1. 23 2
Nutrition, Metabolism, and Body Temperature Regulation

2. Oxidation of Amino Acids
Transamination – switching of an amine group from an amino acid to a keto acid (usually -ketoglutaric acid of the Krebs cycle)
Typically, glutamic acid is formed in this process

3. Oxidation of Amino Acids
Oxidative deamination – the amine group of glutamic acid is:
Released as ammonia
Combined with carbon dioxide in the liver
Excreted as urea by the kidneys
Keto acid modification – keto acids from transamination are altered to produce metabolites that can enter the Krebs cycle

4. Synthesis of Proteins
Amino acids are the most important anabolic nutrients, and they form:
All protein structures
The bulk of the body’s functional molecules

5. Synthesis of Proteins Amounts and types of proteins:
Are hormonally controlled
Reflect each life cycle stage
A complete set of amino acids is necessary for protein synthesis
All essential amino acids must be provided in the diet

6. Summary: Carbohydrate Metabolic Reactions
Table

7. Summary: Lipid and Protein Metabolic Reactions
Table

8. State of the Body
The body exists in a dynamic catabolic-anabolic state
Organic molecules (except DNA) are continuously broken down and rebuilt
The body’s total supply of nutrients constitutes its nutrient pool

9. State of the Body
Amino acid pool – body’s total supply of free amino acids is the source for:
Resynthesizing body proteins
Forming amino acid derivatives
Gluconeogenesis

10. Carbohydrate/Fat and Amino Acid Pools
Figure 23.16

11. Interconversion Pathways of Nutrients
Carbohydrates are easily and frequently converted into fats
Their pools are linked by key intermediates
They differ from the amino acid pool in that:
Fats and carbohydrates are oxidized directly to produce energy
Excess carbohydrate and fat can be stored

12. Interconversion Pathways of Nutrients
Figure 23.17

13. Absoprtive and Postabsorptive States
Metabolic controls equalize blood concentrations of nutrients between two states
Absorptive
The time during and shortly after nutrient intake
Postabsorptive
The time when the GI tract is empty
Energy sources are supplied by the breakdown of body reserves

14. Absoprtive State
The major metabolic thrust is anabolism and energy storage
Amino acids become proteins
Glycerol and fatty acids are converted to triglycerides
Glucose is stored as glycogen
Dietary glucose is the major energy fuel
Excess amino acids are deaminated and used for energy or stored as fat in the liver

15. Absoprtive State
Figure 23.18a

16. Principal Pathways of the Absorptive State
In muscle:
Amino acids become protein
Glucose is converted to glycogen
In the liver:
Amino acids become protein or are deaminated to keto acids
Glucose is stored as glycogen or converted to fat

17. Principal Pathways of the Absorptive State
In adipose tissue:
Glucose and fats are converted and stored as fat
All tissues use glucose to synthesize ATP

18. Principal Pathways of the Absorptive State
Figure 23.18b

19. Insulin Effects on Metabolism
Insulin controls the absorptive state and its secretion is stimulated by:
Increased blood glucose
Elevated amino acid levels in the blood
Gastrin, CCK, and secretin
Insulin enhances:
Active transport of amino acids into tissue cells
Facilitated diffusion of glucose into tissue

20. Insulin Effects on Metabolism
Figure 23.19

21. Diabetes Mellitus
A consequence of inadequate insulin production or abnormal insulin receptors
Glucose becomes unavailable to most body cells
Metabolic acidosis, protein wasting, and weight loss result as fats and tissue proteins are used for energy

22. Postabsorptive State
The major metabolic thrust is catabolism and replacement of fuels in the blood
Proteins are broken down to amino acids
Triglycerides are turned into glycerol and fatty acids
Glycogen becomes glucose
Glucose is provided by glycogenolysis and gluconeogenesis
Fatty acids and ketones are the major energy fuels
Amino acids are converted to glucose in the liver

23. Postabsorptive State
Figure 23.20a

24. Principle Pathways in the Postabsorptive State
In muscle:
Protein is broken down to amino acids
Glycogen is converted to ATP and pyruvic acid (lactic acid in anaerobic states)

25. Principle Pathways in the Postabsorptive State
In the liver:
Amino acids, pyruvic acid, stored glycogen, and fat are converted into glucose
Fat is converted into keto acids that are used to make ATP
Fatty acids (from adipose tissue) and ketone bodies (from the liver) are used in most tissue to make ATP
Glucose from the liver is used by the nervous system to generate ATP

26. Principle Pathways in the Postabsorptive State
Figure 23.20b

27. Hormonal and Neural Controls of the Postabsorptive State
Decreased plasma glucose concentration and rising amino acid levels stimulate alpha cells of the pancreas to secrete glucagon (the antagonist of insulin)
Glucagon stimulates:
Glycogenolysis and gluconeogenesis
Fat breakdown in adipose tissue
Glucose sparing

28. Hormonal and Neural Controls of the Postabsorptive State
In response to low plasma glucose, the sympathetic nervous system releases epinephrine, which acts on the liver, skeletal muscle, and adipose tissue to mobilize fat and promote glycogenolysis

29. Liver Metabolism
Hepatocytes carry out over 500 intricate metabolic functions

30. Liver Metabolism A brief summary of liver functions
Packages fatty acids to be stored and transported
Synthesizes plasma proteins
Forms nonessential amino acids
Converts ammonia from deamination to urea
Stores glucose as glycogen, and regulates blood glucose homeostasis
Stores vitamins, conserves iron, degrades hormones, and detoxifies substances

31. Cholesterol
Is the structural basis of bile salts, steroid hormones, and vitamin D
Makes up part of the hedgehog molecule that directs embryonic development
Is transported to and from tissues via lipoproteins

32. Cholesterol Lipoproteins are classified as:
HDLs – high-density lipoproteins have more protein content
LDLs – low-density lipoproteins have a considerable cholesterol component
VLDLs – very low density lipoproteins are mostly triglycerides

33. Cholesterol
Figure 23.22

34. Lipoproteins
The liver is the main source of VLDLs, which transport triglycerides to peripheral tissues (especially adipose)
LDLs transport cholesterol to the peripheral tissues and regulate cholesterol synthesis
HDLs transport excess cholesterol from peripheral tissues to the liver
Also serve the needs of steroid-producing organs (ovaries and adrenal glands)

35. Lipoproteins
High levels of HDL are thought to protect against heart attack
High levels of LDL, especially lipoprotein (a), increase the risk of heart attack

36. Plasma Cholesterol Levels
The liver produces cholesterol:
At a basal level of cholesterol regardless of dietary intake
Via a negative feedback loop involving serum cholesterol levels
In response to saturated fatty acids

37. Plasma Cholesterol Levels
Fatty acids regulate excretion of cholesterol
Unsaturated fatty acids enhance excretion
Saturated fatty acids inhibit excretion
Certain unsaturated fatty acids (omega-3 fatty acids, found in cold-water fish) lower the proportions of saturated fats and cholesterol

38. Non-Dietary Factors Affecting Cholesterol
Stress, cigarette smoking, and coffee drinking increase LDL levels
Aerobic exercise increases HDL levels
Body shape is correlated with cholesterol levels
Fat carried on the upper body is correlated with high cholesterol levels
Fat carried on the hips and thighs is correlated with lower levels

39. Body Energy Balance
Bond energy released from catabolized food must equal the total energy output
Energy intake – equal to the energy liberated during the oxidation of food
Energy output includes the energy:
Immediately lost as heat (about 60% of the total)
Used to do work (driven by ATP)
Stored in the form of fat and glycogen

40. Body Energy Balance
Nearly all energy derived from food is eventually converted to heat
Cells cannot use this energy to do work, but the heat:
Warms the tissues and blood
Helps maintain the homeostatic body temperature
Allows metabolic reactions to occur efficiently

41. Regulation of Food Intake
When energy intake and energy outflow are balanced, body weight remains stable
The hypothalamus releases peptides that influence feeding behavior
Orexins are powerful appetite enhancers
Neuropeptide Y causes a craving for carbohydrates
Galanin produces a craving for fats
GLP-1 and serotonin make us feel full and satisfied

42. Feeding Behaviors
Feeding behavior and hunger depend on one or more of five factors
Neural signals from the digestive tract
Bloodborne signals related to the body energy stores
Hormones, body temperature, and psychological factors

43. Nutrient Signals Related to Energy Stores
High plasma levels of nutrients that signal depressed eating
Plasma glucose levels
Amino acids in the plasma
Fatty acids and leptin

44. Hormones, Temperature, and Psychological Factors
Glucagon and epinephrine stimulate hunger
Insulin and cholecystokinin depress hunger
Increased body temperature may inhibit eating behavior
Psychological factors that have little to do with caloric balance can also influence eating behaviors

45. Control of Feeding Behavior and Satiety
Leptin, secreted by fat tissue, appears to be the overall satiety signal
Acts on the ventromedial hypothalamus
Controls appetite and energy output
Suppresses the secretion of neuropeptide Y, a potent appetite stimulant
Blood levels of insulin and glucocorticoids play a role in regulating leptin release

46. Control of Feeding Behavior and Satiety
Figure 23.23

47. Metabolic Rate
Rate of energy output (expressed per hour) equal to the total heat produced by:
All the chemical reactions in the body
The mechanical work of the body
Measured directly with a calorimeter or indirectly with a respirometer

48. Metabolic Rate Basal metabolic rate (BMR)
Reflects the energy the body needs to perform its most essential activities
Total metabolic rate (TMR)
Total rate of kilocalorie consumption to fuel all ongoing activities

49. Factors that Influence BMR
Surface area, age, gender, stress, and hormones
As the ratio of surface area to volume increases, BMR increases
Males have a disproportionately high BMR
Stress increases BMR
Thyroxine increases oxygen consumption, cellular respiration, and BMR

50. Regulation of Body Temperature
Body temperature – balance between heat production and heat loss
At rest, the liver, heart, brain, and endocrine organs account for most heat production
During vigorous exercise, heat production from skeletal muscles can increase 30–40 times
Normal body temperature is 36.2C (98.2F); optimal enzyme activity occurs at this temperature
Temperature spikes above this range denature proteins and depress neurons

51. Regulation of Body Temperature
Figure 23.25

52. Core and Shell Temperature
Organs in the core (within the skull, thoracic, and abdominal cavities) have the highest temperature
The shell, essentially the skin, has the lowest temperature
Blood serves as the major agent of heat transfer between the core and shell
Core temperature remains relatively constant, while shell temperature fluctuates substantially (20C–40C)

53. Mechanisms of Heat Exchange
The body uses four mechanisms of heat exchange
Radiation – loss of heat in the form of infrared rays
Conduction – transfer of heat by direct contact
Convection – transfer of heat to the surrounding air
Evaporation – heat loss due to the evaporation of water from the lungs, mouth mucosa, and skin (insensible heat loss)
Evaporative heat loss becomes sensible when body temperature rises and sweating produces increased water for vaporization

54. Role of the Hypothalamus
The main thermoregulation center is the preoptic region of the hypothalamus
The heat-loss and heat-promoting centers comprise the thermoregulatory centers
The hypothalamus:
Receives input from thermoreceptors in the skin and core
Responds by initiating appropriate heat-loss and heat-promoting activities

55. Heat-Promoting Mechanisms
Low external temperature or low temperature of circulating blood activates heat-promoting centers of the hypothalamus to cause:
Vasoconstriction of cutaneous blood vessels
Increased metabolic rate
Shivering
Enhanced thyroxine release

56. Heat-Loss Mechanisms
When the core temperature rises, the heat-loss center is activated to cause:
Vasodilation of cutaneous blood vessels
Enhanced sweating
Voluntary measures commonly taken to reduce body heat include:
Reducing activity and seeking a cooler environment
Wearing light-colored and loose-fitting clothing

57. Mechanisms of Body Temperature Regulation
Figure 23.27

58. Hyperthermia
Normal heat loss processes become ineffective and elevated body temperatures depress the hypothalamus
This sets up a positive-feedback mechanism, sharply increasing body temperature and metabolic rate
This condition, called heat stroke, can be fatal if not corrected

59. Heat Exhaustion
Heat-associated collapse after vigorous exercise, evidenced by elevated body temperature, mental confusion, and fainting
Due to dehydration and low blood pressure
Heat-loss mechanisms are fully functional
Can progress to heat stroke if the body is not cooled and rehydrated

60. Fever
Controlled hyperthermia, often a result of infection, cancer, allergic reactions, or central nervous system injuries
White blood cells, injured tissue cells, and macrophages release pyrogens that act on the hypothalamus, causing the release of prostaglandins
Prostaglandins reset the hypothalamic thermostat
The higher set point is maintained until the natural body defenses reverse the disease process