Diabetes Mellitus Quiz

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Which mechanism best explains the development of hyperglycaemia in type 2 diabetes mellitus?

A Defective insulin receptors due to a congenital mutation present from birth
B Acute pancreatic inflammation causing sudden loss of insulin production
C Excess glucagon secretion from pancreatic alpha cells as the primary abnormality
D Progressive insulin resistance with a gradual decline in pancreatic beta-cell insulin secretion ✓
E Autoimmune destruction of pancreatic beta-cells leading to absolute insulin deficiency

The answer is D: Progressive insulin resistance with a gradual decline in pancreatic beta-cell insulin secretion

Explanation

Why D is correct

See Type 2 Diabetes Mellitus. Option D is correct because type 2 diabetes begins with insulin resistance: liver, muscle and fat respond poorly to insulin, so the liver keeps producing glucose when it should stop and muscle takes up too little glucose. Insulin resistance is strongly linked to obesity. At first the pancreas compensates by making more insulin (hyperinsulinaemia, meaning a high blood insulin level), so glucose stays normal. Over time beta-cell function declines, because the cells are overworked and high glucose itself impairs them, and insulin secretion can no longer overcome the resistance. Glucose then rises into the diabetic range. At diagnosis only about half of the beta cells may still be working, and function keeps falling afterwards, which explains the gradual onset and why treatment usually has to be stepped up over the years. Metformin works mainly by reducing insulin resistance, while sulfonylureas stimulate the beta cells to release more insulin.

Starting point: insulin resistance in liver, muscle and fat, strongly linked to obesity.
Early compensation: the pancreas makes more insulin, so glucose stays normal at first.
Later: beta-cell function declines, insulin secretion cannot overcome the resistance and glucose rises into the diabetic range.

Why the other options are incorrect

A. Defective insulin receptors due to a congenital mutation present from birth: Type 2 diabetes is an acquired condition linked to obesity and insulin resistance, not a receptor fault present from birth. Rare inherited receptor defects exist but do not explain the common disease. A congenital cause would show from infancy.
B. Acute pancreatic inflammation causing sudden loss of insulin production: Acute pancreatic inflammation can damage insulin-making tissue and cause diabetes, but it produces sudden loss of insulin after an acute illness. Type 2 diabetes develops gradually over years. This option describes a different, secondary cause.
C. Excess glucagon secretion from pancreatic alpha cells as the primary abnormality: Glucagon raises blood glucose and can contribute to hyperglycaemia, but excess glucagon is not the primary abnormality in type 2 diabetes. The primary problem is insulin resistance followed by declining beta-cell function.
E. Autoimmune destruction of pancreatic beta-cells leading to absolute insulin deficiency: Autoimmune destruction of beta cells with absolute insulin deficiency defines type 1 diabetes. In type 2 diabetes insulin is initially raised, not absent. It would be the answer in a lean young person who becomes unwell over weeks.

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1
Which of the following best describes metabolic syndrome?
2
A 42-year-old woman attends her GP for a routine health check. She feels well and has no symptoms of hyperglycaemia. A random venous plasma glucose sample returns at 12.0 mmol/L. What is the most appropriate next step to confirm or refute a diagnosis of diabetes mellitus?

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