Carbohydrates Assignment

1. Describe the chemical structure of the four biologically important polysaccharides:

amylose, amylopectin, cellulose and glycogen.

Amylose

Amylose is a linear (unbranched) polymer consisting of between100 – 400 α D-glucose

units connected by α-1,4-glycosidic bonds (Horton et al. 2006, Timberlake 2009). It, along
with amylopectin form the starch plants use for energy storage.

Figure 1: Structure of amylase (from Nelson and Cox 2004)

Amylose, due to its linear structure, is preferable for plants to use as energy storage due to
a better packing fraction. In plants, on average, 30% of the starch is in the form of amylose
(Nelson and Cox 2004).

Amylopectin

Amylopectin’s structure is different to that of amylose’s, in that its polymer chain is

branched. It is effectively a branched version of amylose. Amylopectin molecules generally
contain between 300 and 6000 glucose residues. It shares the same α-1,4-glycosidic
bonds between D-glucose units but every 25 glucose units branching chains bonded by α-
1,6-glycosidic bonds occur (Horton et al. 2006, Timberlake 2009).

Starch represents an important source of carbohydrates in the human diet and it is found
in plants like potatoes and rice. Raw starch is resistant to digestion but cooking allows it to
absorb water and swell. Once ingested it is degraded in the gastrointestinal tract by the
enzyme α-amylase which is excreted (in humans) both in the mouth (salivary amylase)
and by the pancreas (pancreatic amylase)(Crowe et al. 2006, Horton et al. 2006, Nelson
and Cox 2004)

Luke Clews Biological Chemistry 1B CIT 066213

 Figure 2: Structure of amylopectin (from Nelson and Cox 2004)

Cellulose

Cellulose is what is known as a structural polysaccharide, in that it forms the structural

components of wood and plants. It is a linear polymer of D-glucose but unlike starch bonds
the glucose residues are joined by β-1,4-glycosidic linkages. Cellulose molecules vary
greatly in size, containing between 300 and 15000 glucose units (Nelson and Cox 2004,
Timberlake 2009).

The α-amylase humans use to degrade the α-1,4-glycosidic bonds in amylose and
amylopectin cannot break the β-glucosidic linkages in cellulose, therefore it is indigestible
to humans. Ruminant animals such as sheep and cows have microorganisms in their
gastrointestinal tracts that produce β-glucosidase enzymes allowing them to derive energy
from eating cellulose. Humans do derive some benefit from eating cellulose though, with it
representing a good source of insoluble fibre (Crowe et al. 2006, Nelson and Cox 2004,
Timberlake 2009).

Figure 3: Structure of cellulose (from Nelson and Cox 2004)

Luke Clews Biological Chemistry 1B CIT 066213

 Glycogen

Glycogen is known as animal starch and is a branched glucose residue polymer. It is

similar to amylopectin in structure with α-1,4-glycosidic bonds and α-1,6-glycosidic bonds
but in glycogen the branches occur more frequently, every 8 to 12 residues. Also, the
molecules are generally larger that starch, containing up to 50000 glucose sub-units
(Horton et al. 2006).

Glycogen is the form in which glucose is stored in our body to eliminate the need for
humans to eat constantly. It is stored predominantly in the liver with supplies also being
kept in muscle tissue (Crowe et al. 2006, Timberlake 2009).

Figure 4: Structure of glycogen (from Crowe et al. 2006)

2. How does the structure of carbohydrates affect their digestion and absorption?

The key enzyme to digestion of carbohydrates by humans is amylase (both in its α and β
forms). This enzyme is responsible for the cleaving of α-1,4-glycosidic bonds in amylose
and amylopectin. This process converts starch into a mix of di- and trisaccharides which
are then converted by other enzymes into glucose. However, amylase is unable to cleave
α-1,6-glycosidic bonds or α-1,4-glycosidic bonds adjacent to them (Horton et al. 2006,
Nelson and Cox 2004, Timberlake 2009).

The procedure for digestion of starch is as follows: salivary amylase, mechanical

breakdown (chewing) and moisturisation with saliva begin the process of digesting
starches in the mouth breaking them into dextrins (short chain polysaccharides) and
maltose. This process continues in the stomach until the acidic environment renders the
enzyme inactive. Once the material moves to the duodenum it is acted upon by pancreatic
amylase which converts amylose to maltose and maltotriose (a trisaccharide) and
amylopectin to glucose and maltose as well as isomaltose. This last by-product is created

Luke Clews Biological Chemistry 1B CIT 066213

 as a direct result of amylase being unable to cleave the 1,6-glycosidic bonds of
amylopectin. The final stage of digestion is completed at the brush border of the small
intestine by the enzymes maltase and isomaltase (also known as α-dextrinase which
cleaves the remaining 1,6-glycosidic bonds of isomaltose)(Crowe et al. 2006, Gropper et
al. 2009).

The structure of starches is such that even after amylase has acted upon them further
enzymatic work is required to yield a bio-available form of glucose, however the end result
is that most, if not all, of the starch is broken down to a useful form of carbohydrate
(Nelson and Cox 2004).

Glycogen catabolism is much more straightforward; to affect the release of glucose

residue from the storage polymer an enzyme known as glycogen phophorylase
phophorylises a glucose residue attached to the glycogen molecule. The resulting
molecules from this reaction are a α-D-glucose 1-phosphate molecule and a glycogen
molecule less 1 residue. This reaction is only possible for monomers attached with α-1,4-
glycosidic bonds. At the branching points of glycogen (created by α-1,6-glycosidic bonds)
this reaction will not work so another enzyme (glucogen-debranching enzyme) is used to
break the branch into catalysable components (Gropper et al. 2009).

As previously stated, cellulose monomeric units are bound with β-glucosidic linkages, for
which humans do not possess an applicable enzyme to affect catabolism, hence its
indigestible nature.

As can be seen, the chemical structure of the carbohydrates described above dictates the
body’s ability to digest them and how much energy the digestion will require.

3. Describe the condition known as “hypoglycaemia” and explain why it occurs.

Hypoglycaemia is a condition whereby a person’s blood glucose level falls below its
normal range. The name itself literally means “under sweet blood” from the Greek (Dorland
2007). It can be caused by a wide range of endogenous and exogenous factors. Among
these are complications with diabetes mellitus treatment, excessive insulin production,
medications, alcohol, starvation and metabolic disruptions caused by injury or illness
(Cryer 1997).

Symptoms of hypoglycemia can be broken down into 3 categories: adrenergic (adrenaline

is a counterregulatory hormone released in response to low blood glucose levels),
glucagonic (another hormone released in response to hypoglycaemia designed to trigger

Luke Clews Biological Chemistry 1B CIT 066213

 glycogenolysis) and neuroglycopenic (triggered when blood sugar levels drop in the brain)
(Cryer 1997, Gropper et al. 2009). Adrenergic symptoms include shaking, sweating and
tachycardia while glucagonic symptoms range from hunger and borborygmus to nausea
and headache. Neuroglycopenic symptoms are the most dangerous and include impaired
cognition, aggressiveness, amnesia and blurred or double vision through to ataxia,
paralysis, coma and death (Cryer 1997, Cryer 2003).

A common syndrome mistaken for hypoglycaemia is known as postprandial syndrome.

Typically, the patient is a woman of 20–50 years whose weight falls in the normal range.
The patient usually presents with symptoms of a vague feelings of distress occurring
predominantly midmorning, about 11am to 12pm, but occasionally mid afternoon or
evening. These episodes are characterised by feeling of faintness, anxiety, nervousness,
irritability, tachycardia, headache, and sweatiness, either alone or in combination. Usually
they describe themselves as suffering from increased tiredness, lacking in zest for life, and
apathy. Blood glucose tests rarely show actual low blood glucose levels and the disease
usually psychogenic in nature (Caballero et al. 2006, Charles et al. 1981).

4. What types of carbohydrates would you include in a diet to prevent hypoglycaemia?

The concept of glycaemic index (GI) can help in deciding which foods are appropriate for
maintaining adequate blood sugar levels. The GI of a food gives an indication of how
greatly it will affect blood glucose levels after being ingested; the lower the GI, the lower
perturbation of levels. With regard to the carbohydrates mentioned above, the most
desirable would be starches with a higher proportion of amylase because it has a better
packing fraction i.e. higher molecular density, leading to a more prolonged period of
digestion and less marked shifts in blood glucose levels (Cryer 1997, DeBruyne et al.
2007, Gropper et al. 2009).

In general, to avoid large swings in blood sugar levels the carbohydrates necessary are of
the complex variety. Examples include soy, linseed and whole wheat grains. Simple
carbohydrates such a white bread, lollies, sugary drinks and some fruits are considered
high-GI and therefore inappropriate for persons who are hypoglycaemic (Cryer 1997). Also
inappropriate is consumption of excessive amounts of alcohol as it can produce
pronounced spikes in blood sugar (DeBruyne et al. 2007).

Luke Clews Biological Chemistry 1B CIT 066213

Bibliography

Caballero, B, Allen, L & Prentice, A (eds.) 2006, Encyclopedia of Human Nutrition, Elsevier,
Charles, M et al. 1981, Comparison of oral glucose tolerance tests and mixed meals in patients with
apparent idiopathic postabsorptive hypoglycemia: absence of hypoglycemia after meals, Diabetes,
Vol.30, no.6, pp. 465-70.
Crowe, J, Bradshaw, T & Monk, P 2006, Chemistry for the biosciences, 1st edn., Oxford University Press,
Oxford.
Cryer, P 1997, Hypoglycemia: pathophysiology, diagnosis and treatment, 1st edn., Oxford University Press,
Oxford.
Cryer, P 2003, Glucose homeostasis and hypoglycemia, In: LARSEN, P. (ed.) Williams textbook of
endocrinology. 10th edn., W.B. Saunders, Philadelphia.
Debruyne, L, Pinna, K & Whitney, E 2007, Nutrition and diet therapy, 7th edn., Cengage Learning, Toronto.
Dorland, W 2007, Dorland's illustrated medical dictionary, 31st edn., Saunders, New York.
Gropper, S, Smith, J & Groff, J 2009, Advanced nutrition and human metabolism, 5th edn., Cengage
Learning, Toronto.
Horton, H et al. 2006, Principles of biochemistry, 4th edn., Pearson Education, London.
Nelson, D & Cox, M 2004, Lehninger Principles of biochemistry, 4th edn., WH Freeman & Co., St Louis.
Timberlake, K 2009, Chemistry: An introduction to general, organic and biological chemistry, 10th edn.,
Pearson Education, London.

Luke Clews Biological Chemistry 1B CIT 066213