MU 3.2 - Biochemical Aspects of Nutrition PDF

 NUTRIENTS IN FOODS [ESSENTIAL NUTRIENTS] [REGULATORY NUTRIENTS] WATER CARBOHYDRATES VITAMINS PROTEINS MINERALS LIPIDS CARBOHYDRATES IN NUTRITION Monosaccharides: Oligosaccharide: Glucose Raffinose Fructose...

 NUTRIENTS IN FOODS [ESSENTIAL NUTRIENTS] [REGULATORY NUTRIENTS] WATER CARBOHYDRATES VITAMINS PROTEINS MINERALS LIPIDS CARBOHYDRATES IN NUTRITION Monosaccharides: Oligosaccharide: Glucose Raffinose Fructose Stachyose Galactose (in beans and other legumes) (cannot be digested well by Disaccharides: humans = gas-producing Sucrose (table sugar) effects) Lactose (milk sugar) Maltose CARBOHYDRATES IN NUTRITION The amount of carbohydrate is required in the diet:  at least 50- 100 grams/day  most diets contain more than enough carbohydrates CARBOHYDRATES IN NUTRITION DIETARY FIBER: the structural parts of plant-based foods that cannot be digested or absorbed by the body. (Lack of necessary enzymes) A polysaccharide an essential nutrient, which must be eaten in the diet CARBOHYDRATES IN NUTRITION DIETARY FIBER: There are two types of fiber that your body needs: Insoluble fiber Soluble fiber CARBOHYDRATES IN NUTRITION Insoluble fiber does not dissolve in water or gastrointestinal fluids remains more or less unchanged as it moves through the digestive tract. provides bulk, or roughage sensation of being full. accelerates the exit from the body of harmful substances in food cellulose, hemicelluloses CARBOHYDRATES IN NUTRITION Insoluble fiber Preventing constipation: sits in the gastrointestinal tract, absorbing fluid and sticking to other by products of digestion that are ready to be formed into the stool. Improving bowel-related health problems: like constipation, hemorrhoids, and fecal incontinence, and colorectal cancer. Helping weight management CARBOHYDRATES IN NUTRITION Soluble fiber dissolves in water and gastrointestinal fluids It attracts water and turns to a gel-like substance slows down foods are digested feel full longer CARBOHYDRATES IN NUTRITION Soluble fiber Lowering fat absorption and helping weight management Lowering cholesterol Stabilizing blood glucose levels Reducing the risk of cardiovascular disease Feeding healthy gut bacteria Healthy bowel movements MAINTENANCE OF BLOOD GLUCOSE Maintenance of blood glucose DISCUSSED IN TWO STATES: 1) Absorptive State (lasts about 4 hours after a meal) 2) Postabsorptive State (fasting) Maintenance of blood glucose 1) Absorptive State Blood glucose is readily available for ATP synthesis (Excessive glucose is stored as glycogen in the liver and muscles or as body fat) Fats are taken by the tissues (especially adipose and muscular tissue) Amino acids become available for protein synthesis. REGULATED largely by INSULIN, which stimulates nearly all cells to absorb glucose. The well-fed state: the lipogenic liver. Maintenance of blood glucose 2) Postabsorptive State (fasting) Prevails hours after meals and overnight: - The essence of this state is to regulate blood glucose levels, which is especially critical to the brain - Glucose - drawn from the body's glycogen reserves in liver and muscles - synthesized from fats (gluconeogenesis) Maintenance of blood glucose 2) Postabsorptive State (fasting) After 4 to 5 days of fasting, the brain begins to use ketone bodies as supplemental fuel. - from fat - acidosis After glycogen and fat reserves are depleted - The body begins to burn proteins. (skeletal muscle proteins are first). Maintenance of blood glucose Postabsorptive State is regulated by the sympathetic nervous system and several hormones. Glucagon promotes: 1) glycogenolysis glycogen  glucose 2) gluconeogenesis AA/FFA  glucose 3) lipolysis triglyceride  FFA Growth hormone also raises blood glucose concentrations. The fasting state: the glucogenic liver LIPIDS IN NUTRITION LIPIDS IN NUTRITION LIPIDS IN NUTRITION FATTY ACIDS in the human diet and in body tissues 4 carbons to 22 or more each chain have an even number of carbon atoms LIPIDS IN NUTRITION FATTY ACIDS classified as SATURATED or UNSATURATED LIPIDS IN NUTRITION FATTY ACIDS Fats and oils usually contain MIXTURES OF FATTY ACIDS Butter and other animal fats: saturated Olive and canola oil: monounsaturated fish, corn, safflower, soybean, and sunflower oil: polyunsaturated MONOUNSATURATED and POLYUNSATURATED (cis) fats tend to lower LDL LIPIDS IN NUTRITION ESSENTIAL FATTY ACIDS alpha-linolenic acid: 18-carbon polyunsaturated fatty acids omega-3 fatty acid (the location of the first double bond from the methyl end of the fatty acid) linoleic acid: 18-carbon, polyunsaturated fatty acids omega-6 fatty acid LIPIDS IN NUTRITION ESSENTIAL FATTY ACIDS required in small amounts in the diet needed for the formation of cell membranes needed for the synthesis of hormone-like compounds (eicosanoids, prostaglandins, thromboxane, leukotrienes) (important regulators of blood pressure, blood clotting, and the immune response) SOURCES: vegetable oil (safflower or corn oil), grains, nuts, seeds, vegetables, fish (omega-3 fatty acids) LIPIDS IN NUTRITION HYDROGENATION IN THE FOOD INDUSTRY: Hydrogen can be added to the carbon-carbon double bond using a nickel catalyst in a process called HYDROGENATION LIPIDS IN NUTRITION HYDROGENATION IN THE FOOD INDUSTRY: Saturated fats tend to be more stable than unsaturated ones resistant to rancidity (oxidation) more solid and spreadable (margarine) a change in the shape of some unsaturated fatty acids (from cis form to trans form) undesirable health consequences LIPIDS IN NUTRITION CIS FATTY ACIDS Occurs naturally TRANS FATTY ACIDS Produced by hydrogenation (A small portion of trans fat can occur naturally) LIPIDS IN NUTRITION TRANS FATTY ACIDS are known to raise LDL, and lower HDL promote systemic inflammation increase triglycerides MICROBIOTA GUT MICROBIATA complex, diverse, and vast microbial community in human intestine composed of approximately 1,100 prevalent species, Four main bacterial phyla in the healthy human gut: - Firmicutes* gram (+) - Bacteroidetes* gram (-) - Actinobacteria gram (+) - Proteobacteria gram (-) GUT MICROBIATA produce various kinds of metabolites (beneficial and harmful compounds for the host)  SHORT CHAIN FATTY ACIDS  TRIMETHYLAMINE N-OXIDE (TMAO)  BILE ACIDS  BRANCHED CHAIN AMINO ACIDS GUT MICROBIATA SHORT-CHAIN FATTY ACIDS (SCFAs) Fatty acids ranging from 1 to 6 carbon chains the vast majority of SCFAs produced in the healthy gut in the colon and stool acetate 60% propionate 20% butyrate 20% GUT MICROBIATA SHORT-CHAIN FATTY ACIDS (SCFAs) produced in the distal small intestine and colon by anaerobic fermentation of undigested nutrients by microbiota (resistant starch, dietary fiber, and various complex polysaccharides GUT MICROBIATA SHORT-CHAIN FATTY ACIDS (SCFAs) are absorbed in the intestines are used as ENERGY by the host function as regulators of food or energy intake and inflammation are associated with increased satiety and reduced food intake are also signaling molecules GUT MICROBIATA SHORT-CHAIN FATTY ACIDS (SCFAs) ENDOGENOUS RECEPTORS for SCFAS (G protein-coupled receptors) Free fatty acid receptor 2 (FFAR2, GPR43) Free fatty acid receptor 3 (FFAR3, GPR41) GPR109A Olfactory receptor 78 (Olfr78) Acetate preferentially activates FFAR2 in vitro Propionate preferentially activates FFAR2 and FFAR3 Butyrate preferentially activates FFAR3. GUT MICROBIATA SCFAs bind to GPR41 and GPR43 on enteroendocrine cells: Inducing secretion of PYY, and GLP-1 Peptide YY (PYY) inhibits gut motility increases intestinal transit rate reduces the harvest of energy from the diet increases satiety Glucogon-like peptide 1 (GLP-1) increase insulin sensitivity GUT MICROBIATA SCFAs bind to GPR43 in adipose tissue suppress insulin signaling in the adipose tissue prevent of fat accumulation. GUT MICROBIATA SCFAs activate INTESTINAL GLUCONEOGENESIS (IGN) Glucose is detected by a portal vein glucose sensor that signals to the brain (via a gut- brain neural circuit) Glucose tolerance is improved Food intake is reduced GUT MICROBIATA SCFAs suppresses fasting-induced adipose factor (Fiaf) expression in the ileum: Fiaf inhibits lipoprotein lipase (LPL) activity and fat storage in white adipose tissue. GUT MICROBIATA TRIMETHYLAMINE N-OXIDE (TMAO) another metabolite derived from gut microbes’ metabolic activity. a contributor of atherosclerosis. GUT MICROBIATA Trimethylamine (TMA) generated by the altered microbiota through metabolizing choline, phosphatidylcholine, L-carnitine and betaine via TMA lyases. enters the liver through the portal circulation oxidized into TMAO by hepatic flavin monooxygenases (FMO3) GUT MICROBIATA HIGH FAT DIET induces gut microbial alteration increases gut permeability reduces the expression of tight junction proteins in the intestinal epithelial cells. disruption of the gut barrier function leakage of lipopolysaccharide into the portal blood circulation. obesity, insulin resistance, and type 2 diabetes mellitus. GUT MICROBIATA PREBIOTICS non-digestible but fermentable polysaccharides inulin, fructo-oligosaccharides, galato-oligosaccharides, lactulose. Foods artificially enriched with these fibers are defined as prebiotics promote SCFA production and the growth of beneficial bacteria improve gut barrier function reduces hunger and enhances satiety GUT MICROBIATA PROBIOTICS Lactobacillus and Bifidobacterium live microorganisms confer a beneficial health effect on the host when administered in proper amounts. ameliorate obesity and metabolic disorders. beneficial actions on the enteric nervous system regulating gut contractility PROTEINS IN NUTRITION PROTEINS IN NUTRITION basic structural material of the body (in cell membranes and blood) enzymes antibodies collagen in connective tissue many hormones (insulin) PROTEINS IN NUTRITION FOOD CONTAINS APPROXIMATELY 20 COMMON AMINO ACIDS ESSENTIAL AMINO ACIDS INDISPENSABLE AMINO for humans: ACIDS Histidine Arginine Isoleucine Cysteine Leucine Tyrosine Lysine (in premature infants or in Methionine people with liver disease) Phenylalanine Threonine Tryptophan Valine PROTEINS IN NUTRITION PROTEIN SOURCES Foods of animal origin (meat, fish, eggs, and dairy product) Foods of plant origin (soybeans) Vegetarian Diet legumes (beans): high in lysine and low in methionine grains have complementary strengths and weaknesses PROTEINS IN NUTRITION The World Health Organization recommends a daily intake of 0.75 gram of protein per kilogram of body weight for adults of both sexes Additional protein needs  endurance athletes  Infants  Children  Pregnant  Lactating women PROTEINS IN NUTRITION POSITIVE NITROGEN BALANCE  more protein is being retained than excreted  during periods of rapid growth, pregnancy and lactation, or recovery after illness or depletion NEGATIVE NITROGEN BALANCE  more tissue is being broken down than synthesized  during illness or wasting VITAMINS IN NUTRITION VITAMINS IN NUTRITION Vitamin A: for embryonic development, growth, reproduction, proper immune function, the integrity of epithelial cells, vision. B Vitamins: coenzymes that assist in energy metabolism Folic acid (Vitamin B9): helps protect against birth defects Vitamin C: building connective tissue, antioxidant Vitamin D: calcium and phosphorus homeostasis, bone metabolism Vitamin E: antioxidant, heme synthesis Vitamin K: blood clotting VITAMINS IN NUTRITION Humans are able to synthesize certain vitamins to some extent Vitamin D Niacin Vitamin K Biotin Humans depend on their diet to supply vitamins specific deficiency syndrome results Irreversible Some vitamins are found in foods in precursor forms They must be activated in the body beta(β)-carotene, found in plants, is converted to vitamin A in the body. VITAMINS IN NUTRITION water-soluble vitamins are more easily destroyed during cooking than are fat-soluble vitamins. water-soluble vitamins are synthesized by plants and found in both plant and animal foods. BUT VITAMIN B12: supplied by only foods of animal origin Vegetarians are at risk of vitamin B12 deficiency MINERALS IN NUTRITION MINERALS IN NUTRITION simple inorganic elements 4 - 6 % of body weight in the form of salts in the body not themselves metabolized MINERALS IN NUTRITION not a source of energy function broadly in metabolism controlling the movement of water in and out of cells regulate fluid balance, osmotic pressure, and acid-base balance components of enzyme systems MINERALS IN NUTRITION MACROMINERALS in amounts of 100 mg or more per day calcium, phosphorus, magnesium, sulfur, sodium, chloride, and potassium. MICROMINERALS trace elements required in amounts of 15 mg per day or less iron, zinc, copper, manganese, iodine, selenium, fluoride, molybdenum, chromium, and cobalt ULTRATRACE ELEMENTS Foun in extremely small quantities in diet (micrograms each day) arsenic, boron, nickel, silicon, and vanadium. MINERALS IN NUTRITION The levels of different minerals in foods are influenced by growing conditions (soil and water composition) not destroyed during food preparation MINERALS IN NUTRITION better absorbed from animal foods than from plant foods FIBRES in plants interfere with absorption PHYTIC ACID can form complexes with some minerals and make them insoluble and thereby indigestible MINERALS IN NUTRITION Some minerals, particularly those of a similar size and charge, COMPETE with each other for absorption iron supplementation may reduce zinc absorption excessive intakes of zinc can interfere with copper absorption the absorption of iron from plants (nonheme iron) is enhanced when vitamin C is simultaneously present in the diet calcium absorption is improved by adequate amounts of vitamin D MINERALS IN NUTRITION minerals can be toxic if taken in doses not far above recommended levels (iron and copper) ENERGY Energy Balance HUMAN BODY IS AN ENGINE releases THE ENERGY present in the foods This ENERGY is utilized for the mechanical work (muscles, secretory processes) for the work necessary to maintain the body’s structure and functions Energy Balance FOOD is the fuel source of the body CARBOHYDRATE: 4 kilocalories (17 kilojoules) per gram PROTEIN: 4 kilocalories (17 kilojoules) per gram FAT: 9 kilocalories (38 kilojoules) per gram THE ENERGY IN THE DIET from protein : 12-15 % from fat : 30-40 % from carbohydrate : 50-60 % Energy Balance Energy is needed not only when a person is physically active but even when the body is lying motionless. BASAL METABOLIC RATE Minimum amount of energy required by the body to maintain life at physical and mental rest in post absorptive state. Basal Metabolic Rate (BMR) Several functions within the body occurs at basal condition Working of heart and other organs Conduction of nerve impulse Reabsorption by renal tubulus GI motility Ion transport across membranes Basal Metabolic Rate (BMR) BASAL METABOLIC RATE BMR= Total heat production in kcal per hour / body surface area in square meters Basal Metabolic Rate (BMR) NORMAL RANGE OF BMR ADULT MAN : 35-38 cal/sq.m/hr or 1600 cal/day ADULT WOMAN : 32-35 cal/sqm/hr or 1400 cal/day Basal Metabolic Rate (BMR) FACTORS AFFECTING BMR 1. Age: BMR decreases with advancing age. (more surface area in children) 2. Sex: Males have high BMR. (more muscle mass and lower body weight). 4. Body Surface area :. Tall, thin people have a higher BMR than short persons. (BMR is proportional to surface area) 5. Environmental conditions: Exposure to cold causes an increase in BMR. (extra need for heat for the maintenance of body temperature) 6. Body Temperature: Increased rate of chemical reactions causes increased BMR. 7. Exercise: The increase in BMR is also due to burning calories and increased cardiac output. Basal Metabolic Rate (BMR) FACTORS AFFECTING BMR 8. Drugs: Caffeine, Benzedine, alcohol, epinephrine and nicotine increase BMR. Certain anesthetics decrease BMR 9. Pregnancy: The BMR of pregnant mother rises after 6 months of gestation. 10. Racial variations: BMR varies with different racial groups. Higher values have been reported in Eskimos. 11. Barometric pressure: A fall of pressure to half an atmosphere as occurs in mountain climbing increases BMR. 12. State of nutrition: BMR is lowered in starvation, malnutrition and wasting diseases. 13. Hormones: Thyroid hormone, adrenaline, catecholamines, growth hormone, male sex hormone increase BMR APPETITE HUNGER and SATIETY are regulated by a complex interaction of multiple brain centers, hormones, and sensory and motor pathways. Central appetite control Hypothalamus Brain stem Hypothalamic messengers Peripheral signals of appetite Hormones  Central appetite control Central appetite control e body’s appetite control centers are located in HYPOTHALAMUS The body’s appetite control centers are located in HYPOTHALAMUS ENTROMEDI AL HYPOTHALAMUS: atiety center VENTROMEDIAL HYPOTHALAMUS: satiety center TERAL HYPOTHALAMUS: LATERAL eeding (hunger)HYPOTHALAMUS: center feeding (hunger) center Central appetite control Arcuate nucleus in HYPOTHALAMUS control fuel intake and metabolism receive signals from the circulation (Blood–brain barrier surrounding the arcuate nucleus is not complete) Central appetite control Two types of neurons in the Arcuate nucleus 1- Orexigenic NPY/AgRP neurons 2- Anorectic POMC neurons Central appetite control 1- Orexigenic NPY/AgRP neurons APPETITE-STIMULATING PEPTIDES: Neuropeptide Y (NPY) Aouti-related peptide (AgRP) Central appetite control 1- Orexigenic NPY/AgRP neurons Neuropeptide Y (NPY) stimulates the neurons that trigger eating behavior Central appetite control 1- Orexigenic NPY/AgRP neurons Agouti-related protein released from arcuate NPY/AgRP neurons at the PVN stimulates food intake Central appetite control 2- Anorectic POMC neurons APPETITE INHIBITING PEPTIDES: Cocaine and amfetamine-regulated transcript (CART) Pro-opiomelanocortin (POMC) (precursor of α-melanocyte stimulating hormone: α MSH) Central appetite control 2- Anorectic POMC neurons Melanocortins cleaved from the POMC precursor molecule by tissue specific post-translational cleavage Central appetite control 2- Anorectic POMC neurons Melanocortins Alpha-melanocyte stimulating hormone (α- MSH) is released from POMC-expressing neurons acts through MC3-R and MC4-R in PVN inhibits food intake Central appetite control Cocaine- and amfetamine- regulated transcript (CART) inhibits food intake Central appetite control Orexigenic NPY/AgRP neurons inhibit anorectic POMC neurons Agouti-related protein blocks the anorectic effect of α-melanocyte stimulating hormone FASTING increases NPY and AgRP expression reduces CART and POMC expression Peripheral signals of appetite PERIPHERAL HORMONES Insulin Cholecystokinin Peptide YY Pancreatic polypeptide (PP) Leptin Ghrelin Glucagon-like peptide-1  Peripheral signals of appetite PERIPHERAL HORMONES Short-term regulators: GHRELIN, CHOLECYSTOKININ determine individual meals constitute a meal-to-meal control system regulates the onset and end of eating behavior Long-term regulators: INSULIN, LEPTIN stabilize the levels of body fat deposits inhibit eating and promote energy expenditure Peripheral signals of appetite INSULIN signals caloric abundance is produced in response to food excess and the well- fed state. inhibits eating decreases fuel intake increases thermogenesis achieve the usual long-term stability of body weight and fat mass (Blood insulin levels correlate with body fat amounts.)  Peripheral signals of appetite INSULIN acts on INSULIN RECEPTORS in the hypothalamus: in the orexigenic neurons: inhibit the release of NPY in the anorexigenic neurons: stimulate the release of α MSH Peripheral signals of appetite CHOLECYSTOKININ a peptide hormone produced in response to the intraluminal presence of protein and fats by I cells in jejunum and duodenum can cross the BBB and bind directly to its specific receptors transmit the signal of nutrient intake to the brain inhibits food intake inhibits gastric emptying  Peripheral signals of appetite PEPTIDE YY a peptide hormone secreted from L cells of the small and large bowel Produced in response to food entering from the stomach. Blood levels are increased after a meal and remains high for some hours. Postprandial PYY concentrations are proportional to meal energy content  Peripheral signals of appetite PEPTIDE YY carried to the arcuate nucleus and acts on orexigenic neurons inhibits NPY release inhibits appetite stimulates POMC neurons inhibits secretion of gastric acid and pancreatic enzymes inhibits gallbladder emptying Peripheral signals of appetite PANCREATIC POLYPEPTIDE (PP) produced by PP cells of the pancreatic islets produced in response to ingestion of food Obese subjects have lower PP Anorexia nervosa subjects have higher PP Peripheral signals of appetite LEPTIN from the Greek word lepto (thin) produced predominantly by adipose tissue circulating leptin concentrations are directly proportional to adiposity Peripheral signals of appetite LEPTIN moves through the blood to the brain, acts on receptors in arcuate neurons of the hypothalamus inhibits appetite. LEPTIN carries the message that fat reserves are sufficient, and it promotes a reduction in fuel intake and increased expenditure of energy.  Peripheral signals of appetite Blood LEPTIN levels; communicate the status of triacylglycerol levels in the adipocytes to the central nervous system When the mass of adipose tissue increases, released leptin inhibits feeding and fat synthesis and stimulates oxidation of fatty acids. When the mass of adipose tissue decreases, a lowered leptin production favors a greater food intake and less fatty acid oxidation. If leptin levels are low (“starvation”), appetite increases; If leptin levels are high (“overfeeding”), appetite is suppressed. Peripheral signals of appetite LEPTIN regulates fat metabolism in adipocytes: inhibits fatty acid biosynthesis induces fatty acid oxidation increases expression of UCP2 (energy of oxidation is lost as heat: thermogenesis). Peripheral signals of appetite LEPTIN binding to leptin receptors in the hypothalamus inhibits release of NPY (orexic) essential for pituitary function, growth hormone secretion, and normal puberty stimulates the sympathetic nervous system: increasing blood pressure, heart rate, Insulin RECEPTORS in the hypothalamus Leptin makes the cells of liver and muscle more sensitive to insulin. Insulin also stimulates fat cells to make leptin. LEPTIN - ob/ob genotype LEPTIN product of the ob gene ob/ob genotype: completely deficient in leptin a constant state of starvation hyperphagic serum cortisol levels are elevated unable to stay warm severely obese have metabolic disturbances (hyperinsulinaemic, insulin-resistant) When leptin is injected into ob/ob mice, they lose weight and increase their locomotor activity and thermogenesis. Peripheral signals of appetite LEPTIN OBESE PEOPLE: normal leptin genes elevated leptin concentrations (reflecting their high adiposity) Peripheral signals of appetite GHRELIN a peptide hormone Synthesized  in the endocrine cells of the stomach  in the hypothalamus (in much smaller amounts). Receptors:  in the pituitary gland  in the hypothalamus (affecting appetite),  in heart muscle and adipose tissue. Peripheral signals of appetite GHRELIN increase NPY and AgRP increase appetite important in long-term regulation of body weight in normal individuals. Production of ghrelin is maximal when the stomach is empty. Plasma levels fall quickly once food is consumed.  Peripheral signals of appetite PROGLUCAGON in the pancreas results in the formation of glucagon glicentin related pancreatic polypeptide major proglucagon fragments PROGLUCAGON in intestinal L-cells results in the formation of glicentin Oxyntomodulin glucagon- like peptide-1 spacer peptide-2 glucagon- like peptide-2  Peripheral signals of appetite GLUCAGON-LIKE PEPTIDE-1 co-secreted with PYY in response to the presence of nutrients in the gut stimulate the release of insulin inhibit the release of glucagon reduces gastric emptying inhibits gastric acid secretion regulate food intake produce a small, dose-dependent reduction in food intake in humans GLP-1 receptor agonists are used in the treatment of type 2 diabetes THANK YOU