Minerals Exam Final Study Guide
Minerals Exam Final Study Guide NUTR 4550
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This 22 page Study Guide was uploaded by Victoria Hills on Thursday April 28, 2016. The Study Guide belongs to NUTR 4550 at Clemson University taught by Dr. Elliot Jesch in Spring 2016. Since its upload, it has received 16 views. For similar materials see Nutrition and Metabolism in Nutrition and Food Sciences at Clemson University.
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Clemson University Spring 2016 NUTR 4550 Minerals Exam Study Guide Calcium and Phosphorous Slide 3 • Vitmain D and calcium work together • Calcium is also related to vitamin K since it is involved in the blood clotting cascade • Figure shows how calcium can interact with an inactive protein and convert it to its active form • Calmodulin: Calcium-‐binding protein -‐ Calcium-‐bound calmodulin is what binds to an inactive protein to activate it • Curved arrow towards the top right indicates that a secondary messenger system -‐ A first messenger can be a substance such as a hormone that delivers a message to a cell and binds to a specific receptor à Activation of a secondary messenger inside the cell à Takes the message from outside the cell and illicits a change in a function, gene expression, metabolic activity of an enzyme or metabolic pathway -‐ Calcium would be the secondary messenger in this case in sending on the signal from the initial hormone Slide 4: Hormonal Control of Calcium and Phosphate Metabolism Calcium • Relation to Vitamin D: -‐ If there is an increase in vitamin D à Works to maintain concentration of calcium in the blood through increasing calcium levels in the blood • Thyroid gland: -‐ Can produce PTH (Means more calcium is needed in the blood) that can affect: a) Bone: o Have hydroxyapatite: Primary compound stored in bone § Mineral aggregate so that calcium, phosphorous, and magnesium come together to form bone § (Most calcium stores are in bone) § Removes calcium from bone to help increase blood-‐calcium concentrations b) Kidney: o Signaling occurs to produce 1,25-‐dihydroxyvitamin D o Specifically: 1,25-‐hydroxylase activity and therefore active vitamin D are increased to signal the intestine to increase calcium absorption o PTH can also signal reabsorption of calcium from filtrate o Only 10% of calcium filtered daily is excreted à Most is reabsorbed • Intestine: -‐ There are many ways to increase the uptake of calcium absorption -‐ Transporters on the apical and basolateral side of the enterocyte bind calcium -‐ Vitamin D up regulates transporters -‐ *Consumption of a lot of calcium à expression and uptake of calcium is relatively lower vs. a dairy free person where the expression of proteins increases and relative uptake if higher Phosphorus • Uses: -‐ Formation of ATP and transferring high energy phosphate groups à AKA trapping nutrients inside cells -‐ Ex: Phosphorylation of glucose -‐ Used in cell membranes with phosphoglycerides and phosphatidyl choline -‐ Regulation of metabolism à Phosphorous cascade of any number of enzymes helps to regulate metabolic pathways • Thyroid gland: -‐ Opposite of calcium occurs: Increased plasma phosphorous à Increase of PTH production to ultimately reduce phosphorous in the blood -‐ PTH signals the kidney to illicit a number of different changes: a) Reabsorption of phosphorous is decreased so that it is excreted b) Decrease in 1-‐a-‐hydroxylase and an increase in 24-‐hydroxylase • PTH acting on the intestine: -‐ Decrease phosphorous absorption -‐ Due to vitamin D signaling à Reduces phosphorus transporters and therefore reduction in the uptake and absorption of phosphorous to effectively reduce concentration in the blood Slide 5: Osteoclastogenesis vs. osteoblast-‐mediated regulation • Bone metabolism shown • At the bottom of the figure is bone • Compounds in the pro-‐resorptive and calciotropic factors box + anti-‐ resorptive or anabolic factors box à Signaling compounds (Ligands) for each that will inform cells, bone, etc. what should be occurring • Osteoblasts: -‐ Function to be on the anabolic side in laying down mineral in bone -‐ Increases the mineral content of bone -‐ *Osteoclasts (What is looked at here) remove mineral from bone • Progenitor cell (Precursor cell) à Preosteoclast à Mature osteoclast à Activated osteoclast -‐ If there is an osteoclast progenitor cell + RANK on the cell à Ligands in boxes are where they bind to RANK à Stimulation or inhibition of maturation and activation of osteoclasts (Depends on the ligand) • Pro-‐resorptive and calciotropic factors: -‐ Starting with the preosteoclast: Cascade that signals the maturation of becoming an osteoclast à Later activated osteoclast -‐ Factors work with RANKL (Ligand for RANK receptor that is an activator of nuclear factor kappa beta) and pRANKL (Ligand carried within the plasma) à Signal for the maturation and activation of osteoclast to break down bone mineral density -‐ Ligands that bind to RANK to promote osteoclast formation: o Vitamin D (1,25-‐dihydroxyvitamin D): § Active vitamin D increases the concentration of calcium in the blood by increasing the absorption in the intestine, increase reabsorption in the kidneys, and increase reabsorption from bone o PTH o PTHrP o IL1 o IL6 o TNF o Corticosteroids o Prolactin • Anti-‐resorptive or anabolic factors: -‐ Factors work with OPG to inhibit osteoclast maturation and activation à Ultimately inhibits the removal or absorption of calcium from bone -‐ Ligands that bind to OPG for inhibiting osteoclast formation: o Calcium: § When consuming calcium, it is not needed to be taken out of bone because there is another pathway available for increasing the concentration of calcium in the blood o Estrogens: § Before 25, estrogen is very beneficial in depositing bone mineral density § Less available after menopause à Bone mineral density drops off o Calcitonin o BMPs o TGFB o PDGF Slide 6: Figure 32.5-‐ Calcium and phosphorous balance in normal physiology • Absorption of calcium and phosphorous shown • Calcium: -‐ 300 mg of 1,000 mg consumed will be absorbed into the extracellular fluid -‐ 150 mg of endogenous calcium can be moved from the extracellular fluid to the GI tract -‐ Why there is a net absorbance of 150 mg of calcium -‐ 850 mg of calcium exits in the feces à Accounts for what was not absorbed from the diet + the endogenous calcium that was lost -‐ Extracellular fluid pool of 1000 mg of calcium: o From the extracellular fluid pool à Formation of hydroxyapatite: Depositing of mineral into bone o Resorption of calcium from bone à extracellular fluid pool to maintain blood calcium concentrations § Regulator of calcium = Blood o 2% of calcium is excreted via urine • Phosphorous: -‐ 700 mg of phosphorous is consumed per day -‐ A greater amount is consumed than calcium (550 mg) into the extracellular fluid -‐ 150 mg of endogenous phosphorus is sloughed off into the GI tract -‐ Net absorption of 400 mg into the extracellular fluid pool -‐ 10% is excreted via urine Slide 7: Model of para-‐cellular and trans-‐cellular calcium transport • Para-‐cellular transport: Between cells • Trans-‐cellular transport: Nutrient transporters on membranes in a cell remove calcium from the lumen of the intestine into circulation through cells • In the intestine: -‐ Duodenum o 20% of calcium absorbed goes through para-‐cellular transport o 80% of calcium absorbed goes through trans-‐cellular transport -‐ Jejunum o 80% of calcium absorbed goes through para-‐cellular transport o 20% of calcium absorbed goes through trans-‐cellular transport -‐ Ileum o 100% of calcium absorbed goes through para-‐cellular transport • AKA: Trans-‐cellular transport is highest in the duodenum but drops off towards the jejunum and ileum -‐ Proximal portion of the small intestine is where the calcium is taken up through trans-‐cellular means • Uptake of nutrients is largely dependent at different points where proteins are expressed at those points • Apical side of enterocyte: -‐ TRPB6 and TRBP5: Calcium transporters that can facilitate the transport of calcium across the plasma membrane (Trans-‐cellular transport) • Cytoplasm: -‐ Calbindin: Calcium binding protein that moves calcium across the cytoplasm from the apical side to the basolateral side of the enterocyte • Basolateral side of enterocyte: 2 pathways for transporting calcium a) NCX1: Sodium calcium transporter b) PMCA1: Energy dependent calcium transporter • 1,25-‐dihydroxyvitamin D: -‐ Functions to increase the concentration of calcium in the blood -‐ Signals the enterocyte to increase the uptake and absorption of calcium by increasing the expression of these proteins -‐ Steps: Enters the enterocyte and attaches to ultimately to VDR-‐RXR nuclear receptor complex à Response element of DNA à Production of mRNA à Proteins expressed to take up calcium: TRBP6, NCXI, and calbindin Slide 8: Percentage of Calcium Absorbed and total Calcium Absorbed from Various Food Sources • In terms of rate of absorption vs. absolute mass being absorbed • Whole wheat bread is one of the best sources of calcium absorption (% calcium absorption) BUT the total calcium absorbed/absolute amount of calcium taken up is very low • Milk or yogurt: -‐ % of absorption of calcium is not greatà Only 25% -‐ Total calcium amount is very high à 80-‐90 mg • Overall: When looking at minerals, it is important to recognize the rate of absorption vs. total mass of the nutrient that is absorbed—Just because something says 100% absorbed does not mean that a ton (mg) is actually put into the body • If a lot of calcium is absorbed (Or any mineral), the rate of absorption will be lower • If a little amount of calcium is absorbed, the rate of absorption is higher Magnesium Slide 3: Figure 33.1 • Intestinal uptake of magnesium is shown • Apical side of the enterocyte (Left): -‐ Have TRPM6 transporter -‐ Used for the trans-‐cellular uptake of magnesium • Movement of magnesium through the cytoplasm is next • Basolateral side of the enterocyte (Right): -‐ 2 transporters that transport magnesium into the plasma a) Sodium co-‐transporter b) Mystery transporter • Between 2 cells: Claudin-‐16/19 -‐ Facilitates para-‐cellular uptake and absorption of magnesium -‐ Work to regulate the movement of magnesium and other nutrients between cells Slide 4: Figure 33.2-‐ Summary of the Tubular Handling of Magnesium • Kidneys shown along with the secretion and absorption of magnesium à One of the primary pathways for maintain magnesium concentrations in the blood • 100% of 80% of magnesium from the body that enters the glomerulus enters the proximal convoluted tubule • Ascending limb of Loop of Henle: -‐ Where most (60-‐75%) of filtered magnesium is reabsorbed here • Distal convoluted tubule: -‐ 5-‐10% of the filtered magnesium is reabsorbed here • 3-‐5% of magnesium that was filtered is excreted in the urine once it reaches the collecting duct • Overall: Most magnesium is reabsorbed back into to the blood stream Slide 5: Skipped Slide 6: Figure 33.4-‐ Distribution of Magnesium in the Body • Soft tissues: 45% (450 mmol) of magnesium -‐ Functions in stabilizing phosphate groups of ATP -‐ Any time there is an enzyme or protein that binds to or uses ATP, it will use magnesium as a cofactor -‐ Ex: Succinyl CoA dehydrogenase will convert GDP à GTP and it donates a phosphate group to ADP à ATP -‐ Role of soft tissues in the body: To generate or maintain energy for the body o Ex: Adipose tissue o Kidneys o Liver • Skeleton: 54% (540 mmol) of magnesium -‐ Magnesium in bone: o Is part of the hydroxyapatite à Crystalline structure that makes up bone • Extracellular fluid: 1% (10 mmol) of magnesium • Pretty even distribution between tissue and bone Slide 7: Figure 33.5 • Function of magnesium is to stabilize phosphate groups • It is associated with the oxygens on the phosphate groups in ATP and ADP • ATP has a negative charge (Anion) à Magnesium helps keep this molecule stable in the cell so that when enzymatic reactions are occurring, they are much more stable reactions (Won’t bind an enzyme) • Specifically: Magnesium stabilizes the beta and gamma phosphate groups on ATP Slide 8: Figure 33.6 • Magnesium is going to help stabilize any reaction that uses ATP and GTP in this case • Shows 2 ways that lead to intracellular signaling where magnesium plays a role • Left side: cAMP Mechanism -‐ Hormone binds and activates a G protein coupled receptor à Activates adenylate cyclase à Buildup of cAMP à Increase in PKA (Protein kinase A) + downstream functions that depend on the hormone that’s binded such as gluconeogenesis • Right side: Another cell signaling pathway -‐ Uses PI where a hormone binds to a G protein coupled receptor à Phospholipase C acts to stimulate downstream pathways à Ultimately turns on protein kinase C Slide 9: Figure 19.7 • Glucagon shown as a hormone attaching to a G protein coupled receptor (7 transmembrane G protein couple receptor) à Stimulate adenylate cyclase to produce cAMP (Secondary messenger) à Increase PKA (Protein kinase A) Sodium and Potassium Slide 1: Figure 34.1-‐ Ionic composition of plasma, interstitial, and intracellular compartments • Electrolytes: Charged molecules (Sodium and potassium have charges) • Electrolytes work in proton gradients -‐ There is a difference in charge between inside and outside cell membranes -‐ The extracellular compartment outside of cell has a more positive charge than inside the cell where there is a more negative charge à This creates a resting membrane potential • Any time there is an excitability of a neuron and there is a need to stimulate a muscle, there is an interaction between the resting membrane potential à The change in resting membrane potential is used to initiate movement • What causes the difference between inside and outside a cell: -‐ In the plasma: o The principle electrolyte is sodium so that there is more sodium outside the cell o Sodium is 110 mmol/L in the blood o Potassium is 4 mmol/L outside the cell o Also in the plasma: Magnesium, organic acids, and proteins -‐ In the interstitial fluid: o Similar to the plasma but has slightly more sodium present o Also in the interstitial fluid: Bicarbonate, chlorine, and a fairly even number of potassium and calcium -‐ Intracellular compartment (Inside the cell): o The principle electrolyte is potassium o Also in the intracellular compartment: More organic phosphates like ATP phosphates, more proteins, more magnesium (Needed to help stabilize ATP and ADP), less sodium and chloride o Potassium is 150 mmol/L o Sodium is 12 mmol/L -‐ *Sodium-‐potassium ATPase is what creates this charge across the plasma membrane Slide 2: Figure 34.2-‐ Schematic representation for sodium-‐potassium ATPase • Sodium-‐potassium ATPase: Responsible for primary active transport of sodium and potassium in opposite directions across plasma membranes • It is a protein that is a heterodimer with 2 alpha subunits and 2 beta subunits that spans the plasma membrane • Steps for sodium-‐potassium ATPase: 1) Transporter protein picks up 3 sodium molecules 2) ATP, under the guidance of magnesium, will phosphorylate one of the residues on the alpha subunit of sodium-‐potassium ATPase -‐ After the alpha subunit is phosphorylated, ADP is created which releases sodium into the extracellular space to move it out of the cell 3) 2 potassium molecules will be picked up 4) De-‐phosphorylation of residues occurs + 2 potassium molecules are taken up into the cell • Ultimately: -‐ 3 sodium molecules (positive charges) are taken out of the cell per 1 ATP -‐ 2 potassium molecules (negative charges) are brought back into the cell per 1 ATP -‐ Sodium-‐potassium ATPase is used to maintain the resting membrane potential since a difference is desired across the membrane • Later: -‐ There are channels that can direct sodium and potassium inside the cell via electrochemical gradient -‐ The more negative charge of potassium will cause sodium to flow down towards it since sodium has a positive charge à AKA the more positive charge of sedum is attracted to the more negative charge of potassium inside the cell so that sodium moves in Slide 5: Figure 33.6-‐ Physiological regulation of sugar absorption • In addition to sodium playing a role in creating a resting membrane potential, it is involved in carbohydrate metabolism as a sodium-‐glucose transporter • Sodium-‐glucose transporter facilitates the uptake of glucose • SGLT1 (Sodium glucose transporter 1) is present in conditions of a low-‐ sugar meal and sugar-‐rich meal -‐ Located on the apical side of the enterocyte and takes up glucose from the lumen of the small intestine -‐ Every time SGLT1 takes up a molecule of glucose, 2 sodium molecules are also taken up -‐ Sodium is ultimately taken up from a higher concentration to a lower concentration à Want to keep sodium higher on the outside of the cell than inside though • If sodium is being shuttled inside the cell along with glucose, ATPase is needed to get sodium back out of the cell -‐ Energy (ATP) is now being used to pump sodium out against its concentration gradient -‐ ATP needs to be around to maintain a resting membrane potential à Push sodium out and bring potassium back into the cell -‐ More ATPases will be seen on the basolateral side of the enterocyte than the apical side Slide 6: Figure 34.3 • Potassium has a greater concentration inside the cell • Sodium has a greater concentration on the outside of the cell in the interstitial fluid • Apical side of the enterocyte: -‐ Have different transporters -‐ Sodium-‐glucose transporter is shown -‐ There is a co-‐transporter with facilitated diffusion that moves sodium and potassium inside the cell o Facilitated diffusion of chlorine moving inside the cell is shown as well -‐ NaCl: o Chlorine will be piggy-‐backed to sodium when NaCl is absorbed (facilitated diffusion) o Chlorine can also use the para-‐cellular pathway and go in between cells -‐ Counter transporter shown where sodium is moved into the cell and H+ are moved out • Basolateral side of the enterocyte: -‐ Sodium-‐potassium ATPase à Creates resting membrane potential -‐ Sodium-‐potassium channels are important in making action potentials à AKA these are voltage gated channels for sodium and potassium Slide 7: Figure 9.4-‐ Amino Acid Transporters • As nutrients such as glucose and sodium are taken up into a cell, sodium needs to be pumped back out through ATPase (3 at a time) -‐ For every ATP, 2 potassium molecules are pumped back into the cell -‐ Multiple ATPases are located throughout the plasma membrane • Amino acid transporter and co transport of sodium: -‐ Sodium is now needed for the uptake of amino acids in addition to carbohydrate such as glucose and fructose • One can be sodium deficient due to excessive sweating and excessive vomiting • Americans consume about 6 g of sodium per day (US is not sodium deficient) Slide 8: Figure 34.4-‐ Reabsorption of sodium, potassium, and chlorine and secretion of potassium at different parts of the nephron • Kidney: -‐ Cortex region -‐ Medulla region -‐ Nephron -‐ Kidney’s job is to filter blood • Proximal convoluted tubule: -‐ Reabsorbs sodium, chlorine, and potassium • Filtrate that flows through the ascending limb of the Loop of Henle à By the time it reaches the collecting duct, about 90% of the electrolytes have been reabsorbed • When excess sodium is consumed, there is less reabsorption of sodium due to adequate intake • Also for chlorine and potassium, not much will be reabsorbed is adequate intake is met • At the collecting duct: 95% of what has been filtered is reabsorbed • Baroreceptors help the kidney to sense changes in blood volume that can signal nephrons to reabsorb or not reabsorb certain electrolytes depending on the status of the individual • The amount of water one drinks affects what will affect the reabsorption of electrolytes à Depends on blood volume and how much sodium, chlorine and potassium are being taken up (All work together) • Leftover filtrate that is not reabsorbed à Bladder to be excreted Slide 9: Figure 34.5-‐ Schematic representation of the control of renal excretion of sodium and water during salt deficit • Baroreceptors are found in the distal convoluted tubule next to Bowman’s capsule where changes in blood volume can be sensed and signals are sent to the CNS • Decrease in plasma volume and therefore a decrease in blood pressure can be sensed by baroreceptors: -‐ Signals sent to the CNS that will lead to activate sympathetic nervous activity: a) Increase in renin secretion by the kidneys + the cells within the kidneys that house renin o Renin: Pro-‐hormone à Stimualtes angiotensin mechanism where angiotensinogen (Angiotensin in notes?) à angiotensin 1 à angiotensin 2 via ACE (Angiotensin converting enzyme) secreted from the lungs o Angiotensin 2 will act on the adrenal glands to cause the production of aldosterone that will also act to increase blood pressure and increase plasma volume through stimulating sodium reabsorption o Aldosterone acts on the distal convoluted tubule to promote sodium and chlorine reabsorption b) Decrease in glomerular filtration rate: o GFR: Rate of filtrate that enters Bowman’ capsule o As GFR decreases, signals will be sent to the CNS that will cause a release of an enzyme that will activate the cascade of events c) AVP (ADH): o AKA arginine vasopressin hormone o Released from the pituitary gland o Functions in helping water to be reabsorbed into the blood stream from the tubule via opening aquaporins d) Water can be reabsorbed also in the colon that helps regulate blood pressure, plasma volume, and sodium retention • Summary: -‐ Anytime there is low sodium or decrease in plasma volume à Renin is released from the kidney à Signals the conversion of angiotensinogen (Angiotensin in notes?) à Angiotensin 1 à Angiotensin 2 via ACE from the lungs à Increase in plasma levels of aldosterone à Act on the kidneys to reabsorb sodium and chloride -‐ Ultimately increasing blood volume and therefore blood pressure Body Fluids and Water Balance Slide 2: Figure 35.1-‐ Major Fluid Compartments of an Adult • Extracellular fluid: -‐ Cavity fluids: < 2% o Hollow tubes + fluid within the tube o Most is made up by the GI tract due to water -‐ Plasma: 4% (3L) -‐ Interstitial fluid: 16% (11 L) • Intracellular fluid: -‐ 40% (28 L) -‐ Most of the fluid in our body is contained within our cells • In any of these compartments, the fluid’s function is to facilitate enzymatic reactions, maintain electrolyte balance, transport function, temperature regulation, etc. -‐ Primary objective though: Water that acts as a solvent that dissolves solutes like electrolytes so that they are distributed throughout the body (Water acts as a carrier in the blood) Slide 3: Figure 35.2-‐ Osmosis and osmotic pressure illustrated by two compartments separated by a semipermeable membrane, permeable to water but not to solutes • Semi-‐permeable membrane: -‐ Allows some substances through and not others -‐ Water is allowed to freely pass -‐ Dissolved solutes such as sodium and chloride are not allowed through • Top: -‐ U-‐shaped vessel with semipermeable membrane between sides A and B -‐ Side A is more concentrated than side B, but the volume is same on both sides -‐ The concentration of solute will remain the same on both sides since the solutes aren’t allowed to pass through the membrane à It is the volume of water (Fluid) that changes and therefore the osmolarity can change -‐ Dashed arrows: Movement of water (fluid) -‐ Solid arrows: Pressure opposing water movement • Bottom left in terms of top image: -‐ Net movement of water: o Water moves from side A à side B o AKA: Water passes from side A (Area of less concentration) to side B (Area of higher concentration) -‐ Osmotic process shown à Goal is to create an equilibrium to have the same concentration of solutes on both sides o Even though there are 5 Osm of solute on side A and 15 Osm of solute on side B, water volume changes so that side A now has 0.5 L of fluid and side B has 1.5 liters of fluid à Ultimately an equal osmolarity value of 10 Osm/L is created (Equilibrium) • Bottom right in terms of top image: -‐ Solid arrow points down on side B à Represents opposing pressure -‐ Less concentration of solute is on side A than B -‐ 1 L of water is on both A and B -‐ There will not be a net movement of water from side A to side B due to the pressure opposing water • Figure shows open vessel examples, but in mammals they are closed systemsà Cells -‐ If have a cell, pressure opposing water movement is likely the cell wall -‐ There is ability of a cell wall to expand and contract, but it is limited movement Slide 4: Slide 5: Illustration of Starling forces across the capillary endothelium • Capillary with arteriole and venous sides • Movement from the arteriole to the venous side à Filtration movement will occur from the lumen of the capillary into the interstitial space (On the arteriole side) -‐ Assumption is this is the delivery system for nutrients and oxygen • Venous side: -‐ Wastes are removed from the cell on the venous side -‐ Movement from the interstitial space into the lumen of the capillary • 4 pressures affecting fluid movement: a) Capillary hydrostatic pressure: P c -‐ AKA blood pressure -‐ Pushes fluid into the interstitial space b) Capillary colloid osmotic pressure: O c -‐ Resistive to fluid leaving the lumen à interstitial space -‐ Has to do with proteins that are contained within a solvent -‐ Plays a role in filtration -‐ Draws fluid back towards the lumen of the capillary since proteins can’t pass out of the capillary -‐ Ex: Albumin à 1 protein contained within the water solvent in the plasma c) Interstitial hydrostatic pressure: P If -‐ Pushes fluid from the interstitial space into the lumen of the capillary d) Interstitial colloid osmotic pressure: O If -‐ Pulls fluid into the interstitial space -‐ Also relates to proteins (?) • Net filtration pressure: -‐ NFP = (P c If – c If O ) -‐ AKA: (Capillary hydrostatic pressure – Interstitial fluid hydrostatic pressure) – (Capillary colloid osmotic pressure – Interstitial fluid colloid osmotic pressure) • If net filtration pressure is positive: Movement from the lumen of the capillary to the interstitial space • If net filtration pressure is negative: Movement from the interstitial space back into the lumen of the capillary • Filtration: -‐ Movement of solutes filtered from the capillary to the interstitial space • Reabsorption: -‐ Movement from the interstitial space to the lumen of the capillary • There is a difference between the arteriole and venous ends in terms of filtration and reabsorption • Disease conditions: -‐ Reabsorption inhibited à Fluid will be in the interstitial fluid à Build up = Edema Slide 6: Daily water balance to illustrate minimal required drinking water intake • Water intake: 1.44 -‐ Preformed water: 0.85 L -‐ Metabolic water: 0.37 L o From products of respiration at the end of the ETC when oxygen is reduced to water -‐ Drinking-‐minimum: 0.22 L • Water loss: 1.44 L -‐ Insensible water loss in the lungs (0.3 L) -‐ Insensible water loss in the skin when not purposely sweating (0.4 L) -‐ Feces: 0.1 L -‐ Urine: 0.64 L • Recommended to drink 8 cups of water a day, but based on this table, we only need to take in 0.22 due to fluid balance Slide 7: Figure 35.5-‐ Establishment of an osmotic gradient in the medullary region of the kidney by the countercurrent multiplier system of the Loop of Henle • Nephron is the structural unit of the kidney -‐ The concentration of filtrate in the proximal convoluted tubule is much less concentrated than as the filtrate moves down the descending limb of the Loop of Henle o The further the descending limb goes into the medulla, the more concentrated the filtrate -‐ As the filtrate moves back up the ascending limb, the concentration of the filtrate decreases and becomes more dilute again in the distal convoluted tubule and collecting duct like when it first was in the proximal convoluted tubule -‐ Filtrate moving down the collecting duct à Inner medulla where the filtrate is concentrated more again • Function of the nephron is to regulation the filtration and reabsorption of solutes (And therefore water) • Descending limb: Permeable to water and impermeable to solutes (Such as sodium and chloride) -‐ More water moves out to work to maintain equilibrium as the concentration of solute outside the tubule increases • Ascending limb: Impermeable to water and permeable to solutes -‐ Moving up the ascending limb à Urea moves into the nephron • As get to the collecting duct, some urea is able to move out Slide 8: Integration of the osmoreceptor—AVP and thirst mechanisms in the regulation of water balance in water deficit • Excess water loss à Negative water balance -‐ Could be due to sweating, breathing, exercise, diluting urine, etc. • Excess water loss can lead to an increase in plasma osmolarity: a) Concentrations of solutes increased in a solvent so that the solute concentration remain the same but the water volume decreases -‐ Osmoreceptors sense this increase in osmolarity à Leads to the secretion of AVP -‐ AVP (Arginine Vasopressin = ADH) à Increases water reabsorption b) Signal of a thirst sensation to increase the intake of water or fluid -‐ 1% of one’s body weight of fluids is lost before signifying the thirst sensation • Baroreceptors respond to pressure à If there is a decrease in plasma volume: -‐ AVP signaled to increase water reabsorption Slide 9: Proposed mechanism of some major events that result from the action of AVP on the collecting tubule to increase its water permeability • AVP (ADH): Use of a secondary messenger system -‐ Hormone that binds to AVP-‐receptor à Activates adenylate cyclase to generate cAMP (Secondary messenger) à Activates protein kinase that phosphorylates substances (Covalent regulation) à Translocation of a vesicle with aquaporin 2 inside to the cell membrane à Aquaporins are embedded in the cell membrane to allow the transport of water across the membrane • Apical side: Aquaporin 2 presence • Basolateral side: Aquaporins 3 and 4 present that transport water • Dashed lines on the apical side: Means there will be some removal of the protein from the membrane + recycling so that is goes back into one of the intracellular vesicles -‐ Faster to already have the aquaporins in cells ready for when they are needed rather than using signaling of synthesis of aquaporin proteins Iron Slide 3 • Heme compound shown • Ex: Hemoglobin and myoglobin • Fe 2+ à Ferrous form of iron (Middle of this heme compound) • Fe 3+ à Ferric form of iron • Ferrous form (Fe 2+) is more highly reduced than the ferric form (Fe 3+) à AKA the difference between the two has to with a loss or gain of electrons • Relation à ETC: Purpose is to move electrons through the ETC from the matrix of the mitochondria to the inner membrane space Slide 4: Figure 36.2-‐ Iron-‐Sulfur Cluster Proteins • 2 proteins shown that contain iron and sulfur • Interaction between iron and sulfur is key • Left protein: -‐ Contains 2 iron and 2 sulfur • Right protein: -‐ Contains 4 iron and 4 sulfur • In either of these proteins à There is the cysteine AA • Cysteine importance: -‐ One of the sulfur containing AA (Other is methionine) -‐ Both proteins use cysteine to anchor the iron-‐sulfur cluster within the protein -‐ Iron bound to sulfur on cysteine + 2 more sulfur molecules can bridge the gap o AKA there is an iron-‐sulfur cluster within a protein and 2 other sulfur molecules can bridge 2 sides of the protein • Hemoglobin and myoglobin involve iron and play an important role in metabolism -‐ Their function is to carry oxygen in the blood (hemoglobin) and in the muscle (myoglobin) -‐ Iron works to bind to and transport the oxygen • Proteins in the ETC: -‐ Coenzyme Q, succinate dehydrogenase, ATP synthase, cytochrome B and C -‐ Cytochromes C and B à Where there is primarily iron-‐sulfur clusters to allow REDOX reactions to occur -‐ Again: Cytochromes work to move electrons through the ETC to ultimately reduce oxygen to water and create ATP from ADP and inorganic phosphate Slide 5: BOX 36-‐2-‐ Proteins involved in Iron Transport, Storage, and Recycling • Proteins involved in transport, storage, and recycling are listed • Ex: Lactoferrin and transferrin • Transferrin binding proteins: -‐ Transferrin receptor 1 and 2: o Principle protein for iron uptake o Transferrin is responsible for transporting iron in circulation o Transferrin binds to the transferrin receptor so that the iron can be taken up into a cell and used, stored, or recycled • Proteins of iron recycling: -‐ Ceruloplasmin: o Second compound that functions to convert iron in the ferrous
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