FNH 350 Fundamentals of Nutrition Lecture Notes PDF

1. ORGANS ACCESSORY ORGANS ORGANS ORGANS OFTRACT OF GI GI TRACT Salivary glands Oral cavity + tongue Pharynx Upper...

1. ORGANS ACCESSORY ORGANS ORGANS ORGANS OFTRACT OF GI GI TRACT Salivary glands Oral cavity + tongue Pharynx Upper digestive Liver Liver Esophagus tract Gallbladder Stomach Stomach Pancreas Small intestine Lower digestive Large intestine tract LECTURE 1 -‐ SLIDE 35 1.1. ORAL CAVITY and SALIVARY GLANDS * Main enzyme in saliva: salivary amylase (hydrolysis of starch) LECTURE 1 -‐ SLIDE 36 1.2. ESOPHAGUS KEY FACTS Length: 10 inches or 25 cm Function: moves bolus (= food mixed with saliva) from oral cavity to stomach Passage of bolus involves: Swallowing: 1) voluntary 2) pharyngeal 3) esophageal Peristalsis: moving of bolus by wavelike motions Gastroesophageal sphincter: entrance to stomach LECTURE 1 -‐ SLIDE 37 1.3. STOMACH Stomach is ﬂexible in size can expand from 50mL (resting) Rugae = folds; allow to 1.0 -‐ 1.5L (fed) stomach to expand ©2009 Cengage-‐Wadsworth LECTURE 1 -‐ SLIDE 38 1.3. STOMACH Stomach consists of four main regions: Cardia Fundus Body Antrum ©2009 Cengage-‐Wadsworth LECTURE 1 -‐ SLIDE 39 DISCUSSION QUESTION What is the key digestive role of the gastric juices? LECTURE 1 -‐ SLIDE 40 1.3. STOMACH Millions of gastric glands located in the Neck cells: mucus mucosa Chief cells: enzymes produce Parietal cells: HCl; IF gastric G-cells: Gastrin juice. LECTURE 1 -‐ SLIDE 41 er Session 2016/2017 1.3. STOMACH Hydrochloric acid secretion Reason for high acidity of gastric juice; pH = 2 Function: -‐ Denaturation of proteins -‐ Activates pepsinogen to pepsin - Release of nutrients from organic complexes -‐ Antibacterial LECTURE 2 -‐ SLIDE 11 LECTURE 1 -‐ SLIDE 42 CLICKER QUESTION Why pepsin is produced as an inactive proenzyme, pepsinogen? A. To protect the stomach lining B. To protect pepsin from inactivation C. To stimulate release of other enzymes LECTURE 1 -‐ SLIDE 43 1.3. STOMACH Stomach consists of four main regions: Cardia region Fundus Body gastric juices mixing of bolus with circular, longitudinal and diagonal smooth muscles Antrum ©2009 Cengage-‐Wadsworth Grinds food & mixes with gastric juices to form chyme Strong peristalsis for gastric emptying LECTURE 1 -‐ SLIDE 44 1.3. STOMACH Peristalsis of the stomach in the gastric antrum: https://www.youtube.com/watch?v=o18UycWRsaA LECTURE 1 -‐ SLIDE 45 1.3. STOMACH Chyme leaves the stomach through the pyloric sphincter. 1-‐5mL (1tsp) chyme twice per min.  into the Duodenum ©2009 Cengage-‐Wadsworth Gastric emptying following a meal takes: somatostatin release LECTURE 1 -‐ SLIDE 46 1.4. SMALL INTESTINE = Main site for nutrient digestion and absorption Small intestine is composed of Duodenum < 0.3 m (1 ft) long Ileum approx. 3 m (9 ft) long Jejenum Special inner membrane and structure of the small intestine yields a surface of: 300 m2 or 3-ft wide sidewalk three football ﬁelds in length LECTURE 1 -‐ SLIDE 47 1.4. SMALL INTESTINE LECTURE 1 -‐ SLIDE 48 ssion 2016/2017 1.4. SMALL INTESTINE Digestion of nutrients usually completed in brush border. Some nutrient digestion completed in 17 cytoplasm of enterocyte. LECTURE 21 -‐ SLIDE 49 1.4. SMALL INTESTINE Mixing ©2009 Cengage-‐Wadsworth LECTURE 1 -‐ SLIDE 50 1.4. SMALL INTESTINE Propelling LECTURE 1 -‐ SLIDE 51 2017 1.4. SMALL INTESTINE Some of the secretory products in duodenum Alkaline and viscous mucus  to protect mucosa from damage  to neutralize highly acidic chyme Secretin (hormone)  inhibits gastric secretions  stimulates pancreas and gallbladder secretions Somatostatin (hormone)  Released by D-cells in duodenum, pancreas and antrum of the stomach LECTURE 1 -‐ SLIDE 52  diminishes secretion by stomach cells 1.5. ACCESSORY ORGANS LECTURE 1 -‐ SLIDE 53 1.5. PANCREAS Two types of active cells Stimulated by secretin 2016/2017 ©2009 Cengage-‐Wadsworth LLEECCTTUURERE LECTURE 1 -‐ SLIDE 54 1.5. PANCREAS Pancreatic enzymes digest: 50% of all ingested carbohydrates 50% of all proteins 80-90% of ingested fat LECTURE 1 -‐ SLIDE 55 1.5. LIVER/GALLBLADDER LECTURE 1 -‐ SLIDE 56 1.5. LIVER LECTURE 1 -‐ SLIDE 57 1.5. GALLBLADDER Functions: -‐ concentrates -‐ stores -‐ secretes bile Bile = greenish‐yellow ﬂuid -‐ produced in liver, stored in gallbladder -‐ mostly contains bile acids and salts to emulsify lipids -‐ cholesterol, phospholipids, bile pigments LECTURE 1 -‐ SLIDE 58 1.5. GALLBLADDER Importance of cholecystokinin in bile release FFNNHH335500TTeermm12WWinnteterr SSeessssioonn 22001161//22001172 LECTURE 1 -‐ SLIDE 59 1.6. LARGE INTESTINE 1 liter of chyme becomes 200 grams of defecated material LECTURE 1 -‐ SLIDE 60 2. ABSORPTION LECTURE 1 -‐ SLIDE 61 FFNNHH335500TTeermm12WWinnteterr SSeessssioonn 22001161//22001172 2. ABSORPTION MECHANISMS LECTURE 1 -‐ SLIDE 62 2. ABSORPTION MECHANISMS LECTURE 1 -‐ SLIDE 63 SUMMARY ACCESSORY ORGANS ORGANS ORGANS OFTRACT OF GI GI TRACT Salivary glands Oral cavity + tongue Pharynx Upper digestive Liver Liver Esophagus tract Gallbladder Stomach Stomach Pancreas Small intestine Lower digestive Large intestine tract LECTURE 1 -‐ SLIDE 64 NEXT CLASS Carbohydrates -‐ function, classes, structures, food sources, and digestion Textbook Chapter 3 LECTURE 1 -‐ SLIDE 65 FNH 350 – Fundamentals of Nutrition Food, Nutrition and Health Program Term 1 W2024/2025 Lecture 2: Carbohydrates - function, classes, structures, food sources, and digestion FNH 350 Term 1 Winter Session 2016/2017 LECTURE 2 -‐ SLIDE 1 TODAY'S LECTURE Learning Objectives:  Deﬁne the role of carbohydrates in human nutrition.  Describe the major classes of carbohydrates.  Deﬁne carbohydrates and explain the structures of the diﬀerent carbohydrate classes and their individual units.  List food sources for individual carbohydrate classes.  Discuss carbohydrate and sugar intake in Canada.  Describe organs and speciﬁc enzymes involved in carbohydrate digestion.  Explain why some carbohydrates cannot be digested. LECTURE 2 -‐ SLIDE 4 Textbook: Chapter 3 CLASSES OF CARBOHYDRATES Two major classes: I. Simple carbohydrates Monosaccharides Disaccharides II. Complex carbohydrates Oligosaccharides Polysaccharides LECTURE 2 -‐ SLIDE 6 I. SIMPLE CARBOHYDRATES Monosaccharides  = simple sugars  structurally the simplest  ‘one sugar unit’ = ‘monosaccharide unit’  most important in human nutrition: - Glucose - Fructose - Galactose LECTURE 2 -‐ SLIDE 7 I. SIMPLE CARBOHYDRATES Monosaccharides  Monosaccharides occur from triose through heptose  Classiﬁcations: position of functional carbonyl-group: aldose contains aldehyde group ketose contains ketone group number of carbons: aldohexose, ketohexose, ketopentose LECTURE 2 -‐ SLIDE 8 I. SIMPLE CARBOHYDRATES Carbohydrates are optically active. Optical activity due to presence of one or more chiral carbon atoms in the molecule. Polarized light passing through solution of optically active substances is rotated to the right or the left. Sugar content in food products, e.g. marmalade, can be measured with the use of a polarimeter. LECTURE 2 -‐ SLIDE 9 I. SIMPLE CARBOHYDRATES LECTURE 2 -‐ SLIDE 10 I. SIMPLE CARBOHYDRATES Form of monosaccharides in solution: = in ring‐form * Anomeric carbon LECTURE 2 -‐ SLIDE 11 I. SIMPLE CARBOHYDRATES * Anomeric carbon LECTURE 2 -‐ SLIDE 12 I. SIMPLE CARBOHYDRATES * Anomeric carbon LECTURE 2 -‐ SLIDE 13 I. SIMPLE CARBOHYDRATES Pentose Very little source of dietary energy (only few available in the diet) Synthesized in the cell from hexose precursors Transformed into metabolically important compounds LECTURE LECTURE 2 -‐ SLIDE 14 I. SIMPLE CARBOHYDRATES Disaccharides two sugar units Maltose formed from partial hydrolysis of starch β-Maltose LECTURE 2 -‐ SLIDE 15 I. SIMPLE CARBOHYDRATES Disaccharides α-Lactose LECTURE 2 -‐ SLIDE 16 II. COMPLEX CARBOHYDRATES Oligosaccharides ‘oligo‘ = few must be digested to be utilized raﬃnose (trisaccharide) stachyoses (tetrasaccharide) verbascose (pentasaccharide)  made of glucose, galactose, fructose  digestion: no enzyme available intestinal bacteria digest them LECTURE 2 -‐ SLIDE 17 II. COMPLEX CARBOHYDRATES Dextrins oligo- or polysaccharides depending on the chain length composed of glucose additives in foods, pharmaceuticals and nutritional supplements from hydrolysis of starch or glycogen LECTURE 2 -‐ SLIDE 18 II. COMPLEX CARBOHYDRATES Polysaccharides Starch exists in the form of amylose + amylopectin Glycogen storage form of glucose (liver, skeletal muscle) Cellulose not digestible considered a dietary ﬁber not considered an energy source LECTURE 2 -‐ SLIDE 19 II. POLYSACCHARIDES Amylose LECTURE 2 -‐ SLIDE 20 II. POLYSACCHARIDES Amylopectin LECTURE 2 -‐ SLIDE 21 II. POLYSACCHARIDES Glycogen LECTURE 2 -‐ SLIDE 22 CLASSES AND UNITS OF CARBOHYDRATES Dextrins Glucose LECTURE 2 -‐ SLIDE 23 CASE SUDY What is the average carbohydrate intake in grams per day for an adult consuming 2700 kcal/day ? LECTURE 2 -‐ SLIDE 24 Carbohydrates Lipids Proteins SOURCES OF CARBOHYDRATES Does not occur in isolated form in our diet LECTURE 2 -‐ SLIDE 26 SOURCES OF CARBOHYDRATES LECTURE 2 -‐ SLIDE 27 SOURCES OF CARBOHYDRATES LECTURE 2 -‐ SLIDE 28 SOURCES OF CARBOHYDRATES Cellulose LECTURE 2 -‐ SLIDE 29 DIETARY FACTS FOR CANADA, 2015 LECTURE 2 -‐ SLIDE 30 DIETARY FACTS FOR CANADA, 2015 The Canadian Sugar Institute LECTURE 2 -‐ SLIDE 31 DIETARY FACTS IN CANADA Sugar consumption in Canada: 1. What compounds are meant by ‘sugar‘? 2. What are ‘added sugars‘? LECTURE 2 -‐ SLIDE 32 DIETARY FACTS IN CANADA Sugar consumption in Canada: 1. What compounds are meant by ‘sugar‘? SUGAR = Table Sugar = Sucrose, Saccharose TOTAL SUGARS = Simple Carbohydrate (All Mono-/Disaccharides) = NATURAL + ADDED (FREE) LECTURE 2 -‐ SLIDE 33 DEFINITIONS What are ‘free sugars’? "all monosaccharides and disaccharides added to foods by the manufacturer, cook, or consumer, plus sugars naturally present in honey, syrups, fruit juice concentrates, and fruit juices” https://www.ages.at/en/human/nutrition-food/nutrition- recommendations/who-sugar-recommendations LECTURE 2 -‐ SLIDE 34 DIETARY FACTS IN CANADA Sugar consumption in Canada: 2. What are ‘added sugars‘? SUGARS ADDED to food and beverages during food processing: - Sugars, syrup sugar beets/cane - High fructose corn syrup, dextrose - Fruit juice, concentrated fruit juice LECTURE 2 -‐ SLIDE 35 DIETARY FACTS IN CANADA Natural sugars in foods 1 (avg.) peach 15 grams / 180 grams 1 (avg.) apple 23 grams / 220 grams 1 cup of milk 12 grams / 250 mL Free sugars in foods 1 cup of soda 27 grams / 250 mL 10 jelly beans 10 grams / 11 grams Modiﬁed from USDA Nutrient Database LECTURE 2 -‐ SLIDE 36 SUMMARY Carbohydrates are the major source of energy in human diet. Carbohydrates are classiﬁed in simple and complex carbohydrates. Monosaccharides are stereoisomers and optically active. Polysaccharides including cellulose (a dietary ﬁber) consist of glucose only. Polysaccharides account for nearly 50% of dietary carbohydrate intake. Foods contain unreﬁned carbohydrates (whole grains, beans, fruits, and vegetables) and/or reﬁned carbohydrates (simple sugars LECTURE 2 -‐ SLIDE 37 and processed grains). DIGESTION OF CARBOHYDRATES Dextrins Glucose LECTURE 2 -‐ SLIDE 38 DIGESTION OF CARBOHYDRATES Within GI tract, carbohydrate digestion starts in… Salivary glands Oral cavity Contributing accessory organ LECTURE 2 -‐ SLIDE 39 DIGESTION OF CARBOHYDRATES Saliva contains enzyme that digests polysaccharides. α 1-4 amylase = glycosidase Speciﬁcally hydrolyzes α 1-4 glycosidic bonds (optimum pH 6.9) LECTURE 2 -‐ SLIDE 40 DIGESTION OF CARBOHYDRATES α 1-‐4amylase LECTURE 2 -‐ SLIDE 41 DIGESTION OF CARBOHYDRATES Branch point α 1-6 α 1-4 LECTURE 2 -‐ SLIDE 42 DIGESTION OF CARBOHYDRATES LECTURE 2 -‐ SLIDE 43 DIGESTION OF CARBOHYDRATES Next phases of carbohydrate digestion in GI tract: Pancreatic α 1-4amylase Speciﬁcally hydrolyzes α 1-4 glycosidic bonds Pancreatic bicarbonate alkalinizes the chyme -‐ duodenal pH close to pH optimum of amylase LECTURE 2 -‐ SLIDE 45 DIGESTION OF CARBOHYDRATES Intraluminal phase: Digestion of starch and dextrins in duodenum occurs in the interior of the lumen. + Maltotriose Limit dextrin = isomaltose LECTURE 2 -‐ SLIDE 46 DIGESTION OF CARBOHYDRATES Pancreatic α 1-4 amylase = very fast and eﬃcient enzyme; responsive to diet composition: after a high‐carbohydrate diet, amount of enzyme is higher than after a high‐protein diet; secretion regulated by cholecystokinin LECTURE 2 -‐ SLIDE 47 DIGESTION OF CARBOHYDRATES Intraluminal phase Brush border phase LECTURE 2 -‐ SLIDE 48 DIGESTION OF CARBOHYDRATES Brush border contains oligo-‐ saccharidases = glycoprotein enzymes LECTURE 2 -‐ SLIDE 49 DIGESTION OF CARBOHYDRATES = Isomaltase LECTURE 2 -‐ SLIDE 50 DIGESTION OF CARBOHYDRATES Most of the digestion of disaccharides starts in the small intestine, in the brush border. Maltose Isomaltose Lactose Sucrose Maltase Isomaltase Lactase Sucrase Glucose Glucose Galactose Glucose Glucose Glucose Glucose Fructose LECTURE 2 -‐ SLIDE 51 NEXT CLASS - CARBOHYDRATES Carbohydrate absorption Glucose transport Insulin / Control of blood glucose levels Glycemic index Textbook: Chapter 3 LECTURE 2 -‐ SLIDE 52 FNH 350 – Fundamentals of Nutrition Food, Nutrition and Health Program Term 1 W2024/2025 Lecture 3: Carbohydrates – Absorption, Glucose Transport, Blood Glucose Control, Glycemic Index FNH 350 Term 1 Winter Session 2016/2017 LECTURE LECTURE34-‐ -‐SLIDE SLIDE11 TODAY'S LECTURE Learning Objectives:  Describe in what form carbohydrates are absorbed.  Describe how the monosaccharides glucose, galactose and fructose are absorbed in the small intestine and reach the blood stream.  Explain the corresponding absorption and transport mechanisms and why those mechanisms are used.  Describe the structure and role of glucose transporters and list their major sites of expression. Textbook: Chapter 3 LECTURE 3 -‐ SLIDE 4 TODAY'S LECTURE Learning Objectives cont.:  Describe the role of blood glucose.  Describe acute and long-term parameters of blood glucose concentrations.  Explain acute and chronic symptoms of elevated and low blood glucose levels.  Describe regulatory compounds and pathways involved in blood glucose control.  Explain glycemic index and glycemic load and how they are calculated. Discuss the use of these two indicators. Textbook: Chapter 3 LECTURE 3 -‐ SLIDE 5 ABSORPTION OF CARBOHYDRATES Absorption = process by which the digestive products pass out of the digestive tract, enter the cells lining the digestive tract, and enter the blood stream or lymphatics. LECTURE 3 -‐ SLIDE 6 ABSORPTION OF CARBOHYDRATES Absorption capacity for glucose and fructose: up to 5,400 g/day of glucose up to 4,800 g/day of fructose What contributes to high absorption capacities? LECTURE 3 -‐ SLIDE 7 ABSORPTION OF GLUCOSE & GALACTOSE Glucose and galactose are absorbed into the mucosal cell against a concentration gradient This absorption mechanism requires energy and a speciﬁc receptor. Active transport LECTURE 3 -‐ SLIDE 8 ABSORPTION OF GLUCOSE & GALACTOSE Mucosal cell Lumen LECTURE 3 -‐ SLIDE 9 ABSORPTION OF GLUCOSE & GALACTOSE Mucosal cell Lumen SGLT1 GLU GLU GLU Glucose molecule GLU (or Galactose) Sodium ion (Na+) Potassium ion (K+) LECTURE 3 -‐ SLIDE 10 ABSORPTION OF GLUCOSE & GALACTOSE Mucosal cell Lumen SGLT1 GLU GLU [Na+]ext GLU [Na+]ext [Na+]int GLU Glucose molecule (or Galactose) Sodium ion (Na+) Potassium ion (K+) 2016/2017 LECTURE 3 -‐ SLIDE 11 ABSORPTION OF GLUCOSE & GALACTOSE Blood stream Mucosal cell Lumen Of 100% SGLT1 absorbed… GLU GLU GLU GLU GLU GLU GLU GLU GLU GLU GLU 15% back to lumen [Glu]ext [Glu]int LECTURE 3 -‐ SLIDE 12 ABSORPTION OF GLUCOSE & GALACTOSE Blood stream Mucosal cell Lumen 25% diﬀusion Of 100% SGLT1 absorbed… GLU GLU GLU GLU GLU GLU GLU GLU GLU GLU GLU GLU GLU GLU 15% back to lumen [Glu]ext [Glu]int LECTURE 3 -‐ SLIDE 13 ABSORPTION OF GLUCOSE & GALACTOSE Blood stream Mucosal cell Lumen 60% facilitated Of 100% SGLT1 diﬀusion absorbed… GLU GLU GLU GLU GLU GLU GLU GLU GLU GLU GLU GLU GLUT2 GLU 15% back to lumen [Glu]ext [Glu]int LECTURE 3 -‐ SLIDE 14 ABSORPTION OF GLUCOSE & GALACTOSE LECTURE 3 -‐ SLIDE 15 ABSORPTION OF GLUCOSE & GALACTOSE Once leaving the mucosal cell, Glucose and Galactose are quickly transported via portal vein to the liver Glucose and Galactose are taken up by hepatocytes through facilitated diﬀusion. Galactose is phosphorylated in the hepatocytes = ‘trapped’ in the liver. Galactose can be converted into glucose derivatives: enter glucose metabolism and stored as liver glycogen. LECTURE 3 -‐ SLIDE 16 ABSORPTION OF GLUCOSE & GALACTOSE Glucose extensively metabolized in the liver; Glucose is not as withhold from further distribution as galactose (and fructose). Portions of glucose go through blood stream to be distributed in various tissues: muscle kidney Insulin‐dependent uptake via GLUT4 adipose tissue LECTURE 3 -‐ SLIDE 17 ABSORPTION OF FRUCTOSE Blood stream Mucosal cell Lumen GLUT5 FRU FRU FRU FRU FRU FRU FRU FRU FRU FRU FRU [Fru]int [Fru]int [Fru]ext LECTURE 3 -‐ SLIDE 18 ABSORPTION OF FRUCTOSE Blood stream Mucosal cell Lumen Facilitated GLUT5 diﬀusion FRU FRU FRU FRU FRU FRU FRU FRU FRU FRU FRU FRU FRU FRU FRU FRU FRU GLUT2 [Fru]int [Fru]int [Fru]ext LECTURE 3 -‐ SLIDE 19 ABSORPTION OF FRUCTOSE 1. Fructose transport:  down the concentration gradient  diﬀusion mechanisms are possible 2. Once fructose leaves the mucosal cell, fructose in blood stream is quickly transported via portal vein into the liver LECTURE 3 -‐ SLIDE 20 ABSORPTION OF FRUCTOSE Fructokinase ATP ADP LECTURE 3 -‐ SLIDE 21 ABSORPTION OF FRUCTOSE enabling 1. Fructose transport:  down the concentration gradient  diﬀusion mechanisms are possible 2. Once fructose leaves the mucosal cell, fructose in blood stream is quickly transported via portal vein into the liver 3. Fructose in the liver is phosphorylated = ‘trapped’ in the hepatocytes. 4. Fructose concentrations = ‘kept low’ LECTURE 3 -‐ SLIDE 22 SPECIFICS TO FRUCTOSE Public health issues with increasing fructose intake Not everybody can absorb fructose eﬃciently. 60% of healthy adults show intestinal distress after consumption of 50 gram of pure fructose. LECTURE 3 -‐ SLIDE 23 ABSORPTION OF FRUCTOSE More fructose can be absorbed in combination with high glucose intake: Disaccharidase‐related transport system Fructose Less intestinal discomfort when fructose and glucose consumed together; or fructose in mixed diet. Glucose Balancing dietary fructose and glucose can mitigate clinical symptoms for those individuals with apparent sensitivity to fructose. LECTURE 3 -‐ SLIDE 24 FOOD FOR THOUGHTS After eating a large strawberry ice‐cream, how much fructose and galactose do you expect to measure in your blood? LECTURE 3 -‐ SLIDE 25 GLUCOSE TRANSPORTERS How does glucose enter cells? Epithelial cells including small intestine and kidney: SGLT / active transport required Nearly all cells in the body: facilitated diﬀusion with glucose transporters (GLUT) = carriers LECTURE 3 -‐ SLIDE 26 GLUCOSE TRANSPORTERS LECTURE 3 -‐ SLIDE 27 GLUCOSE TRANSPORTERS GLUT1 Deﬁciency Syndrome Rare genetic disorder 500 cases worldwide GLUT1 is responsible for transport of glucose through blood brain barrier; gene mutation leads to lack of transport protein and “glucose deﬁciency in brain” Symptoms related to cognition, behaviour and movement LECTURE 3 -‐ SLIDE 28 GLUCOSE TRANSPORTERS GLUT1 Glucose transporter in erythrocytes Erythrocyte glucose uptake test = diagnostic tool for GLUT1 Deﬁciency: Low rate of glucose uptake in erythrocytes indicates GLUT1 deﬁciency LECTURE 3 -‐ SLIDE 29 BLOOD GLUCOSE Blood glucose = fuel for Brain Main glucose Central nervous system transporter for Erythrocytes glucose entry = GLUT1 (the most Placenta ubiquitously expressed) Lungs Other tissues, e.g. skeletal Insulin-dependent uptake into tissues muscle, heart, adipose with GLUT4 tissue LECTURE 3 -‐ SLIDE 31 BLOOD GLUCOSE How much glucose does circulate in the bloodstream at any point in time? Blood glucose concentration 4-5.4 mmol/L (72-99 mg/dL) up to 7.8 mmol/L (140 mg/dL) 2 hr after a meal LECTURE 3 -‐ SLIDE 32 BLOOD GLUCOSE Measurement of blood glucose concentration Acute parameter: Plasma glucose concentrations Measured with glucometer Long‐term parameter: HbA1c = Hemoglobin A1c Glycated Hemoglobin Test LECTURE 3 -‐ SLIDE 33 BLOOD GLUCOSE Blood glucose levels above normal range = hyperglycemia Acute symptoms: dehydration Chronic symptoms: glycosylation of proteins organ damage Hemoglobin HbA1c Excess glycosylation of proteins, as indicator of e.g. in cell membranes, disrupts long‐term glucose levels normal membrane integrity. LECTURE 3 -‐ SLIDE 34 REGULATION OF GLUCOSE DISPOSAL OTHER THAN BY INSULIN GLUCOSE LECTURE 3 -‐ SLIDE 35 BLOOD GLUCOSE Blood glucose levels below normal range = hypoglycemia Acute symptoms: fatigue dizziness unconsciousness seizures Chronic symptoms: brain damage LECTURE 3 -‐ SLIDE 36 GLUT4 transporter CONTROL OF β-cells BLOOD GLUCOSE glycogenesis glycogenolysis α-cells gluconeogenesis Adrenal glands release glucocorticoids LECTURE 3 -‐ SLIDE 37 (cortisol) CONTROL OF BLOOD GLUCOSE Glucose production to Glucose disposal to lower increase blood blood glucose levels: through glucose levels: Glycolysis/TCA through Glycogenesis (glycogen Glycogenolysis synthesis) (glycogen breakdown) Blood [glucose] Hexose mono‐ Gluconeogenesis phosphate shunt (glucose synthesis) Fatty acid synthesis Urinary excretion LECTURE 3 -‐ SLIDE 38 CONTROL OF BLOOD GLUCOSE Glucose production: Glucose disposal: Stimulated by Stimulated by Glucagon Insulin Blood Insulin- Catecholamins [glucose] independent Glucocorticoids pathways LECTURE 3 -‐ SLIDE 39 EFFECT OF CARBOHYDRATE CLASSES ON BLOOD GLUCOSE LECTURE 3 -‐ SLIDE 40 GLYCEMIC INDEX Classiﬁcation of dietary carbohydrates by ‘their ease of absorption and their eﬀect on the elevation of blood glucose levels’ Concept: ‘to provide a numerical value for the eﬀect of food on blood glucose levels.’ LECTURE 3 -‐ SLIDE 41 GLYCEMIC INDEX Deﬁnition: increase in blood glucose level over the baseline level during a 2‐hour period following the consumption of a deﬁned amount of carbo‐ hydrate (usually 50g) compared with the same amount of carbo- hydrate in a reference food. LECTURE 3 -‐ SLIDE 42 Fasting Food intake Blood sampling in small intervals over 2 hours blood within sample 5-‐10min LECTURE 3 -‐ SLIDE 43 GLYCEMIC INDEX 50 grams of glucose compressed into cubes = 16 glucose cubes LECTURE 3 -‐ SLIDE 44 GLYCEMIC INDEX 2 slices of white bread contain 50 grams of carbohydrates. LECTURE 3 -‐ SLIDE 45 GLYCEMIC INDEX Calculation of glycemic index: 50g glucose Reference = Area‐under‐the curve (AUC) for 50g glucose Food product = AUC for 50g carbohydrates 50g carbs in Glycemic Index = brown rice AUCFood/AUCGlucose x 100 LECTURE 3 -‐ SLIDE 46 GLYCEMIC INDEX White bread or Glucose as the reference LECTURE 3 -‐ SLIDE 47 GLYCEMIC INDEX White bread or Glucose as reference LECTURE 3 -‐ SLIDE 48 GLYCEMIC INDEX Low GI Foods (55 or less) Oatmeal (rolled or steel‐cut), oat bran, muesli, barley, bulgar, milk Sweet potato, corn, yam, lima/butter beans, peas, legumes, lentils Most fruits (e.g., mango GI=51), non-‐starchy vegetables, all-bran cereal Medium GI (56-‐69) Whole wheat, rye and pita bread Quick oats Brown, wild or basmati rice, couscous High GI (70 or more) White bread or bagel, corn ﬂakes, puﬀed rice, bran ﬂakes, instant oatmeal Shortgrain white rice, rice pasta, macaroni and cheese from mix Russet potato, pumpkin Melons and pineapple LECTURE 3 -‐ SLIDE 49 GLYCEMIC LOAD Critique: Glycemic index (GI) of a mixed meal is diﬃcult to predict; GI reﬂects glucose response on 50g carbohydrates but not on a food portion Concept of glycemic load (GL) to address this limitation: Considers both quantity and quality of carbohydrate in a meal GL = GI x grams of carbohydrate in a serving of food LECTURE 3 -‐ SLIDE 50 GLYCEMIC LOAD What is the value of GL for these foods? Chickpeas/Garbanzo beans, canned, in brine Serving size ¾ cup (125 grams) 34 grams of carbohydrate GI of chickpeas = 38 Baked russet potato Serving size ½ cup (150 grams) 35 grams of carbohydrate GI of baked russet potato = 111 Glycemic Load = ? LECTURE 3 -‐ SLIDE 51 Clicker Question #4 What is the value of GL for these foods? A. Chickpeas GL=13, Baked potato GL=39 B. Chickpeas GL=10, Baked potato GL=26 C. Chickpeas GL=30, Baked potato GL=74 LECTURE 3 -‐ SLIDE 52 GLYCEMIC LOAD Ranking of GL GL < 10 best food choice with respect to blood glucose GL 10 – 20 moderate eﬀect on blood glucose GL > 20 can lead to spikes in blood glucose and insulin LECTURE 3 -‐ SLIDE 54 FOOD FOR THOUGHT Carrots have a high glycemic index but a low glycemic load. Why? LECTURE 3 -‐ SLIDE 55 FOOD FOR THOUGHT GL = GI x g CHO/g serving size GL = 71 x 10 g CHO/ 120 g = 6 Carrots have a high glycemic index (=71) but low glycemic load (= 6) because carrots contain only a small amount of carbohydrates per serving size. LECTURE 3 -‐ SLIDE 56 NEXT CLASS – CARBOHYDRATES Glycolysis TCA cycle Textbook: Chapter 3 LECTURE 3 -‐ SLIDE 57 FNH 350 – Fundamentals of Nutrition Food, Nutrition and Health Term 1 Winter Session 2024/2025 Lecture 4: Carbohydrate Metabolism Glycolysis Tricarboxylic Acid Cycle LECTURE 4 -‐ SLIDE 1 TODAY'S LECTURE Learning Objectives:  Name the production and disposal pathways of glucose, and explain which hormones regulate these pathways in the diﬀerent stages of the fed‐fast cycle.  Explain how cells turn glucose into energy in dependence of the cell type and oxygen supply.  Name the regulatory steps (with the speciﬁc intermediary products and enzymes) of glycolysis and TCA cycle pathways.  Explain how and in which format energy is produced from carbohydrates and other macronutrients. Textbook: Chapter 3 LECTURE 4 -‐ SLIDE 2 CARBOHYDRATE METABOLISM LECTURE 4 -‐ SLIDE 6 CARBOHYDRATE METABOLISM Metabolic Pathways of Carbohydrate Metabolism Gluconeogenesis LECTURE 4 -‐ SLIDE 7 GLYCOLYSIS Which cell types? In which cell compartment? LECTURE 4 -‐ SLIDE 8 GLUCOSE -‐SOURCE OF ENERGY Littleenergy Glucose Pyruvate Large amounts of energy H 2O Pyruvate CO2 = ‘conversion of all energy that is in glucose’ (complete oxidation) LECTURE 4 -‐ SLIDE 9 GLUCOSE -‐SOURCE OF ENERGY Glucose Pyruvate Lactate O2 = providing energy in the absence of oxygen LECTURE 4 -‐ SLIDE 10 GLUCOSE -‐SOURCE OF ENERGY Glucose Pyruvate Lactate = sole source of energy from glucose in erythrocytes due to lack of mitochondria LECTURE 4 -‐ SLIDE 11 GLYCOLYSIS Primary role of glycolysis in energy metabolism: Production of pyruvate (1 glucose will lead 2 pyruvate molecules) Initial reaction in glucose oxidation followed by TCA cycle LECTURE 4 -‐ SLIDE 12 1st Regulatory Step – Glucose Phosphorylation 1 Glucose Glucose ‐6‐P ATP ADP LECTURE 4 -‐ SLIDE 13 1st Regulatory Step – Glucose Phosphorylation 1 1 Glucose Glucose‐6‐P ATP ADP 1 Glucokinase in liver: induced by insulin reaches maximum speed at high blood glucose concentrations (high Km) NOT inhibited by its product (G‐6‐P) LECTURE 4 -‐ SLIDE 14 1st Regulatory Step – Glucose Phosphorylation 1 Glucose Glucose‐6‐P ATP ADP Hexokinase in 1 muscle/adipose tissue/brain: insulin independent reaches maximum speed at normal blood glucose concentrations (low Km) allosterically inhibited by its product (G‐6‐P) LECTURE 4 -‐ SLIDE 15 Glucose stored as Glycogen Glycogenolysis Glucose Glucose‐6‐P Glucose‐1‐P Glycogenesis LECTURE 4 -‐ SLIDE 16 2nd Regulatory Step – Phosphofructokinase Glucose Glucose-6-P Fructose-6-P 3 Phosphofructokinase ATP ADP 3 allosterically regulated − ATP, citrate Fructose-1,6-bisP + ADP, AMP LECTURE 4 -‐ SLIDE 17 Stimulation of GLYCOLYSIS Glucose-6-P + Enzyme: Phosphofructokinase 2 Fructose-6-P Fructose 2,6- bisphosphate 3 + Fructose-1,6-bisP LECTURE 4 -‐ SLIDE 18 Inhibition of GLYCOLYSIS Glucose-6-P Phosphofructokinase 2 Low blood glucose level Glucagon + Fructose 2,6- Fructose-6-P bisphosphate Enzyme: Fructose bisphosphatase 2 3 Fructose-1,6-bisP LECTURE 4 -‐ SLIDE 19 GLYCOLYSIS – FIRST PHASE 1 1 Glucokinase/hexokinase Glucose Glucose-6-P 3 Phosphofructokinase ATP ADP Fructose-6-P ATP 3 ADP Fructose-1,6-bisP Glyceraldehyde-3-P (G-3-P) + Dihydroxyacetone-P (DHAP) LECTURE 4 -‐ SLIDE 20 GLYCOLYSIS – SECOND PHASE DHAP Glyceraldehyde-3‐-P NAD NADH + H+ 1,3‐bis‐P‐glycerate ADP ATP 3-P‐glycerate 2-P-glycerate Phosphoenolpyruvate (PEP) Pyruvate kinase 10 (substrate-level ADP phosphorylation) 10 ATP Pyruvate LECTURE 4 -‐ SLIDE 21 3rd Regulatory Step – Pyruvate Kinase P Eﬀect of glucagon is Pyruvate LIVER speciﬁc: kinase Low blood glucose glucagon release H2O + cAMP ADP glucagon activates Glucagon dependent cAMP dependent Pi protein kinase ATP protein kinase phosphorylates pyruvate kinase (inactivates it) Pyruvate kinase Phosphoenolpyruvate + ADP + H+ Pyruvate + ATP + Fructose 1,6-‐bisphosphate ATP AMP Alanine Acetyl-‐ CoA (modiﬁed from Lehninger; 4th edition; Figure 15-‐19; page 580) LECTURE 4 -‐ SLIDE 22 GLYCOLYSIS – SECOND PHASE Glucose Glucose-6-P Fructose-6-P Fates of pyruvate: 2 Phosphoenolpyruvate TCA cycle Lactate formation 2 Pyruvate Amino acid metabolism Glucose formation LECTURE 4 -‐ SLIDE 23 GLYCOLYSIS Net reaction: Glucose + 2 ATP + 2 NAD+ + 4 ADP + 2 Pi 2 Pyruvate + 2 ADP + 2 NADH + 2H+ + 4 ATP + 2 H2O 2.5 ATP can be formed from 1 NADH by oxidative phosphorylation Net (aerobic) = 2 ATP + 2*2.5 ATP = 7 ATP Net (anaerobic) = 2 ATP LECTURE 4 -‐ SLIDE 24 ENTRY OF FRUCTOSE IN GLYCOLYSIS Glucose Glucose‐6‐P ATP ADP Fructose‐6‐P Fructose ATP 3 13 ADP Fructose-1-P Fructose-1,6-bisP Glyceraldehyde + Glyceraldehyde‐3‐P + Dihydroxyacetone-P Dihydroxyacetone-P 3 Phosphofructokinase 13 Fructokinase LECTURE 4 -‐ SLIDE 25 ENTRY OF FRUCTOSE IN GLYCOLYSIS Hepatocyte MUSCLE/KIDNEYS: Hexokinase 12 less important LIVER: Fructokinase 13 after absorption, most fructose is “trapped“ in liver LECTURE 4 -‐ SLIDE 26 FNH 350 Term 1 Winter Session 2018/2019 ENTRY OF FRUCTOSE IN GLYCOLYSIS Entry of fructose in glycolysis pathway after regulatory step Hepatocyte of phosphofructokinase LIVER: Fructokinase 13 after absorption, most fructose is “trapped“ in liver LECTURE 4 -‐ SLIDE 27 FNH 350 Term 1 Winter Session 2018/2019 FRUCTOSE METABOLISM Fructose Hepatocyte Fructose Fructose-1-P Trioses-P Gluconeo Glycolysis De novo -genesis lipogenesis TCA cycle Pyruvate Fatty Acids Glucose Triglycerides Glucose in VLDL LECTURE 4 -‐ SLIDE 28 Systemic circulation FNH 350 Term 1 Winter Session 2018/2019 FRUCTOSE IN THE SPOTLIGHT Hepatic metabolism of fructose favours lipogenesis. ANIMAL MODELS: High consumption of fructose (up to 60% of energy intake) leads to non-alcoholic fatt y liver and obesity. HUMAN TRIALS: High fructose consumption can induce hyperlipidemia, especially in those with metabolic syndrome (i.e., existing hyperlipidemia) LECTURE 4 -‐ SLIDE 29 TCA CYCLE Tricarboxylic acid (TCA) cycle = Citric acid cycle = Krebs cycle ‘Final catabolic pathway‘ of carbohydrates, amino acids, and fat 90% of energy from macronutrients released in TCA cycle LECTURE 4 -‐ SLIDE 30 TCA CYCLE From amino acid catabolism Activated by: -‐insulin, -‐pyruvate, -‐ ADP, NAD+ Inhibited by: -‐acetyl‐CoA, -‐ ATP, NADH LECTURE 4 -‐ SLIDE 31 TCA CYCLE + more active cycle: pyruvate, ADP -‐ less active cycle: ATP LECTURE 4 -‐ SLIDE 32 Malate dehydrogenase Succinate dehydrogenase Succinyl-CoA- Isocitrate synthetase dehydrogenase NH 350 Term 1 Winter α-ketoglutarate dehydrogenase LECTURE 4 -‐ SLIDE 33 NADH/FADH2 ATP Net gain of energy in TCA cycle: 2 pyruvate (from 1 glucose) 2 ATP + (8 NADH + 8H+) + 2 FADH2 1.5 ATP are formed from 1 FADH2 by oxidative phosphorylation 20 ATP 3 ATP Net gain = 2 + 8*2.5 + 2*1.5 = 25 ATP LECTURE 4 -‐ SLIDE 34 FORMATION OF ATP LECTURE 4 -‐ SLIDE 36 Macronutrients as Source of Energy LECTURE 4 -‐ SLIDE 37 Summary: Net Energy Gain / GLUCOSE Cytosol Mitochondrion LECTURE 4 -‐ SLIDE 38 Net Energy Gain – Anaerobic Glycolysis Cytosol Glucose ANAEROBIC Glycolysis 2 ATP 2 NADH + H+ Pyruvate Lactate Mitochondrion LECTURE 4 -‐ SLIDE 39 Net Energy Gain – Aerobic Glycolysis Cytosol Glucose AEROBIC Glycolysis 2 ATP 2 NADH + H+ Pyruvate ETC 2 NADH + H+ O2 5 ATP Mitochondrion LECTURE 4 -‐ SLIDE 40 Net Energy Gain – Aerobic Glycolysis Cytosol Glucose AEROBIC Glycolysis 2 ATP 2 NADH + H+ ETC Pyruvate 2 NADH + H+ O2 5 ATP 8 NADH + H+ 2 FADH2 23 ATP Pyruvate H2O, CO2 TCA 2 ATP O2 Mitochondrion LECTURE 4 -‐ SLIDE 41 Net Energy Gain – GLUCOSE Net reaction (aerobic): Glucose + 6 O2 6 CO2 + 6 H2O + energy Glycolysis 7 ATP TCA Cycle 25 ATP 1 molecule of glucose provides 32 ATP. LECTURE 4 -‐ SLIDE 42 Macronutrients as Source of Energy Energy through food intake = macronutrients (+ alcohol) Cellular oxidation Electron transport Oxidative phosphorylation ATP heat LECTURE 4 -‐ SLIDE 43 CONTENT REVIEW LECTURE 4 -‐ SLIDE 44 CASE STUDY Sarah and her daughter Melissa are enjoying a breakfast together. Sarah eats 1 serving of whole grain cereals with milk and fruit. Melissa decides to start her day with coﬀee and a mango milk shake (with honey added). Describe carbohydrate digestion and absorption on these two examples in the following ﬁgures. Describe organs and speciﬁc enzymes involved. LECTURE 4 -‐ SLIDE 45 LECTURE 4 -‐ SLIDE 46 LECTURE 4 -‐ SLIDE 47 Case Study – Change in blood glucose Sarah: Melissa: coﬀee, a mango milk shake whole grain cereals, milk, fruit (honey) LECTURE 4 -‐ SLIDE 48 LECTURE 4 -‐ SLIDE 49 NEXT CLASS – CARBOHYDRATES HMP Shunt Gluconeogenesis Glycogenesis Glycogenolysis Textbook: Chapter 3 LECTURE 4 -‐ SLIDE 50 FNH 350 – Fundamentals of Nutrition Food, Nutrition and Health Term 1 Winter Session 2024/2025 Lecture 5: Carbohydrate metabolism: HMP shunt, Gluconeogenesis, Glycogenolysis, Glycogenesis LECTURE 5 – SLIDE 1 TODAY'S LECTURE Learning Objectives:  Describe the hexosemonophosphate shunt and name the key products. Explain why the pathway is more active in certain tissues.  Explain gluconeogenesis and how it is regulated. Name precursors for glucose formation.  Describe the structure, function, and distribution of glycogen.  Explain the formation and breakdown of glycogen and describe how those pathways are regulated. Textbook: Chapter 3 LECTURE 5 – SLIDE 2 CARBOHYDRATE METABOLISM (Pentose phosphate pathway) LECTURE 5 – SLIDE 4 HMP SHUNT Hexosemonophosphate shunt DNA = pentose phosphate pathway Two important products: 1. Pentose phosphates -‐ synthesis of nucleic acids (DNA, RNA) RNA Ribose-5’-phosphate (RNA) 2’-deoxyribose-5’-phosphate (DNA) LECTURE 5 – SLIDE 5 HMP SHUNT Hexosemonophosphate shunt = pentose phosphate pathway Two important products: 1. Pentose phosphates required for -‐ synthesis of nucleic acids (DNA, RNA) -‐ formation of other nucleotides (ATP, ADP, AMP) LECTURE 5 – SLIDE 6 HMP SHUNT Hexosemonophosphate shunt = pentose phosphate pathway Two important products: 1. Pentose phosphates required for -‐ synthesis of nucleic acids (DNA, RNA) -‐ formation of other nucleotides (ATP, ADP) 2. Reduced co-substrate NADPH used for -‐ biosynthesis of fatty acids -‐ maintenance of reducing substrates in erythrocytes -‐ drug metabolism in liver LECTURE 5 – SLIDE 7 HMP SHUNT Hexosemonophosphate shunt = pentose phosphate pathway NADPH + H+ NADPH + H+ Glucose‐6‐P D‐ribulose 5‐phosphate D‐xylose 5‐phosphate Fructose‐6‐P D‐ribose 5‐phosphate LECTURE 5 – SLIDE 8 HMP SHUNT Activity of HMP shunt: High in liver These tissues are active adipose tissue in the synthesis of fatty adrenal cortex acids and thus have a lactating mammary gland high demand for NADPH Low in skeletal muscle (limited demand for NADPH) LECTURE 5 – SLIDE 9 GLUCONEOGENESIS (Pentose phosphate pathway) LECTURE 5 – SLIDE 10 GLUCONEOGENESIS Gluconeogenesis = synthesizing of glucose from non‐carbohydrate intermediates Glucose is an essential nutrient for most cells. Tissues particularly dependent on glucose supply: Brain Central nervous system Erythrocytes LECTURE 5 – SLIDE 11 GLUCONEOGENESIS Sources for glucose production: Pyruvate Lactate Glycerol Amino acids Major site of gluconeogenesis Liver Blood (Kidney) glucose LECTURE 5 – SLIDE 12 GLUCONEOGENESIS Glucose Glucose Glucose‐6‐P Fructose‐6‐P Oxaloacetate Fructose‐1,6‐bisP Malate Dihydroxyacetone‐P Glyceraldehyde‐3‐P 1,3‐bisP‐glycerate Malate* 3‐P‐glycerate Oxaloacetate* 2‐P‐glycerate GLUCONEOGENESIS Phosphoenolpyruvate Pyruvate* Pyruvate 2016/2017 *Entrance of amino acids to gluconeogenesis LECTURE 5 – SLIDE 13 GLUCONEOGENESIS Bypass of pyruvate kinase step LECTURE 5 – SLIDE 14 GLUCONEOGENESIS Phosphatases are enzymes that remove phosphate by hydrolysis. Glucose ‐ 6 ‐ phosphatase is expressed in: liver, kidney is not expressed in: muscle, adipose tissue Glucose-6-P X Glucose LECTURE 5 – SLIDE 15 LACTATE AS GLUCOGENIC PRECURSOR Anaerobic glycolysis Lactate Glucose-6‐P CORI CYCLE Uptake of lactate in liver; Blood conversion to glucose glucose via gluconeogenesis LECTURE 5 – SLIDE 16 LACTATE AS GLUCOGENIC PRECURSOR Lactate Glucose-‐6-‐P Uptake of lactate in liver; conversion to glucose‐6‐P via gluconeogenesis; formation of glycogen LECTURE 5 – SLIDE 17 CARBOHYDRATE METABOLISM (Pentose phosphate pathway) LECTURE 5 – SLIDE 18 GLYCOGEN Purpose: Glucose storage for Glucose disposal at high blood glucose concentrations Maintaining blood homeostasis Glucose release at low blood glucose concentrations Rapid demand of energy LECTURE 5 – SLIDE 19 GLYCOGEN Distribution (and function) of glycogen in body Liver (blood glucose homeostasis) 100‐150 grams; 7% of net weight Muscle (reserve of instant energy) 75% of body’s 250‐400 grams; 1‐2% of net weight glycogen stored in muscle. Adipose tissue Erythrocytes LECTURE 5 – SLIDE 20 GLYCOGENESIS LIVER -‐Glucokinase MUSCLE -‐Hexokinase Glycogenesis is initiated by glucose-6- phosphate LECTURE 5 – SLIDE 22 GLUCONEOGENIC PRECURSOR Glucose Absorption / Transport via Portal Vein Liver Uptake of lactate in Conversion to Lactate into liver – conversion to glycogen glucose-6-phosphate circulation via gluconeogenesis Release of glucose Uptake by Anaerobic into circulation erythrocytes glycolysis Uptake by the brain LECTURE 5 – SLIDE 23 GLYCOGENESIS LIVER -‐Glucokinase MUSCLE -‐Hexokinase Glycogen synthase LECTURE 5 – SLIDE 24 GLYCOGENESIS Phosphorylated = less active P Dephosphorylated Attaches 2-‐7 = more active glucose molecules Which regulatory compounds impact the phosphorylation of glycogen synthase and how? LECTURE 5 – SLIDE 25 GLYCOGENESIS 1 2 LECTURE 5 – SLIDE 26 GLYCOGENESIS Glycogenin as core in glycogen molecule: Glycogenin remains in the core of the glycogen molecules in muscle. In the liver, glycogen breaks of the glycogenin because less glycogenin than glycogen molecules are present. http://en.wikipedia.org/wiki/Glycogen LECTURE 5 – SLIDE 27 GLYCOGENOLYSIS Glycogenolysis = cleavage of glycogen One at a time to glucose molecules Regulated by: Glucagon (at low blood glucose concentrations) Catecholamins/epinephrine in „ﬁght or ﬂight“ situations (rapid demand for energy) LECTURE 5 – SLIDE 28 GLYCOGEN REGULATION Glucagon Insulin Epinephrine Stored glucose Free glucose LECTURE 5 – SLIDE 29 GLYCOGENOLYSIS Cleavage of α 1-‐4 glycosidic bonds Cleavage of α 1-‐6 glycosidic bonds by debranching enzyme LECTURE 5 – SLIDE 30 GLYCOGENOLYSIS P Phosphorylated = more active Glucagon (liver, adipose tissue) Epinephrine (liver, muscle) Dephosphorylated = less active LECTURE 5 – SLIDE 31 GLYCOGENOLYSIS Glucose-6-phosphatase (only liver or kidney) At high rates of glycogenolysis, glucose-6-P is formed. Blood glucose GLYCOLYSIS LECTURE 5 – SLIDE 32 GLYCOGENOLYSIS Distribution (and function) of glycogen in body Liver (blood glucose homeostasis) Blood Glycogenolysis to Glucose-1-P glucose Glucose -6-P Glucose (release into circulation) Muscle (reserve of instant energy) ATP Glycogenolysis to Glucose-1-P Glucose-6-P (intracellular usage) LECTURE 5 – SLIDE 33 CASE STUDY Sarah and her daughter Melissa are enjoying a breakfast together. Sarah eats 1 serving of whole grain cereals with milk and fruit. Melissa decides to start her day with coﬀee and a mango milk shake (with honey added). Describe carbohydrate digestion and absorption on these two examples in the following ﬁgures. Describe organs and speciﬁc LECTURE 5 – SLIDE 34 enzymes involved. NEXT CLASS – CARBOHYDRATES Carbohydrate metabolism: Fasting state Fed state Textbook: Chapter 3 LECTURE 5 – SLIDE 40 FNH 350 – Fundamentals of Nutrition Food, Nutrition and Health Term 1 Winter Session 2024/2025 Lecture 6: Carbohydrate metabolism at fasting and fed state; Review of CHO metabolism LECTURE 6 – SLIDE 1 TODAY'S LECTURE Learning Objectives: Describe carbohydrate metabolism at the diﬀerent stages of the fed-fast cycle:  Name the regulatory compounds that are secreted in the diﬀerent stages.  Describe the pathways that are activated (by naming key steps and regulatory enzymes if any).  Explain the purpose of the pathways and their products/ outcomes, and state in what tissues they are active. Textbook: Chapter 3 Chapter 7 LECTURE 6 – SLIDE 2 CARBOHYDRATE METABOLISM (Pentose phosphate pathway) Textbook (2018 Edition) Figure 3.12 Page 77 LECTURE 6 – SLIDE 3 Present a scheme of carbohydrate metabolism pathways taking place in the liver LECTURE 6 – SLIDE 4 STAGES OF FED-FAST CYCLE Fed‐fast cycle has the following four stages: 1. Fed state = during a meal and about 3 hours after a meal 2. Postabsorptive or early fasting state = from about 3 hours to 12‐18 hours following a meal 3. Fasting state = from 18 hours -‐2 days without food intake 4. Starvation state (or long - term fast) = fully adapted state of food deprivation (several weeks) LECTURE 6 – SLIDE 5 CASE STUDY Sarah M. wishes her children to eat breakfast prior to going to school. She is worried that they don’t have enough energy when leaving the house with an empty stomach. Sarah oﬀers her kids whole grain cereals with milk and orange juice for breakfast. What happens with the carbo-‐ hydrates (in regards to their metabolism) upon digestion of this breakfast? LECTURE 6 – SLIDE 6 CASE STUDY Describe carbohydrate metabolism at fed stage.  Name the regulatory compound(s) that are secreted.  Describe the pathways that are activated (by naming key steps and regulatory enzymes if any).  Explain the purpose of the pathways and their products/ outcomes, and state in what tissues they are active. LECTURE 6 – SLIDE 7 LECTURE 6 – SLIDE 8 Fed State LECTURE 6 – SLIDE 9 Summary of the eﬀects of insulin LECTURE 6 – SLIDE 11 CASE STUDY Three hours after breakfast, the absorbed glucose has been used for. What happens in carbo-‐ hydrate metabolism during postabsorptive state (i.e., 3 hours after food consumption up to 12‐18 hours following the last meal)? LECTURE 6 – SLIDE 12 CASE STUDY Describe carbohydrate metabolism at postabsorptive stage.  Name the regulatory compound(s) that are secreted.  Describe the pathways that are activated (by naming key steps and regulatory enzymes if any).  Explain the purpose of the pathways and their products/ outcomes, and state in what tissues they are active. LECTURE 6 – SLIDE 13 Post-absorptive State LECTURE 6 – SLIDE 14 Summary of the eﬀects of glucagon Metabolic Eﬀect Target Enzyme  Glycolysis  Fructose ‐ bisphosphatase 2  Glucose formation GLUT4 (gluconeogenesis)  Glycolysis (liver)  Pyruvate kinase (inactivation)  Glycogen breakdown  Glycogen phosphorylase  Glycogen formation  Glycogen synthase LECTURE 6 – SLIDE 16 NEXT LECTURE - FIBER Fiber Deﬁnition Properties Physiological Eﬀects Role in Chronic Disease LECTURE 6 – SLIDE 22 FNH 350 – Fundamentals of Nutrition Food, Nutrition and Health Term 1 Winter Session 2024/2025 Lecture 7: Fiber – Deﬁnition, Properties, Physiological Eﬀects, Fiber and Chronic Diseases LECTURE 7 -‐ SLIDE 1 QUIZ #1 Held on CANVAS in class (closed-book) October 3 Topics: everything covered until and including Lecture 7 (Fiber) LECTURE 7 -‐ SLIDE 2 PROJECT 1 Project 1 posted on CANVAS Due on Thursday, October 10 LECTURE 7 -‐ SLIDE 3 TODAY'S LECTURE Learning Objectives:  Deﬁne the diﬀerent categories of ﬁber.  Name the diﬀerent forms/classes of ﬁber.  Describe the structure of diﬀerent ﬁbers.  Explain why ﬁber is non-digestible.  Describe the properties and physiological functions/eﬀects of soluble and insoluble ﬁbers.  Give examples of dietary sources for the various ﬁbers. Textbook: Chapter 4 LECTURE 7 -‐ SLIDE 5 TODAY'S LECTURE Learning Objectives cont.:  Identify diﬀerent ﬁbers on a random dietary supplement and describe the expected physiologic and metabolic eﬀects after regular consumption of this product.  Describe fermentability of ﬁber and the role of short‐chain fatty acids.  Explain the diﬀerence between pre‐ and probiotics and their potential health impact.  Describe the suggested metabolic eﬀects of high ﬁber intake and how it could contribute to chronic disease prevention.  List the dietary recommendations for ﬁber intake for adult men and women and give examples of ﬁber rich food sources. Textbook: Chapter 4 LECTURE 7 -‐ SLIDE 6 FIBER What is ﬁber?  Fiber is the non-digestible portion of plants.  Animal ﬁbers include collagen and keratin.  Nowadays, ﬁber can be manufactured in laboratories as food additives (novel fibers). LECTURE 7 -‐ SLIDE 7 FIBER Deﬁnition according to the Dietary Reference Intakes (Institute of Medicine)  DIETARY FIBER (e.g., cellulose, hemicellulose, pectin, beta-glucans) consists of non-digestible carbohydrates and lignin that are intrinsic and intact in plants.  FUNCTIONAL FIBER (e.g., cellulose, pectin, beta-glucans) consists of isolated, non-digestible carbohydrates that have beneﬁcial physiological eﬀects in humans. LECTURE 7 -‐ SLIDE 8 https://www.canada.ca/en/health-canada/services/food-nutrition/healthy-eating/dietary-reference-intakes/tables.html FIBER Plant cell wall = 95% of dietary ﬁbers -‐ primary and secondary wall -‐ contain cellulose and hemicellulose Lignin in specialized cells providing structural support Pectins - intercellular cement, between and around the cell walls LECTURE 7 -‐ SLIDE 9 FIBER Composition of dietary ﬁber inﬂuenced by  Plant species  Part of the plant (leaf, root, stem)  Plant’s maturity Cereals/wheat bran - high in hemicellulose, lignin and cellulose Fruits and vegetables -‐ high in cellulose and pectin LECTURE 7 -‐ SLIDE 10 FIBER CELLULOSE β 1‐4–linked glucose units Dietary and functional ﬁber Main component of plant cell walls DIETARY SOURCES: bran, legumes, nuts, Water insoluble peas, root veggies, Poorly fermented by colonic cabbage family, skin of bacteria seeds and apples, whole grains LECTURE 7 -‐ SLIDE 11 FIBER HEMICELLULOSE β 1‐4; α 1‐2; α 1‐3 glycosidic bonds backbone DIETARY SOURCES: bran, whole grains, nuts, legumes, some fruits and veggies side chain Dietary ﬁber, component of cell walls Sugars in side chains determine characteristics Can be water soluble or insoluble Fermentability varies LECTURE 7 -‐ SLIDE 12 FIBER Dietary and functional ﬁber Part of plant cell wall Water soluble with ion-binding potential, gel forming Completely metabolized by bacteria Backbone PECTINS = α 1-4 galacturonic acid Dietary and functional ﬁber Structural component of plants Backbone Insoluble in water, poorly fermented LIGNIN = phenol units Metabolized by intestinal bacteria to enterolactone (phytoestrogen) LECTURE 7 -‐ SLIDE 13 FIBER GUMS β 1‐3 galactose β 1-6 galactose GUM ARABIC Dietary and functional fibers Secreted at site of plant injury Water soluble and highly fermented by bacteria Used as gelling, thickening agent LECTURE 7 -‐ SLIDE 14 FIBER BETA ‐ GLUCANS β‐D‐glucopyranosyl (β 1‐4 and 1‐3 linkages) Dietary and functional ﬁber Water soluble Reduce serum cholesterol, postprandial blood glucose Highly fermentable Form viscous gels within GI tract LECTURE 7 -‐ SLIDE 15 FIBER RESISTANT STARCH (RS) Starch which cannot be easily enzymatically digested and absorbed by humans – RS1/ RS2 (dietary fibers) – When cooked/chemically modiﬁed = RS3/RS4 (functional and partially fermentable) RS1 = whole or partially milled grains and seeds RS2 = potato, unripe (green) banana, maize, some legumes RS3 = cooked/cooled starchy foods (growth of beneficial bacteria, improved glycemic response) RS4 = chemical modiﬁcation of starch LECTURE 7 -‐ SLIDE 16 FIBER RESISTANT STARCH Glycemic index of warm versus cold potato RS3 = cooked/cooled starchy foods LECTURE 7 -‐ SLIDE 17 (growth of beneficial bacteria, improved glycemic response) FIBER FRUCTANS (inulin, oligofructose, fructooligosaccharides) Fructose units DIETARY SOURCES: Promote growth of biﬁdobacteria artichokes, onions, (prebiotic) chicory, wheat barley, rye Considered dietary ﬁber -‐not included in most food composition databases LECTURE 7 -‐ SLIDE 18 FIBER CHITIN and CHITOSAN β 1‐4 glucose units, similar to cellulose Insoluble, could be functional ﬁber Bind dietary lipids in the stomach – Bind unesterified cholesterol and phospholipids promoting their excretion in the feces – Has been observed to reduce serum cholesterol and triglycerides – May have some immune enhancing functions, may reduce adverse side eﬀects of cancer drugs LECTURE 7 -‐ SLIDE 19 FIBER PSYLLIUM (Mucilages) Similar structure to gums Bind water = adds viscosity Functional ﬁber (laxative properties) Promote reduction in serum lipids *Labels must indicate to have with liquid or there could be risk of choking LECTURE 7 -‐ SLIDE 20 Major physiological eﬀects of ﬁber Some ﬁbers form a gel: Other ﬁbers -‐ delay and lower speed up nutrient absorption digestion -‐ earlier satiation LECTURE 7 -‐ SLIDE 21 FIBER -‐ Properties Aﬀecting Physiological and Metabolic Effects 1. Solubility in water 2. Water holding capacity and viscosity 3. Adsorption or binding ability 4. Degradability or fermentability (by intestinal bacteria) LECTURE 7 -‐ SLIDE 22 SOLUBLE vs. INSOLUBLE 1. SOLUBILITY SOLUBLE: INSOLUBLE: Delay gastric emptying Increase fecal bulk  Increase transit time  Decrease transit time (through slower movement) (speed up movement)  Decrease nutrient  Decrease of nutrient absorption (e.g. glucose) absorption LECTURE 7 -‐ SLIDE 23 SOLUBLE vs. INSOLUBLE 1. SOLUBILITY LECTURE 7 -‐ SLIDE 24 2. SOLUBLE vs. INSOLUBLE WATER HOLDING CAPACITY Deﬁnition: = ability of ﬁber to bind water as it moves through the gastrointestinal tract = describes how much the ﬁber is able to act as a sponge. Water holding capacity can be impacted by: – pH of gastrointestinal tract/bolus/chyme – Size of particles – Level of food processing LECTURE 7 -‐ SLIDE 25 2. SOLUBLE vs. INSOLUBLE WATER HOLDING CAPACITY EFFECTS OF WATER HOLDING CAPACITY: 1. Delayed gastric emptying.  This slows down the movement from stomach to small intestine.  RESULT: you feel full! and the digestion is slowed down. 2. Reduced mixing of chyme with digestive enzymes Gels act as a ‘physical barrier’ preventing digestive enzymes from accessing the food 3. Reduced enzyme function High water holding capacity causes gels to form in the stomach. Digestive enzymes (e.g., peptidases, lipases) may be functionally depressed by gel forming ﬁbers LECTURE 7 -‐ SLIDE 26 2. SOLUBLE vs. INSOLUBLE WATER HOLDING CAPACITY 4. Decreased nutrient diﬀusion – Increased thickness of water layer on surface of enterocytes Less movement of nutrients into enterocytes – Decreased peristaltic movements (convective movements) Less nutrients brought from lumen to epithelial surface Decreased absorption of amino acids and fatty acids Decreased glucose absorption, decreased blood glucose (benefit for diabetic patients) 5. Transit time – Soluble ﬁbers typically delay transit time LECTURE 7 -‐ SLIDE 27 FIBER -‐ Properties Aﬀecting Physiological and Metabolic Effects 1. Solubility in water 2. Water holding capacity and viscosity 3. Adsorption or binding ability 4. Degradability or fermentability (by intestinal bacteria) LECTURE 7 -‐ SLIDE 28 3. ADSORPTION / BINDING ABILITY = ability to bind inorganic and organic molecules, for example enzymes or nutrients, in the GI tract. Adsorption/binding ability of certain ﬁbers results in: A. Diminished absorption of lipids B. Increased fecal bile excretion C. Lowered serum cholesterol concentrations D. Altered mineral, carotenoid, and phytochemical absorption LECTURE 7 -‐ SLIDE 29 3. ADSORPTION / BINDING ABILITY A. Diminished absorption of lipids Types of ﬁber: soluble ﬁbers (especially pectin, gums, β ‐ glucans, and some hemicellulose); lignin, chitosan Mechanism: ﬁber adsorbs and interact with fatty acids, cholesterol and bile acids  prevents formation of micelles (fat transport molecules required for transport into enterocytes) Result: more fat components excreted LECTURE 7 -‐ SLIDE 30 3. ADSORPTION / BINDING ABILITY B. Increased fecal bile excretion Types of ﬁber: soluble ﬁbers (especially pectin, gums, β ‐ glucans, and some hemicellulose); lignin, chitosan Mechanism: ﬁber adsorbs bile acids preventing recirculation and use in the formation of micelles Result: more bile acids degraded (by bacteria) and excreted LECTURE 7 -‐ SLIDE 31 3. ADSORPTION / BINDING ABILITY C. Lowered serum cholesterol concentrations Types of ﬁber: Psyllium, gums, β ‐ glucans, pectin Mechanism: 1)  bile/cholesterol excretion: decreases [cholesterol] in liver,  more LDL removed from blood to make new bile 2) bile composition changes: inhibits HMG CoA reductase enzyme required for cholesterol synthesis 3) production of short chain fatty acids: inhibit cholesterol and fatty acid synthesis Result: lower serum cholesterol! LECTURE 7 -‐ SLIDE 32 3. ADSORPTION / BINDING ABILITY D. Altered mineral, carotenoid, and phytochemical absorption Types of ﬁber: Hemicellulose, pectins, gums, some oligosaccharides; lignin Mechanism: Either enhance or inhibit mineral absorption which depends on the degree of fermentability Generally: slow fermentable ﬁber: inhibitory eﬀect rapidly fermentable: enhancing eﬀect Result: Fluctuations in the absorption of minerals, carotenoids, and phytochemicals LECTURE 7 -‐ SLIDE 33 3. ADSORPTION / BINDING ABILITY Mineral absorption Slowly fermentable fiber: → growth of new microbial cells → uptake of minerals into new microbial cells Highly fermentable fiber: → high production of SCFA → creation of an acidic environment → increase in mineral solubility → increase in absorption of Ca, Mg, Zn, Fe in colon LECTURE 7 -‐ SLIDE 34 FIBER -‐ Properties Aﬀecting Physiological and Metabolic Effects 1. Solubility in water 2. Water holding capacity and viscosity 3. Adsorption or binding ability 4. Degradability or fermentability (by intestinal bacteria) LECTURE 7 -‐ SLIDE 35 4. DEGRADABILITY or FERMENTABILITY 1. NON FERMENTABLE: cellulose and lignin (some hemicellulose) Beneﬁcial Eﬀects: 1. Detoxiﬁcation 2. Increased fecal volume 2. HIGHLY FERMENTABLE: fructans, pectin, gums, psyllium, resistant starch, beta-glucans (some hemicellulose and cellulose (slow)) Beneﬁcial Eﬀects: 1. Generation of short-chain fatty acids 2. Prebiotic capacity LECTURE 7 -‐ SLIDE 36 4. Non‐fermentable ﬁber 1a) Detoxiﬁcation  microbial scavenging of toxins =  excretion of toxins Potential inhibition of proliferation of tumour cells and enzymes that convert pro-carcinogens to active carcinogens 1b) Increased Fecal Volume wheat bran, rice bran; most eﬀective ﬁber laxatives More frequent defecation (laxative), reduced transit time, decreased intraluminal pressure LECTURE 7 -‐ SLIDE 37 4. Highly fermentable ﬁber Fermentation process Anatomic: in colon “Initiators“: bacteria Products: gases: hydrogen (H2), carbon dioxide (CO2), methane (CH4) SCFA: acetic acid (2-carbon) -‐ATP formation in most tissues propionic acid (3‐carbon) -‐ liver converts it to glucose butyric acid (4‐carbon) -‐ source of energy for colon cells LECTURE 7 -‐ SLIDE 38 4. Highly fermentable ﬁber 2a) Generation of short‐chain fatty acids (SCFA) during bacterial metabolism Eﬀects of SCFA (acetic, butyric, and propionic acid):  H2O and Na absorption in colon Mucosal cell diﬀerentiation and proliferation Provision of energy: SCFAs can provide a source of energy for various body tissues Acidiﬁcation of luminal environment in colon:  pH = less soluble bile and less bile conversion  Calcium binding of bile and fatty acids This could be protective in colon cancer (bile and fatty acids cause chronic inflammation in the colon epithelium which can progress to cancer) LECTURE 7 -‐ SLIDE 39 4. Highly fermentable ﬁber 2b) Prebiotic capacity Fermented by beneficial gut bacteria and hence promote growth of the beneﬁcial bacterial species  Lactobacilli, Biﬁdobacterium  Clostridium and Salmonella IMPORTANT: resist digestion in the small intestine and reach May be useful in several diseases the colon, where they are (e.g., protective against colon cancer) fermented by the gut microﬂora In particular: oligosaccharides found in beans and legumes (Raﬃnose, Stachyose, Verbascose) LECTURE 7 -‐ SLIDE 40 PREBIOTICS – PROBIOTICS Probiotics live bacteria (mostly lactobacillus casei) important characteristic: bacteria reach the intestine intact; are not digested ﬁrst probiotic product created in 1935: YAKULT; by Japanese scientist Dr. Minoru Shirota (L. casei Shirota) available as supplements or in foods (for example yoghurt) LECTURE 7 -‐ SLIDE 41 FIBER SOLUBLE vs INSOLUBLE DISEASE PREVENTION AND MANAGEMENT Diabetes mellitus Hypo‐glycemic eﬀects Heart disease Hypo‐lipidemic Hypo‐cholesterolemic eﬀects Obesity Increased satiety Reduced absorption of macronutrients Gastrointestinal disorders (e.g., inflammatory bowel syndrome) Prebiotic eﬀects (support growth of beneﬁcial bacteria) Colon cancer Beneﬁcial bacterial species protective against cancer; likely through formation of SCFA  binding of bile and fatty acids LECTURE 7 -‐ SLIDE 42 FIBER SOLUBLE vs INSOLUBLE DISEASE PREVENTION AND MANAGEMENT Diabetes mellitus Food matrix issue: Hypo‐glycemic eﬀects In some cases food sources of fiber as opposed to Heart disease isolated fiber (supplements) seem to be more beneficial. Hypo‐lipodemic For example: whole wheat cereal vs. cereal fiber Hypo‐cholesterolemic eﬀects Obesity Increased satiety Reduced absorption of macronutrients Gastrointestinal disorders Prebiotic eﬀects (support growth of beneﬁcial bacteria) Colon cancer Beneﬁcial bacterial species protective against cancer; likely through formation of SCFA  binding of bile and fatty acids LECTURE 7 -‐ SLIDE 43 Activity SOLUBLE vs INSOLUBLE FIBER - DISEASE PREVENTION AND MANAGEMENT Name two properties of pectins. Explain the physiological effects related to these properties, and explain how these physiological effects might contribute to the prevention of cardiovascular disease (e.g., atherosclerosis). You may follow a scheme below to answer: Property 1: Physiological effect: How this might prevent cardiovascular disease: Property 2: Physiological effect: LECTURE 7 -‐ SLIDE 44 How this might prevent cardiovascular disease: SOLUBLE vs INSOLUBLE FIBER -‐RECOMMENDED INTAKES Adequate Intakes were created based on the amounts of ﬁber shown to protect against heart disease Suggested intake = 14 grams ﬁber / 1,000 kcal Age 19‐50years Men: 38 grams Women: 25 grams LECTURE 7 -‐ SLIDE 45 SOLUBLE vs INSOLUBLE FIBER -‐RECOMMENDED INTAKES Mean ﬁber intake in Canadian adults (Canadian Community Health Survey 2004-2015) Men 19+ years 19 grams/day Women 19+ years 16 grams/day < 10% meet the adequate intake for ﬁber!!! Adequate Intake Men: 38 grams/day Women: 25 grams/day LECTURE 7 -‐ SLIDE 46 Food Labeling TOTAL FIBER Labeling and claims of food products: Dietary ﬁber = 1 of 13 core nutrients that must be declared in the Nutrition Facts table. Food and Drug Regulations, B.01.401 Amount of both soluble and insoluble ﬁber may be separately declared as additional information. Food and Drug Regulations B.01.402 Total ﬁber = dietary ﬁber + functional ﬁber+ novel fiber https://www.canada.ca/content/dam/hc-sc/migration/hc-sc/fn- an/alt_formats/pdf/legislation/pol/fibre-label-etiquetage-eng.pdf https://www.canada.ca/en/health- canada/services/publications/food-nutrition/labelling- LECTURE 7 -‐ SLIDE 47 advertising-dietary-fibre-food-products.html Fiber Highly fermentable Non-fermentable and soluble and insoluble Beta-glucans * Cellulose Fructans Some hemicellulose Pectin * Lignin Gums * Chitin and chitosan Psyllium * Resistant starch Some hemicellulose Oligosaccharides (raffinose, stachyose, verbascose) * Forming gels in GI LECTURE 7 -‐ SLIDE 49 Fiber Food source Fiber type Strawberries Lignin, pectin Whole grains, wheat Cellulose, bran hemicellulose, lignin Barley, Oat Beta-glucans Artichoke, asparagus, Fructans bananas Citrus fruits, apple Pectin Beans and legumes Oligosaccharides (raffinose, stachyose, verbascose) Carrots Cellulose, lignin, pectin LECTURE 7 -‐ SLIDE 50 SOLUBLE FIBER -‐vs INSOLUBLE SUMMARY In human nutrition, we distinguish between dietary and functional ﬁbers. Physiological eﬀects determined largely by the type and amount of ﬁber. Fiber has numerous beneﬁcial characteristics to which its role in disease can be attributed to. Fiber may have a role in disease prevention and treatment. Fiber in the diet should be varied and complementary to ensure adequate intake of other nutrients. LECTURE 7 -‐ SLIDE 51 CASE STUDY Your friend is interested in loosing weight and found this dietary ﬁber supplement advertised for eﬀective weight loss. She wants to get your advice on how this product might be eﬀective in weight loss and what side eﬀects this product might have. She consumes an omnivorous diet but is not meeting the recommended daily fruit and vegetable intake (5-a‐day). LECTURE 7 -‐ SLIDE 52 CASE STU

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