Pancreatic Islets and Glucose Homeostasis
Key facts on islet cell types, β-cell glucose sensing, insulin signalling and diabetes physiology.
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Questions Covered in This Set
10 cards to master
What percentage of pancreatic mass and blood flow do the islets of Langerhans represent?
Only 1–2% of pancreatic mass, but they receive ~10% of pancreatic blood flow (~1 million islets).
Which islet cells secrete insulin, glucagon and somatostatin, and in what proportions?
β cells ~60% (insulin, C-peptide, amylin), α cells ~30% (glucagon), δ cells ~10% (somatostatin).
List the six steps of glucose-stimulated insulin secretion in a β cell.
1) Glucose enters via GLUT2/GLUT1; 2) glucokinase phosphorylates it; 3) metabolism raises ATP/ADP; 4) K_ATP channel (Kir6.2 + SUR1) closes; 5) depolarisation opens voltage-gated Ca²⁺ channels; 6) Ca²⁺ triggers biphasic exocytosis of insulin granules.
Why is glucokinase called the β-cell 'glucose sensor'?
It has a high K_m (~8 mmol/L) and no product inhibition, so glycolytic flux is proportional to plasma glucose across the physiological range.
Why is C-peptide clinically useful?
It is co-secreted 1:1 with insulin and escapes hepatic first-pass extraction, so it marks endogenous insulin production (distinguishes type 1 diabetes or exogenous insulin from insulinoma).
What is the incretin effect?
GLP-1 and GIP released from the gut amplify insulin secretion, so oral glucose releases far more insulin than the same IV glucose load.
How do sulfonylureas and diazoxide act on the K_ATP channel?
Sulfonylureas (and glinides) close K_ATP directly — insulin release even without glucose, risking hypoglycaemia; diazoxide opens it, used for insulinoma.
Describe insulin's two intracellular signalling branches.
Receptor tyrosine kinase → IRS-1/2, then PI3K→Akt metabolic arm (GLUT4 translocation, glycogen synthase via GSK-3 inhibition, FoxO suppression of gluconeogenesis, lipogenesis, Na⁺/K⁺-ATPase) and MAPK growth arm.
Which tissues do NOT require insulin for glucose uptake?
Brain, liver, kidney, RBCs and gut (GLUT1/2/3); only muscle and adipose depend on insulin-regulated GLUT4.
Which channel mutations cause neonatal diabetes, congenital hyperinsulinism and MODY2?
Activating Kir6.2 mutations → neonatal diabetes; inactivating Kir6.2/SUR1 → congenital hyperinsulinism; glucokinase mutations → MODY2 (mild, reset-thermostat hyperglycaemia).
