Energy Metabolism Chapter 7

Introduction Energy Metabolism Heat, mechanical, electrical, and chemical Metabolism How the body uses foods to meet its needs

Chemical Reactions in the Body Energy metabolism How body obtains and uses energy from food Photosynthesis Cells Liver cells most metabolically active Anabolism: building body compounds Requires energy Catabolism: breaking down body compounds Releases energy

A Typical Cell Figure 7-1 A typical cell

Anabolic and Catabolic Reactions Compared Figure 7-2 Anabolic and catabolic reactions compared

Transfer of Energy in Reactions ATP Released during breakdown of glucose, fatty acids, and amino acids Form of phosphate groups Negative charge – vulnerable to hydrolysis Provides energy for all cell activities Coupled reactions Efficiency Heat loss

ATP (Adenosine Triphosphate) Figure 7-3 Adenosine triphosphate

Capture and Release of Energy by ATP Figure 7-4 The capture and release of energy by ATP

Helpers in Metabolic Reactions Enzymes Facilitators of metabolic reactions Coenzymes Organic Associate with enzymes Without coenzyme, an enzyme cannot function

Breaking Down Nutrients for Energy Digestion Carbohydrates → glucose (and other monosaccharides) Fats (triglycerides) → glycerol and fatty acids Proteins → amino acids Molecules of glucose, glycerol, amino acids, and fatty acids Catabolism breaks bonds Carbon, nitrogen, oxygen, hydrogen

Two New Compounds Pyruvate Acetyl CoA 3-carbon structure Can be used to make glucose Acetyl CoA 2-carbon structure Cannot be used to make glucose TCA cycle and electron transport chain

Simplified Overview of Energy-Yielding Pathways Figure 7-5 Simplified overview of energy-yielding pathways

Glucose-to-Pyruvate Glycolysis 2 pyruvate molecules Hydrogen atoms carried to electron transport chain Pyruvate can be converted back to glucose Liver cells and (to some extent) kidneys

Glycolysis: Glucose-to-Pyruvate Figure 7-6 Glycolysis: glucose-to-pyruvate

Pyruvate’s Options Quick energy needs – anaerobic Pyruvate to lactate Slower energy needs – aerobic Pyruvate to acetyl CoA

Pyruvate-to-Lactate Pyruvate accepts hydrogens Converts pyruvate to lactate Occurs to a limited extent at rest Produces ATP quickly Mitochondrial ability Lactate accumulation in muscles Effects Cori cycle

Pyruvate-to-Lactate and the Cori Cycle Figure 7-7 Pyruvate-to-lactate and lactate-to-glucose (the Cori Cycle)

Pyruvate-to-Acetyl CoA Pyruvate enters mitochondria of cell Carbon removed Becomes carbon dioxide 2-carbon compound joins with CoA becoming acetyl CoA Irreversible Acetyl CoA pathways

Pyruvate-to-Acetyl CoA Illustrated Figure 7-8 Pyruvate-to-acetyl CoA

The Paths of Pyruvate and Acetyl CoA Figure 7-9 The paths of pyruvate and acetyl CoA

Glucose Enters the Energy Pathway Figure 7-10 Glucose enters the energy pathway

Breaking Down Glycerol and Fatty Acids Glycerol-to-pyruvate Glycerol can be converted Glucose Pyruvate Fatty acids-to-acetyl CoA Fatty acid oxidation 2-carbon units at a time join with CoA Hydrogens and electrons carried to electron transport chain

Fatty Acids-to-Acetyl CoA Figure 7-11 Fatty acids-to-acetyl CoA

Fats Enter the Energy Pathway Figure 7-12 Fats enter the energy pathway

Breaking Down Amino Acids Deamination of amino acids Amino acids-to-energy Several entry points in energy pathway Converted to pyruvate Converted to acetyl CoA Enter TCA cycle directly Amino acids-to-glucose

Amino Acids Enter the Energy Pathway Figure 7-13 Amino acids enter the energy pathway

Review of Energy-Yielding Nutrient Endpoints Yields energy? Yields glucose? Yields amino acids and body proteins? Yields fat stores? Carbohydrates (glucose) Yes Yes—when nitrogen is available, can yield nonessential amino acids Lipids (fatty acids) No Lipids (glycerol) Yes—when carbohydrate is unavailable Proteins (amino acids) Table 7-2 Review of energy-yielding nutrient endpoints

Final Steps of Energy Metabolism TCA Cycle Inner compartment of mitochondria Circular path Acetyl CoA Oxaloacetate – made primarily from pyruvate Carbon dioxide release Hydrogen atoms and their electrons Niacin and riboflavin

A Mitochondrion Figure 7-14 A mitochondrion

Electron Transport Chain Captures energy in ATP Series of proteins Electron “carriers” Inner membrane of mitochondria Electrons passed to next carrier Join oxygen at end of chain Water released ATP synthesis

Electron Transport Chain and ATP Synthesis Figure 7-16 Electron transport chain and ATP synthesis

The kCalorie-Per-Gram Secret Revealed Fat provides most energy per gram Carbon-hydrogen bonds More ATP = more kcalories Figure 7-17 Chemical structures of a fatty acid and glucose compared

Feasting – Excess Energy Metabolism favors fat formation Regardless of excess from protein, fat, or carbohydrates Excess protein Excess carbohydrate Excess fat – most direct and efficient conversion Fuel mix

Transition from Feasting to Fasting Glucose, glycerol, and fatty acids are used then stored Fasting state draws on these stores Glycogen and fat are released Basal metabolism Fasting versus starving

Feasting and Fasting Illustrated Figure 7-19 Feasting and fasting

Fasting – Inadequate Energy Carbohydrate, fat, and protein All eventually used for energy Begins with release of glucose and fatty acids Acetyl CoA Low blood glucose levels signal: Fat breakdown Release of amino acids from muscles

Adaptations Making glucose Creating an alternate fuel Nervous system and red blood cells Amino acids yielding pyruvate Breakdown of body proteins Creating an alternate fuel Use fat to fuel brain Ketone bodies Slows the rate of body protein breakdown Ketosis induces appetite loss

Energy Balance During Fasting Conserving energy Hormones Reduced energy output Fasting supports weight loss Not best option for fat loss Symptoms of starvation Physical symptoms Psychological symptoms

Low-Carbohydrate Diets Metabolism similar to fasting Uses glycogen stores first Gluconeogenesis when glycogen is depleted Body tissues used somewhat even when protein provided in diet Urine monitoring Ketosis

Adverse Side Effects of Low-Carbohydrate, Ketogenic Diets Nausea Fatigue (especially if physically active) Constipation Low blood pressure Elevated uric acid (which may exacerbate kidney disease and cause inflammation of the joints in those predisposed to gout) Stale, foul taste in the mouth (bad breath) In pregnant women, fetal harm and stillbirth Table 7-3 Adverse side effects of low-carbohydrate, ketogenic diets

Alcohol in the Body Highlight 7

Alcohol in the Body, continued Potential health benefits Alcohols Glycerol Ethanol Lipid solvents Moderation Definition of “drink” Proof Figure H7-1 Two alcohols: glycerol and ethanol

Alcohol’s Influence Alcohol’s special privileges Stomach No digestion Quick absorption Slowing absorption Stomach Alcohol dehydrogenase Small intestine Priority over nutrients

Alcohol in the Liver Liver cells first to receive alcohol-laden blood Alcohol dehydrogenase Disrupts liver activity Can permanently change liver cell structure Rate of alcohol metabolism Acetaldehyde Acetate

Alcohol Metabolism Figure H7-4 Alcohol metabolism

Effects on the Liver Niacin coenzyme co-opted and normal processes suffer Glycolysis TCA cycle Electron transport chain Fat accumulates in the liver Even after one night of heavy drinking Fatty liver → fibrosis → cirrhosis

Alcohol’s Influence in the Brain Sedates inhibitory nerves Central nervous system depressant Blood alcohol levels and brain responses Death of liver and brain cells Depression of antidiuretic hormone (ADH) Loss of body water Loss of important minerals

Alcohol’s Effects on the Brain Figure H7-6 Alcohol’s effects on the brain

Alcohol Blood Levels and Brain Responses Blood Alcohol Concentration Effect on Brain 0.05 Impaired judgment, relaxed inhibitions, altered mood, increased heart rate 0.10 Impaired coordination, delayed reaction time, exaggerated emotions, impaired peripheral vision, impaired ability to operate a vehicle 0.15 Slurred speech, blurred vision, staggered walk, seriously impaired coordination and judgment 0.20 Double vision, inability to walk 0.30 Uninhibited behavior, stupor, confusion, inability to comprehend 0.40 to 0.60 Unconsciousness, shock, coma, death (cardiac or respiratory failure) Table H7-2 Alcohol blood levels and brain responses NOTE: Blood alcohol concentration depends on a number of factors, including alcohol in the beverage, the rate of consumption, the person's gender, and body weight. For example, a 100-pound female can become legally drunk (≥=0.10 concentration) by drinking three beers in an hour, whereas a 220-pound male consuming that amount at the same rate would have a 0.05 blood alcohol concentration.

Alcohol’s Effects on Weight Contributes to body fat and weight gain One ounce of alcohol represents 0.5 ounce of fat Central obesity (“beer belly”) Substituted energy Seven kcalories per gram Nutrient displacement B vitamins Wernicke-Korsakoff syndrome

Signs of Alcoholism Tolerance: the person needs higher and higher intakes of alcohol to achieve intoxication. Withdrawal: the person who stops drinking experiences anxiety, agitation, increased blood pressure, or seizures, or seeks alcohol to relieve these symptoms. Impaired control: the person intends to have 1 or 2 drinks, but has 9 or 10 instead, or the person tries to control or quit drinking, but fails. Disinterest: the person neglects important social, family, job, or school activities because of drinking. Time: the person spends a great deal of time obtaining and drinking alcohol or recovering from excessive drinking. Impaired ability: the person’s intoxication or withdrawal symptoms interfere with work, school, or home. Problems: the person continues drinking despite physical hazards or medical, legal, psychological, family, employment, or school problems. The presence of three or more of these conditions is required to make a diagnosis. These conditions suggest that a person may have an alcohol problem and might benefit from an abstinence program or professional help. SOURCE: Adapted from Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (Washington, D.C.: American Psychiatric Association, 1994). Table H7-4 Signs of alcoholism