Nutrition (9 page)

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Authors: Sarah Brewer

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BOOK: Nutrition
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Briefly, it combines acetyl-coenzyme A with another substance, oxaloacetate, to make citric acid. Citric acid then goes through a series of eight chemical reactions which convert it back into oxaloacetate, to complete one turn of the cycle (see
Diagram 4
).
During the citric acid cycle (in a similar process to glycolysis), hydrogen ions are released and passed to special carriers, NAD+ and FAD+ (flavine adenine dinucleotide, derived from vitamin B2) to form NADH and FADH
2
. These carriers take the hydrogen to the next metabolic pathway, the electron transport chain, which also takes place within the mitochondria.
THE CITRIC ACID CYCLE AS A SOURCE OF BUILDING BLOCKS
As well as being involved in energy production, the chemicals involved in the citric acid cycle can leave, when needed, to act as building blocks for the production of fatty acids, sterols, amino acids, haem (needed to make the red blood pigment haemoglobin), purines and pyrimidines (needed to make genetic material) and glucose. The citric acid cycle is therefore known as an amphibolic pathway, as it can be used both to break down body chemicals (catabolism) and to build them up (anabolism).
The electron transport chain
The electron transport chain acts rather like a turbo-charged, fuel-injection system, using the energy within the NADH and FADH
2
molecules to drive the production of ATP from ADP. Three molecules of ATP are formed from the processing of each molecule of NADH, and two from each molecule of FADH
2
. The freed hydrogen is ultimately combined with oxygen to produce water.
The latest research suggests that the breakdown of 1 molecule of glucose ultimately yields 31 molecules of ATP via these three routes: glycolysis, the citric acid cycle and the electron transport chain (previously the value was thought to be 38).
That, in a nutshell, explains what happens when your cells ‘burn’ glucose to produce energy plus waste carbon dioxide gas and water. A more complete version of our earlier simplified equation for cell respiration is therefore:
Glucose + oxygen
carbon dioxide + water + 31 ATP (energy)
C
6
H
12
O
6
+ 6 O
2
6 CO
2
+ 6 H
2
O + 31 ATP (energy)
Producing energy from dietary proteins
Dietary proteins (and, during starvation, the body’s own muscle proteins) are also used to provide energy. When you are well fed, dietary proteins may first be converted to glycogen or to triglycerides for fuel storage.
To release energy from amino acids, they are first stripped of their ‘amino’ groups and converted into substances known as alpha-keto acids. Some of these amino groups are used to produce new amino acids (e.g. glutamine), or genetic material (nucleotides) but most are sent to the liver and made into urea, which is then excreted via the kidneys.
The alpha-keto acid part of each amino acid then enters a specific chemical pathway (one for each of the different amino acids) to form an end product (pyruvate, acetyl-coenzyme A, succinate, oxaloacetate or fumarate) that can feed into the citric acid cycle.
Once entered into the citric acid cycle, they are either oxidized to carbon dioxide and water, or used as building blocks to make glucose.
Some amino acids are used to make other products such as ketones, purines and creatine phosphate – a substance well known to athletes, who take creatine supplements to boost muscle strength, especially during weightlifting.
Producing energy from dietary fats
Because the body can only store a small amount of carbohydrate as glycogen for immediate emergency use, glucose is treated as a premium fuel that must be reserved for use by the brain (that’s why muscle and fat cells are only ‘allowed’ to take it up if the hormone insulin is present). So, when possible, your muscle cells use fats as their preferred energy source. Fats are also burned in your liver cells to produce energy – in fact, most of your cells, except brain and mature red blood cells can use fats as an energy source.
Most dietary fats, and your own body-fat stores, are in the form of triglycerides. These have a glycerol backbone to which three fatty acids are attached (to resemble a capital E).
When your glucose levels are low and cells need energy, your pancreas stops making the fat-storage hormone insulin, and instead makes the fat-burning hormone glucagon. As well as telling the liver to start releasing glucose from its glycogen stores, glucagon switches off fat storage and switches on the mobilization of free fatty acids from body fat. It does this indirectly by activating an enzyme known as hormone-sensitive lipase, which breaks down triglycerides into their building blocks of glycerol and free fatty-acid chains. During exercise, and in times of stress, another hormone, adrenaline (epinephrine) made in your adrenal glands also activates hormone-sensitive lipase to release additional fats for energy.
The glycerol released from triglycerides is taken to your liver, where it enters the glycolysis pathway and is broken down to yield a small amount of energy (only 5 per cent of the total energy contained within the triglyceride molecule). The main energy contribution comes from the released free fatty acids. These are transported in your circulation by a blood protein (albumen) and taken to tissues needing energy, such as your skeletal and heart muscle cells. Once escorted inside these cells, the fatty acids are taken into the mitochondria by a transport system called the carnitine shuttle (so called because carnitine is the molecule used to escort the fatty acids inside).
Once within the mitochondria, fatty acids don’t feed directly into the citric acid cycle. First, they are processed in a separate series of reactions known as beta-oxidation. During this chain of reactions, molecules of acetyl-coenzyme A are sequentially pinched off the end of the fatty acids. As acetyl-coenzyme A contains only two carbon atoms, a fatty acid such as palmitate, for example, which has a chain of 16 carbon atoms, will yield 8 molecules of acetyl-coenzyme A. Slightly different processes are needed to derive acetyl-coenzyme A from unsaturated fatty acids and from those with an uneven number of carbon atoms, but the end result is the same.
The released acetyl-coenzyme A molecules feed directly into the citric acid cycle (see
Diagram 4
). Additional NADH and FADH
2
are also generated during beta-oxidation. In this way, a molecule of a fatty acid, such as palmitate, yields as much as 104 packets of energy (ATP) compared with the 31 molecules of ATP formed from burning 1 molecule of glucose. As one triglyceride contains three fatty-acid chains plus glycerol, you can see why fat is such an energy-rich storage molecule.
However, there is a down side. Fatty-acid oxidation only delivers this energy at half the rate at which glycogen breakdown supplies energy. So once an athlete uses up his or her glycogen stores during an initial burst of energy, they ‘hit the wall’ when muscle (and liver) glycogen stores run out. A long-distance runner, for example, is then forced to slow down dramatically once they start burning fat for fuel rather than glucose.
Producing new glucose
The average person has 70 g of carbohydrate stored as glycogen in their liver, and 200 g stored as glycogen in their muscle cells for emergency use. When needed, this glycogen is quickly processed to release glucose. This liver glycogen is enough to see you through the night during your overnight fast so that your brain receives the glucose it needs. During longer periods of not eating, however, you need to raid your protein stores to make energy and glucose instead. Why? Because, as discussed below, you cannot make glucose from your most abundant fuel reserves – the fatty acids within your triglyceride fat stores.
The production of new glucose from non-carbohydrate building blocks such as amino acids (especially alanine), lactate and glycerol (the backbone of triglyceride fats) is known as gluconeogenesis. This process ensures that blood glucose levels remain topped up even when dietary intakes of carbohydrate are low, and your stores of starchy glycogen (in liver and muscle cells) are depleted. Gluconeogenesis mainly occurs in liver cells, but in prolonged starvation it also occurs in the kidney.
The production of glucose is not simply the reverse of the metabolic reactions that broke down glucose to pyruvate (glycolysis), however. Pyruvate must first be converted into oxaloacetate within the mitochondria before following its pathway up to glucose (see
Diagram 5
). This is important, as it stops you wasting valuable energy in ‘futile cycling’ where glucose is simultaneously broken down by glycolysis and then remade by gluconeogenesis in the same cell. This mechanism ensures that one or the other pathway takes priority depending on the cells’ needs, and is mainly regulated by the amount of glucagon hormone present.
The conversion of milk and meat proteins to glucose is quite efficient, and your body can make as much as 50 g of glucose from 100 g of these proteins. The liver can also make approximately 10 g of glucose from the glycerol present within 100 g of triglyceride fat. Unfortunately, as mentioned above, it cannot make any net glucose gains from most fatty acids. This is because every time a two-carbon acetyl-coenzyme A splits off from a fatty acid and feeds into the citric acid cycle, two molecules of carbon dioxide are generated as it works its way round the cycle. As a result, there are no spare carbon atoms remaining to act as building blocks for new glucose.

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