17.4.6: Claudia's new lipid page - here Feast or Famine ?
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Copied from "Blake, J. S., Munoz, K. D., & Volpe, S. (2019). Nutrition: From Science to You (4th ed.). Pearson." . . . I love the pictures and am wondering if Delmar's graphic champ might be able to reproduce?
How Does Metabolism Change during the Absorptive and Postabsorptive States?
Explain how metabolism changes during the absorptive, postabsorptive, and starvation stages of food intake.
Once food has been digested, the amino acids, monoglycerides, and triglycerides are absorbed and available to be used by the body. We refer to this as the absorptive state, or that period within 4 hours following a meal in which anabolic processes exceed catabolic processes. During the absorptive state, the body uses glucose as the primary source of energy (see the Table Tips, Important Advice for Maintaining Energy Levels). Later, when you need energy during sleep, between meals, or when you’re too busy to eat, your body uses the glucose stored as glycogen, and the fatty acids and glycerol stored in triglycerides, for fuel. This is referred to as the postabsorptive state, or the period of time usually more than 4 hours after eating, such as during the late afternoon or overnight. Hormones regulate both the absorptive and postabsorptive states.
TABLE TIPS
Important Advice for Maintaining Energy Levels
During the Absorptive State, Metabolism Favors Energy Storage
Metabolism adjusts to either provide energy for immediate use or store it for later, depending on your energy needs and intake. In the normal process of eating, if you consume more kilocalories than you require for your immediate energy needs, your metabolism favors anabolic reactions for the sake of storing the excess kilocalories for later use. For instance, if you eat excess protein, the excess is converted to fatty acids and stored as a triglyceride. If you overconsume carbohydrates, the anabolic reactions include converting the excess carbohydrates to glycogen. Once the glycogen stores are full, carbohydrates are converted to fatty acids.
Take a close look at Focus Figure 8.15, which illustrates the catabolic and anabolic pathways of the absorptive state.
FOCUS Figure 8.15 Metabolism during the Absorptive State
Figure 8.15 Full Alternative Text
Carbohydrates Are Stored as Glycogen
Although glucose is essential to red blood cells and neural (nervous system) cells, neither of these cell types can convert glucose to its storage form, glycogen, nor can they convert excess glucose to fat. Only liver and muscle cells can convert excess glucose to glycogen for storage.
Remember that dietary glucose arrives first at the liver from the portal vein. If glucose levels are high, the liver converts glucose to glycogen through glycogenesis or releases the glucose for circulation to other tissues. Enzymes in muscle cells can also convert excess glucose to glycogen. The body has a limited ability to store glycogen, however, and only about 1 percent of body weight is in the form of glycogen.
Liver glycogen plays an important role in maintaining glucose homeostasis. When intake of dietary carbohydrate is low, blood glucose levels drop. The glycogen stored in the liver can be broken down into glucose through glycogenolysis and released into the blood. However, about 12–18 hours after eating, liver glycogen levels are nearly depleted.
Even though muscle cells have a high storage capacity for glycogen, they lack the enzyme that can release glucose into the blood. In essence, glucose is “trapped” in the muscle to be used for energy or stored as glycogen; it is not used to maintain blood glucose levels.
Excess Carbohydrates and Amino Acids Are Stored as Triglycerides
Carbohydrates are first stored as glycogen. After those stores are full and energy needs are met, excess carbohydrates form triglycerides. Once glucose has been oxidized to acetyl CoA, it enters lipogenesis, forming fatty acids that are stored in the adipocytes. This conversion is very costly—almost 25 percent of the kilocalories glucose provides must be used to generate enough ATP to convert the glucose to fatty acids—and inefficient.
The same is true for excess amino acids. Protein is first used for the numerous functions it provides to the body before excess is converted to fatty acids. In this process, amino acids are first deaminated, then the remaining carbons are converted to acetyl CoA and formed into fatty acids. Both ketogenic and glucogenic amino acids can be catabolized and converted to fatty acids through pyruvate and acetyl CoA pathways, but the process is highly inefficient.
Fatty Acids Are Stored as Triglycerides
The body stores excess kilocalories in any form as triglycerides through the process known as lipogenesis, or fatty acid synthesis. Fatty acid synthesis begins with the two-carbon gateway molecule acetyl CoA. This molecule eventually becomes a long-chain fatty acid that attaches to a glycerol backbone and is stored as a triglyceride in fat cells.
The metabolic pathway to store dietary fat requires little energy (only about 5 percent of the stored energy within the fatty acid) and only a few steps; therefore dietary fat is easier to store as body fat than are dietary carbohydrate or protein. Lipogenesis is a separate anabolic pathway that synthesizes fatty acids to be stored and is not just a reversal of the reactions involved in the breakdown of fat. In fact, the two processes take place in different parts of the cell. Fatty acids are synthesized in the cytoplasm rather than in the mitochondria, where fats are oxidized. Lipogenesis also differs from fat oxidation in the way it’s affected by glucagon and insulin. Glucagon stimulates lipolysis, which provides the fatty acids for beta-oxidation. Insulin has the opposite effect: It inhibits the breakdown of fat and promotes fatty acid synthesis.
During the Postabsorptive State, Metabolism Favors Energy Production
Many Americans consume more than enough kilocalories to meet their energy demands, a fact which is reflected in the current obesity crisis. But what happens when the opposite is true? That is, you’re too busy to consume enough food or you choose not to eat? Some people choose not to eat for a period of time, often for spiritual or religious reasons. For example, Muslims fast during the month of Ramadan, there are seven fasting days in the Jewish religion, and some Christians may fast during Lent. Regardless of the reason, when you do not consume enough kilocalories to meet your energy needs, your body enters a postabsorptive state—usually more than 4 hours after eating. The stomach and small intestine are empty and the need for energy is met from stored energy. Focus Figure 8.16 illustrates the metabolic pathways that are active during the postabsorptive state.
Figure 8.16 Full Alternative Text
Stores Are Depleted during Fasting
Whereas glycogen stores supply energy during short periods of fasting, such as overnight or between meals, the body adapts differently if you go more than 18 hours without consuming carbohydrates. Again, the body maintains blood glucose levels initially by tapping into liver glycogen through glycogenolysis. At the same time, an increase in lipolysis provides fatty acids for energy, thus reducing the use of glucose by the cell. Once liver glycogen has been depleted, gluconeogenesis is initiated, using amino acids, glycerol, pyruvate, and lactate to meet the body’s glucose needs.
Fat reserves are broken down faster as fasting continues. The brain must switch to an alternative source of energy—ketone bodies—derived from the fatty acids. A severe, prolonged fast, or starvation, depletes fat reserves and begins to break down muscle tissue to provide energy.
Ketogenesis Generates Energy during Prolonged Fasting
As you’ve learned in this chapter, acetyl CoA is generated from glucose (glycolysis) or fatty acid breakdown (lipolysis), both of which produce oxaloacetate that enters the TCA cycle. When deprived of carbohydrates, less oxaloacetate is available. The body depends less and less on glucose, and the TCA cycle slows. This allows acetyl CoA to accumulate because it is not metabolized in the TCA cycle. Some of the acetyl CoA produced by fatty acid oxidation in the liver is converted to ketone bodies, namely acetone, acetoacetate, and β-hydroxybutyrate.β-hydroxybutyrate.
Ketogenesis (the formation of ketone bodies, illustrated in Figure 8.17) occurs when there is an excess buildup of acetyl CoA. Ketogenesis reaches peak levels after an individual has fasted or consumed a limited-carbohydrate diet for 3 days. By the fourth day of a fast, the ketone bodies are providing almost half of the fuel used by the mitochondria.2 The presence of ketone bodies is referred to as ketosis (described in Chapter 4). As you continue to fast, your brain switches from glucose to ketone bodies for fuel, thereby preserving blood glucose. Eventually, about 30 percent of the brain’s energy comes from ketone bodies, with the rest provided by blood glucose.
Figure 8.17 The Formation of Ketone Bodies
Figure 8.17 Full Alternative Text
Ketogenesis is a normal metabolic response to fasting, and ketosis is not life-threatening. The kidneys reabsorb ketone bodies to be used by other tissues for energy or excrete excess ketone bodies in the urine, thereby maintaining a balanced pH. Ketogenesis can be used therapeutically: A ketogenic diet is sometimes prescribed to control seizures in patients who have epilepsy and don’t respond to medications. A ketogenic diet is difficult to follow and must be strictly monitored by a registered dietitian nutritionist. It is much stricter than the Atkins diet, another form of a ketogenic diet, requiring careful control of kilocalorie intake, fluids, and proteins.3
When very high concentrations of ketone bodies—which are acidic—accumulate in the blood, they lower the body’s pH to dangerous levels. This condition, called ketoacidosis, most commonly occurs in individuals with untreated type 1 diabetes because, without insulin, glucose is not available to the cells. The body responds with hyperventilation, rapid and shallow breathing that increases excretion of CO2,CO2, which in turn increases the blood pH. If the level of ketone bodies continues to rise, diabetic ketoacidosis can lead to deep and labored breathing, impaired heart activity, coma, and even death.
THE TAKE-HOME MESSAGE
The differences in metabolism between the absorptive, or feeding, state and the postabsorptive, or fasting, state are listed in Table 8.5. During the absorptive state, anabolic reactions are favored. Carbohydrates are first used for ATP synthesis with excess stored as glycogen or triglycerides in the adipose tissue. Excess amino acids and dietary fat are also converted to triglycerides and stored. During the postabsorptive state, metabolism shifts to favor catabolic reactions. Fat is broken down to fatty acids to be used for ATP synthesis, while liver glycogen, glycerol, and glucogenic amino acids are used to maintain blood glucose levels. As fasting continues, glycogen stores are depleted, and muscle is broken down to provide amino acids for energy and gluconeogenesis. A lack of sufficient glucose in the blood can lead to excess breakdown of fat and the synthesis of ketone bodies, which can be used by the brain and muscles for energy, but are acidic. If ketogenesis is prolonged, ketoacidosis—an excessive level of ketones in the blood—can develop, leading to coma and even death.
Table 8.5 Metabolism during Feeding and Fasting
