenesis (ly′-poh-JEN-eh-sis). Lipogenesis takes place in the cytosol. It involves a large enzyme complex called fatty acid synthase, which catalyzes reactions that progressively lengthen the fatty acid chain by two-carbon units. Most of the fatty acids are attached to glycerol and assembled into triglycerides in the endoplasmic reticulum, after which they are stored in adipocytes.

Define metabolic rate and explain how it is regulated.

The total amount of energy expended by the body to power all its processes is called the metabolic rate. Indeed, metabolism is the primary source of body heat, and metabolic processes are an important part of body temperature regulation, or thermoregulation. Stimulus: Body temperature increases above the normal range. Receptor: Thermoreceptors in the skin and the hypothalamus detect the increased body temperature. Many factors can cause body temperature to rise, including stimulation from the sympathetic nervous system, muscle activity, inflammation, and elevated environmental temperature. Temperature-sensitive thermoreceptors are located throughout the body, particularly in the skin and hypothalamus. These receptors detect the current higher temperature, and then send this information to the hypothalamus. Control center: The heat-loss center in the hypothalamus is activated. The hypothalamic thermoregulatory centers, which act as the control center, compare the current temperature with the temperature set point, and find that they are too far apart. This stimulates a hypothalamic nucleus, the heat-loss center, which sends signals to effectors. Effector/response: Blood vessels in the skin dilate, and sweat glands release sweat. Several effectors then produce responses that reduce body temperature. One response is dilation of blood vessels in the skin. Recall that this increases blood flow through the skin and promotes heat loss (see Chapter 5). Another response is increased sweating from the skin's sweat glands. However, sweating only produces significant heat loss if the humidity in the air isn't too high. In high-humidity conditions, the rate of evaporation decreases, which is why humid heat feels hotter than "dry heat." Homeostatic range and negative feedback: As body temperature returns to the homeostatic range, the hypothalamus stops stimulating the effectors, which decreases the responses. When the thermoreceptors detect a return to the homeostatic body temperature range, they stop stimulating the hypothalamus through negative feedback, which in turn ends stimulation of the effector organs, decreasing or shutting down the responses.

Explain glucose anabolism.

There are two anabolic processes involving glucose. The first is glycogenesis, which is the storage of excess glucose taken in from the diet. The second is gluconeogenesis, which is the formation of new glucose from noncarbohydrate precursors. When the glucose concentration in the bloodstream decreases, hormones such as glucagon and epinephrine trigger the breakdown of glycogen, a catabolic process called glycogenolysis (gly′-koh-jen-AWL-ih-sis). This releases glucose molecules into the bloodstream, which raises the concentration of blood glucose. Glycogen stores do not last long, however, and are depleted after about half a day (much faster when a person is engaged in strenuous activity). When glycogen supplies are exhausted, the body needs to turn to alternative methods to keep up with the needs of cells that require glucose. The body's main method of doing so is gluconeogenesis (gloo′-koh-nee-oh-JEN-eh-sis; literally, "making new glucose"), or synthesis of glucose from noncarbohydrate precursors (Figure 23.13). During gluconeogenesis, the hepatocytes and certain cells of the kidney perform reactions that convert three- and four-carbon compounds into glucose. Sources of these compounds include the following: glycerol from triglyceride catabolism, pyruvate and lactate from glycolysis, intermediate compounds from the citric acid cycle, and certain amino acids called glucogenic amino acids.

Explain amino acid anabolism.

We have already discussed protein synthesis and seen how strings of amino acids are joined by peptide bonds in a sequence determined by the DNA of one gene (see Chapter 3). The body can synthesize 11 of the 20 amino acids found in human proteins. These amino acids are primarily synthesized by reactions that add an amino group to carbon skeletons such as α-ketoglutarate, pyruvate, and oxaloacetate. The remaining amino acids (known as essential amino acids) must be supplied by the diet, which we discuss in Module 23.7. Unlike carbohydrates and lipids, amino acids are not stored to any significant extent in the body's proteins. A cell needs to synthesize only so many proteins; once this limit has been reached, any excess amino acids obtained by the diet are converted to other compounds for storage. All nucleated cells produce proteins, although some cells, such as skeletal muscle cells, undergo higher than average rates of protein synthesis due to the composition of their cells. Some amino acids are converted to glucose by gluconeogenesis and either used immediately or incorporated into glycogen. Others are converted to fatty acids and stored in the body's adipose tissue. You may have heard the claim by individuals promoting high-protein diets that proteins cannot be stored as fat. This is, of course, untrue.

Explain fatty acid catabolism.

When fatty acids are released from adipocytes, they are transported through the bloodstream bound to protein carriers and delivered to tissues that can oxidize fatty acids, such as skeletal muscle and the heart. Inside these cells, the fatty acids enter the mitochondrial matrix. As shown in Figure 23.9, each fatty acid ❶❶ is bound to coenzyme A. From here, fatty acid oxidation proceeds by a series of reactions known as β-oxidation. ❷❷ In the reactions of β-oxidation, the fatty acid chain is oxidized by NAD1 and FAD, and two carbons are removed. ❸❸ The products of this reaction are FADH2, NADH, acetyl-CoA, and a fatty acid with two fewer carbons. FADH2 and NADH go to the electron transport chain, and acetyl-CoA goes to the citric acid cycle. ❹❹ Another CoA binds to the shorter fatty acid, and rounds of β-oxidation are repeated until the entire fatty acid has been converted into two-carbon acetyl-CoA subunits—fatty acids that have six carbons yield three acetyl-CoA molecules, fatty acids with four carbons yield two acetyl-CoA molecules, and so forth. The released acetyl-CoA molecules are then fed into the citric acid cycle and further oxidized by the same pathway that we discussed with glucose catabolism. The NADH and FADH2 from β-oxidation and from the citric acid cycle donate their electrons to the electron transport chain, and ATP is generated.

Define Diabetes Mellitus, type I and II and explain the impact on metabolism.

a disorder characterized by defects in the production of or response to the pancreatic hormone insulin. Insulin causes most cells to take in glucose; in its absence, these cells are unable to bring glucose into their cytosol. This leads to a high level of circulating blood glucose, or hyperglycemia, which results in excessive amounts of glucose in the filtrate and ultimately in the urine.

Explain the role of insulin and glucagon in the absorptive and postabsorptive states of metabolism.

abdorptive state: As we discussed in the endocrine chapter, insulin release is triggered by a rising level of glucose in the blood (see Chapter 16). This hormone targets most body cells and stimulates the uptake of glucose by cells, lowering the concentration of glucose in the blood. It also acts on the liver and several other tissues, initiating the anabolic processes we just covered. In the absorptive state, then, cells take in fuels and, under the control of insulin, use or store them. postobsorptive state: Several hormones help the body adapt during the postabsorptive state. One of these is the pancreatic hormone glucagon, which is released in response to a decreasing blood glucose concentration. Its main target tissue is the liver, where it triggers glycogenolysis and gluconeogenesis (see Chapter 16 for a review of how blood glucose homeostasis is maintained). Other hormones that play a role during the postabsorptive state include the catecholamines epinephrine and norepinephrine, which stimulate lipolysis in adipose tissue and glycogenolysis in skeletal muscle. In addition, cortisol stimulates gluconeogenesis and processes that release glucogenic precursors into the blood.

Distinguish between the metabolic states of the absorptive state and postabsorptive state.

absorptive state: The absorptive state occurs right after feeding, from the time that ingested nutrients enter the bloodstream to as many as 4 hours after feeding (Figure 23.15a). It is called the absorptive state because it is the period during which the nutrients from food are absorbed from the small intestine into the blood. During the absorptive state, the following processes occur: Oxidation of nutrients, primarily glucose, provides fuel to cells. Glucose is the main fuel used by cells. Glucose is usually readily available during the absorptive state, and it enters cells rapidly to be oxidized as the main fuel. A small fraction of the absorbed fatty acids and glycerol are oxidized by different tissues for fuel; similarly, a small percentage of amino acids are deaminated and oxidized for fuel. Synthesis of amino acids into proteins provides structural materials to cells. Many ingested amino acids enter cells, where they are used for protein synthesis. Glycogenesis stores excess glucose in skeletal muscle cells and hepatocytes. Glucose that is not oxidized for energy is stored as glycogen. Lipogenesis stores triglycerides in adipocytes and hepatocytes. The majority of triglycerides are simply stored in adipose tissue or the liver. Excess glucose is also converted into fatty acids or glycerol and stored as fat, and some amino acids are converted to fatty acids and stored as well. postabsorptive state:Once nutrient absorption is complete, the body enters the postabsorptive state (Figure 23.15b). The postabsorptive state generally begins about 4 hours after feeding, although this varies depending on the amount and types of nutrients ingested. For most individuals, the body is generally in the postabsorptive state in late morning, late afternoon, and most of the night. During this state, the body slows and then ceases anabolic processes such as glycogenesis, lipogenesis, and protein synthesis because the steady supply of nutrients ends during the postabsorptive period. In their place, the following processes occur: Breakdown of proteins in muscle cells releases glucogenic amino acids into the blood. If necessary, muscle proteins are broken down to release glucogenic amino acids that can be taken up by cells and converted to glucose. See A&P in the Real World: Fasting and Protein Wasting to find out more about protein breakdown during the postabsorptive state. Ketogenesis in hepatocytes converts fatty acids to ketone bodies and releases them into the blood. Many of the fatty acids oxidized in the liver are converted to ketone bodies, which are released into the blood. The advantage to releasing ketones is that cells of the nervous system are able to oxidize them for fuel when glucose is unavailable, whereas these cells are not capable of oxidizing fatty acids to any significant extent. Gluconeogenesis and glycogenolysis in hepatocytes release glucose into the blood. The concentration of blood glucose begins to decline during the postabsorptive state. To ensure that cells requiring glucose, such as those of the brain, are not deprived of their primary fuel, gluconeogenesis and glycogenolysis in hepatocytes begin to raise the concentration of blood glucose. Lipolysis in adipocytes releases fatty acids into the blood. The limited concentration of blood glucose means that cells will need another source of fuel, namely, the fuel in fats. For this reason, lipolysis begins and fatty acids are released into the bloodstream from adipocytes. Oxidation of nutrients such as fatty acids provides most cells with fuel. When fatty acids are delivered to cells, most cells preferentially begin to catabolize them in order to conserve glucose for cells of the nervous system, a phenomenon called glucose sparing. Cells outside the nervous system can also use ketone bodies and amino acids for fuel.

Explain the difference between exergonic and endogonic reactions.

exergonic: Reactions that release energy are known as exergonic reactions. The products of these reactions have less energy than their reactants, and the remaining energy is released during the reaction. To understand why energy is released, we need to discuss the law of conservation of energy, which states that energy cannot be created or destroyed; it can only change forms. This means that the energy present before the reaction must equal the energy present after the reaction. Since the products of an exergonic reaction have less energy than the reactants, energy must be released so that the total energy is the same before and after the reaction. Most catabolic reactions are exergonic. endogonic: An endergonic reaction is one that requires the input of energy to proceed. This is because the products of the reaction have more energy than the reactants. To be in line with the law of conservation of energy, energy must be added to the reactant side so that the energy on both sides of the equation is equal. Anabolic reactions tend to be endergonic.

Identify the 3 main nutrient monomers used to make ATP.

glucose, amino acids, and fatty acids broken down via catabolism and provide ATP such reactions are called oxidation-reduction reactions (see Chapter 2). The substance that loses electrons is oxidized, and the substance that gains electrons is reduced The energy released from glucose catabolism can be used to produce ATP in two ways: Substrate-level phosphorylation. Substrate-level phosphorylation involves the transfer of a phosphate group directly from a phosphate-containing chemical (the substrate) to ADP, to form ATP. A simple example is one that you saw in the muscle tissue chapter—that of creatine phosphate (see Chapter 10). Recall that creatine phosphate donates its phosphate group to ADP, producing ATP: Oxidative phosphorylation. During oxidative phosphorylation, the energy from the flow of electrons is harnessed in a process that generates ATP (recall our earlier battery example). Oxidative phosphorylation produces a great deal more ATP for the cell than does substrate-level phosphorylation. Note that oxidative phosphorylation occurs in the mitochondria as part of the ETC. The reactions of glucose catabolism in glycolysis and the citric acid cycle reduce electron carriers, which are then fed into the ETC and participate in oxidative phosphorylation.

summarize glucose catabolism and it's three stages: glycolysis, citric acid cycle and ETC.

glycolysis: a series of reactions in the cytosol that split glucose ❶❶ First phosphorylation: Glucose is phosphorylated by ATP, yielding glucose-6-phosphate and ADP. The six-carbon glucose is phosphorylated in the first reaction of this phase, "spending" an ATP molecule. As you can see in Figure 23.4, a phosphate group is removed from ATP and attached to glucose, producing glucose-6-phosphate (and ADP). This reaction is critical to glucose catabolism because it effectively traps the glucose in the cytosol and prevents it from leaving the cell. ❷❷ Second phosphorylation: The carbon atoms in glucose- 6-phosphate are rearranged, which is then phosphorylated by another ATP, yielding fructose-1,6-bisphosphate and ADP. In reactions two and three, the carbons of glucose- 6-phosphate are rearranged and a second phosphorylation reaction takes place, which consumes another molecule of ATP. This reaction yields the six-carbon sugar fructose-1,6-bisphosphate (and ADP). ❸❸ Cleavage: The six-carbon fructose-1,6-bisphosphate is split, and two three-carbon compounds are formed. During reactions four and five, the six-carbon sugar fructose is split, yielding two three-carbon compounds: glyceraldehyde-3-phosphate and dihydroxyacetone-3-phosphate. The latter compound undergoes another reaction and converts into a molecule of glyceraldehyde-3-phosphate. ❹❹ Oxidation: Glyceraldehyde-3-phosphate is phosphorylated and oxidized by NAD+ to yield NADH and 1,3-bisphosphoglycerate, which then donates a Pi to ADP, yielding ATP. During reaction six, each of the glyceraldehyde-3-phosphates is given a second phosphate group, after which they are oxidized and their electrons are transferred to NAD+. This produces two molecules of the reduced NADH. In reaction seven, one of the phosphate groups of each 1,3-bisphosphoglycerate is transferred to ADP, yielding two molecules of 3-phosphoglycerate and two molecules of ATP by substrate-level phosphorylation. ❺❺ ATP synthesis: The carbon atoms in the two molecules of 3-phosphoglycerate are rearranged to form phosphoenolpyruvate, which donates a Pi to ADP, yielding ATP and pyruvate. After rearranging the carbon atoms in the two molecules of 3-phosphoglycerate to produce two molecules of phosphoenolpyruvate in reactions eight and nine, the remaining phosphate groups on the phosphoenolpyruvate are transferred to ADP via substrate-level phosphorylation in reaction ten. This produces two ATP and two three-carbon pyruvates. spent two ATP, synthesized four ATP, synthesized two NADH, and split glucose into two three-carbon pyruvates. citric acid cycle: a series of reactions in the mitochondrial matrix that breaks down glucose further ❶❶ Citrate synthesis: Acetyl-CoA combines with oxaloacetate to form citrate and CoA. In reaction one, the acetyl-CoA "donates" its two-carbon acetyl group to a four-carbon compound called oxaloacetate, forming the six-carbon compound citrate (for which the cycle was named) and leaving CoA. Acetyl-CoA in this reaction acts a little like an ATP—acetyl-CoA has a great deal of potential energy, as its bond is unstable. When the bond is broken, the resulting CoA and acetate have less energy, and the released energy helps to unite acetate and oxaloacetate. ❷❷ First oxidation: Citrate is rearranged, then oxidized by NAD+, generating CO2 and NADH. In reactions two through four, the atoms in the six-carbon citrate are rearranged and oxidized, eventually forming the four-carbon compound succinyl-CoA (containing the same CoA that was part of acetyl-CoA). The two removed carbons are lost as two molecules of carbon dioxide, and the removed electrons are accepted by two NAD+, producing two NADH. ❸❸ ATP synthesis: Succinyl-CoA is converted to succinate and CoA, while forming ATP. In the fifth reaction, the CoA is removed from succinyl-CoA. In this reaction we again see an unstable bond between CoA and its partner. The energy released when CoA is removed from succinate is used to drive the formation of ATP by substrate-level phosphorylation (sometimes the very similar compound GTP, or guanosine triphosphate, is produced instead). ❹❹ Second oxidation: Succinate is oxidized by FAD and NAD+, generating FADH2 and NADH, and is converted back to oxaloacetate. Reactions six through eight of the citric acid cycle see succinate oxidized to other four-carbon compounds until it is converted back into oxaloacetate. As the compounds are oxidized, their electrons are transferred to FAD and NAD+, generating one each of FADH2 and NADH. ten NADH (two from glycolysis, two from pyruvate oxidation, and six from the citric acid cycle), two FADH2, and four ATP (two from glycolysis and two from the citric acid cycle). ETC: to use the energy liberated by glucose catabolism, a series of oxidation-reduction reactions known as oxidative phosphorylation takes place in the inner mitochondrial membrane. This series of reactions involves the transfer of electrons between electron carriers ❸❸ Electron flow through complexes III and IV continues to drive the pumping of hydrogen ions into the intermembrane space. As you can see in the figure, electrons continue to be transferred, first to complex III and then complex IV. As they gain electrons, the electron carriers in these complexes are reduced and hydrogen ions continue to be pumped into the intermembrane space. ❹❹ Complex IV transfers the electrons to oxygen—the final electron acceptor—to form H2O. Complex IV transfers electrons to the final electron acceptor, oxygen. In this reaction, oxygen is reduced and accepts the electrons while combining with two hydrogen ions. The end result of this reduction is the following reaction: 2H++2e−+12O2→H2O ❺❺ ADP and Pi bind to ATP synthase and form ATP. ATP synthesis begins when ADP and Pi bind to the enzyme portion of ATP synthase, uniting them and forming ATP. Since this enzyme is most stable when bound to ATP, it holds on to it tightly. ATP cannot be used by the cell until it is released from this enzyme. ❻❻ Hydrogen ions flow through the ion channel, causing the rotor to spin and making the enzyme release the ATP. Now the energy from glucose catabolism finally comes into play. The electrochemical gradient causes hydrogen ions to flow into the matrix through the ion channel of ATP synthase, which generates a force called the proton motive force. The electrochemical energy of the proton motive force causes a portion of the enzyme ​called ​the rotor to start spinning just like a turbine. The spinning rotor causes the enzyme to release its ATP. This process is repeated, with a new ADP and Pi binding and joining into ATP, and the spinning rotor causing ATP to be released. So, the majority of the energy harnessed from the oxidation of glucose is used to create a hydrogen ion gradient. The energy of the hydrogen ion gradient then causes ATP synthase to release the newly formed ATP for the cell to use.

Explain the molecule ATP and its importance.

❶❶ Energy is released from exergonic catabolic reactions. Nutrients such as glucose, fatty acids, and amino acids are broken down via catabolic reactions that eventually release energy. ❷❷ This energy is used to fuel the endergonic anabolic reaction of ATP synthesis. Synthesis of compounds such as ATP is an endergonic process. The energy for this reaction comes from the exergonic reactions in the previous step. ❸❸ ATP is broken down in an exergonic catabolic reaction. In another exergonic catabolic reaction, the third phosphate group from ATP is removed and energy is released. ❹❹ The energy from ATP breakdown fuels other endergonic anabolic reactions in the cell. ATP breakdown is a highly exergonic process that can fuel a number of endergonic reactions in the cell. The cell can harness energy from ATP by removing its third phosphate group in a hydrolysis reaction. In this reaction, the bond between the second and third phosphate groups is broken by a water molecule, resulting in free phosphate (Pi) and adenosine diphosphate, or ADP. As we have discussed previously, these reactions are catalyzed by enzymes called ATPases.

Explain amino acid catabolism.

❶❶ In transamination, the amino group is removed from the amino acid and transferred to α-ketoglutarate. The removed amino group is transferred to the five-carbon compound α-ketoglutarate, one of the components of the citric acid cycle. ❷❷ This generates two products: a carbon skeleton and the amino acid glutamate. ❸❸ The carbon skeleton can be converted into a variety of compounds, which can then be oxidized. The carbon skeleton itself may become certain compounds, including pyruvate, acetyl-CoA, other citric acid cycle compounds, and even glucose. These compounds can then be oxidized via the reactions of glycolysis or the citric acid cycle. ❹❹ In the mitochondria of the hepatocyte, glutamate undergoes oxidative deamination, producing NH3 and α-ketoglutarate. Glutamate "carries" the amino group to the mitochondria of the hepatocyte. In the mitochondria, glutamate undergoes a process called oxidative deamination, during which the amino group is removed, forming ammonia (NH3) and re-forming α-ketoglutarate. ❺❺ Some of the amino groups removed as ammonia are used in the synthesis of new amino acids. ❻❻ The remaining ammonia molecules are removed by the urea cycle, which forms urea that is then eliminated by the kidneys in urine. The remaining ammonia must be removed from the body, because it is toxic to cells. This occurs via the Urea cycle (yoo-REE-uh), which takes place in hepatocytes. During the urea cycle, two ammonia groups are combined with carbon dioxide to form the compound urea. Most of the urea resulting from this cycle is then eliminated in the urine by the kidneys.