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SALADIN C. 26 Nutrition & Metabolism, Body Weight & Energy Balance • 30 – 50% of variation in human body weight is heredity, rest is environmental factors – eating & exercise habits. Appetite • Many peptide hormones & regulatory pathways are involved in short & long term appetite control • Short term regulators – Ghrelin – from stomach – sensation of hunger + stimulates hypothalamus to release – GHRH Appetite – Peptide YY [PYY] – from ileum & colon – secreted with feeding – proportional to calories consumed – stop eating signal. – CCK – from SI – stimulates secretion of bile & pancreatic enzymes. – Also causes appetite suppressing effect on vagus – a stop eating signal Appetite • Long term regulators – Leptin – from adipocytes – proportional to levels of body fat – most human obesity related to leptin is due to receptor defect, not hormone defect – Insulin – from pancreas – receptors in brain – functions like leptin - weaker Appetite • Brain center = arcuate nucleus of hypothalamus – 2 groups of neurons 1 – secretes neuropeptide Y – stimulates appetite 2 – secretes melanocortin – inhibits eating Gastric peristalsis also stimulates hunger Control of Feeding & Satiety Figure 24.23 Appetite • Neurotransmitters influence types of food consumed – Norepinephrine – CBH – Galanin – fat – Endorphins - protein Appetite • Obesity – more than 20% above norm for demographic. In US 30% are obese and an additional • 35% are overweight. • Predisposition to obesity is increased by over-feeding in infancy and early childhood. Heat – kinetic energy • Heat = kinetic energy • calorie-amount of heat required to raise one gram of H2O 1oC Energy Yields • Carbohydrates - 4Kcal/g • Lipid- 9 Kcal/g • Protein – 4 Kcal/g Nutrients • Nutrient – a substance that promotes normal growth, maintenance, and repair. • Major nutrients – carbohydrates, lipids, and proteins. • Other nutrients – vitamins and minerals (and technically speaking, water). Nutrition – [see www.mypyramid.gov for details] Figure 24.1 CBH Fates of CBH’s • ATP production – aerobic respiration, anaerobic fermentation • Glycogen & adipose storage • Amino Acid synthesis • Structural component of nucleotides, glycoproteins, glycolipids CBH • Excretion – spill over onto urine • Neurons & erythrocytes depend almost entirely on CBH • Review Insulin/glucagon homeostasis – Ch 17; CBH in API notes Requirements – higher than other nutrients • Sources – plants • Fiber – resist digestion – plant & animal CBH • Promotes intestinal function. Water soluble forms reduce blood cholesterol & LDL’s. • Blood sugar levels – 70 -110 mg/dL = normal Lipids • Fatty acids, glycerol, cholesterol • Meet 80 – 90% of resting energy needs • Required for absorption of fat soluble vitamins • Membrane & hormone structural components. Lipids • Needs – no more than 30% of diet – most should be unsaturated; • Must get linoleic acid from diet – rest appear to be able to be made. Lipids Cholesterol Metabolism • Structural unit of bile salts, steroids, Vitamin D and cell membranes. – 15% of blood cholesterol is from diet – 85% is made by the body Lipids • Cholesterol & Lipoproteins - transported as spheres • The spheres are lipoproteins – hydrophobic triglycerides & cholesterol esters are in interior, hydrophilic phospholipid heads, cholesterol & proteins are on exterior Lipids Classes • Chylomicrons – 2% protein, 90% triglyceride, 3% phospholipid, 5% cholesterol • VLDL – 8% protein, 55% triglycerides, 17% phospholipid, 20% cholesterol Lipids • LDL (bad cholesterol – gets deposited in blood vessels) 20% protein, 6% triglyceride, 21% phospholipid, 53% cholesterol – gets deposited in vessel walls [from adipose]. • HDL – 50% protein, 5% triglyceride, 25% phospholipid, 20% cholesterol (good cholesterol) cleared by liver – no vascular buildup. [transport TO liver] Lipids Desirable levels • Total cholesterol - < 200mg/dL – LDL < 130mg/dL – HDL > 40mg/dL [60 or higher gives some protection against heart disease] – Total <200mg/dL – Ratio of total/HDL <4 desired Lipids • Bad – LDL > 159 mg/dL – Total > 239 mg/dL Lipids Factors regulating plasma cholesterol • Increased dietary cholesterol decreases liver production, BUT doesn’t stop it. • Saturated fatty acids increase liver synthesis and decrease excretion • Unsaturated fatty acids increase excretion • Hydrogenated fats increase LDL’s and decrease HDL [worst effect of all] Proteins Proteins amino acids • 8 essential amino acids - we don't or can't make enough • 12 non-essential - synthesized by the body by transamination. • Not stored – must be present from ingestion. • Nitrogen balance –in = out – positive with growth, negative with insufficiency. Vitamins & Mnerals • Vitamins – review table 26.3 – Fat soluble - A, D, E, K – Water soluble - B1, B2, niacin, B6, B12, Folic acid, C • Minerals – review table 26.2 - Ca, P, Fe, I, Cu, Na, K, Cl, Mg, S, Zn, F, Mn Metabolism • Metabolism – all chemical reactions necessary to maintain life. • Anabolic reactions – synthesis of larger molecules from smaller ones. • Catabolic reactions – hydrolysis of complex structures into simpler ones. CBH Metabolism • All oxidative CBH consumption is essentially glucose catabolism C6H12O6 + 6O2 6H2O +6CO2 + ATP [+heat] • Glucose catabolism – glycolysis, anaerobic fermentation, aerobic respiration Oxidation-Reduction (Redox) Reactions • Oxidation removes electrons. • Reduction adds electrons. • Coenzymes act as hydrogen (or electron pair) acceptors. • Two important coenzymes are nicotinamide adenine dinucleotide (NAD+) and flavin adenine dinucleotide (FAD). Carbohydrate Metabolism • Glucose is catabolized in three pathways: – Glycolysis & anaerobic fermentation – Krebs cycle – The electron transport chain & oxidative phosphorylation Carbohydrate Catabolism Figure 24.5 Glycolysis • A three-phase pathway in which: – Glucose is oxidized into pyruvic acid. – NAD+ is reduced to NADH + H+. – ATP is synthesized by substrate-level phosphorylation. Glycolysis • Glycolysis – occurs in cytoplasm – converts glucose to pyruvate • Immediately upon entry into the cell, glucose is converted to glucose-6-phosphate • 10 steps –SEE HANDOUT and Figure 26.3 • Ends [for 1 glucose] 2 pyruvates, 2 net ATP and 2NADH + 2H+ Glycolysis Anaerobic fermentation • Glucose Metabolism in the Absence of O2 • Lactic acid fermentation – in muscle cells • Starts with pyruvate and NADH – Produces lactic acid and NAD+. Lactic acid can be used in liver for glucose synthesis. – Renews NAD+ in cytoplasm for continued ATP production. Matrix Reactions • Starts with pyruvate, NAD+ and Coenzyme A [CoA] --> AcetylCoA + CO2 + NADH + H+ • Runs twice per original glucose 2 Acetyl CoA’s Matrix Reactions • Kreb’s Cycle – in matrix of mitochondrion – 8 steps – SEE Handout – Starts with Acetyl CoA, oxaloacetic acid, NAD+, FAD+ – Runs twice per original glucose molecule – Ends - [with 2 pyruvates] 6CO2 + 2 ATP + 8 NADH + 8H+ + 2FADH2 Figure 24.7 Membrane Reactions • Membrane reactions - oxidize NADH & FADH2 to move electrons, & regenerate NAD+ & FAD+ • Electron Transport System – on inner mitochondrial membrane – cristae pumps H+ ions for Chemiosmosis. Membrane Reactions • Need electron carriers – pass electrons from one carrier to another by paired redox reactions. • Carriers = Flavin Mononucleotide [FMN], cytochromes, Fe-S centers, Cu, Coenzyme Q. Electronic Energy Gradient Figure 24.9 Membrane Reactions 3 pumps present • 1 – NADH dehydrogenase complex – FMN & 5 Fe-S centers – start – NADH + H+ is oxidized to NAD+ and FMN is reduced to FMNH2. Ends with Coenzyme Q – a mobile carrier that transports the electrons it receives to the next pump. Membrane Reactions • 2 – Cytochrome b-c1 complex – electrons passed from Q to cyt b --- to cyt c –> passes electrons to next pump • 3 – cytochrome oxidase complex – receives electrons from cyt c & passes them o Cu then to cyt a, cyt a3 & then to O. The negative O picks up 2 H+ H2O [only place in respiration where O is consumed!!!] Chemiosmosis • Energy from step-wise release powers pumping H+ into intermembrane space by chemiosmosis – The concentration of H+ outside > than that inside – this produces an electrostatic gradient and a net voltage. – Since it is positive charges – it is called proton motive force instead of electromotive force (from electron distribution). Chemiosmosis – Facilitated diffusion channels containing enzymes for ATP formation [ATP synthase] allow the H+ to move back across the membrane driven by this force. – The energy from the force is used for the ATP production. • Figure 24.8 Energy Yield of Cellular Respiration Step Product Glycolsis Energy (O) Energy (no O) 2 ATP 2 NADH Transition 2NADH Krebs 2ATP 6NADH 2ATP 4-6ATP 6ATP 2ATP 18ATP 2FADH2 4ATP Totals 36-38ATP 2ATP 2ATP Glycogen Metabolism Gluconeogenesis • Forms glucose from non-CBH molecules. • In the liver. • Protects the body, especially the brain, from the damaging effects of hypoglycemia by ensuring ATP synthesis can continue. • Stimulated by insulin Glycogen Metabolism • Glycogenolysis – breakdown of glycogen in response to low blood glucose • Stimulated by glucagon Figure 24.12 Glycogen Metabolism Glycogenesis Glucose is converted to Glucose – 6 – P Glucose –6 – P is converted to glucose -1-P which is converted to glycogen Liver Disorders Liver disorders • Hepatitis - inflammation - viral usually - 5 strains – A most common - transmitted in large restricted groups & by foods – B & C are sexually transmitted & by blood and fluids. – Symptoms - Fatigue, malaise, nausea, weight loss Hepatitis C Lipid Metabolism Lipid transport • Most non-polar lipids complex with protein to produce water soluble spheres Lipogenesis • Excess glycerol & fatty acids undergo lipogenesis to form triglycerides in the liver. • Glucose or amino acids converted into lipids Glucose glyceraldehyde glyceraldehyde3-phosphate glycerol or to acetyl CoA which can go on to form fatty acids • Amino acids Acetyl CoA fatty acids, etc. • Stimulated by Insulin Lipid Catabolism Lipolysis • Lipids are split into glycerol & fatty acids. • Fatty acids undergo beta oxidation which produces 2-carbon acetic acid fragments, that can enter the Krebs cycle, or form ketone bodies Lipid Metabolism Figure 24.13 Protein Metabolism • Excess protein results in amino acids being used to make other proteins, glucose, triglycerides or ATP. • Proteins are not stored. Protein Catabolism Use as fuel: • Deaminated amino acids can be converted into pyruvic acid & into one of the keto acid intermediates of the Krebs cycle. Proteins Transamination, ammonia & urea • Amino group ammonia urea • Amino group is transferred to citric acid -> --> glutamic acid --> liver --> removal of NH2 --> ammonia --> urea Protein synthesis - occurs on ribosomes, directed by DNA and RNA • Stimulated by GH, Insulin, T3, T4, estrogen and testosterone Summary: Carbohydrate Metabolic Reactions Table 24.2.1 Summary: Lipid and Protein Metabolic Reactions Table 24.2.2 Absorptive and Postabsorptive States • Metabolic controls balance blood concentrations of nutrients between two states: – Absorptive • The time during & shortly after nutrient intake Absorptive and Postabsorptive States – Postabsorptive • The time when the GI tract is empty. • Energy sources are supplied by the breakdown of body reserves. Absorptive State • Ingested nutrients enter blood and lymphatic system --> hepatic portal system to liver • Lasts about 4 hours after completing a meal Absorptive State Events: • Glucose – Glucose uptake by liver converted to triglycerides and glycogen (10%) – Adipose tissues store fat take up blood glucose to triglycerides (40%) – Muscles take up glucose and store as glycogen (50%) Absorptive State Events: • Amino Acids liver Kreb's cycle or gluconeogenesis or protein synthesis • Lipids most packaged VLDL lipoproteins and are carried to adipose. • Hormones -mostly, insulin [hypoglycemic hormone] Absorptive State Figure 24.18a Principal Pathways of the Absorptive State Figure 24.18b Postabsorptive State • Need to maintain normal blood glucose level [90-100mg/100mL] • Very important for nervous system can only use glucose for energy. Postabsorptive State EVENTS: • Liver glycogen is converted to glucose - lasts about 4 hrs. • Muscle glycogen is converted to lactic acid glucose in liver • Adipose breaks triglycerides to glycerol glucose Postabsorptive State • Muscle protein aa converted by liver into glucose [gluconeogenesis] • Hormone – glucagon; Neural Control – ANS via epinephrine Postabsorptive State Figure 24.20a Principle Pathways in the Postabsorptive State Figure 24.20b Metabolic Rate • Basal metabolic rate [BMR] - rate of metabolism measured under standard conditions - awake, resting, fasting. • Units = Kcal/m2/hr. Can be indirectly measured by monitoring oxygen consumption per unit time. [averages ~2000 kcal/day] Factors that Influence BMR • Surface area, age, gender, stress, & hormones. • Ratio of surface area to volume [if increases, BMR increases]. • Sex. [Males have a high BMR]. Factors that Influence BMR • Stress. [Increases BMR]. • Thyroxine increases oxygen consumption, cellular respiration, & BMR. Thermoregulation Imbalances • Hyperthermia – elevated body temperature Heat stroke, fever • Hypothermia - too low --> death Thermoregulation Body temperature • Core temperature =~ 37.2 - 37.6 oC [can be higher with high activity] • Shell temperature =~ 36.6 - 37.0 oC [can be higher with high activity] Mechanisms of Heat Exchange • The body uses four mechanisms of heat exchange: – Radiation – Conduction – Convection – Evaporation Regulation of Body Temperature Figure 24.25 Role of the Hypothalamus • The chief thermoregulation center is the pre-optic region of the hypothalamus. • Thermoregulatory areas include heat-loss & heat-promoting centers. Heat-Promoting Mechanisms • Activation of heat-promoting centers of the hypothalamus causes: – Vasoconstriction of cutaneous blood vessels. – Shivering. – Increased metabolic rate. – Enhanced thyroxine release. Heat-Loss Mechanisms • When core temperature rises, the heat-loss center is activated to cause: – Vasodilation of cutaneous blood vessels, – Enhanced sweating