Diabetes Mellitus

Diabetes mellitus is the commonest endocrine disorder in the world, affecting around 10% of UK adults in some form. It is a condition in which blood glucose becomes chronically elevated because insulin is either absent, deficient or ineffective. Understanding diabetes provides an excellent test of whether you have mastered the blood glucose control mechanisms covered in the previous lesson. OCR A-Level Biology A specification 5.1.4(j)–(k) requires you to distinguish type 1 from type 2 diabetes, know their causes, symptoms and treatments, and understand how recombinant insulin is produced.

Key Definitions:

• Diabetes mellitus — a chronic condition characterised by hyperglycaemia due to insulin deficiency or insulin resistance.
• Type 1 diabetes — autoimmune destruction of β cells; no insulin produced.
• Type 2 diabetes — insulin resistance in target tissues, often with reduced insulin secretion.
• Hyperglycaemia — abnormally high blood glucose (>7 mmol dm⁻³ fasting or >11 mmol dm⁻³ random).
• Glycosuria — glucose in the urine; a classic sign of diabetes.

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Two Diseases with the Same Name

"Diabetes mellitus" is really an umbrella term for several conditions that all result in high blood glucose. Two are important for OCR:

Feature	Type 1	Type 2
Age of onset	Usually childhood/adolescence (but can be adult)	Usually middle age or later
Cause	Autoimmune destruction of β cells	Insulin resistance ± β cell dysfunction
Insulin production	None	Initially normal or high; later declines
Body weight	Often normal or thin	Often overweight or obese
Onset	Rapid (weeks)	Gradual (years)
% of cases	~10%	~90%
Main treatment	Insulin injections	Diet, exercise, oral medication; insulin in late stages
Ketoacidosis risk	High (classic acute presentation)	Low

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Type 1 Diabetes

Type 1 diabetes is an autoimmune disease. For reasons that are incompletely understood, the body's own immune system — T cells, especially — attacks and destroys the β cells of the pancreas, leaving the islets with α cells and δ cells but no insulin-producing cells. The loss is irreversible.

Causes

• Genetic predisposition — certain HLA (human leukocyte antigen) types increase risk.
• Environmental triggers — possibly viral infections (Coxsackie B, mumps, rubella); early cow's milk exposure has been investigated. The exact trigger is debated.
• Not caused by diet or obesity.

Symptoms

The classic "polys" develop rapidly as glucose rises:

• Polyuria — passing large volumes of urine. Glucose in the filtrate exceeds the tubular maximum for reabsorption, so it remains in the filtrate, raising its solute concentration and reducing water reabsorption by osmosis.
• Polydipsia — excessive thirst, caused by the dehydration that follows polyuria.
• Polyphagia — increased hunger, as cells are unable to take up glucose.
• Weight loss — because fat and muscle are broken down for energy as an alternative.
• Fatigue — poor glucose use.
• Ketoacidosis — without insulin, fatty acids are broken down into acidic ketone bodies, lowering blood pH. Untreated, this is fatal within days.

Treatment

Type 1 diabetes is managed with:

• Insulin injections or insulin pumps — several times a day, matched to meals and activity. Modern regimens use rapid-acting insulin analogues with meals and a long-acting basal insulin.
• Blood glucose monitoring — traditionally with finger-prick meters; increasingly with continuous glucose monitors.
• Carbohydrate counting — matching insulin doses to food intake.
• Islet cell or pancreas transplantation — for selected patients.

There is no cure, but tight control of blood glucose greatly reduces long-term complications.

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Type 2 Diabetes

Type 2 diabetes is a different disease altogether. Here, the β cells still produce insulin (at least initially) but the target tissues — liver, muscle and fat — fail to respond adequately. This is called insulin resistance. Over time, the β cells exhaust themselves trying to overcome the resistance by producing more insulin, and eventually insulin secretion falls below what the body needs.

Causes

• Obesity — especially visceral (abdominal) fat, which releases adipokines that impair insulin signalling.
• Physical inactivity — sedentary lifestyles promote insulin resistance.
• Diet — high in refined carbohydrates and sugars.
• Age — risk rises steeply after 45.
• Genetic predisposition — some populations (e.g. South Asian) are at greater risk for any given BMI.
• Pregnancy — gestational diabetes in pregnancy is often a precursor.

Symptoms

Symptoms are often milder and develop more slowly. They include:

• Polyuria, polydipsia — similar mechanism to type 1.
• Fatigue.
• Blurred vision.
• Frequent infections (e.g. thrush) because glucose in tissues promotes fungal growth.
• Slow wound healing.
• Numbness in hands and feet (neuropathy, from chronic nerve damage).