Question
What is the role of insulin in the body? What happens when insulin production or action is insufficient? Distinguish between Type 1 and Type 2 diabetes mellitus.
Solution — Step by Step
Insulin is a peptide hormone produced by the β cells of the islets of Langerhans in the pancreas. It is secreted in response to rising blood glucose levels (after a meal).
Key actions of insulin:
- Stimulates uptake of glucose from blood into cells (especially muscle and fat cells) via glucose transporter proteins (GLUT4)
- Stimulates glycogenesis (conversion of glucose to glycogen) in liver and muscle
- Inhibits gluconeogenesis (production of new glucose) in the liver
- Promotes lipogenesis (fat synthesis) from excess glucose
- Net result: blood glucose returns to normal (fasting level ~70-100 mg/dL)
Insulin is often called the “key that opens the cell door for glucose.”
When insulin is absent or ineffective:
- Hyperglycaemia: Blood glucose rises persistently (above 126 mg/dL fasting)
- Glycosuria: Glucose spills into urine (exceeds renal threshold)
- Osmotic diuresis: Glucose in urine draws water with it → excessive urination (polyuria) → dehydration → excessive thirst (polydipsia)
- Polyphagia: Cells cannot use glucose → perceived starvation → excessive hunger
- Fat catabolism: Body breaks down fat for energy → produces ketone bodies → can lead to ketoacidosis (dangerous drop in blood pH)
- Long-term: damage to blood vessels (retinopathy, nephropathy, neuropathy, cardiovascular disease)
Cause: Autoimmune destruction of β cells. The immune system mistakenly attacks and destroys the cells that produce insulin.
Insulin production: Absent or severely deficient
Age of onset: Usually childhood/adolescence (“juvenile diabetes”) — but can occur at any age
Body weight: Usually normal or lean
Treatment: Requires daily insulin injections or insulin pump — no other treatment can replace the missing insulin
Ketoacidosis: Common if insulin is missed (without insulin, the body switches entirely to fat metabolism)
Genetic component: Yes, but triggered by environmental factors (possibly viral infection)
Cause: Combination of insulin resistance (cells don’t respond properly to insulin) and gradual decline in β-cell function
Insulin production: Initially normal or even elevated (body compensates), later decreases
Age of onset: Usually adults (but increasingly in obese youth) — “adult-onset diabetes”
Body weight: Usually obese or overweight
Treatment: Begins with lifestyle changes (diet, exercise), then oral medications (metformin, sulfonylureas), insulin in advanced stages
Ketoacidosis: Rare (some insulin still present)
Strong lifestyle connection: Obesity, sedentary lifestyle, and poor diet are major risk factors. Type 2 diabetes is largely preventable and manageable.
Why This Works
The body regulates blood glucose within a narrow range because both extremes are harmful: too high (hyperglycaemia) damages blood vessels; too low (hypoglycaemia) deprives the brain of fuel.
Insulin and glucagon (from α cells) work as opposing hormones:
- Insulin: lowers blood glucose (fed state)
- Glucagon: raises blood glucose (fasting state)
Common Mistake
Students often write that “Type 2 diabetics don’t need insulin.” In advanced Type 2 diabetes, the pancreas eventually burns out and insulin production falls, requiring insulin therapy. The early distinction — Type 1 always needs insulin, Type 2 may not — is valid for early-stage disease. Also note: both types are called “diabetes mellitus” (sweet urine), distinct from “diabetes insipidus” (caused by ADH deficiency, producing large amounts of dilute urine without glucose).