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Almost exactly two centuries before Tutankhamun died in 1352BC, Hesy-Ra, an Egyptian physician, had described diabetes and had understood its symptoms, if not the pathology that caused them. About one in 20 of the UK population, but a much higher percentage of older, plumper people, have diabetes. But a third of those with the condition, presumably including many attending the current Tutankhamun exhibition at the O2, London, won’t know that they have it.

This is a sad reflection on medicine, when it is remembered that some of its symptoms and the problems they can cause were known to the goldsmiths, silversmiths and craftsmen who, more than 3,000 years ago, created the works of art on show at the O2. In Britain at that time, we were only just reaching the Iron Age and busy with developing a better axe with which to hit our neighbours.

It was nearly 2,000 years after Hesy-Ra that Arataeus, a Greek physician, described diabetes as the disease that made someone pass water so ceaselessly that to him it seemed that the ever-thirsty patient’s flesh was becoming liquefied and expelled with copious quantities of urine. Throughout the Middle Ages it had been recognised that the urine of diabetic patients was loaded with sugar.

However, the modern history of diabetes only really began with Paul Langerhans’s discovery that the pancreas has two different types of cell, only one of which is concerned with digestion. Twenty years later it was demonstrated that the cells without a digestive role, now named the islets of Langerhans or beta pancreatic cells, affects glucose metabolism. A shortage of these cells, a total absence of them or a resistance in the body to insulin, the hormone that they secrete, leads to diabetes.

Insulin affects every cell and tissue in the human body, hence the widespread damage that occurs in a variety of organs in patients suffering from diabetes. Insulin controls metabolism of glucose. It stimulates the uptake of glucose by muscles to provide energy, and by fatty tissue for conversion to fatty acid and trigylcerides for storage. Insulin also controls the utilisation of glucose in the body’s cells and its level in the blood.

Muscle wasting, unaccountable tiredness, loss of weight, thirst, frequency of urination, cataracts, retinal damage, blurred vision, dry skin, loss of peripheral skin sensitivity (especially in the feet and fingers) and a liability to itchy skin infections (especially in the damp and clammy, often hidden areas of the body, such as the skin creases, groin, belly button and the feet) are often early warning signs of diabetes.

There are two types of diabetes. Type 1 usually affects people before the age of 30. It is apparently of acute onset, although the exposure to precipitating factors, whether environmental or infective, may have been several weeks before.

A patient with type 1 diabetes notices that they are having to pass large quantities of urine and are drinking more to make up for this. They might also have become dehydrated, cripplingly tired, have lost weight, have blurred vision and will eventually develop mental changes, including confusion and finally coma. Type 1 diabetes is caused by failure of the beta cells of the pancreas as the result of an autoimmune response to a trigger experienced by a vulnerable patient.

Type 2 diabetes is the type that used to be called non-insulin-dependent late-onset diabetes. This description is now largely abandoned, because some cases of type 2 diabetes need insulin and as young people, even children, become fatter and more slothful, it is increasingly affecting young adults, including adolescents, especially if there is a family history of it.

Diabetes is responsible for early death from strokes, coronary arterial disease, peripheral arterial disease and kidney failure in many people because of damage to arteries caused by furring up with atheroma.

Raised cholesterol levels are frequently associated with diabetes. Diabetic men are twice as likely to have coronary arterial disease and strokes and four times more likely to have peripheral vascular disease. Women fare even worse. They are three times more likely to have coronary heart disease and six times more likely to have peripheral vascular disease. A sixth of men and a quarter of women already have heart disease when diabetes is diagnosed.

The early deaths from strokes, heart attacks and kidney failure obscures the damage done to the eyes in diabetes, the most common complication in people who have had diabetes for more than 20 years. It is also the most frequent cause of blindness in people under 65.

Sufferers have recently been given hope by the evidence of the efficacy of Fenofibrate in the protection of diabetic eyes. Fenofibrate modifies levels of blood fats, and thereby reduces the risk of damage to the retinal arteries.

A recent trial showed that Fenofibrate reduces the risk of blindness and/or deteriorating vision in patients with type 2 diabetes, reduces their need for laser treatment and slows progress of any loss of vision. The advantages of Fenofibrate were apparent after only eight months’ treatment and increased during the five years of the trial.