Download Differentiate between glucose and fructose

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.

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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:
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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
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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:
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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.