1. Energy Metabolism
Chapter 7

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

3. 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

4. A Typical Cell
Figure 7-1 A typical cell

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

6. 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

7. ATP (Adenosine Triphosphate)
Figure 7-3 Adenosine triphosphate

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

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

10. 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

11. 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

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

13. 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

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

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

16. 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

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

18. 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

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

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

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

22. 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

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

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

25. 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

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

27. 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

28. 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

29. A Mitochondrion
Figure 7-14 A mitochondrion

30. 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

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

32. 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

33. 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

34. 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

35. Feasting and Fasting Illustrated
Figure 7-19 Feasting and fasting

36. 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

37. 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

38. 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

39. 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

40. 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

41. Alcohol in the Body
Highlight 7

42. 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

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

44. 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

45. Alcohol Metabolism
Figure H7-4 Alcohol metabolism

46. 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

47. 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

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

49. 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.

50. 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

51. 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