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David Oluwatobi Tobechukwu Human Nutrition and Dietetics 14/MHS01/145 NTD 201- Introduction to Food Nutrition Assignment: 1. Differentiate between glucose and fructose 2. Write short notes on raffinose and stachyose (state their importance and significance) 3. Explain: Complementary value of protein, supplementary value of protein, limiting amino acid 4. Write notes on cholesterol plaque, hyperglycaemia 5. Explain digestion of yam 6. Write on lactose intolerance and kwashiorkor Differentiate between glucose and fructose Glucose Glucose is a sugar with the molecular formula C6H12O6. It is also known as grape sugar. With 6 carbon atoms, it is classed as a hexose, a sub-category of monosaccharides. α-D-glucose is one of the 16 aldose stereoisomers. The D-isomer (D-glucose), also known as dextrose, occurs widely in nature, but the L-isomer (L-glucose) does not. Glucose is made during photosynthesis from water and carbon dioxide, using energy from sunlight. The reverse of the photosynthesis reaction, which releases this energy, is a very important source of power for cellular respiration. Glucose is stored as a polymer, in plants as starch and in animals as glycogen. Glucose can be obtained by hydrolysis of carbohydrates such as milk, cane sugar, maltose, cellulose, glycogen etc. It is however, manufactured by hydrolysis of corn-starch by steaming and diluting acid. D-Glucose α-D-glucopyranose (chair form) Haworth projection of α-D-glucopyranose Fischer projection of D-glucose Fructose Fructose, or fruit sugar, is a simple ketonic monosaccharide found in many plants, where it is often bonded to glucose to form the disaccharide sucrose. It is one of the three dietary monosaccharides, along with glucose and galactose, that are absorbed directly into the bloodstream during digestion. Fructose was discovered by French chemist Augustin-Pierre Dubrunfaut in 1847. The name "fructose" was coined in 1857 by the English chemist William Miller. Pure, dry fructose is a very sweet, white, odourless, crystalline solid and is the most water-soluble of all the sugars. Fructose is found in honey, tree and vine fruits, flowers, berries, and most root vegetables. Commercially, fructose is frequently derived from sugar cane, sugar beets, and corn. Crystalline fructose is the monosaccharide, dried, ground, and of high purity. High-fructose corn syrup (HFCS) is a mixture of glucose and fructose as monosaccharides. Sucrose is a compound with one molecule of glucose covalently linked to one molecule of fructose. All forms of fructose, including fruits and juices, are commonly added to foods and drinks for palatability and taste enhancement, and for browning of some foods, such as baked goods. Excess fructose consumption has been hypothesized to be a cause of insulin, resistance, obesity, elevated LDL cholesterol and triglycerides, leading to metabolic syndrome. Fructose encourages visceral adipose tissue build-up and ectopic fat deposition. The majority of studies indicate there may be an increased risk of cardiovascular disease from a high intake of fructose. D-Fructose Fructose is a 6-carbon polyhydroxyketone. Crystalline fructose adopts a cyclic six-membered structure owing to the stability of its hemiketal and internal hydrogen-bonding. This form is formally called D-fructopyranose. In solution, fructose exists as an equilibrium mixture of 70% fructopyranose and about 22% fructofuranose, as well as small amounts of three other forms, including the acyclic structure. Differences between Glucose and Fructose 1. Glucose forms cyclic 6-carbon ring structure glucopyranose, while fructose forms both 5 sided ring structure fructofuranose and 6-carbin ring structure fructopyranose. 2. Glucose is and aldose sugar while fructose is a ketone sugar. 3. Glucose is the body’s main source of energy. Write short notes on raffinose and starchyose (state their importance and significance) Raffinose Raffinose Raffinose is a trisaccharide composed of galactose, glucose, and fructose. It can be found in beans, cabbage, brussels sprouts, broccoli, asparagus, other vegetables, and whole grains. Raffinose can be hydrolysed to D-galactose and sucrose by the enzyme α-galactosidase (αGAL), an enzyme not found in the human digestive tract. α-GAL also hydrolyses other αgalactosides such as stachyose, verbascose, and galactinol, if present. The enzyme does not cleave β-linked galactose, as in lactose. The raffinose family of oligosaccharides (RFOs) are alpha-galactosyl derivatives of sucrose, and the most common are the trisaccharide raffinose, the tetrasaccharide stachyose, and the pentasaccharide verbascose. RFOs are almost ubiquitous in the plant kingdom, being found in a large variety of seeds from many different families, and they rank second only to sucrose in abundance as soluble carbohydrates. Humans and other monogastric animals (pigs and poultry) do not possess the α-GAL enzyme to break down RFOs and these oligosaccharides pass undigested through the stomach and upper intestine. In the lower intestine, they are fermented by gas-producing bacteria that do possess the α-GAL enzyme and make carbon dioxide, methane or hydrogen—leading to the flatulence commonly associated with eating beans and other vegetables. α-GAL is present in digestive aids. Stachyose Stachyose Stachyose is a tetrasaccharide consisting of two α-D-galactose units, one α-D-glucose unit, and one β-D-fructose unit sequentially linked. Together with related oligosaccharides such as raffinose, Stachyose occurs naturally in numerous vegetables (e.g. green beans, soybeans and other beans) and other plants. Stachyose is less sweet than sucrose, at about 28% on a weight basis. It is mainly used as a bulk sweetener or for its functional oligosaccharide properties. Stachyose is not completely digestible by humans and delivers 1.5 to 2.4 kcal/g (6 to 10 kJ/g). Explain: Complementary value of protein, supplementary value of protein, limiting amino acid Complementary value of protein This is the combination of two or more incomplete protein foods such that the essential amino acids that are lacking in one of them will be supplied by the other e.g. rice and beans or maize and beans will give a complete protein. Complementary proteins do not need to be eaten together, so long as the day's meals supply them all. Supplementary value of protein This is the combination of plant and animals protein food in such manner that the animal’s protein supplies the essential amino acids lacking in the plant protein e.g. milk and cereal pap in a meal. Limiting amino acids If a diet is inadequate in any essential amino acid, protein synthesis cannot proceed beyond the rate at which that amino acid is available. This is called a limiting amino acid. Therefore a limiting amino acid is any essential amino acid which controls the rate of protein metabolism. Write notes on cholesterol plaque, hyperglycaemia Cholesterol plaque Cholesterol plaques are caused by the build-up of cholesterol deposits in the body tissues especially the arteries by low density lipoproteins(LDLs). Cholesterol plaques start developing in the walls of arteries. Long before they can be called plaques, hints of atherosclerosis can be found in the arteries. Even some adolescents have these "fatty streaks" of cholesterol in their artery walls. These streaks are early precursors of cholesterol plaques. They can't be detected by tests. But researchers have found them during autopsies of young victims of accidents and violence. Atherosclerosis develops over years. It happens through a complicated process of cholesterol plaque formation that involves: Damaged endothelium. The smooth, delicate lining of blood vessels is called the endothelium. High cholesterol, smoking, high blood pressure, or diabetes can damage the endothelium, creating a place for cholesterol to enter the artery's wall. Cholesterol invasion. "Bad" cholesterol (LDL cholesterol) circulating in the blood crosses the damaged endothelium. LDL cholesterol starts to accumulate in the wall of the artery. Plaque formation. White blood cells stream in to digest the LDL cholesterol. Over years, the toxic mess of cholesterol and cells becomes a cholesterol plaque in the wall of the artery. Hyperglycaemia Hyperglycemia, or high blood sugar (also spelled hyperglycaemia or hyperglycæmia, not to be confused with the opposite disorder, hypoglycemia) is a condition in which an excessive amount of glucose circulates in the blood plasma. This is generally a blood sugar level higher than 11.1 mmol/l (200 mg/dl), but symptoms may not start to become noticeable until even higher values such as 15–20 mmol/l (~250–300 mg/dl). A subject with a consistent range between ~5.6 and ~7 mmol/l (100–126 mg/dl) (American Diabetes Association guidelines) is considered hyperglycemic, while above 7 mmol/l (126 mg/dl) is generally held to have diabetes. Chronic levels exceeding 7 mmol/l (125 mg/dl) can produce organ damage. Signs and symptoms Temporary hyperglycemia is often benign and asymptomatic. Blood glucose levels can rise well above normal for significant periods without producing any permanent effects or symptoms. However, chronic hyperglycemia at levels more than slightly above normal can produce a very wide variety of serious complications over a period of years, including kidney damage, neurological damage, cardiovascular damage, damage to the retina or damage to feet and legs. Diabetic neuropathy may be a result of long-term hyperglycemia. In diabetes mellitus (by far the most common cause of chronic hyperglycemia), treatment aims at maintaining blood glucose at a level as close to normal as possible, in order to avoid these serious long-term complications. This is done by a combination of proper diet, regular exercise, and insulin or other medication such as metformin, etc. Acute hyperglycemia involving glucose levels that are extremely high is a medical emergency and can rapidly produce serious complications (such as fluid loss through osmotic diuresis). It is most often seen in persons who have uncontrolled insulin-dependent diabetes. The following symptoms may be associated with acute or chronic hyperglycemia, with the first three composing the classic hyperglycemic triad: Polyphagia - frequent hunger, especially pronounced hunger Polydipsia - frequent thirst, especially excessive thirst Polyuria - increased volume of urination (not an increased frequency for urination) Blurred vision Fatigue (sleepiness) Weight loss Poor wound healing (cuts, scrapes, etc.) Dry mouth Dry or itchy skin Tingling in feet or heels Erectile dysfunction Recurrent infections, external ear infections (swimmer's ear) Cardiac arrhythmia Stupor Coma Seizures Frequent hunger without other symptoms can also indicate that blood sugar levels are too low. This may occur when people who have diabetes take too much oral hypoglycemic medication or insulin for the amount of food they eat. The resulting drop in blood sugar level to below the normal range prompts a hunger response. This hunger is not usually as pronounced as in Type I diabetes, especially the juvenile onset form, but it makes the prescription of oral hypoglycemic medication difficult to manage. Polydipsia and polyuria occur when blood glucose levels rise high enough to result in excretion of excess glucose via the kidneys, which leads to the presence of glucose in the urine. This produces an osmotic diuresis. Signs and symptoms of diabetic ketoacidosis may include: Ketoacidosis Kussmaul hyperventilation: deep, rapid breathing Confusion or a decreased level of consciousness Dehydration due to glycosuria and osmotic diuresis Acute hunger and/or thirst 'Fruity' smelling breath odor Impairment of cognitive function, along with increased sadness and anxiety Explain digestion of yam Digestion is both a mechanical process (chewing) and a chemical process (enzymic actions). The class of enzymes that hydrolyze carbohydrates are broadly known as carbohydrases. Digestion can be broken down into 4 stages; 1. 2. 3. 4. Mouth Stomach Small intestine Large intestine Mouth While the digestion of all types of foods (proteins, carbohydrates, fats, etc.) begins in the mouth with the mechanical process of mastication, certain carbohydrates—namely, starches and dextrins—are the only food types whose chemical digestion begins in the mouth. Here an enzyme known as salivary amylase or ptyalin, secreted by the parotid glands, is mixed with the food during the chewing process and begins the conversion of glycogen, starch and dextrins into the disaccharide maltose. Stomach What happens when the starches, dextrin, and glycogens that were not converted to maltose in the mouth and what happens to the maltose when these carbohydrates reach the stomach depends upon several factors—what other types of foods are eaten with the starch, how much food is being eaten and how fast, the emotional condition of the eater and the condition of the eater’s digestive system. If a relatively uncomplicated starch such as potatoes or yams is eaten alone or with non-starchy vegetables, and no proteins (as meats, cheese or milk, or even nuts or seeds or acids (as tomatoes, lemon or lemon juice or vinegar—as in salads or salad dressings) are consumed with the starchy food, salivary amylase (ptyalin) can and will continue the digestion of starches and dextrins in the stomach for a long period. In the stomach, in response to other food groups such as protein, hydrochloric acid is secreted which halts the action of ptyalin. Small intestine Whatever carbohydrates make it to the intestine quickly enough to escape fermentation by bacterial action will be acted upon in the first part of the small intestine, the duodenum, by pancreatic amylase. This enzyme, secreted by the pancreas, converts any remaining dextrin and starch to maltose. The reason this amylase can act in the intestine is because of the more alkaline medium which prevails there. As stated earlier, amylase must have a somewhat alkaline medium to do its job and is destroyed by acids. At this stage in the digestive process, that is, after the polysaccharides (starch, dextrin and glycogen) have been converted to the disaccharide maltose, maltose and the other disaccharides (sucrose and lactose) must be converted to monosaccharides since, as stated earlier, the body can absorb and use sugars only as monosaccharides. This is accomplished by the amylases maltase (to convert maltose), sucrase (to convert sucrose) and lactase (to convert lactose). These amylases are secreted by the wall of the small intestine and are capable of splitting the particular sugars for which they were designed to the monosaccharide stage. Large intestine Carbohydrates that were not digested and absorbed by the small intestine reach the colon where they are partly broken down by intestinal bacteria. Fiber, which cannot be digested like other carbohydrates, is excreted with feces after being partly digested by the normal intestinal flora. Write on lactose intolerance and kwashiorkor Lactose intolerance Lactose intolerance is the inability of adults and children to digest lactose, a sugar found in milk and to a lesser extent dairy products, causing side effects. It is due to a lactase deficiency, or hypolactasia. In some (rare) cases, babies have congenital lactase deficiency, which prevents them from being able to digest even human milk. Lactose intolerant individuals have insufficient levels of lactase, an enzyme that catalyzes the hydrolysis of lactose into glucose and galactose, in their digestive system. In most cases, this causes symptoms which may include abdominal bloating and cramps, flatulence, diarrhea, nausea, borborygmi (rumbling stomach), or vomiting after consuming significant amounts of lactose. It is common for patients with inflammatory bowel disease to experience gastrointestinal symptoms after lactose ingestion, although the prevalence of lactase deficiency in this population has not been well studied. The frequency of lactose intolerance ranges from 5% in Northern European to more than 90% in some African and Asian countries. Kwashiorkor Kwashiorkor is a form of severe protein–energy malnutrition characterized by edema, irritability, anorexia, ulcerating dermatoses, and an enlarged liver with fatty infiltrates. Sufficient calorie intake, but with insufficient protein consumption, distinguishes it from marasmus. Kwashiorkor cases occur in areas of famine or poor food supply. Cases in the developed world are rare. Signs and symptoms The defining sign of kwashiorkor in a malnourished child is pitting edema (swelling of the ankles and feet). Other signs include a distended abdomen, an enlarged liver with fatty infiltrates, thinning hair, loss of teeth, skin depigmentation and dermatitis. Children with kwashiorkor often develop irritability and anorexia. Victims of kwashiorkor fail to produce antibodies following vaccination against diseases, including diphtheria and typhoid. Generally, the disease can be treated by adding protein to the diet; however, it can have a long-term impact on a child's physical and mental development, and in severe cases may lead to death. In dry climates, marasmus is the more frequent disease associated with malnutrition. Another malnutrition syndrome includes cachexia, although it is often caused by underlying illnesses.