Question
What is diabetes mellitus? Compare Type 1 and Type 2 diabetes. How does insulin regulate blood glucose? Why does glucose appear in urine (glycosuria) in diabetic patients?
(NEET 2023, similar pattern)
Solution — Step by Step
Insulin is produced by the beta cells of the Islets of Langerhans in the pancreas. It is the only hormone that lowers blood glucose.
How insulin works:
- Stimulates cells (especially muscle and fat) to take up glucose from blood
- Promotes glycogenesis (glucose → glycogen storage in liver and muscles)
- Promotes lipogenesis (glucose → fat)
- Inhibits gluconeogenesis (stops production of new glucose from non-sugar sources)
Normal fasting blood glucose: 70-100 mg/dL. Diabetes is diagnosed when fasting glucose exceeds 126 mg/dL.
Cause: Autoimmune destruction of beta cells → pancreas produces little or no insulin.
- Also called juvenile-onset diabetes (typically starts in childhood/adolescence)
- Accounts for ~5-10% of diabetes cases
- Treatment: lifelong insulin injections (cannot be managed by diet alone)
- Sudden onset, patients are usually lean
Cause: Body cells become resistant to insulin — they don’t respond properly even though insulin is produced. Over time, the pancreas may also produce less insulin.
- Also called adult-onset diabetes (though increasingly seen in younger people)
- Accounts for ~90% of diabetes cases
- Strongly associated with obesity, sedentary lifestyle, and family history
- Treatment: lifestyle changes (diet, exercise), oral hypoglycaemic drugs, sometimes insulin in advanced cases
Normally, the kidneys reabsorb all filtered glucose back into the blood. But when blood glucose exceeds the renal threshold (~180 mg/dL), the kidney tubules can’t reabsorb all of it.
The excess glucose spills into the urine — this is glycosuria. It carries extra water with it (osmotic diuresis), causing:
- Polyuria — frequent urination
- Polydipsia — excessive thirst (to compensate water loss)
- Polyphagia — excessive hunger (cells are starving despite high blood glucose)
These are the classic “3 Ps” of diabetes.
Why This Works
Insulin acts as the key that unlocks cells to let glucose in. In Type 1, there is no key (no insulin). In Type 2, the lock is jammed (insulin resistance). Either way, glucose accumulates in the blood while cells starve — that’s the paradox of diabetes: plenty of fuel in the blood, but cells can’t use it.
The body responds by breaking down fats and proteins for energy, leading to weight loss (Type 1) and ketone body production (diabetic ketoacidosis — a medical emergency).
Alternative Method — Comparison Table
| Feature | Type 1 | Type 2 |
|---|---|---|
| Age of onset | Childhood | Adult (usually > 40) |
| Cause | Autoimmune beta cell destruction | Insulin resistance |
| Insulin level | Very low/absent | Normal or high (initially) |
| Body type | Lean | Often obese |
| Treatment | Insulin injections | Diet, exercise, oral drugs |
| Prevalence | 5-10% | 90% |
| Ketoacidosis risk | High | Low |
For NEET: remember the hormonal pair — insulin (lowers glucose, from beta cells) and glucagon (raises glucose, from alpha cells of islets). Together they maintain glucose homeostasis. NEET may ask about glucagon’s role — it promotes glycogenolysis (glycogen → glucose) and gluconeogenesis.
Common Mistake
Students write “diabetes is caused by excess sugar intake.” While high sugar diet can contribute to obesity (a risk factor for Type 2), diabetes is fundamentally a hormonal/metabolic disorder — not simply a dietary one. Type 1 has nothing to do with diet at all. Also, don’t confuse diabetes mellitus (sugar in urine, insulin problem) with diabetes insipidus (dilute urine, ADH deficiency from posterior pituitary). They share the name “diabetes” (meaning siphon/excessive urination) but are completely different diseases.