HSC1008 Anatomy and Physiology 2 - Metabolism PDF

HSC1008 ANATOMY AND PHYSIOLOGY 2 METABOLISM - ENERGY BALANCE ANDY LEE (PHD) ASSISTANT PROFESSOR FACULTY HALL #04-17 OFFICE PHONE: 6592 2524 [email protected] LEARNING OUTCOMES  At the end of the lesson, you should be able to:  List the standardized basal conditions for determining...

HSC1008 ANATOMY AND PHYSIOLOGY 2 METABOLISM - ENERGY BALANCE ANDY LEE (PHD) ASSISTANT PROFESSOR FACULTY HALL #04-17 OFFICE PHONE: 6592 2524 [email protected] LEARNING OUTCOMES  At the end of the lesson, you should be able to:  List the standardized basal conditions for determining BMR  Explain the factors influencing BMR  Discuss the regulation of food intake  Define BMI and obesity  Discuss the metabolism of carbohydrates, lipids (including lipoproteins), proteins and vitamins ENERGY INPUT AND OUTPUT  First law of thermodynamics  Energy can be neither be created nor destroyed  Energy input Energy OUT  Ingested food Energy IN  Energy output  External work  Internal work  ENERGY INPUT AND OUTPUT  Internal work 1. Skeletal muscle used other than external work 2. Life sustaining energy requiring processes Fig 17-1; Sherwood MOST FOOD ENERGY IS ULTIMATELY CONVERTED INTO HEAT  Biochemical processing of nutrients  50% of energy from food transferred to ATP Food Energy  50% lost as heat  Usage of ATP 50% 50%  50% lost as heat  Net lost as heat ATP 50%  = 50% + (50% x 50%) HEAT 50%  =75% of energy from food USE Net lost = 75% METABOLIC RATE  Metabolic rate = energy expenditure/unit of time  Rate at which energy is expended by the body during both external and internal work  calorie: basic unit of heat energy  Amount of heat required to raise the temperature of 1g of H2O by 1°C  Kilocalorie or Calorie: used when discussing the human body  Equivalent to 1000 calories METABOLIC RATE BASAL METABOLIC RATE (BMR)  Metabolic rate under standardized basal conditions  Metabolic activity necessary to maintain basic body functions at rest  65 – 70 Calories/hr in an average 70kg man  Usually corrected for differences in body size STANDARDIZED BASAL CONDITIONS 1. Subject not eaten any food for at least 12 hrs 2. At physical rest (no physical activity) 3. No strenuous activity or exercise for at least 30min to 1hr before the test 4. All mental and physical factors that cause excitement must be eliminated 5. Comfortable room temperature (no shivering, no sweating) 6. After a night of restful sleep (8hrs sleep) METHODS OF MEASURING METABOLIC RATE  Direct calorimetry  Measure total quantity of heat given out by the body per unit time  Indirect calorimetry  Food + O2 → CO2 + H2O + energy (mostly transformed into heat)  Energy equivalent of O2 (4.8 Calories/L energy liberated per litre of O2 consumed)  Estimated BMR = O2 consumption (L/hr) x 4.8 Calories/L FACTORS INFLUENCING THE METABOLIC RATE  Thyroid hormone - ↑ MR  Testosterone - ↑ MR  Growth hormone - ↑ MR  Fever - ↑ MR  Sleep - ↓ MR  Malnutrition - ↓ MR ENERGY BALANCE  Energy input must equal energy output to maintain a neutral energy balance  Neutral energy balance: energy intake equals output  Positive energy balance: energy intake exceeds output  Negative energy balance: energy intake is less than immediate requirements External work Energy in food Energy Energy Internal heat consumed input output production Stored energy REGULATION OF FOOD INTAKE 1. Short-term regulation  Food intake from meal to meal (Feeding pattern)  Appetite signals – sensation of hunger  Satiety signals – fullness, suppress desire to eat 2. Long-term regulation  Energy balance and body weight 3. Psychosocial / environmental factors LONG TERM MAINTENANCE OF ENERGY BALANCE  Food intake is controlled primarily by the hypothalamus  Role of the arcuate nucleus: NPY and melanocortins  Arcuate nucleus: central role in long-term control of energy balance and body weight and short-term control of food intake from meal to meal  Neuropeptide Y (NPY): potent appetite stimulator  Melanocortins: group of hormones shown to play a role in energy homeostasis LONG TERM MAINTENANCE OF ENERGY BALANCE  Regulatory inputs to the arcuate nucleus in long-term maintenance of energy balance: Leptin and Insulin  Leptin: essential for normal body-weight regulation  Adipokines: hormones secreted by adipose tissue that play important roles in energy balance and metabolism  Insulin: Important role in long-term control of body weight LONG TERM MAINTENANCE OF ENERGY BALANCE  Leptin  Indication of amount of triglyceride fat stored in adipose tissue  Molecular satiety signal  Suppress appetite, ↓ food consumption, ↑ weight loss  Act on the arcuate nucleus  ↓ NPY production and ↑ melanocortin release  Long term matching of food intake to energy expenditure LONG TERM MAINTENANCE OF ENERGY BALANCE Food Intake Fig 17-2; Sherwood SHORT TERM REGULATION OF EATING BEHAVIOR  Ghrelin: potent appetite stimulator  PYY3-36 : inhibits appetite-stimulating NPY secreting neurons  Cholecystokinin  Released from duodenum during digestion  activates the satiety center in brainstem to signal satiety  Stomach distension: activates the satiety center in brainstem PUTTING IT ALL TOGETHER Fig 17-2; Sherwood SUMMARY OF FACTORS INVOLVED IN APPETITE OBESITY  Obesity occurs when more kilocalories are consumed than are burned  Body mass index (BMI): mathematical means of assessing the proportion of body fat  BMI = Weight (Kg) / Height2 (Meters) BODY MASS INDEX (BMI) Asian BMI cut-off points for action BMI (kg/m2) Cardiovascular Disease Risk Below 18.5 18.5-22.9 Low 23 – 27.4 Moderate 27.5 – 32.4 High 32.5 – 37.4 Very High Above 37.5 Adapted from HPB-MOH Clinical Practice Guidelines 1/2016 CAUSES OF OBESITY  Complex, involves physiological, lifestyle and environment factors  Sedentary lifestyle  Abnormal feeding behavior  Genetic factors  Leptin-signaling pathway dysfunction  Childhood overnutrition  Hypothyroidism – deficiency of thyroid hormone TREATMENT OF OBESITY  Lifestyle modification  Increase energy output  Decrease energy input  Drugs  Decreasing degree of hunger  Altering lipid absorption in gut  Surgery  Gastric bypass surgery etc METABOLISM  Chemical processes or reactions in an organism required to sustain life  Functions 1. Metabolic turnover 2. Growth and cell division 3. Special processes such as secretion, contraction and the propagation of action potentials METABOLISM  Catabolism  Is the breakdown of organic substrates  Releases energy used to synthesize high- energy compounds (e.g., ATP) ENERGY  Anabolism  Is the synthesis of new organic molecules  Uses energy (ATP) produced by mitochondria OVERVIEW OF ORGANIC COMPOUNDS IN METABOLISM (Fig. 25-1; Martini) METABOLISM  Functions of Organic Compounds 1. Perform structural maintenance and repairs 2. Support growth 3. Produce secretions 4. Store nutrient reserves ORGANIC COMPOUNDS AS NUTRIENT RESERVE Fig. 25-2; Martini (10th ed) CARBOHYDRATE METABOLISM  Generates ATP and other high-energy compounds by breaking down carbohydrates  Glucose + Oxygen = Carbon dioxide + Water  For one glucose molecule processed, cell gains 30-32 molecules of ATP  2 from glycolysis  5 from NADH generated in glycolysis (ETC)  2 from citric acid cycle (GTP)  23 from NADH and FADH2 generated in citric acid cycle (ETC) CARBOHYDRATE METABOLISM Fig 25-5; Martini CARBOHYDRATE METABOLISM  Gluconeogenesis  Is the synthesis of glucose from noncarbohydrate precursors  Lactic acid, Glycerol, Amino acids  Stores glucose as glycogen in liver and skeletal muscle  Glycogenesis  Is the formation of glycogen from glucose  Occurs slowly  Glycogenolysis  Is the breakdown of glycogen  Occurs quickly LIPID METABOLISM  Lipid Catabolism (Lipolysis)  Hydrolysis splits triglyceride into components  One molecule of glycerol and Three fatty acid molecules  Enzymes in cytosol convert glycerol to pyruvate  Different enzymes convert fatty acids to acetyl-CoA (beta-oxidation) LIPID METABOLISM  Lipids and Energy Production  For each 2-carbon fragment removed from fatty acid, cell gains:  12 ATP from acetyl-CoA in citric acid cycle  5 ATP from NADH  Cell can gain 120 ATP molecules from breakdown of one 18-carbon fatty acid molecule  Fatty acid breakdown yields about 1.3 times the energy of glucose breakdown LIPID METABOLISM  Lipid Synthesis (Lipogenesis)  Essential fatty acids  Cannot be produced by the body, must be consumed  Linoleic acid, Linolenic acid (Unsaturated 18-carbon fatty acid from plants)  Glycerol  Is synthesized from dihydroxyacetone phosphate (intermediate product of glycolysis)  Nonessential fatty acids and steroids  Are synthesized from acetyl-CoA  Can use almost any organic substrate LIPID METABOLISM  Most lipids are not soluble in water  Most lipids circulate through bloodstream as lipoproteins  Free fatty acids are a small percentage of total circulating lipids  Generally bound to albumin in blood  Can diffuse easily across plasma membranes LIPID METABOLISM  Lipoproteins  Lipid–protein complexes 1. Chylomicrons 2. Very low-density lipoproteins (VLDLs) 3. Intermediate-density lipoproteins (IDLs) 4. Low-density lipoproteins (LDLs) 5. High-density lipoproteins (HDLs) triglyceride LDL = Total cholesterol − HDL − (mg/dL) 5 LIPOPROTEINS AND LIPID TRANSPORT AND DISTRIBUTION (Fig. 25-8; Martini) PROTEIN METABOLISM  Cellular proteins are recycled in cytosol  Peptide bonds are broken  Free amino acids are used in new proteins  When glucose and lipid reserves are inadequate, liver cells:  Break down internal proteins  Absorb additional amino acids from blood PROTEIN METABOLISM  Three Factors against Protein Catabolism 1. Proteins are more difficult to break apart than complex carbohydrates or lipids 2. A by-product, ammonium ion, is toxic to cells 3. Proteins form the most important structural and functional components of cells PROTEIN METABOLISM  Protein Synthesis  The body can synthesize half of the amino acids needed to build proteins  Non-essential amino acids  11 Amino acids made by the body on demand  Nine essential amino acids  Cannot make or cannot make in sufficient quantity  Histidine, Isoleucine, leucine, lysine, threonine, tryptophan, phenylalanine, valine, and methionine VITAMINS  Essential organic nutrient that functions as a coenzyme in vital enzymatic reactions  Deficiency in diet may cause metabolic deficits  Vitamins are assigned to either of two groups based on their chemical structure and characteristics 1. Fat-soluble vitamins 2. Water-soluble vitamins FAT-SOLUBLE VITAMINS  Vitamins A, D, E, and K  Are absorbed primarily from the digestive tract along with lipids of micelles  Normally diffuse into plasma membranes and lipids in liver and adipose tissue  The body contains significant reserves of fat-soluble vitamins (stored to a major extent in the liver)  Normal metabolism can continue several months without dietary sources FAT-SOLUBLE VITAMINS  Vitamin A  A structural component of visual pigment retinal  Vitamin D  Is converted to calcitriol, which increases rate of intestinal calcium and phosphorus absorption  Vitamin E  Stabilizes intracellular membranes  Vitamin K  Helps synthesize several proteins, including four clotting factors FAT-SOLUBLE VITAMINS Martini WATER-SOLUBLE VITAMINS  Components of coenzymes  Rapidly exchanged between fluid in digestive tract and circulating blood  Excesses are excreted in urine  Relatively less storage as compared to Fat-soluble vitamins  Absence of vitamin C can cause symptoms within a few week WATER-SOLUBLE VITAMINS Martini VITAMIN DEFICIENCY Scurvy (Ascorbic acid deficiency) Pellagra (Niacin deficiency) REFERENCES  Chapter 16. Sherwood, L. (2016) Human Physiology: From Cells to Systems. 9th edition. Cengage  Chapter 25. Martini, F. H., Nath, J.L., & Bartholomew, E. F. (2018). Fundamentals of Anatomy and Physiology. 11th Global Edition. Pearson.  Hall, J. E., & Hall, M. E. (2020). Guyton and Hall textbook of medical physiology. 14th Edition. Elsevier Health Sciences.