Nutrition Physiology Exam 2 Study Guide PDF

NUTRITION PHYSIOLOGY EXAM 2 STUDY GUIDE Incretins ○ GLP-1 and GIP Secreted after food ingestion Stimulates insulin secretion ○ DPP-4 (Dipeptidyl Peptidase) Breaks down GLP-1 and GIP on lymphocytes and endo...

NUTRITION PHYSIOLOGY EXAM 2 STUDY GUIDE Incretins ○ GLP-1 and GIP Secreted after food ingestion Stimulates insulin secretion ○ DPP-4 (Dipeptidyl Peptidase) Breaks down GLP-1 and GIP on lymphocytes and endothelial cells DPP-4 inhibitors blocks the enzyme DPP-4 to help treat T2D Additional Info ○ The dual GIP/GLP-1 receptor co-agonist combing agonist at both incretin hormones’ receptors “twincretin” was originally designed as a novel treatment for T2D Triglyceride Structure and Function ○ Major form of lipids in the body and food ○ Body’s main storage form of energy and source of fuel for cells ○ Composed of three fatty acids attached to a glycerol backbone Cholesterol Structure and Function ○ Hydrocarbon and a Hydroxyl Group (-OH) ○ Amphipathic molecule Has both hydrophilic and hydrophobic properties ○ Aids in Vitamin D synthesis ○ Used by the liver to manufacture bile salts  2 Cholesterol Ester Structure and Function ○ Connects tail to another structure creating an ester bond Attaching a fatty acid to Hydroxyl Group (-OH) ○ Storage and transport form of cholesterol within the body ○ How cholesterol is found in food ○ Packaged into lipoproteins LDL and HDL Bioactive Lipids Function Act as signal molecules in the cells and participate in many cellular reactions Sterols ○ Class of lipids characterized by their complex four ring structure Hydrocarbon ○ Major structural component of all cell membranes and is abundant in nerve and brain tissue ○ Example: cholesterol Phospholipids ○ Glycerol molecule bonded to two fatty acids and a phosphate group Has a nitrogen-containing compound ○ Amphipathic molecule ○ Synthesized in the body and not needed in the diet ○ Soluble in oil and water ○ Functions Emulsifiers Lipid transport Structural element for cell membranes Temporary storage of fatty acids Phosphatidylcholine whose choline component becomes part of the major neurotransmitter Acetylcholine  3 Types of Fat Saturated Fat ○ No double bonds ○ Commonly Found Meat Dairy Some plant oils ○ Solid at room temperature Short chains are liquid ○ High intake can increase levels of LDL Unsaturated Fat ○ Monounsaturated Fat Contains one double bond Missing some hydrogens Liquid at room temperature ○ Polyunsaturated Fat Contains two or more double bonds Missing some hydrogens Liquid at room temperature Cis and Trans Configurations CIS ○ Hydrogen atoms are on the same side of the double bond ○ Can not pack closely together ○ More susceptible to oxidation Liquid state at room temperature Decreases shelf stability TRANS ○ Hydrogen atoms are on the opposite sides of the double bond ○ Straighter chains can pack more tightly Less prone to oxidation Increases shelf stability  4 Fatty Acid Structure Chain Length ○ Lengths of 4 to 24 carbons and most have an even number of carbons ○ Short, medium, and long chains Two Ends ○ Carboxyl End (α-Carbon) Contains a carboxyl group (-COOH) ○ Methyl AKA Omega End (w-Carbon) Contains a methyl group (-CH3) Naming ○ Based on the number of carbon atoms and double bonds Hydrogenation and Creation of Trans Fats and Health Effects Hydrogenation ○ Addition of hydrogen atoms to unsaturated fats to convert them into saturated fats Converts double bonds to single bonds Makes fats more shelf stable Creation of Trans Fats ○ Double bonds from a cis configuration are converted to a trans configuration during hydrogenation Health Effects ○ Raises LDL  5 ○ Increases risk of CVD Essential and Nonessential Fatty Acids Essential ○ Body can not synthesize and must be consumed in diet Linoleic acid (LA): Omega-6 Alpha-linolenic acid (ALA): Omega-3 Nonessential ○ Fatty acids that the body can make Oleic acid: Omega-9 Lipid Dietary Recommendations Dietary Fat ○ 20 to 35% of total calories ○ Children Aged 1 to 3 30 to 40% of total calories ○ Children Aged 4 to 18 25 to 35% of total calories Saturated Fat ○ No more than 10% of total calories or ⅓ of fat calories Goal: Lower Blood Cholesterol ○ Saturated fat intake reduced to no more than 5% or 6% of total calories ○ No more than 300 mg/day of cholesterol Trans Fat ○ Limit as much as possible Infants ○ Birth to 6 months 31g fat per day ○ 7 to 12 months 30g per day AIs and RDAs ○ Not set for children or adults Fat-Free or Low-Fat Dairy  6 ○ Milk ○ Yogurt ○ Cheese ○ Fortified soy beverages Variety of Protein Foods ○ Seafood ○ Lean meats ○ Poultry ○ Eggs ○ Legumes ○ Nuts ○ Seeds Limit ○ Saturated fat ○ Trans fat ○ Added sugars ○ Sodium Lipid Digestion Example: Consumed a fatty hamburger STEP 1 ○ Lingual lipase (enzyme) is activated at oral intake to begin lipid breakdown STEP 2 ○ Bolus enters the stomach and becomes Chyme AKA Fat Globules ○ Fat Globules Consist Of: Diglycerides Monoglycerides Cholesterol and FFA Phospholipids STEP 3 ○ Chief Cells secrete gastric lipase enzyme Acts on fat globules and releases some fatty acids STEP 4 ○ Pancreatic Juice Secretion  7 Pancreatic lipase and Colipase enzymes are activated Acts on triglycerides Phospholipase A enzyme is activated Acts on phospholipids Cholesterol Ester Hydrolase enzyme is activated Acts on cholesterol esters STEP 5 ○ Bile Releases Lecithin and Cholic Acid Stimulated by CCK Lecithin ○ Phospholipid ○ Amphipathic molecule Polar head and two nonpolar tails Cholic Acid ○ Bile Salts Emulsifies fat STEP 6 ○ Lecithin pulls apart the tiny fat globules ○ Cholic acid “coats” the globules Colipase enzyme sticks on top of the globules followed by Pancreatic Lipase enzyme ○ Cholic Acid (Bile Salts) → Colipase → Pancreatic Lipase STEP 7 ○ Pancreatic Lipase enzyme further breaks down the fat globules Creates More: Monoglycerides Free fatty acids Cholesterol STEP 8 ○ Generation of Micelles Tiny fat droplets ○ Bile gets recycled and goes back to the liver STEP 9 ○ Fat soluble vitamins ADEK get dissolved into the Micelles STEP 10  8 ○ Micelles enter Enterocyte Endocytosis: Passive Diffusion STEP 11 ○ Micelles enter the smooth ER within the Enterocyte STEP 12 ○ LIPOGENESIS Smooth ER resynthesizes the Micelles back into triglycerides, cholesterol esters, and phospholipids STEP 13 ○ Lipid moves into the Rough ER and Golgi Apparatus for further processing Addition of protein carrier molecule (apolipoprotein B48) ○ Creates Chylomicrons Lipoprotein Protein and fat coated structure STEP 14 ○ EXOCYTOSIS Chylomicrons enter lymphatic capillaries and are carried to the liver, muscle, or adipocytes Lipolysis Occurs In ○ Adipose tissue ○ Liver Entire Process is Reversible* ○ Triglyceride → Glycerol + Fatty Acids = Lipolysis ○ Fatty Acids + Glycerol → Triglyceride = Lipogenesis STEP 1 ○ Lipases (Group of Enzymes) attack ester bonds and release them Creates Glycerol and FFA STEP 2 ○ Glycerol → Glycerol-3-Phosphate (G-3-P) Enzyme: Glycerol Kinase G-3-P can be converted to DHAP ○ Part of Glycolysis  9 3 Irreversible Steps PEP to Pyruvate F-6-P to F-1-6-BP Glucose to G-6-P STEP 3 ○ FFA can go directly to mitochondria for energy Beta Oxidation Broken down to get a tail that is two carbon short Produce Acetyl CoA molecules TCA Metabolites ○ OAA → Malate → OAA ○ OAA → PEP Enzyme: PEPCK ○ PEP → Pyruvate ○ Availability of OAA can determine the ketogenesis pathway in the liver and cholesterol biogenesis Beta Oxidation Occurs In ○ Liver ○ Muscle ○ Heart INTRO STEP 1 ○ ACTIVATION CoASH (Coenzyme A) is added to the head of the FFA Enzyme: Fatty Acyl CoA Synthetase ATP is broken down Becomes Fatty Acyl CoA AKA CoASH INTRO STEP 2 ○ TRANSPORTATION ○ Outside Mitochondria Carnitine replaces CoASH and CoASH becomes free Carnitine is transported into the mitochondria Enzyme: CAT-1  10 CoASH is transported into the mitochondria Enzyme: CAT-2 INTRO STEP 3 ○ Inside Mitochondria Carnitine is removed and CoASH is reattached to the FFA Enzyme: CAT-2 Carnitine goes back and brings another FFA into the mitochondria FOUR STEP PROCESS ○ STEP 1 CoASH Hydrogens are removed Double bond is created between the α and β carbons FAD → FADH2 Creates Enoyl CoA ○ Enzyme: Fatty Acyl CoA Dehydrogenase ○ STEP 2 Water is added to Enoyl CoA Enzyme: Enoyl CoA Hydratase Enoyl CoA becomes β-Hydroxy Acyl CoA ○ STEP 3 H is removed from β carbon of β-Hydroxy Acyl CoA NAD → NADH Creates C=O Creates β-Keto Acyl CoA Enzyme: Keto Acyl CoA Dehydrogenase ○ STEP 4 β-Keto Acyl CoA is broken down into two molecules Cuts β carbon and adds CoASH Enzyme: Thiolase ○ PRODUCTS Product A: 2 Carbon Short Fatty Acyl CoA Goes through 7 rounds of Beta Oxidation ○ Provides 8 Acetyl CoA Product B: Acetyl CoA Goes into Krebs Cycle  11 Chain Length of Fatty Acids Short Chain Fatty Acids (SCFA) ○ < 6 carbon atoms ○ Foods Oats Rye Barley ○ Examples Acetate Propionate Butyrate Medium Chain Fatty Acids (MCFA) ○ 6 to 12 carbon atoms ○ Foods Coconut Dairy Products ○ Examples Caproic acid Caprylic Acid Lauric Acid Long Chain Fatty Acids (LCFA) ○ > 12 carbon atoms ○ Foods Olive Oil Soybeans Fish Avocado ○ Examples Palmitic Oleic Linoleic DHA EPA  12 Autosomal Recessive Genetic disorders where a child inherits two copies of a mutated gene (one from each parent) ○ Fatty Acid Oxidation Disorder (FAOD) is inherited Autosomal Dominant Genetic disorders where a child inherits a mutated gene from one parent that causes a condition Chylomicrons, VLDL, LDL, and HDL ○ Chylomicrons Make their way to the central lacteal of the villi Enter lymph system and are propelled through the thoracic duct and emptied into veins in the neck ○ VLDL Triglyceride-rich lipoproteins Synthesized In Liver Acted upon by enzyme lipoprotein lipase Releases triglycerides to cells ○ LDL Cholesterol rich lipoproteins Result from the breakdown and removal of triglycerides from IDLs Special receptors on the cell walls bind LDL Cell engulfs and ingests by Endocytosis Inside The Cell LDL is broken down release cholesterol LDL Receptors Bind LDL Help control blood cholesterol levels  13 ○ Lack of LDL receptors reduces the uptake of cholesterol Forcing cholesterol to remain in circulation at dangerously high levels ○ HDL Lipoproteins that contain high levels of protein and low levels of triglycerides Synthesized In Liver Small Intestine Action Picks up cholesterol released from dying cells and other sources ○ Transfer it to other lipoproteins such as IDL Returns cholesterol to the liver for recycling High HDL Levels Protective effect Ketogenesis Produces ketone bodies to provide a secondary form of energy Occurs When ○ Prolonged starvation ○ Low blood glucose levels ○ Uncontrolled diabetes ○ Carbohydrate restriction Where Does It Occur ○ Liver Krebs Cycle Metabolites ○ Low Krebs Cycle activity due to low blood glucose ○ OAA levels are low due to making glucose Acetyl CoA can not react with OAA Citrate ↓ Accumulation of Acetyl CoA molecules STEP 1  14 ○ Acetyl CoA Alternative Pathway 2 Acetyl CoA molecules are fused together and creates AcetoAcetyl CoA Enzyme: Acetyl CoA Acyl Transferase STEP 2 ○ AcetoAcetyl CoA is added to another Acetyl CoA and creates HMG-CoA RATE LIMITING STEP* Enzyme: HMG-CoA Synthase STEP 3 ○ HMG-CoA loses an Acetyl CoA and creates Acetoacetate: Ketone Body Enzyme: HMG-CoA Lyase STEP 4 ○ Acetoacetate: Ketone Body receives (H) from NADH and creates β-Hydroxy Butyrate: Ketone Body Enzyme: β-Hydroxy Butyrate Dehydrogenase NADH becomes NAD+ STEP 5 ○ Acetoacetate and β-Hydroxy Butyrate go into bloodstream and are taken to muscle or brain cells MORE STEPS ○ Acetoacetate can be acted on by another enzyme and creates Acetone: Ketone Body Enzyme: Acetoacetate Decarboxylase Removes a carbon ○ Acetone creates Acetone Breath Ketone Bodies can donate protons into blood Makes blood acidic EXCESS AMOUNTS ○ Acetoacetate and β-Hydroxy Butyrate stimulate brain Outcomes Vomiting Ketonuria: blood in the urine Severe can lead to Comatose State Diabetic Ketoacidosis  15 Body does not have enough insulin to allow blood sugar into cells for energy ○ Blood sugar levels are too high* ○ Life threatening ○ Pathology Insulin deficiency Hyperglycemia Metabolic acidosis ○ Outcomes Acetone Breath Fruity odor in the breath Results from the presence of acetone Kussmaul Breathing Rapid, deep, and labored breathing ○ Indication that the blood is too acidic Body is trying to get CO2 out of the body Caused by low blood pH Medical emergency Ketolysis Process of breaking down ketone bodies to produce energy Where Does It Occur ○ Muscle ○ Brain STEP 1 ○ β-Hydroxy Butyrate break downs to Acetoacetate Enzyme: B-Hydroxy Butyrate Dehydrogenase NAD+ → NADH STEP 2 ○ Acetoacetate breaks down to AcetoAcetyl CoA Enzyme: Thiophorase Succinyl CoA from Krebs Cycle drops off CoA ○ Results in Succinate STEP 3 ○ AcetoAcetyl CoA breaks down to 2 Acetyl CoA Molecules  16 Enzyme: Acetyl CoA Acyl Transferase STEP 4 ○ Acetyl CoA Molecules go into Krebs Cycle Generates NADH Generates FADH2 Generates ATP Thiophorase vs. Thiolase Enzymes Thiophorase ○ Transfers CoA from Succinyl CoA during Ketolysis Acetoacetate breaks down to AcetoAcetyl CoA Thiolase ○ β-Keto Acyl CoA is broken down into two molecules during Beta Oxidation ○ Cuts β carbon and adds CoASH Produces 2 Carbon Short Fatty Acyl CoA Acetyl CoA Renin Angiotensin Aldosterone System (RAAS) STEP 1 ○ Decreased BP stimulates kidneys to secrete enzyme renin STEP 2 ○ Renin splits the plasma protein angiotensinogen to Angiotensin I STEP 3 ○ Angiotensin I is converted to Angiotensin II Enzyme: Converting Enzyme Secreted by lung tissue and vascular endothelium STEP 4 ○ Angiotensin II Causes vasoconstriction Stimulates the adrenal cortex to secrete aldosterone  17 DRUGS ○ ACEIs (angiotensin converting enzyme inhibitors) Block active site of angiotensin-converting enzyme ○ ARBs (angiotensin receptor blockers) Block angiotensin II receptor ○ BBs (beta blockers) Block beta-adrenergic receptors β1 and β2 Reduces processing of prorenin into renin Reduces HR ○ CCBs (calcium channel blockers) Inhibits calcium ions going into muscle cells Blocks L-type calcium channels Leads to vasodilation Reduces HR ○ Thiazide-Type Diuretics Inhibit sodium reabsorption  18 Low blood volume Stimulate renin release Activating RAAS Hypertension and CVD Risk Factors Risk Factors ○ Family history ○ Obesity ○ Physical inactivity ○ Diet High In Fat Sodium Sugar ○ Smoking ○ Alcohol consumption Symptoms of High Blood Pressure and Recommendations Symptoms ○ Headaches ○ Dizziness ○ Nosebleeds ○ Shortness of breath ○ Chest pain Dietary Changes ○ Consume More Fruits Vegetables Whole grains ○ Limit Saturated fat Trans fat Sugar intake Alcohol  19 Metabolic Syndrome Increases the risk of many chronic diseases ○ Obesity ○ Diabetes ○ Hypertension ○ Cardiovascular complications Presence of any three ○ Waist Circumference > 40” (102 cm) Men > 35” (88 cm) Women ○ Atherogenic Dyslipidemia Increase in Triglycerides > 150 mg/DL Decrease in HDL Cholesterol < 40 mg/DL and < 50 mg/DL in men and women ○ Elevated Blood Pressure > 130 / > 85 mmHg ○ Insulin Resistance and Glucose Intolerance FPG > 100 mg/dL ○ Proinflammatory State Elevated inflammatory markers Cytokines CRP (C-Reactive Protein) ○ Prothrombotic State Increases venous thrombosis Blood clot blocks a vein Hypertension Correlation With Other Disorders Increased BP ○ Requires heart to work harder ○ Potentially leads to left ventricular hypertrophy and heart failure  20 Elevated BP ○ Damages the blood vessel walls by promoting atherosclerotic plaques ○ Dislodge blood clots and atherosclerotic plaques Can block smaller arterioles or capillaries Results in an ischemic attack ○ May damage the small arterioles of the kidneys needed for proper blood filtration and urine excretion Dietary Assessment Tools Associated With Hypertension and CVD CAGE ○ (cheese, animal fats, got it away from home, and eat [extra] high-fat commercial products) for saturated fats and cholesterol Rapid Eating Assessment for Patients (REAP) MEDFICTS Assessment ○ Adequacy in comparison to TLC Diet Therapeutic Lifestyle Changes (TLC) Diet Heart healthy eating plan that aims to lower LDL and risk of CVD via diet, exercise, and weight management ○ Reduce saturated fat intake ○ Increase fiber, fruits, vegetables, and whole grains ○ Limit red meat ○ Aim for 30 minutes of activity most days of the week MEDFICTS Quick screening (questionnaire) that assess dietary fat intake Helps assess adherence to the TLC diet FH Article Important Points  21 Practice Questions What organelle is involved in the resynthesizing of triglycerides? Smooth ER What is the category of lipids categorized with hydrocarbon rings? Sterols ○ Cholesterol ○ Phospholipids True or False: Beta Oxidation can generate electron carriers True True or False: Saturated fats are generally solids at room temperature True True or False: Activation of fatty acids occur in the mitochondria False ○ Activation occurs outside of the mitochondria with CoA being attached to the head of the FFA by enzyme Fatty Acyl CoA Synthetase A decrease in what can lead to ketogenesis? OAA What end of the fatty acyl molecule is activated by the addition of CoA? Carboxy end What type of fat is not suited for fat storage? Ectopic fat How is cholesterol found in foods? Cholesterol esters True or False: Fats can not enter the glycolysis pathway for ATP generation False  22 What are the droplets of liquids that enter the enterocytes? Micelles True or False: Bile salts are involved in lipid digestion and get processed in the Smooth ER of the enterocyte False What is a key step in cholesterol synthesis? Formation of HMG CoA What food is rich in saturated fats? Premium sausages Where does dietary fat-soluble vitamin uptake occur? Small intestine