DurgicalDurgical
EN
Open the app

Pharmacology · Insulins

Regular human insulin !

The body's own hormone, made by recombinant DNA. Regular (short-acting) insulin replaces missing insulin and is the one given intravenously.

Updated 2026-11-01

  • Class: Insulins
  • Receptor: Insulin receptor
  • ATC code: A10AB01
  • WHO Model List of Essential Medicines

Also called: soluble insulin, short-acting human insulin

The figure shows insulin (chains A and B) bound to site 1 of a receptor fragment (L1–CR domains plus the αCT peptide). The antibody fragment used to crystallize it is not part of the receptor.

Target in 3D: Insulin receptor. PDB structure 4OGA (RCSB PDB, public domain). View the structure at RCSB PDB

Mechanism of action

Insulin binds the alpha subunits of the insulin receptor; the beta subunits, a tyrosine kinase, phosphorylate each other and the IRS proteins, switching on the PI3K–Akt pathway (and MAPK for growth signals). In muscle and fat, Akt moves GLUT4 transporters to the cell membrane so glucose enters. In the liver, insulin promotes glycogen synthesis and glycolysis (it induces glucokinase and activates PFK-2, whose product fructose-2,6-bisphosphate activates PFK-1) and suppresses gluconeogenesis, lipolysis and ketogenesis. It also drives potassium into cells through the Na+/K+-ATPase.

  1. Binds the insulin receptor; its tyrosine kinase switches on
  2. IRS, PI3K and Akt relay the signal inside the cell
  3. GLUT4 reaches the membrane; liver glycolysis and glycogen up, glucose output down
  4. Blood glucose, ketones and potassium fall

Pharmacokinetics

Absorption
Given by subcutaneous injection, or intravenously under medical supervision.
Elimination
Kidney impairment raises the risk of hypoglycemia.
Onset and duration
Under the skin: starts in about 30 minutes, strongest at 1.5 to 3.5 hours, ends about 8 hours later. Intravenous: faster than under the skin.

Indications

  • Type 1 diabetes (insulin replacement is essential) Type 1 diabetes mellitus →
  • Type 2 diabetes when other drugs are not enough, and during acute illness, surgery or pregnancy Type 2 diabetes mellitus →
  • Diabetic ketoacidosis and hyperosmolar hyperglycemic state, as a continuous intravenous infusion
  • Hyperkalemia, given with glucose to shift potassium into cells
  • Gestational diabetes when diet alone does not control glucose

Adverse effects

Common

  • Hypoglycemia (tremor, sweating, palpitations, hunger, confusion)
  • Weight gain
  • Lipohypertrophy at repeated injection sites
  • Low potassium

Contraindications

  • During an episode of hypoglycemia
  • Hypersensitivity to insulin or to an excipient of the preparation

Key interactions

Beta-blockers
Can blunt the warning signs of hypoglycemia.
Alcohol
Can increase or decrease the glucose-lowering effect.
Other antidiabetic drugs, ACE inhibitors, ARBs, fibrates, fluoxetine, sulfonamide antibiotics
Can increase the risk of hypoglycemia.
Glucocorticoids, diuretics, atypical antipsychotics, estrogens, thyroid hormones
Reduce the glucose-lowering effect, so insulin needs go up.
Thiazolidinediones (pioglitazone)
Fluid retention that can cause or worsen heart failure.

What is monitored

  • Capillary blood glucose
  • HbA1c
  • Potassium and glucose every few hours during intravenous infusions
  • Injection sites

Test yourself

Think of the answer, then tap the question to see it.

Why does an intravenous insulin infusion in diabetic ketoacidosis require close potassium monitoring?

Insulin drives potassium into cells through the Na+/K+-ATPase. Total body potassium is already depleted in ketoacidosis, so serum potassium can fall to dangerous levels.

Which insulin preparation is the standard for intravenous infusions?

Regular (soluble) human insulin, a clear solution; given intravenously, under supervision, it acts faster than under the skin.

How does insulin speed up glycolysis in the liver?

It induces glucokinase and, by dephosphorylating the bifunctional enzyme, activates PFK-2. Fructose-2,6-bisphosphate rises and activates PFK-1, the key committed step.

Why can beta-blockers make hypoglycemia more dangerous in a patient on insulin?

They can blunt adrenergic warning signs such as tremor and palpitations, so the patient may notice hypoglycemia later.

Add to my cards (4)

← Back to the class: Insulins

Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.

Sources: Human Insulin Injection: MedlinePlus Drug Information (MedlinePlus (U.S. National Library of Medicine), 2026); Insulin in complex with Site 1 of the human insulin receptor (RCSB Protein Data Bank, 2014); eEML - Electronic Essential Medicines List (World Health Organization, 2025); ATCDDD - ATC/DDD Index (WHO Collaborating Centre for Drug Statistics Methodology, 2026).

Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake

Representative model, for educational purposes only.