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Transcript
Food Processing Module 22.2: Nutrient pool substrates Nutrient pool supplies molecules for catabolism, anabolism, and to fuel ATP production ◦ ◦ ATP used for metabolic makeover inside cell Organic compounds used for 2-carbon substrate molecules for mitochondrial activities The centrality of the nutrient pool to both anabolism and catabolism Structural, functional, and storage components Triglycerides Organic compounds that can be absorbed by cells are distributed to cells throughout the body by the bloodstream. Nutrient Fatty acids pool Glycogen Proteins Glucose Amino acids Three-carbon chains Two-carbon chains MITOCHONDRIA KEY Citric acid cycle ATP Coenzymes Electron transport system O2 = Catabolic pathway H2 O = Anabolic pathway CO2 Figure 22.2 1 Module 22.2: Nutrient pool substrates When nutrients absorbed from digestive tract are insufficient for cellular metabolism, energy reserves come from various cells ◦ Liver cells store triglycerides and glycogen ◦ Fatty acids and glucose can be released Adipocytes store triglycerides ◦ Fatty acids can be released Skeletal muscle cells store glycogen Amino acids can be released The use of the body’s metabolic reserves to maintain normal nutrient levels in the blood Nutrients obtained through digestion and absorption Neural tissue requires a continuous supply of glucose. During starvation, other tissues shift to fatty acid or amino acid catabolism, conserving glucose for neural tissue. Liver cells store triglycerides and glycogen reserves. If absorption by the digestive tract fails to maintain normal nutrient levels, the triglycerides and glycogen are broken down and the fatty acids and glucose are released. Nutrients distributed in the blood Adipocytes convert excess fatty acids to triglycerides for storage. If absorption by the digestive tract and reserves in the liver fail to maintain normal nurtient levels, the triglycerides are broken down and the fatty acids released. Skeletal muscles at rest metabolize fatty acids and use glucose to build glycogen reserves. Amino acids are used to increase the number of myofibrils. If the digestive tract, adipocytes, and liver are unable to maintain normal nutrient levels, the contractile proteins can be broken down and amino acids released into the circulation for use by other tissues. Cells in most tissues continuously absorb and catabolize glucose. Figure 22.2 2 Module 22.2: Nutrient pool substrates Cellular catabolic and anabolic pathways ◦ Cells must synthesize some organic molecules ◦ ◦ Insufficient nutrients from nutrient pool and diet Nutrients are often used to create 2-carbon chains for mitochondrial ATP production Oxygen required must be continuously provided by diffusion from ECF CO2 produced must diffuse out of cell to ECF Module 22.2: Nutrient pool substrates Cellular nutrient dynamics ◦ Fatty acids ◦ Can be stored as triglycerides Can be created from acetyl-CoA and triglycerides Glucose Can be stored as glycogen (glycogenesis) Can be created from: Glycogen catabolism (glycogenolysis) Smaller carbon chain anabolism (gluconeogenesis) Can be used to make two 3-carbon chains for ATP production (glycolysis) Module 22.2: Nutrient pool substrates Cellular nutrient dynamics (continued) ◦ Amino acids Can be stored as proteins Can be created from: 3-carbon chains Protein catabolism (only during starvation) KEY = Catabolic pathway A general overview of the catabolic and anabolic pathways of cells = Anabolic pathway Fatty acids can be stored as triglycerides. Nutrient pool Proteins Glycogen Triglycerides Stored triglycerides can be broken down into fatty acids. In glycogenesis, glycogen is synthesized from glucose. Fatty acids The release of glucose from glycogen is called glycogenolysis. Amino acids Glucose The breakdown of a fatty acid releases glycerol and acetyl-CoA suitable for use by mitochondria. Gluconeogenesis: glucose synthesis from smaller carbon chains. Glycolysis: glucose breakdown into two three-carbon molecules/chains The primary use of amino acids is the synthesis of proteins. Amino acids are seldom broken down if other energy sources are available. However, in starvation the proteins of muscle tissues are mobilized, releasing amino acids that can be catabolized by other tissues. Three-carbon chains Two-carbon chains Fatty acid synthesis begins with acetyl-CoA. Because this is the common intermediary for all aerobic catabolic pathways, fatty acids can be synthesized from excess carbohydrates or amino acids. MITOCHONDRIA Citric acid cycle Coenzymes ATP Electron transport system O2 H2O CO2 CO2 must leave the cytosol by diffusion into the ECF, and the bloodstream must continuously absorb CO2 in peripheral tissues and eliminate it at the lungs to prevent potentially dangerous changes in body fluid pH. O2 must be continuously provided by diffusion from the ECF. This requires normal respiratory function and adequate tissue perfusion. Figure 22.2 3 Module 22.2 Review a. Define nutrient pool. b. Why do cells engage in catabolism? c. Why do cells make new compounds? Section 2: Digestion and Metabolism of Organic Nutrients Overview of digestive process ◦ Oral cavity (mechanical processing and chemical digestion of carbohydrates and lipids) ◦ Stomach (acidic chemical digestion) ◦ Duodenum (various enzymes catalyze catabolism of all organic molecules needed by cells) ◦ Jejunum and Ileum (nutrient absorption) Nutrients stored and processed by liver ◦ Large intestine (water reabsorbed, nutrients and vitamins produced by bacteria, feces eliminated) Steps in the Process of Digestion In the oral cavity, saliva dissolves some organic nutrients, and mechanical processing with the teeth and tongue disrupts the physical structure of the material and provides access for digestive enzymes. Those enzymes begin the digestion of complex carbohydrates (polysaccharides) and lipids. In the stomach, the material is further broken down physically and chemically by stomach acid and by enzymes that can operate at an extremely low pH. In the duodenum, buffers from the pancreas and liver moderate the pH of the arriving chyme, and various digestive enzymes are secreted by the pancreas that catalyze the catabolism of carbohydrates, lipids, proteins, and nucleic acids. Nutrient absorption then occurs in the small intestine, primarily in the jejunum, and the nutrients enter the bloodstream. Indigestible materials and wastes enter the large intestine, where water is reabsorbed and bacterial action generates both organic nutrients and vitamins. These organic products are absorbed before the residue is ejected at the anus. Most of the nutrients absorbed by the digestive tract end up in a tributary of the hepatic portal vein that ends at the liver. The liver absorbs nutrients as needed to maintain normal levels in the systemic circuit. Within peripheral tissues, cells absorb the nutrients needed to maintain their nutrient pool and ongoing operations. Figure 22 Section 2 Module 22.3: Carbohydrates Carbohydrates are usually preferred substrates for catabolism and ATP production when resting Steps of carbohydrate digestion ◦ In mouth, salivary amylase digests complex carbohydrates into disaccharides and trisaccharides ◦ Enzyme active only down to pH 4.5 and denatured in stomach At duodenum, pancreatic alpha-amylase continues carbohydrate digestion Module 22.3: Carbohydrates Steps of carbohydrate digestion (continued) ◦ In jejunum, brush border enzymes finish carbohydrate digestion down to simple sugars (monosaccharides) ◦ Maltase (digests maltose: glucose + glucose) Sucrase (digests sucrose: glucose + fructose) Lactase (digests lactose: glucose + galactose) In large intestine, remaining indigestible carbohydrates (such as cellulose) are food source for colonic bacteria Produce intestinal gas (flatus) during metabolic activities Module 22.3: Carbohydrates Carbohydrate absorption and transport ◦ Transported into small intestine epithelial cells ◦ Leave cells by facilitated diffusion through basolateral surface Enter cardiovascular capillaries to transport to liver in hepatic portal vein Processed by liver to maintain glucose levels (~90 mg/dL) Released as glucose or Stored as glycogen Module 22.3: Carbohydrates Cellular use of digested carbohydrates ◦ Generally preferred for catabolism ◦ ◦ Proteins and lipids more important for structural components of cells and tissues In skeletal muscle, stored as glycogen In most tissues, transported into cell by carrier molecule (regulated by insulin) May be converted to ribose May be converted to 2 pyruvate molecules in glycolysis Produces 2 ATP Pyruvates used by mitochondria Uses 3 O2, generates 3 CO2, 6 H2O, 34 ATP The events in carbohydrate catabolism and ATP production from glucose GLUCOSE (6-carbon) ATP Carbohydrates (such as glucose) are generally preferred for catabolism because proteins and lipids are more important as structural components of cells and tissues. In most tissues, the transport of glucose into the cell is dependent on the presence of a carrier protein stimulated by insulin. Inside the cell, the glucose may be converted to another simple sugar, such as ribose, used to Insulin build glycoproteins, other structural materials, or nucleic acids. They may also be converted to glycerol for the synthesis of glycerides. Other simple sugars If needed to provide energy, the 6-carbon glucose molecule is broken down into two 3-carbon molecules of pyruvate. This anaerobic process, called glycolysis, yields a net gain of 2 ATP for every glucose molecule broken down. Pyruvate (3-carbon) Pyruvate (3-carbon) CO2 Coenzyme A Each pyruvate molecule can then be used by mitochondria, after conversion to acetyl-CoA. Acetyl-CoA (2-carbon) Citric acid cycle ATP Coenzymes Electron transport system O2 For each molecule of pyruvate processed by mitochondria, the cell gains 17 ATP, consumes 3 molecules of O2, and generates 3 molecules of CO2 and 6 molecules of water. Thus for each pair of pyruvate molecules catabolized, the cell gains 34 ATP. H2O CO2 Figure 22.3 Module 22.3 Review a. Describe the source of intestinal gas. b. Explain the role of glycogen in cellular metabolism. c. Explain why carbohydrates are preferred over proteins and fats as an energy source. Module 22.4: Catabolism of glucose Glycolysis ◦ Anaerobic process making two 3-carbon pyruvate from one 6-carbon glucose Occurs in cytosol Produces a net gain of 2 ATP ◦ ◦ Also produces hydrogen atoms that are transferred by NAD to mitochondria for ETS Module 22.4: Catabolism of glucose Steps of glycolysis ◦ ◦ ◦ Phosphate group attached to glucose in cytosol 2nd phosphate attached (cost of 2 ATP) 6-carbon molecule split into two 3-carbon molecules Another phosphate attached to each molecule and processed further ◦ ◦ 2 NADH generated 2 ATP generated 2 H2O released Further processing creates an additional 2 ATP The steps in glycolysis, the breakdown of a six-carbon glucose molecule into two three-carbon pyruvate molecules INTERSTITIAL FLUID Glucose ATP CYTOSOL ADP Steps in Glycolysis Glucose-6-phosphate ATP As soon as a glucose molecule enters the cytosol, a phosphate group is attached to the molecule. ADP Fructose-1,6-biphosphate A second phosphate group is attached. Together, steps 1 and 2 cost the cell 2 ATP. The six-carbon chain is split into two three-carbon molecules, each of which then follows the rest of this pathway. Another phosphate group is attached to each molecule, and NAD•H is generated from NAD. Dihydroxyacetone phosphate Glyceraldehyde 3-phosphate 2 2 NAD 2 NAD•H From mitochondria To mitochondria 1,3-Bisphosphoglycerate 2 ADP One ATP molecule is formed for each molecule processed. The atoms in each molecule are rearranged, releasing a molecule of water. 2 ATP 3-Phosphoglycerate 2 H2O Energy Summary Steps 1 & 2: –2 ATP Step 5: +2 ATP Step 7: +2 ATP NET GAIN:+2 ATP Phosphoenolpyruvate A second ATP molecule is formed for each molecule processed. Step 7 produces 2 ATP molecules. 2 ADP 2 ATP Pyruvate To mitochondria Figure 22.4 1 Module 22.4: Catabolism of glucose Summary of aerobic ATP production ◦ ◦ ◦ ◦ ◦ 4 ATP from NADH produced in glycolysis 24 ATP from NADH generated in citric acid cycle 4 ATP from FADH2 generated in citric acid cycle 2 ATP via GTP produced during enzymatic reactions 34 ATP total Figure 22.4 2 Module 22.4 Review a. List the molecular products from a glucose molecule after glycolysis. b. Identify when most of the CO2 is released during the complete catabolism of glucose. c. Explain when glycolysis may be important in cellular metabolism. Module 22.5: Lipids Steps of lipid digestion ◦ In mouth, mechanical processing and chemical digestion by lingual lipase In stomach, lingual lipase continues to function but can only access surface of lipid drops that have formed In duodenum ◦ ◦ Bile salts break up lipid drops into smaller droplets (= emulsification) Pancreatic lipase digests triglycerides into fatty acids, monoglycerides, and glycerol Forms micelles (lipid–bile salt complexes) Module 22.5: Lipids Absorption and transport of digested lipids ◦ ◦ Lipids diffuse from micelle into intestinal epithelial cell Intracellular anabolic reactions synthesize new triglycerides from digested lipids New triglycerides packaged in chylomicrons (chylos, milky lymph, mikros, small) and released via exocytosis Chylomicrons diffuse into intestinal lacteals due to their size ◦ ◦ ◦ Transported through lymphatic vessels (including thoracic duct) to bloodstream Enzyme in capillaries (lipoprotein lipase) breaks down chylomicron and releases digested lipids to tissues Module 22.5: Lipids Digested lipid distribution and processing ◦ Tissues that use or process digested lipids Skeletal muscles Adipose tissue Use fatty acids to generate ATP for contraction and to convert glucose to glycogen Uses fatty acids and monoglycerides to synthesize triglycerides for storage Liver Absorbs intact chylomicrons and extracts triglycerides and cholesterol from chylomicron Module 22.5: Lipids Cholesterol distribution ◦ Released from liver attached to low-density lipoproteins (LDL) for distribution to peripheral tissues LDLs absorbed and broken down by lysosomes in cells ◦ ◦ High-density lipoproteins (HDL) (plasma proteins from liver) absorb peripheral cholesterol and return to liver Cholesterol extracted and used Unused cholesterol released into bloodstream Cholesterol released again with LDLs or excreted in bile Ratio of LDL/HDL and total cholesterol used diagnostically for cardiovascular problems Thoracic duct The chylomicrons enter the bloodstream at the left subclavian vein, then pass through the pulmonary circuit before entering the systemic circuit. Resting skeletal muscles absorb fatty acids and break them down, using the ATP provided both to power the contractions that maintain muscle tone and to convert glucose to glycogen. Capillary walls contain the enzyme lipoprotein lipase, which breaks down the chylomicrons and releases fatty acids and monoglycerides that can diffuse into the interstitial fluid. Adipocytes absorb the monoglycerides and fatty acids, and use them to synthesize triglycerides for storage. Lipoproteins and Lipid Transport and Distribution The liver absorbs chylomicrons, removes the triglycerides, combines the cholesterol from the chylomicron with synthesized or recycled cholesterol, and alters the surface proteins. It then releases low-density lipoproteins (LDLs) into the circulation, which deliver cholesterol to peripheral tissues. Some of the cholesterol is used by the liver to synthesize bile salts; excess cholesterol is excreted in the bile. The HDLs return the cholesterol to the liver, where it is extracted and packaged in new LDLs or excreted with bile salts in bile. From the lacteals, the chylomicrons proceed along the lymphatic vessels and into the thoracic duct. Chylomicrons Triglycerides removed The LDLs released by the liver leave the bloodstream through capillary pores or cross the endothelium by vesicular transport. LDL Cholesterol extracted Excess cholesterol is excreted with the bile salts HDL HDL High cholesterol Low cholesterol Once in peripheral tissues, the LDLs are absorbed. LDL Lysosomal breakdown HDL Cholesterol release Used in synthesis of membranes, hormones, other material Figure 22.5 Module 22.5 Review a. What is the difference between a micelle and a chylomicron? b. What does the liver do with the chylomicrons it receives? c. Describe the roles of LDL and HDL. Module 22.6: Lipid catabolism and synthesis Lipolysis (lipid catabolism) ◦ Triglycerides absorbed into cells through endocytosis Lysosomal enzymes break down to glycerol and fatty acids Glycerol Converted to pyruvate in glycolysis (+ 2 ATP) Fatty acids Enzymes convert two carbons to acetyl-CoA directly (= beta-oxidation) used in mitochondria More efficient than glucose catabolism (6-carbon glucose = 36 ATP; 6 carbons from FAs = 51 ATP) Module 22.6: Lipid catabolism and synthesis Lipid synthesis (lipogenesis) ◦ Begins with acetyl-CoA ◦ Almost any organic substrate (lipids, amino acids, carbohydrates) can be converted to acetyl-CoA Fatty acids synthesized from acetyl-CoA Series of enzymatic steps (different from beta-oxidation) Essential fatty acids ◦ Cannot be synthesized and must be obtained from diet Examples: linolenic acid (omega-3 fatty acid) and linoleic acid (omega-6 fatty acid) Structural and functional lipids created from fatty acids Fatty acids + glycerol (from glycolysis) = triglycerides CYTOSOL The glycerol required for triglyceride production is synthesized from one of the intermediate products of glycolysis. Steroids Triglycerides Glucose All of the other structural and functional lipids can be synthesized from fatty acids. Glycerol Cholesterol Fatty acid synthesis involves a reaction sequence quite distinct from that of beta-oxidation. As a result, body cells cannot build every fatty acid they can break down. For example, our cells lack the enzymes to insert double bonds in the proper locations to synthesize two 18-carbon fatty acids synthesized by plants: linolenic acid (an omega-3 fatty acid) or linoleic acid (an omega-6 fatty acid). However, these fatty acids are needed to synthesize prostaglandins and some of the phospholipids found in plasma membranes throughout the body. They are therefore called essential fatty acids, because they must be included in your diet. Prostaglandins Fatty acids Pyruvate Phospholipids Glycolipids Start The synthesis of most types of lipids, including nonessential fatty acids and steroids, begins with acetyl-CoA. Lipogenesis can use almost any organic substrate, because lipids, amino acids, and carbohydrates can be converted to acetyl-CoA. CO2 Coenzyme A ADP ATP Acetyl-CoA Citric acid cycle MITOCHONDRIA The major pathways for lipogenesis, the synthesis of lipids Figure 22.6 2 Module 22.6: Lipid catabolism and synthesis Lipids as energy reserves ◦ ◦ Beta-oxidation is very efficient Can be easily stored as triglycerides Although water-soluble enzymes cannot access, so not used for quick energy but for long-term storage Module 22.6 Review a. Define beta-oxidation. b. What molecule plays a key reactant role in both ATP production from fatty acids and lipogenesis? c. Identify the fates of fatty acids. Module 22.7: Protein digestion and amino acid metabolism Steps of protein digestion ◦ ◦ In mouth, mechanical processing occurs In stomach: Mechanical processing due to churning Stomach acid denatures protein secondary and tertiary structures Pepsin (from parietal cells) attacks certain peptide bonds Digests proteins to polypeptide and peptide chains Module 22.7: Protein digestion and amino acid metabolism Steps of protein digestion (continued) ◦ In duodenum: Enteropeptidase (from duodenal epithelium) converts trypsinogen (pancreatic proenzyme) to trypsin Trypsin activates other pancreatic proenzymes Chymotrypsin, carboxypeptidase, and elastase Activated pancreatic enzymes digest specific peptide bonds producing short peptides and amino acids Module 22.7: Protein digestion and amino acid metabolism Digested protein absorption and transport ◦ Epithelial brush border enzymes (peptidases) finish protein digestion Amino acids absorbed through: ◦ ◦ ◦ Facilitated diffusion Cotransport Released from epithelial cell basal surface through same cell transport mechanisms Amino acids transported to liver through intestinal capillaries to hepatic portal vein Module 22.7: Protein digestion and amino acid metabolism Amino acid processing in liver ◦ Control of plasma amino acid levels is less precise than glucose ◦ Normal range: 35–65 mg/dL Can increase after protein-rich meal Liver amino acid use Synthesize plasma proteins Create 3-carbon molecules for gluconeogenesis Module 22.7: Protein digestion and amino acid metabolism Amino acid processing in liver (continued) ◦ Amino acid catabolism Deamination (removal of amino group) Ammonium ions released are toxic Liver enzymes convert to urea excreted into urine = Urea cycle The liver does not control circulating levels of amino acids as precisely as it does glucose concentrations. Plasma amino acid levels normally range between 35 and 65 mg/dL, but they may become elevated after a protein-rich meal. The liver itself uses many amino acids for synthesizing plasma proteins, and it has all of the enzymes needed to synthesize, convert, or catabolize amino acids. In addition, amino acids that can be broken down to 3-carbon molecules can be used for gluconeogenesis when other sources of glucose are unavailable. Amino Acid Synthesis Liver cells and other body cells can readily synthesize the carbon frameworks of roughly half of the amino acids needed to synthesize proteins. There are 10 essential amino acids that the body either cannot synthesize or that cannot be produced in amounts sufficient for growing children. In an amination reaction, an ammonium ion (NH4+) is used to form an amino group that is attached to a molecule, yielding an amino acid. NH4+ H2O H+ α–Ketoglutarate Glutamic acid In a transamination, the amino group of one amino acid gets transferred to another molecule, yielding a different amino acid. The remaining carbon chain can then be broken down or used in other ways. Transaminase Glutamic acid Organic acid 1 Organic acid 2 Tyrosine Figure 22.7 Module 22.7 Review a. Name the enzyme secreted by parietal cells that is necessary for protein digestion. b. Identify the processes by which the amino group is removed. c. What happens to the ammonium ions that are removed from amino acids during deamination? Module 22.8: Absorptive and postabsorptive states Absorptive state ◦ ◦ ◦ Period following a meal, when nutrient absorption is occurring Commonly continues for ~4 hours Insulin is primary regulating hormone by stimulating: 1. Glucose uptake and glycogenesis 2. Amino acid uptake and protein synthesis Others can be involved (GH, androgens, estrogens) 3. Triglyceride synthesis ◦ ATP can be produced from nutrient pool The activities during the absorptive state following a meal KEY Glucose levels elevated = Catabolic pathway = Anabolic pathway = Stimulation Insulin CARBOHYDRATES LIPIDS Triglycerides PROTEINS Glycogen Proteins Insulin Glucose Insulin Lipid levels elevated Fatty acids Glycerol G l y c o l y s I s Insulin Androgens Estrogens Growth hormone ATP Amino acids elevated Amino acids Insulin, Growth hormone Pyruvate In the absorptive state: • Insulin stimulates (1) glucose uptake and glycogenesis, (2) amino acid uptake and protein synthesis, and (3) triglyceride synthesis. • Androgens, estrogens, and growth hormone also stimulate protein synthesis. • Glycolysis and aerobic metabolism provide the ATP needed to power cellular activities as well as the synthesis of lipids and proteins. CO2 Insulin Acetyl-CoA Citric acid cycle ATP Coenzymes MITOCHONDRIA Electron transport system O2 O2 H2O CO2 Figure 22.8 1 Module 22.8: Absorptive and postabsorptive states Postabsorptive state ◦ Period when nutrient absorption in not occurring and body relies on energy reserves (~12 hours/day) Metabolic activity focused on mobilizing energy reserves and maintaining blood glucose ◦ ◦ Lipid levels decrease = fatty acids released by adipocytes Amino acid levels decrease = amino acids released by liver Glucose levels decrease = glucose released by liver Coordinated by several hormones Glucagon, epinephrine, glucocorticoids, growth hormone Module 22.8: Absorptive and postabsorptive states Postabsorptive state (continued) ◦ Catabolism of lipids and amino acids in liver produce acetyl-CoA Leads to formation of ketone bodies Diffuse into blood and are used by other cells as energy source Module 22.8: Absorptive and postabsorptive states Postabsorptive state (continued) ◦ Hormone effects Glucocorticoids Glucagon Stimulate mobilization of lipid and protein reserves Enhanced by growth hormone Stimulates glycogenolysis and gluconeogenesis Mainly in liver Epinephrine Glycogenolysis in skeletal and cardiac muscle Lipolysis in adipocytes Module 22.8 Review a. Define absorptive state and postabsorptive state. b. When and how do ketone bodies form? c. How do the absorptive and postabsorptive states maintain normal blood glucose levels? Module 22.9:Vitamins Nutrition ◦ Absorption of nutrients from food Vitamins ◦ ◦ Organic compounds required in very small quantities for essential metabolic activities Two classes 1. Fat-soluble vitamins (A, D3, E, and K) 2. Water-soluble vitamins (B vitamins and C) Module 22.9:Vitamins Fat-soluble vitamins ◦ ◦ Absorbed primarily from digestive tract with micelles Vegetables are potential sources ◦ Vitamin D3 produced in skin Vitamin K produced by intestinal bacteria Stored in lipid deposits Gives large bodily reserves Avitaminosis (vitamin deficiency) rarely occurs with fat-soluble vitamins Hypervitaminosis can occur as metabolism from lipid reserves takes time Figure 22.9 2 Figure 22.9 2 Module 22.9:Vitamins Water-soluble vitamins ◦ ◦ Most are components of coenzymes Nutritional sources ◦ ◦ B vitamins are found in meat, eggs, and dairy products Vitamin C is found in citrus fruits Significant stores of only vitamins B12 and C Intestinal bacteria produce four of nine B vitamins Module 22.9:Vitamins Water-soluble vitamins (continued) ◦ ◦ Readily exchanged between body fluid compartments Most easily absorbed across intestinal wall ◦ B12 requires transport with intrinsic factor Excess amounts excreted in urine Hypervitaminosis rarely occurs with water-soluble vitamins Figure 22.9 4 Figure 22.9 4 Figure 22.9 4 Module 22.9 Review a. Define nutrition. b. Identify the two classes of vitamins. c. If vitamins do not provide a source of energy, what is their role in nutrition? Stop Module 22.10: Nutrition and diet Balanced diet ◦ Contains all ingredients required for homeostasis Substrates for ATP production Essential amino acids Fatty acids Vitamins Electrolytes Water ◦ Malnutrition Unhealthy state from inadequate or excessive nutrient absorption Module 22.10: Nutrition and diet MyPyramid.gov Steps to a Healthier You ◦ U.S. Dept. of Agriculture personalized eating plans based on current Dietary Guidelines for Americans ◦ Color-coded vertical food groups indicate recommended proportions Grains (orange) Vegetables (green) Fruits (red) Milk products (blue) Meat and beans (purple) Oils (yellow) The MyPyramid.gov Steps to a Healthier You Activity GRAINS Make half your grains whole VEGETABLES Vary your veggies FRUITS Focus on fruits O MILK I L Get your calcium-rich foods S MEAT & BEANS Go lean with proteins Figure 22.10 1 Figure 22.10 1 Figure 22.10 1 Module 22.10: Nutrition and diet Food energy content ◦ Common units are calories or joules (0.239 calories) 1 calorie = energy to raise temperature of 1 g of water by 1°C ◦ Kilocalories (kcal or Calorie) or kilojoule (kJ) are used for whole-body metabolism 1 kCal = energy to raise temperature of 1 kg of water by 1°C ◦ Energy yield of different nutrients varies Carbohydrates: 4.18 Cal/g Proteins: 4.32 Cal/g Lipids: 9.46 Cal/g ◦ Average adult needs 2000–3000 Cal daily Figure 22.10 2 Figure 22.10 3 Module 22.10: Nutrition and diet Different nutritional proteins ◦ Complete proteins Provide all essential amino acids From beef, fish, poultry, eggs, and milk ◦ Incomplete proteins Deficient in one or more essential amino acids Mostly from plant sources Vegetarians and vegans must closely monitor sufficient combination of plant protein sources Module 22.10 Review a. Define balanced diet. b. Distinguish between a complete protein and an incomplete protein. c. Of these three—carbohydrates, lipids, or proteins—which one releases the greatest number of Calories per gram during catabolism? CLINICAL MODULE 22.11: Metabolic disorders Disorders related to diet and digestion ◦ Eating disorders (psychological problems resulting in abnormal eating habits) Anorexia nervosa Self-induced starvation or lack/loss of appetite Weights commonly 30% below normal Most common in adolescent Caucasian females Patients convinced they are too fat Bulimia Binge eating followed by vomiting, or use of laxatives or diuretics More common than anorexia CLINICAL MODULE 22.11: Metabolic disorders Disorders related to diet and digestion (continued) ◦ Obesity Condition of being >20% over ideal weight U.S. Centers for Disease Control (CDC) estimate: Due to energy input > energy output 32% of men and 35% of women are obese Two major categories 1. Regulatory obesity (failure to regulate food input) Most common form 2. Metabolic obesity (secondary to underlying malfunction in cell/tissue metabolism) CLINICAL MODULE 22.11: Metabolic disorders Disorders related to diet and digestion (continued) ◦ Elevated cholesterol levels May cause development of atherosclerosis and coronary artery disease Recommended <300 mg/day High LDL levels can lead to deposits in peripheral tissues such as blood vessels CLINICAL MODULE 22.11: Metabolic disorders Nutritional/metabolic disorders ◦ Phenylketonuria (PKU) Inability to convert phenylalanine to tyrosine ◦ Essential to synthesis of: Norepinephrine Epinephrine Dopamine Melanin Protein deficiency disease Liver unable to produce plasma proteins leading to edema Example: kwashiorkor CLINICAL MODULE 22.11: Metabolic disorders Nutritional/metabolic disorders (continued) ◦ Ketoacidosis Acidification of blood due to ketone body production Occurs when glucose supplies are limited ◦ Leads to ketosis Fatty acid and amino acid catabolism in liver leads to acetyl-CoA production and generation of ketones In extreme cases, may cause coma, cardiac arrhythmias, and death Gout (insoluble urea crystal formation) Commonly in joints (gouty arthritis) CLINICAL MODULE 22.11 Review a. Identify and briefly define two eating disorders. b. Define protein deficiency disease and cite an example. c. Briefly describe phenylketonuria (PKU). Section 3: Energetics and Thermoregulation Energetics ◦ Study of energy flow and energy conversion ◦ Basal metabolic rate (BMR) Minimum resting energy expenditure of awake, alert person Various factors can affect BMR Person’s size or weight Level of physical activity Common benchmark for energetics studies Direct measurement method Measuring respiratory activity and assuming 4.825 Cal/L oxygen consumed Average is 70 Cal/hr 1000 800 Calories per hour The approximate number of Calories expended per hour at various levels of physical exertion Estimated Calories expended by a 70-kg individual 600 400 200 0 Resting Slow walking Speed walking Climbing stairs Jogging Competitive swimming Figure 22 Section 3 2 Section 3: Energetics and Thermoregulation Thermoregulation ◦ Homeostatic control of body temperature Maintaining food intake adequate to support body activities ◦ Catabolic reactions generating ATP 40% of energy used to form ATP 60% released as heat ◦ Many enzymes and metabolic activities require a specific temperature range Module 22.12: Appetite regulation Appetite is controlled by two areas of hypothalamus 1. Feeding center 2. Satiety center Causes inhibition of feeding center Regulation of appetite can occur on two levels 1. Short-term regulation 2. Long-term regulation Module 22.12: Appetite regulation Short-term regulation of appetite ◦ Stimulation of satiety center Elevation of blood glucose levels Hormones of digestive tract (like CCK) Digestive tract wall stretching ◦ Stimulation of feeding center Neurotransmitters Example: neuropeptide Y or NPY from hypothalamus Ghrelin Hormone secreted by gastric mucosa when stomach is empty Module 22.12: Appetite regulation Long-term regulation of appetite Leptin Peptide hormone secreted by adipocytes Stimulates satiety center and suppresses appetite Effects are gradual Short-Term Regulation of Appetite Stimulation of Satiety Center Hypothalamus Satiety center Elevated bood glucose levels depress appetite, and low blood glucose stimulates appetite. The likely mechanism is glucose entry stimulating the neurons of the satiety center. Several hormones of the digestive tract, including CCK, suppress appetite during the absorptive state. Feeding center Stimulation of stretch receptors along the digestive tract, especially in the stomach, causes a sense of satiation and suppresses appetite. Long-Term Regulation of Appetite Stimulation of Feeding Center Several neurotransmitters have been linked to appetite regulation. Neuropeptide Y (NPY), for example, is a hypothalamic neurotransmitter that (among other effects) stimulates the feeding center and increases appetite. The hormone ghrelin (GREL-in), secreted by the gastric mucosa, stimulates appetite. Ghrelin levels are high when the stomach is empty, and decline as the stomach fills. When appetite outpaces energy usage, excess calories are stored as fat in adipose tissue. Leptin is a peptide hormone released by adipose tissues as they synthesize triglycerides. In the CNS it stimulates the satiety center and suppresses appetite. The effects are gradual, and it is probably involved in long-term regulation of food intake. Mechanisms in the control of appetite Figure 22.12 Module 22.12 Review a. What hormone inhibits the satiety center and stimulates appetite in the short-term? b. Describe leptin and its effect on appetite. c. How might a lack of Neuropeptide Y in the hypothalamus affect the control of appetite? Module 22.13: Thermodynamics Thermodynamics ◦ About 40% of energy from catabolism is captured as ATP Rest is heat that warms surrounding tissues ◦ To maintain body temperature, heat loss and heat production must be in balance Varying activities and environmental conditions affect heat balance Module 22.13: Thermodynamics Primary heat transfer mechanisms 1. Radiation (infrared radiation from warm objects) ~50% of body heat lost by radiation 2. Convection (conductive heat loss due to air movement) 3. Evaporation (water loss from moist areas) Insensible perspiration (from alveoli and skin) Sensible perspiration (from sweat glands) 4. Conduction (direct transfer through physical contact) Primary Mechanisms of Heat Transfer Radiation: Warm objects lose heat energy as infrared radiation. More than 50 percent of the heat you lose indoors is attributable to radiation. The primary mechanisms of heat transfer between the body and the surrounding environment Convection: This process results from conductive heat loss to the air that overlies the surface of the body. Convection accounts for roughly 15 percent of the body’s heat loss indoors Evaporation: When water changes from a liquid to a vapor, evaporation absorbs energy and cools the surface where it occurs. Insensible perspiration—the evaporation of water across epithelia, from alveolar surfaces, and from the skin—accounts for roughly 20 percent of heat loss indoors. The water in sweat is termed sensible perspiration. Conduction: This process, which is the direct transfer of energy through physical contact, is generally not an effective mechanism for gaining or losing heat. When you are standing, conductive losses are negligible. Figure 22.13 1 The effects of a failure to control body temperature Underlying physical or °F environmental condition 114 CNS damage Heat stroke Disease-related fevers Severe exercise Active children 110 106 102 °C 44 Severely impaired 42 38 98 Early mornings in cold weather 94 36 34 90 32 86 30 82 28 26 Hypothermia for open heart surgery 78 74 Impaired 40 Normal range (oral) Severe exposure Thermoregulatory capabilities 24 Major physiological effects Death Proteins denature Convulsions Cell damage Disorientation Effective Systems normal Impaired Severely impaired Lost Disorientation Loss of muscle control Loss of consciousness Cardiac arrest Death Figure 22.13 2 Module 22.13 Review a. Define insensible perspiration. b. What heat transfer process accounts for about one-half of an individual’s heat loss when indoors? c. How is heat loss different between conduction and convection? Module 22.14: Thermoregulation Thermoregulation ◦ ◦ Heat loss and heat gain involve many systems Coordinated by two centers in hypothalamus preoptic area 1. Heat-loss center 2. Heat-gain center Module 22.14: Thermoregulation Responses to high body temperature ◦ ◦ Behavioral changes (moving to shade, pool, etc.) Vasodilation and shunting of blood to skin surface ◦ Radiational and convective heat loss increases Sweat production ◦ Increases evaporative heat loss Respiratory heat loss Depth of respiration increases to increase evaporative heat loss from lungs Preoptic area Heat-loss center Heat-gain center Responses Coordinated by the Heat-Loss Center When Body Temperature Rises Behavioral Changes: A sense of discomfort leads to behavioral responses—getting into the shade, going into the water, or taking other steps that reduce body temperature. Vasodilation and Shunting of Blood to Skin Surface: The inhibition of the vasomotor center causes peripheral vasodilation, and warm blood flows to the surface of the body. The skin takes on a reddish color, skin temperatures rise, and radiational and convective losses increase. Radiation Convection Sweat Production: As blood flow to the skin increases, sweat glands are stimulated to increase their secretory output. The perspiration flows across the body surface, and evaporative heat losses accelerate. Maximal secretion, if completely evaporated, would remove 2320 Cal per hour. Respiratory Heat Loss: The respiratory centers are stimulated, and the depth of respiration increases. Often, the individual begins respiring through an open mouth rather than through the nasal passageways, increasing evaporative heat losses through the lungs. Figure 22.14 Module 22.14: Thermoregulation Responses to low body temperature ◦ Increased generation of body heat Nonshivering thermogenesis Shivering thermogenesis ◦ Release of hormones that increase metabolic rate Increased muscle tone leading to brief contractions Conservation of body heat Vasoconstriction of vessels near body surface Countercurrent exchange of heat Transfer of heat from deep arteries to deep veins Responses Coordinated by the Heat-Gain Center When Body Temperature Falls The heat-gain center responds to low body temperature in two ways: Increased Generation of Body Heat Nonshivering thermogenesis (ther-mō-JEN-e-sis) involves the release of hormones that increase the metabolic activity of all tissues. Sympathetic stimulation of the adrenal medullae releases epinephrine, which quickly increases the rates of glycogenolysis in liver and skeletal muscle and the metabolic rate of most tissues. In shivering thermogenesis, a gradual increase in muscle tone increases the energy consumption of skeletal muscle tissue throughout your body. Both agonists and antagonists are involved, and muscle tone gradually increases to the point at which stretch receptor stimulation will produce brief, oscillatory contractions of antagonistic muscles. In other words, you begin to shiver. Shivering can elevate body temperature quite effectively, increasing the rate of heat generation by as much as 400 percent. Radiation Convection Conservation of Body Heat Warm Warm blood blood from returns trunk to trunk 37°C 24°C Cooled blood to distal capillaries 36.5°– 37°C The vasomotor center decreases blood flow to the dermis, thereby reducing losses by radiation and convection. The skin cools, and with blood flow restricted, it may take on a bluish or pale color. The epithelial cells are not damaged, because they can tolerate extended periods at temperatures as low as 25°C (77°F) or as high as 49°C (120°F). The deep veins lie alongside the deep arteries, and heat is conducted from the warm blood flowing outward to the limbs to the cooler blood returning from the periphery. This arrangement traps the heat close to the body core and dramatically reduces heat loss. The transfer of heat, water, or solutes between fluids moving in opposite directions is called countercurrent exchange. 23°C Cool blood returns to trunk Figure 22.14 Module 22.14 Review a. Name the heat conservation mechanism that results in the conduction of heat from deep arteries to adjacent deep veins in the limbs. b. Describe the role of nonshivering thermogenesis in regulating body temperature. c. Predict the effect of peripheral vasodilation on an individual’s body temperature.