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Saladin Ch. 26 Nutrition & Metabolism I. NUTRITION 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 appetites control Short term regulators Ghrelin – from stomach – sensation of hunger + stimulates hypothalamus to release GHRH. 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 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 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 Neurotransmitters influence types of food consumed Norepinephrine – CBH Galanin – fat Endorphins - protein 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. Calories Calorie - amount of heat required to raise one gram of water one degree Celsius. Kilocalorie [the dietary Calorie} = 1000 calories. Energy yields of nutrients Carbohydrate - 4Kcal/g Lipid - 9 Kcal/g Protein - 4 Kcal/g Nutrients Any ingested chemical that is used for growth, repair or maintenance. Required dietary Nutrients – review RDA, Table 26.1 Carbohydrates Fates of CBH’s ATP production – aerobic respiration, anaerobic fermentation Glycogen & adipose storage Amino Acid synthesis Saladin Ch. 26 1 of 7 Structural component of nucleotides, glycoproteins, glycolipids 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 forms. Promotes intestinal function. Water soluble forms reduce blood cholesterol & LDL’s. Blood sugar levels – 70 -110 mg/dL = normal range. Lipids Fatty acids, glycerol, cholesterol Meet 80 – 90% of resting energy needs Required for absorption of fat soluble vitamins Membrane & hormone structural components. 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. 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 Cholesterol & Lipoproteins - transported as spheres The spheres are lipoproteins – hydrophobic triglycerides and cholesterol esters are in the interior, hydrophilic phospholipid heads, cholesterol and proteins are on the exterior surface. Classes Chylomicrons – 2% protein, 90% triglyceride, 3% phospholipid, 5% cholesterol VLDL – 8% protein, 55% triglycerides, 17% phospholipid, 20% cholesterol 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] 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 Bad LDL > 159 mg/dL Saladin Ch. 26 2 of 7 Total > 239 mg/dL 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 amino acids 8 essential amino acids - we don't make or can't make enough isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, valine, histidine, arginine 12 non-essential - synthesized by the body by transamination. Not stored – must be present when needed from ingestion. Nitrogen balance – when in = out – positive with growth, negative with insufficiency. Vitamins & Minerals 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 II. CARBOHYDRATE METABOLISM All oxidative CBH consumption is essentially glucose catabolism C6H12O6 + 6O2 6H2O +6CO2 + ATP [+heat] Glucose catabolism – glycolysis, anaerobic fermentation, aerobic respiration Mechanisms - Redox Reduction reactions add electrons to substances. Oxidations remove electrons [stepwise removal of pairs] They are always coupled – the electrons given in the reduction are equal in number to the ones removed in the oxidation. In biologic systems, the most common oxidation process generates 2 H’s plus 2 electrons. These associate with a co-enzyme – either one or both H’s binds [one may be released]. Ex. NAD+ [nicotinamide adenine dinucleotide] is in the oxidized state. It receives the pair to form NADH and H+. Other co-enzymes include NADP+ and FAD+ [flavin adenine dinucleotide] 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’s Anaerobic fermentation Glucose Metabolism in the Absence of Oxygen 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+ Saladin Ch. 26 3 of 7 Runs twice per original glucose 2 Acetyl CoA’s 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 Membrane reactions - oxidize NADH & FADH2 to move electrons, & regenerate NAD+ & FAD+ Electron Transport System – on inner mitochondrial membrane – cristae - pumps H+ ions for Chemiosmosis. 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. 3 pumps present 1 – NADH dehydrogenase complex – FMN and 5 Fe-S centers – start – NADH + H+ is oxidized to NAD+ and FMN is reduced to FMNH2. This is oxidized--- and so on down line – Ends with Coenzyme Q – a mobile carrier that transports the electrons it receives to the next pump. 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 and passes them to Cu then to cyt a, cyt a3 and then to O. The negative O picks up 2 H+ H2O [only place in respiration where O is consumed!!!] Energy from step-wise release powers pumping H+ into intermediate 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). 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. ENERGY YIELD OF CELLULAR RESPIRATION [2-3 ATP/NADH, 2 ATP/FADH2] Step Products Energy[with O] without O Glycolysis 2ATP 2 ATP 2ATP 2NADH 4 - 6 ATP Transition 2NADH 6 ATP Krebs 2ATP 2 ATP 6NADH 18 ATP 2FADH2 4 ATP Totals 36 - 38 ATP 2 ATP Glycogen metabolism [glucose is stored, not ATP] Glycogenesis – glucose converted into glycogen for storage Saladin Ch. 26 4 of 7 In liver and skeletal muscle Stimulated by insulin Glucose is converted to Glucose – 6 phosphate. Glucose –6 – phosphate is converted to glucose -1-phosphate which is converted to glycogen Glycogenolysis – gets glucose out of glycogen In liver Stimulated by glucagon and epinephrine Glycogen cleaved releases glucose-1-phosphate. Glucose-1-phosphate is converted to glucose-6-phosphate Glucose-6phosphate is converted to glucose or can enter glycolysis. Gluconeogensis – In liver, making of new glucose –from protein and or fat Stimulated by cortisol, glucagons, epinephrine 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 III. LIPID & PROTEIN METABOLISM Lipids Lipid Transport – most non-polar lipids complex with protein made in the liver and intestines to produce water soluble spheres [see above] Lipogenesis In liver and adipose Glucose or amino acids converted into lipids Glucose glyceraldehyde glyceraldehyde-3-phosphate glycerol or to acetyl CoA which can go on to form fatty acids Amino acids Acetyl CoA fatty acids, etc. Stimulated by Insulin Lipolysis Liver. First lipids are split into glycerol & fatty acids by lipases. Then, by beta oxidation, cleaves the A's into 2C fragments and attaches them to CoA to form Acetyl CoA for Kreb’s cycle, or converts 2Acetyl CoA’s to acetoacetic acid & then to beta-hydroxybutyric acid and acetone [all 3 are called ketone bodies] Too much acidosis Proteins Protein metabolism Amino Acids are either used to make other proteins, glucose or triglycerides or ATP, they are not stored. Use as fuel Proteins are broken down to amino acids Deamination in liver allows them to enter the Kreb's cycle For Kreb's - aa is converted to acetyl CoA or an acid in the cycle For gluconeogenesis - the amino less acid is converted to pyruvate and Other molecules that can enter the Kreb’s cycle. Saladin Ch. 26 5 of 7 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 Amino acids joined by peptide bonds Stimulated by GH, Insulin, T3, T4, estrogen and testosterone IV. METABOLIC STATES & METABOLIC RATE Absorptive State - During digestion Ingested nutrients enter blood and lymphatic system --> hepatic portal system to liver Lasts about 4 hours after completing a meal 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%) 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] Post Absorptive State - fasting Need to maintain normal blood glucose level [90-100mg/100mL] Very important for nervous system - can only use glucose for energy. 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 Muscle protein aa converted by liver into glucose [gluconeogenesis] Hormone – glucagon; Neural Control – ANS via epinephrine 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 Influences Surface area – greater surface area, higher BMR Age – younger, higher Gender – Male much higher Body Temperature – higher, higher Stress – increases BMR T3 and T4 – increase BMR BODY HEAT & THERMOREGULATION Imbalances Hyperthermia – elevated body temperature - Heat stroke, fever Hypothermia - too low --> death Saladin Ch. 26 6 of 7 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] Heat production & loss Mechanisms of Heat Exchange Radiation - exposed surface area [60%] - heat moves from high to low Conduction - transfer to another object [ice pack, e.g.] [18%] Convection - transfer by moving currents - water, air, etc. Evaporation - sweat, etc. [22%] Thermoregulation Thermostat = hypothalamus [preoptic area] Heat losing center - parasympathetic Heat promoting area - sympathetic Factors Affecting heat Production Vasoconstriction, shivering, Increase in metabolic rate Hormones [T3, T4] ALCOHOLISM - review system effects - p. 1029 Saladin Ch. 26 7 of 7