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Nov 6 - Carbohydrates - Lecture Notes - LIFESCI 2N03

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Life Sciences
Danny M.Pincivero

LECTURE 5 LIFESCI 2N03 Lecture 5: Carbohydrates October 21, 23, 24, 28, 30, Nov 4, 6 2013  Carbohydrate – “hydrate of carbon”; manufactured by plants o Making a glucose molecule o Eg/ making a glucose molecule  6 CO2+ 6 H 2 + Energy  C H6O12 66O 2  Storage form of glucose o Animals – glycogen  Glycogen – branches at points; compact manner; liver higher in glucose; 8-10 glucose units then branch o Plants – starch (amylopectin and amylose) and fiber  Amylopectin – more bioavailable; ¾ starch; branched linear chains 25-30 glucose units, then branch  Amylose – ¼ of all starch available in plant based sources; less bioavailable than amylopectin (more compact)  Fiber – non-digestible carbohydrates (in plants); our bodies do not have the enzymes to breakdown certain fibers o Soluble Fibre  Dissolves in hot water  Forms a gel in GI system – does not move fast  Slows gastric/intestinal motility – advantage; absorbs fatty acids consumed with this fiber  “Fuller” feeling, absorbs FA’s  Decreases cardiovascular disease, because less cholesterol is absorbed into body  Eg/ Oat, bran, dried beans, nuts o Insoluble Fibre  Does not dissolve in hot water  Absorbs water into GI system  Speeds intestinal motility  Decreases Type II DM – because increased motility decreases glucose absorption time  Can lead to nutrient deficiencies  Eg/ Vegetable, fruit skins, whole grains  Function of Carbohydrates 1. Burned for energy 2. Ribose and deoxyribose sugars – serve as part of DNA and RNA 3. Structure and strength of plants 4. Linked to proteins and lipids  Glycoprotein – covalent link between protein and a carbohydrate monomer; found on cell surfaces – help to strengthen outer membrane of cells and for cell-cell adhesion  Glycolipid – forms myelin around neuron axons (insulation barrier for increase in speed of transmission along neuron)  Forms of Carbohydrates o Monosaccharide’s – simple form of CHO  Contains 3-9 carbon atoms  Eg/ Glucose, fructose, galactose,6C12 O6  Sugar alcohols  Derived from monosaccharide  Used as a sweetener (sorbitol made from glucose); sweetness in sugarless gum  Chemical modification of glucose molecule – changes the way our body perceives and senses monosaccharide o Glucose does not provide sweet flavor; fructose provides sweetness o Sorbitol can add the sweet flavor (carries calories, and larger sweet effect – negligible amount needed to be included, negligible about of calories)  Figure:  Monosaccharides enter into cardiovascular system from intestinal villi  Note: lipids and cholesterol do not go directly into cardiovascular system 1 LECTURE 5 LIFESCI 2N03 o Disaccharides – sucrose, lactose, maltose o Oligosaccharides – 3-9 CHO monomers  Considered to be a complex carbohydrate o Polysaccharides (≥ 10 monosaccharides)  Dietary from – starch  Vegetables and fruits  Grains – wheat, corn, oats, barley, rice  Legumes – peas, beans, lentils, soy  Tubers – potatoes, yams, cassava (toxic in raw form) Fiber  Soluble fiber – fermentable (bacteria can break it down anaerobically) becomes short chain fatty acids and can be absorbed to the body (very small amount) Starch  Begins in mouth, salivary glands begins to break down larger chain glucose molecules  Small intestine, pancreatic amylases accelerates breakdown of polysaccharides  Maltase, sucrose, lactase – intestinal cells use these enzymes to breakdown disaccharide in small intestines 2 LECTURE 5 LIFESCI 2N03  Purpose of consuming carbohydrates 1. Energy needs  Fuel source for neurons (only uses glucose except during starvation; can uptake protein); most amino acids are considered to be glucogenic  RBCs only use glucose; anaerobic, lacking mitochondria and nuclei; no ability to regenerate  Need CHO to metabolize other fuels; “fat burns in a flame of carbohydrates”  Ketone Bodies  Major source of production is the liver (in mitochondria)  Accumulation from protein and fat metabolism  Heart and renal cortex cells; ketone bodies are used as fuel  Starvation and Other Diseases o Brain neurons use ketone bodies (water soluble) – converted to Acetyl CoA o High levels of ketone bodies in blood reduces adipocyte lipolysis (regulates fat breakdown; feedback mechanism); increases reliance on CHO for energy  Type I Diabetes Mellitus – characterized by high level of ketones produced, and high lipolysis; no insulin (insulin has the effect of reducing lipolysis; no regulatory mechanism for fat breakdown) 2. Pregnancy  Fetus and placenta “feed” on glucose  Gestational diabetes – elevated blood glucose (inability to regulate glucose) during pregnancy; greater risk of developing Type I diabetes; usually ceases after birth but can persist 3. Spares muscle protein degradation for energy  Glucose must be synthesized from muscle protein when insufficient carbs from diet  proper diet will prevent muscle protein degradation  Amino acids converted to 1) ketone bodies 2) fatty acids 3) glucose o Ketone bodies – when harnessed from muscle tissues; recycle and use tissue o Fatty acids – can only occur when there is a high energy diet – there is a metabolic pathway to convert amino acids to fatty acids if energy needs are met o Glucose – amino acids are glucogenic  Gatorade will spare muscle breakdown o Exercise  glycolysis is elevated; storage of carbs in liver cells are begin metabolized and have to be restocked o Illness  infection  increased WBC (glucose); continues intake of carbohydrates to feed elevated metabolic state Carbohydrates and Energy  Glucose carried in the body o Always supply of glycogen in cardiovascular system o Liver stores glycogen more densely than muscle o Plasma glucose fluctuates with amount eaten, what was eaten, type of carbohydrate o Muscle tissue contains more energy than liver tissue – more muscle cells in the body than liver cells; muscle distributed throughout body  Overall glucose content o Blood glucose – 30 g o Liver glycogen – 90 g o Muscle glycogen – 350 g  ATP yield for CHO and fats 3 LECTURE 5 LIFESCI 2N03 o 5.1 kcal/L of2O (carbohydrates) – better fuel source when metabolized aerobically than fat o 4.8 kcal/L of2O (fats) o Due to substrate level phosphorylation – refers only to glucose; direct making of ATP from transformation of macronutrient; 4 extra ATP from glycolysis in cytoplasm  Minimum intake of CHO: 130 g/day for nervous system function  Figure: Body reactions to ingesting carbohydrates o 2. Glucose in blood binds to B-cells in pancreas which stimulates insulin production  Type I DM – B-cells are destroyed by body; insulin is not produced (#2 inhibition; pancreas)  high blood glucose o 3. Insulin binds muscle and liver cells to promote glucose uptake in cells – remove glucose from blood as glycogen  Type II DM – 9/10 of Canadians with DM; muscle cells not responding to insulin (insulin resistant) (#3 inhibition; muscle tissue)  high blood glucose o 4. Homeostatic level; blood glucose declines but does not deplete (not too high, not too low) o 5. Glucagon from a-cells in pancreas to maintain homeostasis of blood glucose – promotes glycogen breakdown (glycogenolysis) from liver and blood glucose increases  External cellular signal, stimulant of glycogenolysis  Glycemic Index (GI) – a measure (no units) of the potential food to raise blood glucose levels o High GI – blood glucose response is quicker in cardiovascular system  Increase [glucose] fast  increase blood [insulin] fast  7TM (7 transmembrane) receptor binds insulin – deactivates lipase  Diet chronically high in high GI foods – insulin continues to be secreted, muscle cells begin to be resistant to insulin  Exercise causes muscle cell contraction – same effect as insulin, stimulates proteins that pull glucose into cell o Fructose content; have to convert to glucose  lower GI o 2 different standards – one slide of white bread or pure glucose (both taken as 100%) o High GI ≥80 o Mid GI 56-59 o Low GI <56 4 LECTURE 5 LIFESCI 2N03 o Factors affecting the GI of foods 1. Proportion of CHO content of the ingested food  Increased % CHO, increase GI  Examples (compare to pure glucose ingestion) o Ice Cream 61  Fat molecules slow rate of glucose absorption o Baked Potato 85 o Instant Rice 91 o CHO easily broken down and absorbed o If GI is the factor – french fries are healthier than baked potatoes because lower GI 2. Type of carbohydrates  Simple vs. Complex  Role in Fat Storage – insulin action 3. Cooking  Heat helps to disrupt chemical bonds – faster digestion  Eg/ o Pasta GI (5 min boiled) 34 o Pasta GI (10 min boiled) 40  Blood glucose response to feeding  Glycemic Load – amount of carbs, blood glucose will increase (as opposed to rate of blood glucose increase) o GI multiplied by the amount of available carbohydrates in a food source/100 o Predictor of developing Type II diabetes mellitus and cardiovascular disease o Eg/  Corn Muffin GI = 102 (compared to glucose), 29 g carbs/serving, GL = 20  Bran Muffin GI = 60 (compared to glucose), 24 g carbs/serving, GL = 15  High fibre – indigestible o Fruits – high GI, low glycemic load  Watermelon – blood glucose increases quickly, but not by a lot o Blood Glucose Response to Feeding  Eat  blood glucose begins to rise  eventually goes down, undershoots then stabilizes  Baked potatoes  magnitude of increase in blood glucose is much larger and enters system more quickly (dotted line)  Ice cream (red line)  Fat molecules compete with intestinal absorption of glucose  Glycemic Index – slope of curve; how fast blood glucose concentration increases  Glycemic Load – magnitude of blood glucose concentration  Rate of insulin secretion is proportional to rate of [blood glucose] increase  Diagram o Challenge to get glucose out of cardiovascular system into muscle cell  signaled by insulin o Muscle fiber membrane – contains of fatty acids, GLUT1 o GLUT1 (glucose transporters) – protein that transports glucose from outside of cell to interior of cell; always present in cell  Glucose forms chemical bond with asparagine 45 (45 amino acid in sequence from amino end of GLUT1) – protein inverts into interior of cell, glucose pulled into interior of cell  Cells always need glucose – GLUT1 always active, even during rest  Does not transport efficiently enough (after meal, many glucose molecules; GLUT1 not fast enough) o Insulin binds to another membrane protein on muscle fiber membrane – stimulates GLUT4 which is held inside cell in a vesicle, translocates GLUT4 to be embedded in membrane (for ~12 minutes)  DM Type II – no Insulin; cannot bind to GLUT4  GlLUT4 –only recruited when need to internalize more glucose; GLUT1 always expressed  DM Type II – GLUT4 cannot be recruited o Muscle cell eventually becomes resistant to insulin 5 LECTURE 5 LIFESCI 2N03 Pancreatic Hormones  Insulin o Produced by beta cells of the pancreas o Helps cells take in glucose from the blood o Stimulates the liver and muscle cells to take up glucose and convert it to glycogen o Overall effect of lowering blood glucose o 51 amino acid sequence, with 2 chains (A and B) o Disulfide bridges between cysteine residues  Glucagon o Produced by alpha cells of the pancreas o 29 amino acid polypeptide o Signals a physiologically starved state – body has not ingested nutrients o Stimulates the breakdown of glycogen to glucose o Glucagon increase seen in exercise o More glucose is available to cells of the body o Stimulates gluconeogenesis – the production of glucose from amino acids o Overall effect of raising blood glucose CHO Related Disorders  Diabetes Mellitus – a disorder of carbohydrate metabolism, characterized by hyperglycemia and glycosuria and resulting from in adequate production (Type I) or utilization (Type II) of insulin o Hyperglycemia – greater than normal glucose level o 2 million Canadians affected o ~10% Type I diabetes (IDDM; insulin dependent DM)) o ~90% Type II diabetes (NIDDM; non-insulin dependent DM)  Gestational Diabetes o 3.7 % of all pregnancies (more similar to Type II DM) o 8-18% of all pregnancies among Aboriginal women  Diabetes o Gr. “passing through” 6 LECTURE 5 LIFESCI 2N03 o A general term for diseases characterized by excessive urination  Mellitus o Latin “sweetened with honey” o Presence of sugar in the urine (glycosuria)  Diabetes Insipidus o Impaired water re-absorption in kidney (lack of ADH)  Type I Diabetes Mellitus o Autoimmune disorder o Beta-cell ingestion by the immune system 1. No production of insulin 2. Leads to hyperglycemia (abnormally high blood glucose)  Normal range = 80-110 mg/dL (4.4-6.1 mmol/L)  Meal – may rise to 140 mg/dL 3. No insulin, no uptake of glucose into cells  Consequences  Glucose not brought into muscle or liver cells o Muscle – no translocation of GLUT4 o Liver – GLUT2 not activated (insulin is an activator) o Liver interprets this as low blood glucose (even though glucose levels are high)  liver increases rate of glycogenolysis – makes hyperglycemia worse  Renal threshold – 170-200 mg/dL o Kidney filters the blood and “cleans” it; filtration then reabsorption (2ons, H O, glucose) o Can only reabsorb up to a certain point (renal threshold) – Kidneys reabsorb 99% of filtered substances o Blood glucose level in which glucose is not reabsorbed from the kidneys; glycosuria (glucose in the liver) o Exceeds the capacity of renal tubules for re-absorption  Urinary glucose will attract water molecules  takes it out of body and secretes it o Symptom  Consistent thirst and frequent urination (because of lost of water molecules)  First observed 2000+ years ago o Risk Factor  Largely genetic susceptibility  Family history of Type I (or Type II) diabetes mellitus o Energy utilization in Type I Diabetes Mellitus  Problem – not able to get glucose into cells, so the body senses a starvation state o Fuel source for cells  Fatty acids – no insulin, no 7TM receptor binding, no inhibition of TG lipase  With insulin bound to 7TM – inhibited enzyme that breaks down triglycerides (enzyme allows for fatty acids to enter cardiovascular system)  Insulin is a regulator of fat metabolism  Fat metabolism is higher in DM  Eventually use of muscle protein – body attempts to conserve, but eventually leads to muscle wasting Physiological States  Fed state – after digesting a meal; 1. Blood glucose concentration increases 2. GLUT2 activation in liver and pancreas (acceleration of GLUT2 by insulin, due to glucose) 3. Start pulling glucose into liver and signal in the pancreas to secrete insulin  Insulin Secretion  Translocation of GLUT4 in muscle cells  Adipocyte: promotes fatty acid synthesis; inhibits lipase that breaks up triglyceride  Promotes uptake of branched-chain aa by skeletal muscle; stimulates protein synthesis; eg/ not during exercise; after exercise (so eat protein; protein shake, high GI)  Accelerates GLUT2 activation (liver and muscle) accelerates glycogen synthesis  Insulin increases macronutrient storage  Early fasting state – few (2-3) hours after eating a meal o Glucose ingested, then insulin increases; deceleration of glucose because insulin has caused glucose to be pulled out of cardiovascular system into cells 7 LECTURE 5
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