Diabetes & Regulation

Diabetes & Blood Glucose Regulation

Blood glucose is precisely regulated between 70–100 mg/dL in the fasting state. This is achieved through the coordinated actions of hormones, primarily insulin and glucagon, acting on liver, muscle, and adipose tissue.

Hormonal Control

  • Insulin (β-cells of islets of Langerhans): Anabolic hormone. Secreted in response to ↑blood glucose, GLP-1. Actions: ↑Glucose uptake (GLUT4 in muscle/fat), ↑Glycogenesis, ↑Glycolysis, ↑FA synthesis, ↑Protein synthesis; ↓Glycogenolysis, ↓Gluconeogenesis, ↓Lipolysis, ↓Ketogenesis.
  • Glucagon (α-cells): Catabolic hormone. Secreted in response to ↓blood glucose, amino acids. Actions: ↑Glycogenolysis (liver), ↑Gluconeogenesis, ↑Lipolysis, ↑Ketogenesis; ↓Glycolysis, ↓FA synthesis.
  • Cortisol: Raises blood glucose (induces gluconeogenic enzymes, stimulates lipolysis and proteolysis for substrates). Causes insulin resistance.
  • Epinephrine: Stress hormone; rapid glycogenolysis (liver and muscle), lipolysis.
  • Growth Hormone: Stimulates lipolysis; anti-insulin (diabetogenic in excess).

Diabetes Mellitus — Classification

  • Type 1 DM (Insulin-dependent): Autoimmune destruction of β-cells → absolute insulin deficiency. Prone to diabetic ketoacidosis. Treatment: Insulin replacement.
  • Type 2 DM (Non-insulin-dependent): Insulin resistance + relative insulin deficiency. Associated with obesity, aging. No ketoacidosis (some insulin present). Treatment: Lifestyle + Metformin/sulfonylureas/GLP-1 agonists; insulin if needed.
  • Gestational DM: Diagnosed in pregnancy; risk of macrosomia, neonatal hypoglycemia.
  • MODY: Maturity Onset Diabetes of the Young — monogenic, autosomal dominant.

Metabolic Changes in Diabetes

  • ↑Blood glucose → glycosuria (exceeded renal threshold ~180 mg/dL) → osmotic diuresis → polyuria, polydipsia
  • Lack of insulin → ↑Lipolysis → ↑FFA → ↑Ketogenesis (3 ketone bodies: Acetoacetate, β-Hydroxybutyrate, Acetone)
  • Ketoacidosis: Blood pH drops → Kussmaul breathing (rapid deep breathing to blow off CO₂)
  • Hyperglycemia → non-enzymatic glycosylation → HbA1c (3-month average glucose); AGEs cause vascular damage

Complications of Diabetes

  • Microvascular: Retinopathy, Nephropathy (Kimmelstiel-Wilson lesion), Neuropathy
  • Macrovascular: Accelerated atherosclerosis, MI, stroke, peripheral vascular disease
  • Sorbitol pathway: Excess glucose → sorbitol (aldose reductase) → cataracts, neuropathy in DM

HbA1c

Non-enzymatic glycosylation of Hb. Reflects average blood glucose over previous 2–3 months (RBC lifespan ~120 days). Normal <5.7%; Prediabetes 5.7–6.4%; Diabetes ≥6.5%.

Quiz - Exam Preparation Strategy

When studying Quiz for your final board exams, it is critical to focus on the core concepts and fundamental formulas. Relying strictly on NCERT textbook solutions and practicing previous year questions (PYQs) is the proven methodology for scoring high marks. Avoid rote memorization and instead focus on the logical application of the theories presented in this chapter.

⚠️ Common Mistakes to Avoid

❓ Frequently Asked Questions

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Board exams tend to favor conceptual application questions and direct formula-based derivations from the NCERT syllabus. Ensure you have solved every single exercise in the official textbook.

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Yes, the NCERT textbook is the absolute gold standard for board exams. However, to improve your speed and accuracy during the actual exam, you must supplement your reading by solving timed mock tests and objective questions.