• Ingestion (eetin’ an’ swallowin’ it)
• Peristalsis (movin’ it along)
• Digestion (smashin’ it up)
• Absorption (mekin’ it part of you)
• Egestion (defaecation or “shitting”)

The wall of the alimentary canal consists of:

• a lumen through which the food travels
• a mucosa, consisting of epithelium, connective tissue and muscles in the ileum which cause the movement of microvilli
• a submucosa
• circular muscle which contracts behind, and relaxes in front of the bolus. This widens in places to form sphincter muscles, like the cardiac and pyloric sphincter, which keep the food in the stomach for as long as is needed and enables the irregular feeding of carnivores. The anal sphincter keeps faeces in your body until a suitable time; otherwise life could be quite awkward!
• longitudinal muscle which relaxes behind, and contracts in front of the bolus.
• a serosa on the outside which protects the gut from friction. The epithelium surrounding it is called the mesentery and joins the various organs of the gut together.

The buccal cavity (gob) has a tongue (no…!), which rolls food into a bolus so that it passes easily down the oesophagus.
The stomach has cardiac and pyloric sphincters which keep food in and regulate it’s flow into the small intestine in small squirts. It is surrounded by muscle which helps to churn and mix the contents.
The small intestine (duodenum, jujenum, ileum) is long thin and folded, and therefore it has a large area over which to digest food. It has villi and microvilli, which further increase the available surface area. Its cells produce mucous, which lubricates the passage of food and reduce damage and friction.
The large intestine (colon) has the job of re-absorbing all the fluids secreted and ingested into the alimentary canal, and compacting the undigested remains for storing in the rectum. It is fairly wide. Bacteria exist here which use some of the undigested remains (fibre) and synthesise vitamins such as K, B₁₂ and riboflavin.

Digestion of protein, starch and lipids (walk-through) and control of secretions

Physical digestion begins in the mouth with mastication. This process breaks the food up and increases the surface area for enzymes to work on. Saliva from the salivary gland contains amylase, which begins the digestion of starch to maltose. Stimulation of salivary glands is by the nervous system in response to real or imagined food. Saliva also lubricates the movement of the food, which is then rolled into a bolus by the tongue and travels down the oesophagus to the stomach. Here it is mixed with gastric juice (pH 2), which is produced in gastric pits/glands in the stomach epithelium. Gastric juice is released in response to the presence of food in the buccal cavity. As the stimulation by the nervous system wears off, the presence of food stimulates cells in the stomach lining to produce gastrin. This passes into the bloodstream and stimulates the release of gastric juice for several hours. These consist of:
 

• Chief cells, which secrete pepsinogen, which is converted to its active enzyme by hydrochloric acid and pepsin itself. Producing the inactive form first prevents it from digesting the cell cytoplasm contents.
• Oxyntic cells, which produce hydrochloric acid. This converts pepsinogen to its active form as mentioned above, provides optimum pH for pepsin to work in, and kills most bacteria. The stomach epithelium is protected from ulceration by a thick layer of mucous produced by goblet cells.

Gastric juice therefore contains pepsin and pepsinogen, as well as HCl, and chemical digestion begins. Both pepsin and HCl catalyse hydrolysis. Pepsin is an endopeptidase: it is an enzyme which catalyses the hydrolysis of proteins to polypeptides. It does this by hydrolysing the inside of the protein molecule, thus increasing the number of ends for the exopeptidases to work on. The pyloric sphincter opens when the chyme (the mixture of food and gastric juice) is of the correct consistency, and releases the food into the small intestine. Lipid stimulates the production of entergasterone by the stomach mucosa, which has an antagonistic effect on gastrin. Therefore, the more fat the food contains, the longer it remains in the stomach. The first section of this is the duodenum, which runs nearly horizontally across your body below your stomach. When chyme enters the duodenum, its lining releases a number of hormones. One of these is secretin, which stimulates the production of the sodium hydrogencarbonate portion of the pancreatic juice. Cholecystokinin-pancreozymin (CCK-PZ) stimulates the gall bladder to contract, and the release of digestive enzymes from the pancreas. At the beginning of this, ducts running from the gall bladder (bile duct) and the pancreas (pancreatic duct) form the common duct and secrete bile and pancreatic juice into the duodenum. Pancreatic juice

• Is rich in sodium hydrogencarbonate, which neutralises the acidic chyme from the stomach, raising the pH to about 7.
• Is also rich in enzymes. They are summarised in the table below. The bits in bold must be learnt.

Bile

• Is stored in the gall bladder
• Contains no active enzymes
• Contains bile salts which emulsify fats, increasing the surface area for the action of lipase  

The duodenum contains deep folds between its villi, which have Brunner’s glands below them. The latter secrete a viscous fluid containing water, hydrogencarbonate ions and mucoprotein, and serves to protect the wall of the duodenum from the pepsin and chyme. Both extracellular digestion and intracellular digestion occur in the small intestine. The cells of the epithelium contain enzymes in their cytoplasm and embedded within their cell surface membrane. Digestion therefore occurs outside, on the way into, and inside the cytoplasm of, these cells. Resulting from the digestion in the lumen of the small intestine, carbohydrates have been hydrolysed to disaccharides and proteins to dipeptides and tripeptides. Their further digestion takes place in the cell surface membrane of the microvilli of the intestinal mucosa. Disaccharidases break disaccharides down into their constituent monosaccharides. Most of these are released back into the lumen of the gut. A similar process occurs with dipeptides and tripeptides, which are taken up by the microvilli and broken down into their respective amino acids. Some also diffuse into the cytoplasm of the cells of the villi, where they are digested.

The experiment was set up to be as fair as possible. Then the potato chips were cut into 15 cylinders using a cork cutter and then cut to a length of exactly 4cm each with a scalpel. Then three were weighed at one time on a top pan balance to find an average mass, this was done because it did not involve confusion over which potato cylinder was which after the experiment. Once these averages were found and recorded the potato chips were placed into their test tube solutions of 0.0M(distilled water), 0.25M, 0.5M, 0.75M and 1.0M solutions of sucrose. Then the contents, each containing three potato cylinders were left for 50minutes. When the time was over I removed the potato with a pair tweezers and placed them on a paper towel to try and dry of any excess water. Then I weighed the potato again together in their threes on a top pan balance and found the average mass.
 

Prediction
 

 I believe from my past knowledge of a similar experiment involving raw eggs that the potato cylinders placed in the distilled water will be hyperosmotic, therefore the water will diffuse by osmosis into the potato from an area of high concentration down the concentration gradient. This will result in a gain of mass for the potato.
 

    However in the 1.0M solution I think that the opposite will occur as there will be a higher concentration of water within the potato than the solution, containing lots of solute, this will make the potato hpo-osmotic and it will lose its water content as the water diffuses out.Finally, a difference between the egg experiment and the potatoes that the cells will not reach equilibrium (become iso-osmotic). This is because plants have a cellulose cell wall which cannot expand beyond a certain point as it is turgid, therefore the contents will never be able to be equal to the outside or it will not be able to give out all its water as it has a rigid structure. It is the pressure created by the cell wall which stops the cell reaching equilibrium. I think that the contents of the cell will be about 0.3M concentration as it will be in between 0.25M and 0.5MThe experiment has yielded a graph, (see attached) this graph gives me an excellent set of data. The graph shows that in the distilled water the potato gains in mass by approximently 7.4% then it gains 4.4% in the 0.25M solution. In the 0.5 M solution there is a change, the gradient of the graph decreases steeply and the potato loses mass to 4.4% then in the 0.75M solution the gradient decreases as it loses yet more mass to 10.4%.
 

 The first observation I made was after the potato cylinders were placed in their solutions I could see a difference. The ones in the 0.0M and 0.25M solutions were floating and the potatoes in the 0.5M, 0.75M and 1.0M solutions were at the bottom of the test tube, this lead me to drawing my next conclusion.
 

 The graph shows that the potato in the 0.0M solution and in the 0.25M is hyperosmotic, as I said in my prediction, this means that there is a higher water potential in the distilled water and 0.25M solution than in the potato, which has a high concentration of solutes. Therefore this is why the water diffuses by osmosis down the concentration gradient from high concentration to low concentration, resulting in the potato gaining mass.
 

 The opposite occurs in the solutions where the molarity is higher 0.5M, 0.75M and 1.0M, the potato in these is hypo-osmotic because there is a higher concentration of water inside the potato than in the solutions, therefore the water diffused out of the potatoes by osmosis, down the concentration gradient and into the solutions outside, this resulted in the loss of mass.
 

 Another important fact is that the graph makes a shape that will result in the potato not being able to take in any more water or lose any more. Like I said in my prediction the cell wall causes the pressure that prevents this from happening, therefore the cell will never become iso-osmotic like an egg.
 

 On my graph I have marked the point where the graph line crosses the place on the axis where the potato neither loses mass nor gains mass. This happens at 0.36M, therefore the contents of the potato cells in molar strength is 0.36M.
 

 This result is very close to my prediction of 0.3M and it shows that the contents of the cell are between 0.25M and 0.5M which is why in these concentrations they gained mass and lost mass.
 

  I think that the experiment went very well, there were no odd results and they produced a good graph. However there were a few areas where there could be improvement. Firstly, when I dried off the excess water on the potato cylinders after the experiment and before I weighed them, I used a paper towel. This might have either taken some water out of the potato or it might of left some excess water on the potato. This part of the experiment is difficult to     come up with an accurate and fair method, as other ways would also lead to some slight mistakes.
 

     Also the potato itself was not definitely from the same potato and was not exactly the same size, although I did try to cut them to 4cm each, this could have effected the amount of water gained or lost.
 

     Another way of improving the results would have been to leave the experiment running longer, this would have enabled me to find the saturation point (when the potato can no longer take in any more water) and dehydration point (when the potato cannot lose any more water) and therefore get a more accurate result.
 

     Finally, I could extend the experiment to a more exact level by looking at the potato cylinders under a microscope, then I would be able to see the cells in greater detail and draw some more observational results.