Exam 1 Notes
Exam 1 Notes HUN3224
Popular in Intermediary Metabolism
Popular in Nutrition and Food Sciences
This 33 page Bundle was uploaded by Channelle Brown on Saturday April 23, 2016. The Bundle belongs to HUN3224 at Florida State University taught by Dr. Farrell in Spring 2016. Since its upload, it has received 41 views. For similar materials see Intermediary Metabolism in Nutrition and Food Sciences at Florida State University.
Reviews for Exam 1 Notes
Report this Material
What is Karma?
Karma is the currency of StudySoup.
You can buy or earn more Karma at anytime and redeem it for class notes, study guides, flashcards, and more!
Date Created: 04/23/16
GI Tract – HUN3224 Most of immune system is in GI tract Oral Cavity o Mastication – chewing breaks down food Increases surface area o Saliva Enzymes Salivary amylase – carbs Salivary lipase – milk fat (most active in infants) Lysozymes Kill bacteria Our first defense Esophagus o Muscular tube – connect the back of the mouth and stomach Movement of food via peristalsis o Lower esophageal sphincter – circular muscular valve Relaxes to let food into stomach Constricts to keep food from moving back up into esophagus o GERD (gastro esophageal reflux disease) Relaxation of LES (weak LES) Stomach acid comes in contact with esophagus Possible causes: spicy foods, caffeine, fatty foods, pregnancy, pressure from obesity, laying down after eating, etc.( Over time can damage esophagus leading to ulcers and an increased of esophageal cancer Stomach o Holds food o Mechanical mixing and breaking down of food o Gastric secretions Gastrin Release of HCl and pepsinogen Hydrochloric Acid (HCl) Kill bacteria Denatures proteins Inactivates lingual lipase Converts pepsinogen into pepsin Pepsinogen Inactive precursor to pepsin *all proteases are inactive at rest* Protein digestion Mucus Protects stomach lining Contains bicarbonate to neutralize acid Intrinsic Factor Necessary for absorption of B12 Lack of B12 – anemia, lethargy, etc. o Absorption of alcohol and aspirin Pyloric Sphincter o Circular muscular valve separating stomach from duodenum o Regulates movement of food and acid from stomach to small intestine o If it does not work properly”dumping”diarrhea o Chime = food + acid Small Intestine o 3 sections: Duodenum Main site of digestion and absorption Receives secretions from other digestive organs (pancreas, gallbladder) Lining: folded into finger-like projections called villi o Increases surface area, increases absorption o Villi – covered with microvilli o Microvilli = brush border (where digestion is usually completed) o Villi are lined with enterocytes (“gate keepers”) Villar tip cells – slough off (the tip) Midvillar cells – secrete digestive enzymes & hormones for macronutrient digestion (CCK, secretin, GIP) Crypt cells – replicate (bottom) Jejunum Digestion and absorption continue Ileum (longest section) Absorption Enterohepatic circulation of bile We reabsorb most bile Large Intestine o Smooth lining, no villi o Water and electrolyte absorption o Intestinal microflora – bacterial breakdown of fiber; produce vit. K and some B vitamins When we are born, we get a shot of Khelps us produce bacteria in gut o Temporary storage and concentration until defecation Accessory Organs o Pancreas Acini – secrete enzymes into GI tract Zymogens Pancreatic amylase Pancreatic lipase Islet tissue Secrete hormones into blood o Beta – insulin o Alpha – glucagon o Delta – somatostatin Not connected to GI Shares common bile duct with gallbladder gallstoneback system uppancreatitisimbalance of blood glucose o Liver Makes bile Emulsifier for fats, needed for fat digestion Bile o Made in hepatocytes from cholesterol o Stored in gallbladder o After digestion of fats, bile reabsorbed in ileum and sent back to liver (EHC) Metabolizes drugs, alcohol, and toxins Urea synthesis Makes plasma proteins Transport proteins o Albumin: maintains osmotic pressure; low albuminfluid pools in intercellular spaces = edema o Transferrin : transports iron o Lipoproteins: 5 types (chylomicron, VLDL, IDL, LDL, HDL), carries various lipid/cholesterol components to tissues Circulation of Nutrients o Vascular System Carries nutrients in blood to liver and then disperses it to body (EHC) For water-soluble substances o Lymph System Exogenous lipid transport Lacteals (fat/fat-soluble substances go through these) Fatdirectly into bloodstream Carbohydrates – HUN3224 Major source of energy fuel in average diet ½ total caloric intake o Polysaccharides (starches & dextrins) o Monosaccharides (simple sugars – glucose, galactose, fructose) o Some are digestible, some are not Chemical structure (below: most simple carb) o Simple: glyceraldehyde o Complex: glycogen Monosaccharides o Types (based on # of carbons) 3 – triose 4 – tetrose 5 – pentose (made from hexoses; helps made riboses) 6 – hexoses (major energy source: glucose, galactose, fructose) 7 – heptose Dietary Monosaccharides (“simple carbs”) o Glucose Most abundant of the three “blood sugar” o Fructose o Galactose Disaccharides o Formed from condensation of 2 monosaccharides Glucose + glucose = maltose Glucose + galactose = lactose *lactose intolerance = inability to break down lactose, NOT a milk allergy Glucose + fructose = sucrose o High Fructose Corn Syrup 50% glucose + 50% fructose = sucrose Cane and beet sugar Table sugar, processed foods HFCS: 45% glucose + 55% fructose Lquid, made in lab Helps softer foods stay soft/keeps processed food preserved Made from corn Sucrose = less processed than HFCS Oligosaccharides o 3-10 monosaccharides Raffinose (gal-glu-fruc) Stachyose (gal-gal-gluc-fruc) Found in beans, peas, and whole bran Sometimes fermented in gut using healthy bacteria, unable to be enzymatically digested gas Fibers don’t increase blood sugar Polysaccharides o Starch Storage form of carbs in plants Types (we can digest these) Amylose o Alpha 1-4 bonds of glucose units o Linear molecule Amylopectin o Branched alpha 1-6 chain polymer o Also has linear long straight chain (alpha 1-4) o Glycogen Storage form of carbs in animals From all glucose Stored in liver and muscle Highly branched (looks like amylopectin) Energy source Get it when we are starving, high epinephrine, etc. From glycogenolysis o Fiber Non-digestible plant polysaccharides Defined by the USDA Dietary fiber: found intact/intrinsically in plant (e.g. – oats) Functional fiber: isolated & extracted, beneficial (e.g. – “double fiber bread”, Metamucil) Types Insoluble o Doesn’t dissolve in water o Lower transit time (moves through colon faster) o Increases fecal bulk o Helps constipation o E.g. – celluloses, lignans, some hemicelluloses Soluble o Dissolves in water o Increased transit time (slower) o E.g. – pectin, gum, some hemicelluloses o Helps diarrhea Fermented by bacteria in colon Hydrogen, methane gas, CO2, short chain fatty acids o Short chain F.A.’s Acetic acid, butyric acid, propionic acid o Functions of short chain F.A.’s Stimulate water and sodium absorption into mucosa Provide colonocytes with energy Enhanced immune function Increases good bacteria in gut Decreases atrophy of gut Decreases cholesterol Excreted as fecal matter Carries bile with it (soluble fiber does more than insoluble) Sources: Fruits, vegetables, and whole grains DRI: o Men, ages 19-50: 38 g o Men, older than 51: 30 g o Women, ages 19-50: 25 g o Women, older than 51: 21 g Digestion of Carbs o Begins in mouth Salivary glandsalivary amylase Digest alpha 1-4 bonds Amylose digestion Can totally digest it in mouth via amylase Branched starches Only breaks alpha 1-4 linkages, not the alpha 1-6 bonds Action of salivary amylase is incomplete Alpha 1-6 bonds Time spent in mouth can determine how much is digested o Stomach HCl inactivates salivary amylase Does not digest carbs that much Mostly holds fod o Small intestine Pancreatic secretions Bicarbonate – neutralizes chime Pancreatic amylase – breaks only alpha 1-4 bonds Brush border enzymes Sucrase – breaks down sucrose Lactase – breaks down lactose Maltase – breaks down maltose Absorption & Transport o Location Small intestine o Mechanisms of transport Passive diffusion No energy needed Limited by concentration gradient Small molecules and solutes Facilitated diffusion Needs a carrier protein o Integral membrane protein o Functions as a transporter Rate determined by: o Concentration gradient o Amount of carriers (“doors”) available o Rapidity of solute/carrier interaction o Rapidity of conformation change of carrier Active transport Needs a carrier protein Requires energy in form of ATP Pumps against concentration gradient E.g. – Na+K+ pump o Carb Absorption Glucose Sodium dependent Active transport Transporter: SGLT1 To maintain Na+ gradient, Na+ must be pumped out of the cell (K+ comes into cell) Glucose enters hepatic portal system enterocytecapillariesportal systemliver Galactose Same as glucose Can be converted to glucose to meet needs of enterocyte Fructose Facilitated diffusion GLUT5 Transported to liver Glucose Transporters GLUT1 – erthyocytes, placenta GLUT2 – movement across basolateral membrane (enterocytes), fructose transport at liver GLUT3 - brain GLUT4 – muscle, adipocytes GLUT5 – fructose (small intestine) GLUT6 – spleen, brain GLUT7 - unknown GLUT9,10 - liver SGLT1 – uptake of glucose/galactose at lumen *transporters that are insulin stimulated: GLUT2, GLUT4, GLUT5, SGLT1 o Transport Portal circulation (liver) Facilitated diffusion o Fructose o Galactose o Glucose At typical intakes, little to no fructose or galactose in peripheral blood Glucose not taken up by liver: o Facilitated, insulin dependent Skeletal muscle, adipose tissue o Facilitated, insulin independent Kidney, brain Metabolic Pathways of Carbohydrates o Glycolysis Purpose: oxidation of glucose, energy production Location: cytosol Types (2): Anaerobic (no oxygen): glucosepyruvatelactate Aerobic (oxygen): glucosepyruvateacetyl CoA Liver can take up extra glucose (glycogen) Muscle has to have a concentration gradient (if more glucose in cell than outside, then it stops taking anymore in) o Glucokinase Functions in liver and pancreas Upregulated by insulin Liver doesn’t remove large quantities of glucose from blood unless glucose levels are high o Hexokinase Functions in muscle, adipose tissue, and brain Downregulated by G6P Max. enzyme activity at normal blood glucose levels o Anaerobic Glycolysis Energy production: o ATP glucoseG6P = -1 ATP F6PF-1,6-BP = -1 ATP 1,3-BPG3PPG = +2 ATP PEPPyruvate = +2 ATP o NADH G3P1,3-BPG = +2NADH PyruvateLactate = -2 NADH o Net energy production = 2 ATP o Aerobic Glycolysis Energy Production o ATP (same as above) = +2 ATP o NADH G3P1,3-BPG = +2 NADH (x3=6 ATP) Pyruvateacetyl CoA = +2 NADH (x3=6 ATP) o Net energy production = 14 ATP o Krebs Cycle TCA cycle, citric acid cycle, etc. Amphibolic pathway CHO, fats, & proteins can all enter and be completely oxidized into CO2, H2O, and energy Provides precursors for synthesis pathways Location: mitochondrial matrix Products: Co2 – exhaled by lungs H2O Energy o GTP = 1 ATP o FADH = 2 ATP (in reality b/c of uncoupling: 1.5) o NADH = 3 ATP (in reality, b/c of uncoupling: 2.5) Energy Beginning w/ Acetyl CoA 3 NADH x 3 = 9 ATP 1 FADH x 2 = 2 ATP 1 GTP = 1 ATP TOTAL: 12 ATP Beginning w/ Pyruvate 4 NADH x 3 = 12 ATP 1 FADH x 2 = 2 ATP 1 GTP = 1 ATP TOTAL: 15 ATP Total energy production from 1 molecule of glucose under aerobic conditions = 38 ATP (max yield) The Shuttle Systems Malate-Aspartate Shuttle o Moves NADH into mitochondria (ETC) o In liver, kidneys, & heart Glycerol-3-Phosphate Shuttle o NADHFADH o Enters at complex 3 of ETC o FADH yields 2 ATP o In muscle and brain o Electron Transport Chain Purpose: production of mitochondrial ATP; changes FADH & NADH to ATP Location: cristae of mitochondria Oxidative Phosphorylation Oxidation: loss of electrons or hydrogens Phosphorylation: addition of phosphorous Uncoupling: a pathway starts but doesn’t finish and halts action of ATP synthesis Proton Gradient Diffuse from higher to lower concentration Must maintain a higher concentration of protons in outer mitochondrial space (“intermembrane space”) vs. inner mitochondrial space (“mitochondrial matrix”) Maintain gradientuse proton pumps (pump from high to low conc.) Proton Pumps 3 of them: o Complex 1: NADH dehydrogenase o Complex 3: cytochrome B-C o Complex 4: cytochrome oxidase Complexes which removed electrons from coenzymes located in the inner mitochondrial space and/or pump protons into outer mitochondrial space NADH hits all 3 complexeseach one makes 3 ATP FADH starts at complex 3 each one makes 2 ATP Electron Transporters Transport electrons b/t complexes in ETC (electron transport chain) o Ubiquinone: transports electrons b/t complex 1 and 3 o Cytochrome C: transports electrons b/t complexes 3 and 4 ATP Synthase (actual “pumping”) Transports protons across inner mitochondrial membrane into matrix for phosphorylation (ADP + Pi ATP) Uses B vitamins Thyroid Hormone o Associated w/ uncoupling proteins o Uncouple oxidation-phosphorylation reactions o Hyperthyroidism: Increased production of uncoupling proteins Inefficient ETC – heat loss (burn more glucose to make same amount of energy) Higher BMR, weight loss, warmer Lose concentration gradient Can grow out of it o Hypothyroidism Can result in a goiter/enlarged thyroid gland “perfect system” – less glucose to make energy, rest of glucose stored as fat Low production of uncoupling proteins (*everyone has some uncoupling proteins and some that don’t) Lower BMR, weight gain, cold, lethargic, deeper voice Usually around for life Gluconeogenesis o Synthesis of glucose from non-CHO sources (EXCEPT fat) Pyruvate Krebs cycle intermediates Amino acids Lactate o Not just the reverse of glycolysis Acetyl CoA can go back to pyruvate Pyruvate cannot go back to PEP o Why? Makes glucose when CHO isn’t available Hypoglycemia can cause brain dysfunction, coma and death Clears lactate produced by muscle via Cori Cycle o Liver is the only tissue that can use a phosphate to make a glucose to put back in the bloodstream (usually once a cell is phosphorylated, it stays in the cell) Glycogenesis o Glucoseglycogen (storage) o Liver – main site of glycogen metabolism and storage o Induced by: high glucose, G6P, & insulin o Never making and breaking glycogen at the same time o Can only store finite amounts in liver o Extra glucoselipolysisstored as fats Glycogenolysis o Glycogenglucose o Liver-main site of glycogen metabolism and storage o Induced by low glucose, glucagon, epinephrine (need energy for ‘fight or flight’ response) Epi: more energy neededmore glucose; elevated blood glucoseafter stressful events HMP Shunt: o “hexose monophosphate shunt”/”pentose phosphate pathway” o Products Pentose phosphates – used for synthesis of nucleic acids NADPH (NOT used for energy) – synthesis of fatty acids & cholesterol Cori Cycle o Intense exercise (lactate producing) o Clears lactate from the muscleback into glucose in muscle (recycles the glucose) o Uses anaerobic glycolysis & gluconeogenesis o Even though the pathway seems inefficient because of the net -4 ATP for the whole body, the muscle is still getting energy so it’s still a good system. o Not all lactate gets sent to liver; some stays in muscle and continues to build up Regulation of Blood Glucose o Eat a CHO rich meal Digestion to glucose, fructose, and galactose Blood glucose increases (when it is in peripheral bloodstream, the pancreas secretes insulin to help glucose get into cell) o Secretion of Insulin In response to increased blood glucose Released by beta cells of pancreas Insulin binds to receptor in cell GLUT4- allows glucose to enter cell (muscle cells have GLUT4) Blood glucose levels decrease o Secretion of Glucagon In response to low blood sugar Released by alpha cells of pancreas Stimulates glycogenolysis and gluconeogenesis We go to glycogenolysis first because it is free and our main storage compartment (“savings account”) for glucose Integration of CHO cycles (mostly on drawings) o 2 ways to make glucose: Glycogenolysis (1 choice) Gluconeogenesis o We rarely use amino acids (protein) for energy; they are used to make neurotransmitters, muscle fibers, bone tissue, etc. (everything else, mostly) o We mainly use carbs and fat for energy o When the body is fed: Glycogenesis (store glucose in the form of glycogen) o When we need energy: Glycogenolysis (from glycogen) Gluconeogenesis (from lactate, amino acids, etc.) Both above processes then go to glycolysis (aerobic or anaerobic) Fructose: o Sources: Table sugar = 50% fructose + 50% glucose HFCS-42=42% fructose + 53% glucose HFCS-55= 55% fructose + 42% glucose Honey=49% fructose + 43% glucose Apple Juice=59% fructose + 31% glucose o “non-processed foods vs. low fructose” Agave nectar has more fructose than glucose but it non- processed. Whether or not you choose to eat high fructose foods or non-processed foods depends on your diet goals. o HFCS can make food softer (e.g. – cookies, cakes) and can also increase shelf life. o Absorption GLUT5 Enterocyte Converted to glucose Conversion is dose dependent GLUT2 Leaves the cell just like glucose and galactose o Portal Bloodstream At low levels, all fructose is taken up by liver At high levels, it’s found in peripheral bloodstream o Liver Metabolism of fructose Fructokinase Skips rate-limiting enzyme PFK o De novo fatty acid synthesis (pretty much, if there’s extra fructose, it will be turned into fat) o Non-alcoholic fatty liver disease o Triglycerides in peripheral bloodstreamincreased LDLs Excess fructose travels in peripheral bloodstream o Peripheral Bloodstream Fructose doesn’t stimulate insulin Insulin o Low blood glucose o Promotes carb storage o Promotes satiety o “Is fructose really the enemy?” Does HFCS cause disregulation of blood glucose? – can be due to a multitude of factors put together High insulin levels? = insulin resistance? – most likely Build up of TGs in liver, fatty liver? – yes Increased TGs in bloodstream? – yes Increased VLDL hence LDL in bloodstream? – yes Lack of satiety? – maybe o The real enemy is… The amount of carbs total coming into the body, not whether or not it’s specifically glucose or fructose (they’re both sugar). o “Is HFCS worse than sucrose?” Amount per day has increased over the years (24 g/d in 1930’s 73 g/d in present) 1975-1985 HFCS started being used in processed foods (less expensive, more corn available) Total calorie consumption has increased More processed foods than ever before HFCS diet vs. sucrose diet (research – Princeton): Rats that ate more HFCS ate less but gained more weight, especially around abdominal region Other research: No differences between HFCS and sucrose Carbohydrates – Pathways /Charts HUN3224 Diabetes – HUN3224 Blood Glucose Values o Normal Fasting – 60-100 mg/dL o Elevated – 100-125 mg/dL o Hyperglycemia - >126 mg/dL o Hypoglycemia - <50 mg/dL o HbA1C – 7% Glycated hemoglobin Good at determining/examining long-term control of blood glucose levels Types of Diabetes o Diabetes Mellitus Type 1 Causes Autoimmune or viral damage to beta cells Reduced insulin production o Glucose cannot move into cells o Glucose remains in blood Usually diagnosed in children and teens Uncontrolled diabetes o Still has better control than type 2 and there are usually fewer complications than type 2 Symptoms Weight loss (cells use fat instead of glucoseketosisketones provide less energy than CHOburn more fat) Increased urination Ketosis (using fat) Long-term complications Kidney disease, blindness, poor circulation, CVD, impaired nerve conduction Treatment: Insulin (2 peptides together, can be synthetic) o Insulin pumps o Injections – medications need to be refrigerated Diet o Carb controlled (know amount of carbs) o Amount of food o Time of food/know how rapid the insulin is Usually the whole family is involved and educated o One reason type 1 diabetes is so well controlled (more controlled than type 2) Goal: stable blood glucose levels o DM (“Diabetes Mellitus”) Type 2 Causes/Complications o Begins as insulin resistance diabetes o Obesity, diet, genetics, inactivity o Correlation between adipose tissue amounts and diabetes o Genetics can affect it as well (nature vs. nurture conversation) Symptoms/Long-Term Complications o Similar to type 1 o Pancreatic insufficiency – can stop making insulin so they need insulin and resistance medications Treatment o Weight loss o Exercise o Diet o Pharmaceuticals Metformin/Glucophage – prevents gluconeogenesis, glycogenolysis Glipizide/Glucotrol – tells pancreas to make more insulin Insulin o Needs to be diet-controlled while taking meds Medications only work at certain levels Not “fix alls” o Education Type 2 diabetes education – expensive, some people don’t know about it Type 2 diabetics usually aren’t as educated as type 1 diabetes Symptoms of Uncontrolled Diabetes o High blood glucose levels associated with dyslipidemia o Dyslipidemiamicrovascular diseasesdecreased blood flowhigh risk of infection, longer to heal numbness o Neuropathy Decreased blood flow Decreased nerve signaling, lose sensitivity Lose feeling in hands, feet, etc. Sores, bruises, cuts, etc. Infection, gangrene, amputation #1 cause of non-trauma amputations is type 2 diabetes (>60%) Risk is 10x higher in diabetics for amputations GI Tract Intermittent diarrhea, constipation Thickening, cracking, bleeding can lead to infection Gangrene spreads through limbs, can be quick (days) o Retinopathy New capillaries form to compensate for decreased blood flow and increased oxygen New capillaries are fragile Prone to bleeding Microaneurysms Lesions Undergo fibrosis Macular edema – fluid leaks into eye Leading cause of new blindness Usually in type 2 diabetics From high levels of glucose for a long time Short term: blurry vision o Nephropathy Decreased kidney functioning Can cause renal disease Uncontrolled diabetes – leading cause of kidney failure Kidney failure Dialysis o When kidney function decreases to 10-15% at normal o 3-4 hours, 3-4 times a week (time-consuming process) Types of Dialysis o Hemodialysis AV fistula – implanted, move it over a period of time because scar tissue builds up Graft Catheter o Peritoneal Passive diffusion of toxins through peritoneum (abdomen – peritoneal cavity) “wet abdomen” Diet – Diabetes & Dialysis o Diabetes Continue with carb control o Dialysis Fluid They may not urinate anymore Avoid foods with high water content: veggies, soups, fruits, ice cream, jello, drinks Potassium (potatoes, bananas) Phosphorous – take phosphorous binders, patient can feel itchy Protein – kidney gets rid of extra nitrogen but the kidneys are not working properly Sodium o Gestational Diabetes (onset w/ pregnancy) Abnormal glucose tolerance during pregnancy Excess weight gain during pregnancy and obese women pre-pregnancy have high incidence of gestational diabetes Some women with it will develop type 2 diabetes post- pregnancy, especially if they’re overweight Does not seem to be correlated with type 1 It increases risk of: Macrosomia (big babies) o Extra nutrients pass from mom to baby o Baby grows as big as it wants NICU stays o Problems with breathing, developmental issues, prematurity Hypoglycemia after birth o Glucose can pass from the mom to baby but NOT insulin o Baby makes own insulin hyperinsulinemia o After the umbilical cord is cut, the insulin is still high even though there’s no more glucose (only glucose supply is cut off) hypoglycemia o Hypoglycemia Can occur in diabetics (more common) and non-diabetics Considered more dangerous than type 1 and 2 Symptoms: irritability, dizziness, headache, shakiness, confusion, seizures, coma, death, unconsciousness, sweating Prevention: Match insulin and medications with meals If you’re doing more activity than usual, have a snack first Don’t drink excessively and don’t drink on an empty stomach Treatment: 15/15 rule: check blood glucose, eat 15 g of carbs, wait 15 minutes 2-3 glucose tablets ½ cup fruit juice or soda, not milk (mostly fats and proteins) 5-6 pieces of hard candy/pure sugar (e.g. – icing)
Are you sure you want to buy this material for
You're already Subscribed!
Looks like you've already subscribed to StudySoup, you won't need to purchase another subscription to get this material. To access this material simply click 'View Full Document'