Sec 3 Combined Science (Biology) Nutrition in Humans notes

Follow a mouthful of food. Ingestion is the entry itself — food taken into the mouth. The mouth chews it into pieces and salivary amylase starts on starch. Swallowed, the food reaches the stomach, where strong acid kills bacteria and provides the pH at which stomach protease digests protein. The small intestine is the main event: enzymes finish digestion here, and the soluble end-products — glucose, amino acids, fatty-acid fragments — are absorbed through its folded lining into the bloodstream. The large intestine reclaims water and salts from whatever is left. Finally egestion: the undigested residue (fibre, mostly) is passed out through the anus. Assimilation happens after absorption, in the body)s cells, which use the delivered glucose for respiration and amino acids for building new protein.

Digestion is enzyme work, and the exam wants four names with their inputs and outputs. Amylase cuts starch → maltose (it starts in the mouth and continues in the small intestine). Maltase, anchored in the small-intestine lining, finishes the job: maltose → glucose. Protease (pepsin in the acidic stomach, other proteases in the intestine) cuts proteins → amino acids. Lipase cuts fats → fatty acids (and glycerol), helped by bile from the liver, which emulsifies fat into tiny droplets so lipase has a huge surface to work on.

A classic trap: amylase does not make glucose directly — its product is maltose, and maltase must finish. Another: bile is not an enzyme — it emulsifies fat physically, increasing surface area for lipase, but does not digest it chemically.

The small intestine)s lining is folded and folded again, giving an enormous surface area over which glucose, amino acids and fatty-acid fragments cross into the blood — absorption. That nutrient-rich blood does not wander around the body first: the hepatic portal vein delivers it directly from the small intestine to the liver, so the liver inspects and processes everything absorbed from a meal before it reaches the rest of the body.

The liver)s processing jobs, all examinable: (1) glucose–glycogen conversion — storing excess glucose as glycogen and releasing it again when blood glucose falls; (2) fat digestion — making bile, which emulsifies fats in the small intestine; (3) amino-acid metabolism — processing amino acids and forming urea from the nitrogen-containing part, which the blood later carries away; (4) breakdown of alcohol and hormones — detoxifying substances that would otherwise circulate unchecked.

A hormone is a chemical substance produced by a gland, carried by the blood, that alters the activity of specific target organs. Four parts of the definition, four marks: made in a gland; travels in the blood; acts on specific target organs (the ones with matching receptors); and changes what those organs do. Hormones are slower than nerve messages but longer-lasting — ideal for running the body)s chemical balance over minutes and hours.

The two digestive-era hormones to know are insulin and glucagon, both made in the pancreas, both targeting the liver (among other organs). They work as an opposing pair — one lowers blood glucose, the other raises it — which is exactly what regulation needs.

Blood glucose must stay near about 5 mmol/dm³ for cells to have steady fuel. After a sugary meal the level climbs — say towards 8 mmol/dm³. The pancreas detects the rise and secretes insulin, which makes the liver (and muscles) take up glucose and store it as glycogen: the level falls back to normal. Skip a meal and the level sags; the pancreas then releases glucagon, which makes the liver convert glycogen back to glucose and release it, raising the level again. Insulin and glucagon form a negative-feedback pair — one undoes the other)s effect, so glucose stays in a narrow band.

Type 2 diabetes is a condition of persistently high blood glucose. The pancreas may still make insulin, but the body)s cells resist it — the "store this glucose" signal is ignored — or too little insulin is produced. Either way, glucose stays in the blood instead of moving into storage and cells, starving them while the blood stays overloaded.

The main risk factors: obesity, a physically inactive lifestyle, family history and increasing age. Management attacks those factors: a healthy diet low in sugar and refined carbohydrate, regular exercise, weight control — plus medication when lifestyle changes are not enough. Unlike the rarer type 1 form, type 2 is strongly linked to lifestyle, which is why prevention focuses on diet and activity.