Pancreatic islets (islets of Langerhans)

Insulae pancreaticae

Also known as: islets of Langerhans, endocrine pancreas, beta cells, alpha cells, delta cells

About a million microscopic clusters of endocrine cells scattered through the exocrine pancreas (1–2 % of its mass) that secrete insulin, glucagon, somatostatin and pancreatic polypeptide to control fuel metabolism.

Overview

Number≈1 million (estimates 1–3 million)

Proportion of pancreas≈1–2 % of mass

Islet diameter≈50–300 µm

Each islet (≈50–300 µm) is a richly vascularised cluster of a few hundred to a few thousand cells embedded in the acinar tissue, most densely in the tail of the pancreas. Despite their small mass, islets receive ≈10–15 % of pancreatic blood flow through a dense fenestrated capillary network. In humans, the different cell types are intermingled throughout the islet (in rodents β cells form a central core with a mantle of other cells).

Islet cells influence each other through paracrine signalling and blood flow: insulin and zinc suppress α cells, somatostatin inhibits both α and β cells, and glucagon stimulates β cells. Venous blood from the islets drains into the hepatic portal vein, so the liver — the main target of insulin and glucagon — receives hormone concentrations several times higher than the rest of the body and removes ≈50 % of insulin on first pass.

Islets are innervated by both autonomic divisions: vagal parasympathetic fibres stimulate insulin release (the cephalic phase before eating), while sympathetic activity (α2-adrenergic) inhibits insulin and stimulates glucagon during exercise and stress.

Location

Scattered throughout the pancreas (head, body, tail), most concentrated in the tail; PP cells are most abundant in the posterior head/uncinate process (ventral-bud derivative).

Parts & subdivisions

β (beta) cells — ≈60–70 %

Secrete insulin with C-peptide and amylin (islet amyloid polypeptide). Glucose sensing via glucokinase and K_ATP channels.

α (alpha) cells — ≈20–30 %

Secrete glucagon; stimulated by hypoglycaemia, amino acids and sympathetic activity.

δ (delta) cells — ≈5–10 %

Secrete somatostatin, a paracrine brake on insulin and glucagon release.

PP (F/γ) cells — <5 %

Secrete pancreatic polypeptide, which inhibits exocrine pancreatic secretion and gallbladder contraction.

ε (epsilon) cells — <1 %

Secrete ghrelin; most prominent in fetal islets.

Anatomy

Innervation

Parasympathetic (vagus — muscarinic M3, stimulates insulin); sympathetic (α2 inhibits insulin, β2 stimulates insulin and glucagon); intrapancreatic ganglia.

Arterial supply

Branches of the pancreaticoduodenal arteries and splenic artery (pancreatic branches) form glomerulus-like capillary beds in each islet; efferent vessels may perfuse surrounding acini (insulo-acinar portal system).

Venous drainage

Pancreatic veins → splenic and superior mesenteric veins → hepatic portal vein.

Histology

Pale-staining cell clusters among darker basophilic acini on H&E; cell types identified by immunohistochemistry (insulin, glucagon, somatostatin). Islets lack ducts.

Development

Endodermal pancreatic buds (dorsal and ventral); islet progenitors express NGN3 and differentiate from ≈9–10 weeks.

Clinical significance

Type 1 diabetes

Autoimmune insulitis: CD8⁺ T cells destroy β cells while α and δ cells survive; symptoms appear when ≈70–90 % of β-cell mass is lost.

Pancreatic neuroendocrine tumours

Insulinoma (Whipple triad: symptoms of hypoglycaemia, low glucose at the time, relief with glucose; high insulin and C-peptide). Glucagonoma (necrolytic migratory erythema, diabetes, weight loss, venous thrombosis). Somatostatinoma (diabetes, gallstones, steatorrhoea). Gastrinoma (Zollinger–Ellison). VIPoma (watery diarrhoea, hypokalaemia, achlorhydria). Associated with MEN1.

Islet transplantation

Islets isolated from donor pancreases can be infused into the portal vein to treat brittle type 1 diabetes, requiring immunosuppression.