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Chapter 25: Metabolism Primary sources for figures and content: Marieb, E. N. Human Anatomy & Physiology. 6 th ed. San Francisco: Pearson Benjamin Cummings,

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Presentation on theme: "Chapter 25: Metabolism Primary sources for figures and content: Marieb, E. N. Human Anatomy & Physiology. 6 th ed. San Francisco: Pearson Benjamin Cummings,"— Presentation transcript:

1 Chapter 25: Metabolism Primary sources for figures and content: Marieb, E. N. Human Anatomy & Physiology. 6 th ed. San Francisco: Pearson Benjamin Cummings, 2004. Martini, F. H. Fundamentals of Anatomy & Physiology. 6 th ed. San Francisco: Pearson Benjamin Cummings, 2004.

2 Metabolism Digestion + Absorption by GI  monomers (building blocks) for ATP or biomolecule synthesis Metabolism = sum of all chemical reactions in the body

3 Metabolism Figure 25–1

4 Metabolism 1.Catabolism –Breakdown of organic molecules A.Hydrolysis -Large molecules into monomers B.Cellular Respiration -Oxidation of monomers in mitochondria -40% of energy  ATP -60% of energy  heat 2.Anabolism –Synthesis of new organic molecules for Cell maintenance and repair & Growth Formation of secretions & Nutrient reserves

5 Nutrient Use in Cellular Metabolism Figure 25–2 (Navigator) Catabolism supplies ATP and monomers to drive anabolism

6 Carbohydrate Metabolism

7 1. Carbohydrate Metabolism –Carbs are easiest to catabolize for energy, always used first –Cellular respiration Oxidizes glucose + oxygen  carbon dioxide + water and generates ATP

8 Cellular Respiration Review 1. Glycolysis Figure 25–3 (Navigator)

9 Cellular Respiration Review 1. Glycolysis Anaerobic, occurs in the cytoplasm 1 glucose is oxidized into 2 pyruvic acids 2 ATP produced by substrate level phosphorylation 2 NADH produced by reduction of NAD via oxidation of glucose In no Oxygen available, pyruvic acid is reduced to lactic acid (fermentation) –Erythrocytes (RBCs)  glycolysis only (no mitochondria) –Skeletal muscle  fermentation when no Oxygen –Neurons and cardiac muscle cannot ferment, need oxygen

10 Cellular Respiration Review 2. Decarboxylation + Kreb/Citric Acid Cycle Figure 25–4a (Navigator)

11 Figure 25–4b Cellular Respiration Review 2. Decarboxylation + Kreb/Citric Acid Cycle

12 Occur in matrix of mitochondria Decarboxylation: –2 pyruvic acid decarboxylated and oxidized into  2 acetyl CoA + 2 CO 2 + 2 NADH Citric Acid Cycle: –2 acetyl combined with 2 oxaloacetic acids creating 2 citric acids –Citric acid decarboxylated and oxidized  4 CO 2, 6 NADH, 2 FADH 2 – 2 ATP generated by substrate level phosphorylation Cellular Respiration Review 2. Decarboxylation + Kreb/Citric Acid Cycle

13 Cellular Respiration Review 3. Electron Transport Chain/Oxidative Phosphorylation Figure 25–5a (Navigator)

14 Cellular Respiration Review 3. Electron Transport Chain/Oxidative Phosphorylation Figure 25–5b

15 Cellular Respiration Review 3. Electron Transport Chain/Oxidative Phosphorylation Aerobic, occurs on cristae of mitochondria NADH and FADH 2 reduced during glycolysis and citric acid cycle are oxidized Electrons are passed to cytochromes, finally accepted by oxygen 32 ATP generated by chemiosmosis/oxidative phosphorylation 12 H 2 O produced as waste from oxidation of oxygen

16 Summary: Complete Aerobic Cellular Respiration Figure 25–6 With Oxygen 1 glucose =36 ATP Without Oxygen 1 glucose = 2 ATP (0 ATP in neurons and cardiac muscle, where fermentation is not possible)

17 Carbohydrate Metabolism 2. Carbohydrate Anabolism –All carbohydrates and lactic acid can be converted to glucose –Gluconeogenesis Synthesis of glucose from a non- carbohydrate precursor –e.g. glycerol, amino acids, lactic acid

18 Carbohydrate Metabolism 3. Functions of Glucose –Stored as glycogen via Glycogenesis –Used to generate ATP –To create other carbohydrates Cell membrane receptors Nucleic acids

19 Carbohydrate Breakdown and Synthesis Figure 25–7

20 Lipid Metabolism

21 1. Lipid Catabolism –Triglycerides are most common –Lipolysis Triglycerides  glycerol + 3 fatty acids A. Glycerol  pyruvic acid  citric acid cycle  generate 18 ATP B. Fatty Acids  undergo β-oxidation to become 2 carbon acetyl  citric acid cycle  each 2-C fragment generates 17 ATP –Carbon for carbon, lipids have 1.5x the energy of carbohydrates but are more difficult to use

22 Beta–Oxidation Figure 25–8 (Navigator)

23 Lipid Metabolism 1. Lipid Catabolism –Lipolysis is common to hepatocytes, cardiac muscle, skeletal muscle for ATP synthesis –Not possible in neurons –Not water soluble, difficult for enzymes to access –Lipolysis requires oxygen for ATP synthesis, no fermentation

24 Lipid Metabolism 2. Lipid Anabolism A. Lipogenesis Triglycerides synthesized from cellular respiration intermediates –Glycerol from glycolysis products –Fatty acids from Acetyl Co A B. Cholesterol Synthesis From any saturated fat molecule C. Essential Fatty Acids

25 Lipid Metabolism 2.Lipid Anabolism C. Essential Fatty Acids Must be ingested in diet, no synthesis 1. Linolenic acid = Omega 3 fatty acid 2. Linoleic acid = Omega 6 fatty acid **Both used to synthesize arachidonic acid, to synthesize eicosanoids (leukotrienes and protaglandins), for cell signaling

26 Lipid Metabolism 3. Functions of Lipids –Catabolism to generate ATP Breakdown of triglycerides, mostly –Cell membranes phospholipids, glycolipids, cholesterol –Myelin sheaths on axons –Bile salts –Steroid hormones –Cell signaling molecules –Energy reserve, 80% of total = triglycerides –Insulation and protection

27 Lipid Metabolism 4. Lipid Transport –Free fatty acids bound to albumins in blood –Others bound to proteins to form lipoproteins Soluble lipoproteins, bind specific receptors –Five classes of lipoproteins based on size and composition High protein content = High density High lipid content = Low density

28 Lipoprotein Classes Increased lipids = decreased density 1. Chylomicrons –95% triglycerides, from intestinal epithelium –Delivers lipids from gut to liver 2. Very Low Density Lipoproteins –Triglycerides (at high levels), phospholipids and cholesterol –Delivers triglycerides from liver to tissues 3. Intermediate Density Lipoproteins –VLDLs with triglycerides removed –Return to liver for processing

29 Lipoprotein Classes Increased lipids = decreased density 4. Low Density Lipoproteins –High cholesterol, low triglycerides and phospholipids –Deliver cholesterol from liver to tissues 5. High Density Lipoproteins –Equal protein and lipids (cholesterol and phospholipids –Return cholesterols to liver for degradation

30 Lipoprotein Distribution 1.Liver synthesizes VLDLs and releases them into blood 2.Triglycerides are removed in capillaries making IDLs from the VLDLs 3.IDLs return to liver, triglycerides are removed and proteins are altered, making LDLs from the IDLs which are released to blood 4.LDLs travel to peripheral tissues 5.Cells endocytose LDLs and break them down 6.Extra cholesterol diffuses out of the cells and enters the blood

31 Lipoprotein Distribution 7.Cholesterol binds to HDLs in blood and returns to liver 8.HDLs at liver have cholesterol extracted to form -empty HDLs, -new LDLs, -and bile salts 9.Empty HDLs return to the blood to pick up free cholesterol

32 Lipid Transport and Utilization Figure 25–9

33 Cholesterol and Health Normal: –HDLs > 60 mg/ml –LDLs < 160 mg/ml > 260 mg/ml LDLs need immediate medication or risk cardiovascular disease and heart attack Diet rich in saturated fats (animal)  Triggers synthesis of cholesterol and blocks excretion/conversion by liver Diet rich in non-hydrogenated unsaturated fats (plants)  enhance excretion and conversion to bile salts

34 Protein Metabolism

35 Proteins Metabolism Amino acids usually recycled to new proteins When carbs and lipids are lacking or amino acids are in excess, proteins can be catabolized for ATP or stored as fat

36 Protein Metabolism 1. Amino Acid Catabolism Deamination –Amino group is removed, Requires vitamin B6 Generate ammonia = toxic –Converted by liver to urea –Excreted in urine Carbon chain  citric acid cycle for ATP Different amino acids produce different amounts of ATP, some are not used at all Catabolism is difficult, inefficient and toxic Last resort for energy!

37 Protein Metabolism 1. Amino Acid Catabolism

38 Protein Metabolism 2. Amino Acid Anabolism A. Essential Amino Acids –8 for adults, 10 for children –Must be ingested, no synthesis B. Synthesis –12 can be synthesized using carbon backbone from other amino acids –Amination = addition of amino group –We synthesize 500-1000 lbs of protein in our lifetime

39 Protein Metabolism 2. Amino Acid Anabolism Figure 25–11

40 Phenylketonuria Lack of enzyme to convert phenylalanine to tyrosine Tyrosine is needed for melanin Deaminated phenylalanine levels rise  neurotoxic affects

41 Protein Metabolism 3. Functions of Proteins –Cell structural components –Enzymes –hormones

42 Summary: Pathways of Catabolism and Anabolism Figure 25–12

43 Nucleic Acid Metabolism

44 Nucleotides usually recycled for new nucleic acids DNA never catabolized for energy RNA only under extreme conditions Nucleotide hydrolyzed to pentose sugar, nitrogenous base, and phosphate –Sugar  glycolysis for ATP –Pyrimidine bases (C, U)  acetyl  citric acid cycle for ATP –Purine bases (A, G)  deaminated excreted as uric acid NOT USED FOR ATP

45 Gout Crystals of uric acid in joints Causes pain and swelling

46 How would a diet that is deficient in pyridoxine (vitamin B 6 ) affect protein metabolism? A.It would interfere with protein metabolism. B.It would enhance protein metabolism. C.It would cause the use of different coenzymes. D.Pyridoxine is not involved in protein metabolism.

47 Elevated levels of uric acid in the blood can be an indicator of increased metabolism of which organic compound? A.nucleic acids B.proteins C.carbohydrates D.lipids

48 Why are high-density lipoproteins (HDLs) considered beneficial? A.They increase lipid metabolism. B.They decrease blood pressure. C.They increase blood pH. D.They reduce fat and cholesterol in the bloodstream.

49 Metabolic Interactions: 5 regions of metabolism 1. Liver –Site of metabolic regulation and control –Can break down or synthesize most molecules for use by other cells –Stores glycogen reserves 2. Adipose –Stores triglyceride reserves 3. Skeletal Muscle –Stores glycogen reserves –Has contractile proteins that can be catabolized

50 Metabolic Interactions: 5 regions of metabolism 4. Neural Tissue –High energy demand but no reserves –Requires constant supply of glucose 5. Peripheral Tissues –No reserves –Catabolize a wide range of substrates

51 Patterns of Metabolic Activity 1.The Absorptive State - Anabolism exceeds catabolism 2.The Post Absorptive State -Catabolism dominates

52 1. Absorptive State Occurs for ~ 4 hr post meal while nutrients are being transported to liver then tissues Some nutrients are used immediately, some are stored as reserves A. Hormones involved 1.Insulin: -promotes glucose uptake and utilization by cells 2.Growth hormone: -promotes amino acid uptake and protein synthesis by cells 3.Androgens and Estrogens : -promote amino acid utilization in protein synthesis

53 1. Absorptive State B. Tissues involved 1.Liver: -Regulates blood glucose levels -Removes excess glucose from blood and performs glycogenesis (formation of glycogen from glucose) -Excess glucose  triglycerides  VLDLs for storage in adipocytes -Amino acids not tightly regulated -Some absorbed for protein and enzyme synthesis -Some converted to more rare amino acids for use by body cells

54 1. Absorptive State B. Tissues involved 2.Adipose Tissue: -Absorb fatty acids and glycerol from the blood and triglycerides from VLDLs -Absorb glucose for ATP synthesis to drive lipogenesis (triglyceride formation) -All excess nutrients converted and stored as triglycerides 3.Peripheral Tissues: -Absorb glucose for ATP synthesis -Absorb amino acids for protein synthesis

55 2. Post Absorptive State Periods when there is no more absorption from GI Cells must rely on energy reserves –Glycogen: liver and skeletal muscle –Triglycerides: adipose tissue –Proteins: muscle tissue Primary goal is to maintain glucose levels to the brain

56 2. Post Absorptive State A. Hormones involved 1.Glucagon -Promotes release of glucose from liver 2.Epinephrine -Promotes release of glucose from liver -Promotes lipolysis in adipose and release of glycerol and fatty acids 3.Glucocorticoids -Inhibits use of glucose of body tissues -Promotes use of fatty acids 4.Growth Hormone: Complements glucocorticoids *Blood glucose decr.  glucagon + epinephrine incr., insulin decr.

57 2. Post Absorptive State B. Tissues involved A.Liver -Glycogenolysis to cleave glucose from glycogen and release it into blood -Gluconeogensis (via glucocorticoid stimulation) to synthesize glucose from lipids -Triglyceride conversion -Glycerol  glucose -Fatty acids  acetyl  ketone bodies -Amino acid conversion -Amino acids deaminated  ketone bodies

58 2. Post Absorptive State B. Tissues involved A.Liver -Amino acid conversion -Ketone bodies  released into blood, absorbed by peripheral tissues  converted to acetyl  catabolized in Citric Acid Cycle *During starvation High concentrations of ketone bodies will be present in body fluids = Ketosis

59 Ketosis 1. During Starvation –Oxaloacetic acid from Citric Acid Cycle will be converted into glucose for brain –Acetyl and ketone bodies will not be able to enter citric acid cycle –Ketone bodies (acids and acetone) build up –Can lead to ketoacidosis (low blood pH)  death –Long term nonfetal ketosis  bone loss, kidney damage, heart disease 2. Diabetes mellitus –No insulin  no glucose use –Use of lipids and proteins  ketosis

60 2. Post Absorptive State B. Tissues involved B.Adipose -Fat mobilization -Lipolysis converts triglycerides  glycerol + fatty acids are released into blood -Body cells use them for ATP synthesis -Liver used them for gluconeogenesis C.Skeletal Muscle -Catabolism of contractile proteins -Release amino acids for use by liver in gluconeogenesis and ketone body formation

61 2. Post Absorptive State Most peripheral tissue cells in post absorptive state lacking insulin stimulation –Switch from glucose to ketone bodies for ATP synthesis Neurons can only use GLUCOSE

62 Regulatory Hormones: Effects on Peripheral Metabolism Table 25–1

63 KEY CONCEPT In the absorption state after a meal: –cells absorb nutrients to support growth and maintenance –nutrients are stored as energy reserves In the postabsorptive state: –gluconeogenesis in the liver maintains blood glucose levels –cells conserve energy by shifting to lipid based metabolism If necessary, ketone bodies become preferred energy source Metabolic shift reserves circulating glucose for use by neurons

64 What process in the liver would you expect to increase after you have eaten a high-carbohydrate meal? A.glycolysis B.glycogenesis C.lipolysis D.beta-oxidation

65 Why does the amount of urea in blood increase during the postabsorptive state? A.Protein digestion creates urea. B.Lipolysis creates urea. C.Glycolysis creates urea. D.Glycogenesis creates urea.

66 If a cell accumulates more acetyl-CoA than it can metabolize by way of the TCA cycle, what products are likely to form? A.ketone bodies B.uric acid crystals C.lactic acid molecules D.ATP molecules

67 Balanced diet

68 Homeostasis Can be maintained only if digestive tract absorbs enough fluids, organic substrates, minerals, and vitamins to meet cellular demands

69 Nutrition Is the absorption of nutrients from food The body’s requirement for each nutrient varies

70 A Balanced Diet Provides: Provides 1.Substrates for energy (ATP) production 2.Complete proteins (all essential a.a.) 3.Essential lipids 4.Nitrogen: needed for a.a. and nucleotides 5.Minerals = inorganic ions (Ca 2+, Na +, etc.) -Regulation of osmotic conc. -Physiological processes -Cofactors for enzymes -Form compounds 6.Vitamins = organic cofactors

71 Minerals and Mineral Reserves Table 25–3

72 A Balanced Diet Provides: 6. Vitamins = organic cofactors -Tissue maintenance -Coenzymes -Antioxidants -Hormone and neurotransmitter synthesis *Gut bacteria synthesize K, B5, biotin *Skin synthesizes D3 *All other from diet -Fat soluble (A, D, E, K) stored in fat - too much can cause toxicity - Water soluble (B, C, niacin, folacin, biotin) - either used or excreted by kidney

73 The Fat-Soluble Vitamins Table 25–4

74 The Water-Soluble Vitamins Table 25–5

75 Metabolic rate and what factors are involved in determining BMR.

76 Energy Gains and Losses Energy is released: –when chemical bonds are broken In cells: –energy is used to synthesize ATP –some energy is lost as heat

77 Bioenergetics Study of acquisition and use of energy by organisms Measure food energy in Calories 1 C = 1 kcal = amount of energy needed to raise temp of 1 kg H 2 O 1 ⁰ C Lipids  9.46 C/g Carbs  4. 18 C/g Proteins  4.32 C/g

78 Bioenergetics Metabolic Rate –Sum of all catabolic and anabolic reaction energy needs in body Basal Metabolic Rate (BMR) –Minimal energy cost of living to maintain homeostasis –BMR measured 12 hr post food @ 25⁰C room temp Average  70 C/hr, 1680 C/day Increased during healing or pregnancy –Guestimate: Weight in kg x 1.0 for males = BMR C/hr Weight in kg x 0.9 for females = BMR C/hr

79 Metabolic Rate If daily Calorie intake exceeds energy demands: –body stores excess energy as triglycerides in adipose tissue If daily caloric expenditures exceeds dietary supply: –body uses energy reserves (triglycerides) –Loss weight –Loss muscle protein

80 Hormonal Effects Thyroxine: –controls overall metabolism –T 4 assay measures thyroxine in blood Cholecystokinin (CCK): –suppresses appetite Adrenocorticotropic hormone (ACTH): –suppresses appetite Leptin: –released by adipose tissues during absorptive state –binds to CNS neurons that suppress appetite

81 Body Mass Index (BMI) BMI = weight in lb x 705 ÷ (height in inches) 2 BMI < 18 = underweight –18-25 = normal –25-30 = overweight –> 30 = obese (1:3 Americans) Obese = 20% + over ideal body weight Obese Mouse study –Leptin k/o mouse  obesity –Leptin released by adipocytes to trigger satiation in brain –5% of obese people have mutation in leptin gene or leptin receptor

82 Obesity Mouse Study

83 Heat Production BMR estimates rate of energy use Energy not captured is released as heat: –serves important homeostatic purpose Enzymes operate in a limited temperature range Homeostatic mechanisms keep body temperature within limited range (thermoregulation)

84 Thermoregulation Body temperature = 97-104 ⁰ F, for enzymes to function Heat: byproduct of metabolism –110 ⁰F = dead, must lose heat Heat transfer methods 1.Radiation: infrared waves, ~ 50% 2.Conduction: direct heat transfer, low % 3.Convection: warm air rises away from skin, cold air gets heated, ~ 15% 4.Evaporation: water changes to gas vapor using heat energy, ~ 20%, constant 10% loss due to insensible perspiration

85 Thermoregulation Heat regulation is controlled by anterior hypothalamus –Receptors in skin and brain detect temperature change –Hypothalamus responds via ANS stimulation Too hot  triggers heat loss 1.Peripheral vasodilation  incr. radiation & convention 2.Sensible perspiration  incr. evaporation 3.Incr. respiration depth  incr. evaporation Pyrexia –Elevated temp. if too high  heat stroke, cooling mechanism shut down  death

86 Thermoregulation Too cold  triggers heat retention and generation 1.Constrict cutaneous vessels  decr. radiation & convention Frost bite: if flow restricted for too long  tissue dies 2.Nonshivering thermogenesis  hormones -Increase metabolic rate (60% of catabolism = heat) 3.Shivering thermogenesis  muscle contraction -Increase muscle metabolism  incr. heat Hypothermia –Low temp.  slow metabolism  confusion

87 Thermoregulation Fever  Triggered by pyrogens –Resets thermostat  triggers heat generation to elevate body temperature up to 104⁰F  dysfunction, 110⁰F Heat and surface area –Volume to surface are ratio affects heat loss and BMR –Incr. area, decr. Volume = incr. heat loss, incr. BMR Thin people and children Infants/small children have Brown Fat –For heat generation (adipose with mitochondria) –Aerobic respiration produces 60% heat, 40% ATP

88 Age Related Changes 1.Incr. non-insulin dependent diabetes -Cells ignore insulin and won’t use glucose 2.Incr. glucose in blood can cause permanent protein changes by binding -cataracts, glaucoma, capillary blockage  necrosis 3.Decr. Metabolic rate 4.Incr. malnutrition due to decr. appetite

89 How would the BMR of a pregnant woman compare with her own BMR before she became pregnant? A.higher when pregnant B.lower when pregnant difference during pregnancy D.impossible to predict

90 What effect would the vasoconstriction of peripheral blood vessels have on an individual’s body temperature on a hot day? increase in body temperature B.a decrease in body temperature difference D.impossible to predict

91 Why do infants have greater problems with thermoregulation than adults do? A.higher surface to volume ratio B.undeveloped temperature regulation C.expend more energy to remain warm D.all of the above

92 SUMMARY Cellular metabolism Catabolism Anabolism Carbohydrate metabolism Glycolysis Cellular Respiration Mitochondrial ATP production Gluconeogenesis Glycogenesis Lipid catabolism Beta-oxidation Lipid synthesis Lipoproteins

93 SUMMARY Amino acid catabolism Protein synthesis Metabolic components: –liver –adipose tissue –skeletal muscle –neural tissue peripheral tissues Absorptive state Postabsorptive state Ketone bodies

94 SUMMARY Nutrition Minerals Vitamins Kilocalories (kc) Calories (c/g) Metabolic rate Thermoregulation

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