By Dr. Marcus Judge

Next Lesson - Reproductive and Post-Reproductive Health

Pharmacology

Contents

  1. Introduction
  2. Insulin Physiology
  3. Type 1 and Type 2 Diabetes
  4. Insulin Preparations
  5. Insulin Regimens
  6. Adverse Effects of Insulin
  7. Oral and Non-Insulin Antidiabetic Drugs
  8. The NICE Algorithm for Type 2 Diabetes
  9. Hypoglycaemia
  10. Summary
  11. Drug Summary Table
  12. Quiz

Abstract

  • Insulin is a peptide hormone released from pancreatic β-cells (the insulin-making cells of the pancreas) in response to a rise in blood glucose. It promotes glucose uptake into muscle and fat, stores glucose as glycogen in the liver, suppresses hepatic glucose output, and stimulates lipid and protein synthesis.
  • Type 1 diabetes is autoimmune destruction of β-cells: always requires insulin. Type 2 diabetes is insulin resistance (the body's cells respond poorly to insulin) with relative insulin deficiency: managed initially with lifestyle and oral agents, with insulin added later if needed.
  • Insulin preparations differ mainly in how quickly they start to work and how long they last: rapid (aspart, lispro), short (Actrapid), intermediate (NPH/Humulin I), and long-acting (glargine, detemir, degludec).
  • Non-insulin antidiabetic drugs (most are taken by mouth, but GLP-1 receptor agonists are mostly injected) include metformin (first line, usually with an SGLT2 inhibitor), sulphonylureas, DPP-4 inhibitors ("gliptins"), GLP-1 receptor agonists ("-tides": drugs that copy glucagon-like peptide-1, a gut hormone that boosts insulin release after meals), SGLT2 inhibitors ("-flozins"), pioglitazone, and the rarely used acarbose.

Core

Introduction

Diabetes affects almost 6 million people in the UK (Diabetes UK, 2024 to 2025 figures). Almost 1.3 million of them are estimated to have type 2 diabetes that has not yet been diagnosed. Diabetes is one of the most common long-term conditions in the UK. Insulin pharmacology is the foundation of management for everyone with type 1 diabetes and a substantial fraction of those with type 2. The endocrinology of insulin is covered in Metabolic and Endocrine Regulation; this article focuses on the drugs.

Insulin Physiology

Insulin is a peptide hormone of two chains (A: 21 amino acids; B: 30 amino acids) joined by disulphide bonds (strong sulphur-to-sulphur links between the chains). It is synthesised in the β-cells of the pancreatic islets of Langerhans (clusters of hormone-producing cells in the pancreas) as preproinsulin. This is processed to proinsulin (preproinsulin and proinsulin are inactive precursor molecules) and finally cleaved to insulin and a "C-peptide" by-product. Measurement of C-peptide is the standard way to distinguish endogenous insulin (high C-peptide) from injected exogenous insulin (suppressed C-peptide).

Insulin is released in response to a rise in blood glucose. The signalling sequence is worth remembering:

  1. Glucose enters the β-cell through glucose transporters (GLUTs). GLUT2 is the main one in rodents and is shown in the diagram; human β-cells also use GLUT1 and GLUT3, and their relative roles are still debated.
  2. Glucose is metabolised to ATP.
  3. Rising ATP closes ATP-sensitive K+ channels (KATP).
  4. The membrane depolarises.
  5. Voltage-gated Ca2+ channels open, intracellular Ca2+ rises.
  6. Insulin-containing granules fuse with the membrane and release their contents.

The KATP channel is the target of sulphonylureas, which close it directly and trigger insulin release.

Insulin release from the pancreatic β-cell β-cell of pancreatic islet Glucose (plasma) GLUT2 membrane ↑ ATP KATP closed depolarisation VG-Ca2+ opens ↑ Ca2+ Insulin granule exocytosis Insulin (plasma) ▪ Sulphonylureas close KATP directly: trigger insulin release regardless of glucose gliclazide, glimepiride ▪ GLP-1 / DPP-4 inhibitors amplify glucose-driven release via incretin signalling liraglutide, sitagliptin, tirzepatide SimpleMed Original by Dr Marcus Judge

Diagram: Insulin release from the pancreatic β-cell. Glucose → ATP → closure of KATP → depolarisation → calcium influx → insulin exocytosis. Sulphonylureas force the KATP channel closed regardless of glucose; GLP-1 receptor agonists and DPP-4 inhibitors amplify glucose-driven release.

The major effects of insulin are:

  • Stimulates glucose uptake into muscle and adipose (fat) tissue via GLUT4 translocation. GLUT4 is an insulin-responsive glucose transporter that moves to the cell surface when insulin binds. The liver does not use GLUT4: hepatic glucose uptake uses GLUT2 and is largely concentration-driven.
  • In the liver, insulin promotes glycogen synthesis and inhibits gluconeogenesis and glycogenolysis (the breakdown of glycogen to glucose), suppressing hepatic glucose output.
  • Stimulates lipogenesis (making fat) and inhibits lipolysis (breaking down fat) in adipose tissue.
  • Stimulates protein synthesis.

Type 1 and Type 2 Diabetes

  • Type 1 diabetes: autoimmune destruction of pancreatic β-cells, leading to absolute insulin deficiency. Usually presents in childhood or early adulthood. Insulin is the only treatment, given for life.
  • Type 2 diabetes: the dominant abnormality is insulin resistance, with relative β-cell failure that worsens with disease duration. Most patients are managed initially with lifestyle and oral agents; many will eventually need insulin.

The standard UK diagnostic thresholds (NICE Clinical Knowledge Summaries, CKS):

  • HbA1c (glycated haemoglobin, a measure of average blood glucose over the previous 8 to 12 weeks) ≥ 48 mmol/mol (6.5%).
  • Fasting glucose ≥ 7.0 mmol/L.
  • Random glucose ≥ 11.1 mmol/L with symptoms or signs of diabetes.
  • 2-hour glucose ≥ 11.1 mmol/L on an oral glucose tolerance test (OGTT, in which the patient drinks a set amount of glucose).

One abnormal reading can be used if the patient is symptomatic (repeat testing is still sensible); two are needed if asymptomatic.

HbA1c is unreliable in conditions that alter red cell turnover (anaemia, haemoglobinopathies, which are inherited disorders of haemoglobin such as sickle cell disease, and recent blood transfusion). HbA1c should not be used to diagnose diabetes in children and young people under 18, in pregnancy or within 2 months after giving birth, or when symptoms have lasted less than 2 months.

Insulin Preparations

Modern insulin preparations differ in their pharmacokinetic profile (how the body absorbs and clears the drug): the rate of absorption from the subcutaneous tissue and the duration of action. Manufacturers change these in four ways:

  • amino-acid substitutions;
  • fatty-acid acylation (attaching a fatty-acid chain so that the insulin binds to the blood protein albumin and lasts longer);
  • formulation tricks such as protamine complexing (binding insulin to the protein protamine so that it is released slowly, as in NPH or Neutral Protamine Hagedorn insulin);
  • changes in concentration.

Most insulin is supplied at U100 (100 units per mL). Higher strengths also exist: U200 (insulin degludec, Tresiba), U300 (insulin glargine, Toujeo) and U500 (for patients on very high doses). Check the strength carefully, because dosing errors with high-strength insulins can cause harm.

Rapid- and Ultra-Rapid-Acting

Onset within 5-15 minutes; peak at 1-2 hours; duration 3-5 hours. Used for meal-time ("bolus") cover and in continuous subcutaneous infusion pumps.

  • Insulin aspart (NovoRapid).
  • Insulin lispro (Humalog).
  • Insulin glulisine (Apidra).
  • Faster aspart (Fiasp): even quicker onset.

Short-Acting

Onset 30 minutes; peak at 2-3 hours; duration 6-8 hours. Must be taken 15-30 minutes before meals.

  • Soluble (regular) human insulin: Actrapid, Humulin S.

Intermediate-Acting

Onset 1-2 hours; peak at 4-8 hours; duration 12-18 hours. Used as basal (background) cover, often given twice daily.

  • NPH (Isophane) insulin: Humulin I, Insulatard.

Long- and Ultra-Long-Acting

Slow absorption with no marked peak in action, providing background insulin cover for about 16 to 42 hours depending on the insulin. In type 1 diabetes, NICE offers twice-daily insulin detemir as the basal insulin (it is being discontinued, see below) and lists once-daily glargine or degludec as alternatives. In type 2 diabetes, NICE advises a basal insulin given once or twice a day, chosen with the patient.

  • Insulin glargine (Lantus, Toujeo): ~24 hours, and longer with Toujeo (the more concentrated 300 units/mL strength).
  • Insulin detemir (Levemir): ~16-20 hours. It is being discontinued, with supply expected to end in December 2026.
  • Insulin degludec (Tresiba): more than 42 hours, very flat profile.

Biphasic / Mixed Insulins

A pre-mixed combination of a rapid- or short-acting insulin with an intermediate insulin (e.g. NovoMix 30 = 30% aspart + 70% protaminated aspart, which is aspart bound to protamine to slow its absorption). Usually given twice daily before breakfast and the evening meal.

Insulin Regimens

The two main regimens taught at pre-clinical level:

  • Basal-bolus regimen: long-acting insulin once or twice daily as background plus rapid-acting insulin with each meal, typically four or five injections per day. Most physiological; the standard for type 1 diabetes.
  • Biphasic (twice-daily) regimen: pre-mixed insulin before breakfast and evening meal. Less flexible but fewer injections; sometimes used in older or less mobile patients.

Specialist alternatives include continuous subcutaneous insulin infusion (CSII) via pump, used in selected type 1 patients. Another option is hybrid closed loop (HCL) systems. In these, a pump adjusts insulin delivery automatically using readings from continuous glucose monitoring. Some manual dosing is still needed, for example around mealtimes.

NICE recommends HCL systems for some adults with type 1 diabetes. They include people with an HbA1c of 58 mmol/mol (7.5%) or more, or with disabling hypoglycaemia (low blood glucose that happens often or without warning, so the person is constantly anxious about it), despite best possible management with an insulin pump or continuous glucose monitoring.

Adverse Effects of Insulin

  • Hypoglycaemia (abnormally low blood glucose): the most important and most common.
  • Weight gain: insulin is anabolic (it builds up body tissue and stores energy).
  • Lipohypertrophy (lumpy swelling of fatty tissue) at injection sites: reduced if injection sites are rotated.
  • Lipoatrophy (loss of fat under the skin): immunological reaction at injection site, much rarer with modern human and analogue insulins (analogue insulins are modified human insulins, such as aspart and glargine).
  • Local pain, occasional allergy to additives.
  • Hypokalaemia (low blood potassium) with high-dose insulin. This is the basis for giving insulin with dextrose (glucose) to shift potassium into cells in hyperkalaemia (high blood potassium).

Oral and Non-Insulin Antidiabetic Drugs

Used in type 2 diabetes (and some used in type 1 as add-on treatment to insulin). The drug classes are best learned by their suffix where possible.

Metformin

Metformin is a biguanide (the name of its drug class). In NICE guidance, it is one of the two first-line drugs for type 2 diabetes, offered with an SGLT2 inhibitor to most adults. It works by:

  • Reducing hepatic gluconeogenesis (the major effect).
  • Increasing peripheral insulin sensitivity (probably by activating AMP-activated protein kinase, an enzyme that senses low cellular energy).
  • Modestly slowing intestinal glucose absorption.

Metformin does not cause hypoglycaemia when used alone, does not cause weight gain (and may produce modest weight loss), is cheap, and has cardiovascular outcome data.

Side effects:

  • Gastrointestinal (GI) symptoms: nausea, diarrhoea, abdominal discomfort. Reduced by starting at low dose, taking with food, or using modified-release preparations.
  • Vitamin B12 deficiency with prolonged use.
  • Lactic acidosis (a build-up of lactic acid that makes the blood too acidic): rare but serious. Risk increased in renal impairment, sepsis, dehydration and after iodinated contrast (the iodine-containing dye used in CT scans).

Renal precautions: metformin is contraindicated in severe renal impairment because of the risk of lactic acidosis. Check the estimated glomerular filtration rate (eGFR, a measure of kidney function): review the dose if eGFR is below 45 and stop metformin if it is below 30. Withhold around iodinated contrast administration in patients with reduced renal function.

Sulphonylureas

Gliclazide and glimepiride are the most commonly used UK sulphonylureas. They close ATP-sensitive K+ channels in pancreatic β-cells, depolarising the cell and triggering insulin release. They therefore require some functioning β-cell mass to work.

Effective and cheap, but with two important downsides:

  • Hypoglycaemia: risk is real because insulin is released whatever the current blood glucose level is.
  • Weight gain.

Sulphonylureas should be used with care in renal impairment because of the risk of hypoglycaemia, and avoided where possible in severe renal impairment. If one is needed, gliclazide can be used because it is mainly metabolised in the liver, but blood glucose needs careful monitoring.

DPP-4 Inhibitors

The "-gliptin" drugs (sitagliptin, linagliptin, saxagliptin and alogliptin) inhibit dipeptidyl peptidase-4, the enzyme that breaks down the body's own glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). These two gut hormones are called the "incretins" (they boost insulin release after a meal). Higher GLP-1 levels stimulate insulin and suppress glucagon in a glucose-dependent manner.

Modest HbA1c reduction. Weight neutral. Low risk of hypoglycaemia. Watch for: pancreatitis (inflammation of the pancreas, which is rare) and upper respiratory tract infections.

GLP-1 Receptor Agonists

The "-tide" drugs (liraglutide, semaglutide and dulaglutide; exenatide is no longer marketed in the UK) are GLP-1 receptor agonists. Most are given by subcutaneous injection, and semaglutide is also available as a tablet. They are resistant to DPP-4 degradation and produce sustained GLP-1 receptor activation, which:

  • Stimulates glucose-dependent insulin secretion.
  • Suppresses glucagon.
  • Slows gastric emptying.
  • Reduces appetite.

The result is meaningful HbA1c reduction and substantial weight loss (5-15% body weight depending on agent and dose). Several agents (semaglutide, liraglutide) also have proven cardiovascular benefit.

Side effects:

  • GI: nausea is very common, especially on initiation; reduces over weeks.
  • Pancreatitis: in January 2026 the Medicines and Healthcare products Regulatory Agency (MHRA) strengthened its warning about severe acute pancreatitis across the GLP-1 receptor agonist and dual GIP/GLP-1 agonist class. This includes rare necrotising (tissue-destroying) and fatal cases. Stop the drug if pancreatitis is suspected and do not restart if confirmed.
  • Increased risk of cholelithiasis (gallstones) with rapid weight loss.
  • Injection-site reactions.

Higher-dose preparations (semaglutide 2.4 mg as Wegovy) are now licensed for obesity in the UK. Tirzepatide (Mounjaro) is a related but distinct drug: a dual GIP/GLP-1 receptor agonist, with even greater HbA1c and weight-loss effects than the pure GLP-1 agonists; same MHRA pancreatitis warning applies.

SGLT2 Inhibitors

The "-flozin" drugs (dapagliflozin, empagliflozin, canagliflozin and ertugliflozin) block the sodium-glucose cotransporter 2 (SGLT2) in the proximal renal tubule, preventing reabsorption of filtered glucose. Glucose appears in the urine, taking water with it.

The clinical benefits go well beyond HbA1c:

  • Modest weight loss (~3 kg).
  • Modest blood pressure reduction.
  • Reduction in cardiovascular events in patients with established disease.
  • Reduction in hospitalisation for heart failure: dapagliflozin and empagliflozin are also used to treat symptomatic chronic heart failure in adults whether or not they have diabetes (covered in Hypertension and Heart Failure).
  • Slowing of CKD progression: now used independently of diabetes status.

Side effects:

  • Genitourinary infections (thrush, balanitis, which is inflammation of the head of the penis, and urinary tract infections): the predictable consequence of glycosuria (glucose in the urine). NICE puts the chance of a genital infection at roughly 1 to 10 in every 100 people taking an SGLT2 inhibitor.
  • Diabetic ketoacidosis (DKA, a dangerous build-up of acids called ketones): classically euglycaemic DKA (DKA with a normal blood glucose), where the glucose looks reassuring. Rare but serious; warn patients to stop the drug if acutely unwell.
  • Volume depletion (loss of body fluid, causing dehydration), especially with co-prescribed diuretics.
  • Rare but well-known: Fournier's gangrene (necrotising fasciitis, a rapidly spreading infection that destroys tissue, of the genitalia or perineum, the area between the genitals and the anus).

Pioglitazone

Pioglitazone (a thiazolidinedione, "glitazone") activates PPAR-γ, increasing insulin sensitivity in muscle and adipose tissue. PPAR-γ stands for peroxisome proliferator-activated receptor gamma, a receptor in the cell nucleus that regulates genes for glucose and fat handling. It is now a niche drug because of side effects:

  • Weight gain and fluid retention.
  • Heart failure (it can worsen existing heart failure, and it is contraindicated in anyone with a history of heart failure).
  • Increased fracture risk.
  • Bladder cancer: a small increased risk. Pioglitazone is contraindicated (must not be used) in previous or active bladder cancer and in uninvestigated visible blood in the urine.

Acarbose

Acarbose inhibits intestinal α-glucosidase (the gut enzyme that breaks carbohydrate down into glucose), slowing carbohydrate digestion and absorption. Modest HbA1c reduction (~0.5%). Side effects (flatulence, loose stools, diarrhoea) are predictable from the mechanism and limit use; rarely prescribed in UK practice.

The NICE Algorithm for Type 2 Diabetes

NICE updated its type 2 diabetes guideline (NG28) in February 2026, with new recommendations on metformin, SGLT2 inhibitors, GLP-1 receptor agonists, DPP-4 inhibitors, sulphonylureas and pioglitazone. Initial treatment now depends on the person's other conditions, such as heart failure, atherosclerotic cardiovascular disease (fatty build-up in the artery walls), obesity, chronic kidney disease or frailty. For most adults, the pathway is:

  1. Healthy living advice (diet and physical activity) is given alongside medicines.
  2. Offer modified-release metformin (a slow-release form) and an SGLT2 inhibitor. Introduce them one at a time: metformin first, then the SGLT2 inhibitor once metformin is at the highest dose the patient tolerates. This applies to adults with no relevant comorbidity (none of the conditions listed above), with heart failure or with obesity.
  3. If metformin is contraindicated or not tolerated, offer an SGLT2 inhibitor on its own.
  4. If HbA1c rises to 58 mmol/mol (7.5%) or more on the initial treatment, reinforce healthy living and adherence, aim for 53 mmol/mol (7.0%) and intensify treatment. Offer to add a DPP-4 inhibitor. If a DPP-4 inhibitor is contraindicated, not tolerated or not effective, offer a sulphonylurea, pioglitazone (not in heart failure) or an insulin-based treatment. In atherosclerotic cardiovascular disease, NICE does not list a DPP-4 inhibitor at this step and goes straight to the sulphonylurea, pioglitazone or insulin-based options. Targets can be relaxed for people who are older or frailer.
  5. In atherosclerotic cardiovascular disease, also offer subcutaneous semaglutide (Ozempic), up to 1 mg once a week, for its cardiovascular, kidney and blood glucose benefits. In obesity, consider adding a GLP-1 receptor agonist or tirzepatide if further medicines are needed after at least 3 months of initial treatment.
  6. An insulin-based treatment is one of the options when more is needed. The usual first insulin is a basal insulin (background insulin) given once or twice a day. Short- or rapid-acting insulin can be added, especially if HbA1c is 75 mmol/mol (9.0%) or more.

The HbA1c target is agreed with each patient. It is typically 48 mmol/mol (6.5%) with healthy living alone or with an initial medicine regimen that is not associated with hypoglycaemia. It is typically 53 mmol/mol (7.0%) on a medicine that can cause hypoglycaemia, such as a sulphonylurea or insulin.

Hypoglycaemia

Hypoglycaemia (abnormally low blood glucose) is the commonest acute adverse effect of diabetes treatment. It is defined as a plasma glucose below 4 mmol/L, and any glucose below 4 mmol/L should be treated, with or without symptoms. A patient who has symptoms but a glucose of 4 mmol/L or more is given a carbohydrate snack. "Four is the floor" is the standard UK teaching mnemonic.

Symptoms divide into:

  • Autonomic (caused by adrenaline, which the body releases to raise blood glucose): sweating, tremor (shaking), palpitations (a noticeable heartbeat), hunger.
  • Neuroglycopenic (caused by the brain not getting enough glucose): confusion, slurred speech, drowsiness, seizures, coma.

Treatment depends on whether the patient can swallow safely and reliably:

  • Conscious and cooperative: oral fast-acting carbohydrate (e.g. glucose tablets, fruit juice, sugary drink), followed by a longer-acting carbohydrate to prevent recurrence.
  • Unable to swallow safely: intravenous glucose (200 mL of 10% glucose, or 100 mL of 20% glucose, over 15 minutes) or, if no IV access, intramuscular glucagon 1 mg. Glucagon is ineffective when liver glycogen is depleted (for example after prolonged fasting or in alcohol-induced hypoglycaemia) and may be less effective in people taking a sulphonylurea, who need IV glucose instead.
  • Sulphonylurea-induced hypoglycaemia: can be prolonged, so admit and observe. Consider an IV glucose infusion. In refractory cases (those that do not respond to treatment), consider IV octreotide (a drug that reduces insulin release).

The key prescribing point is that beta-blockers (drugs that block the effects of adrenaline), particularly non-selective ones (which block beta-receptors throughout the body), can mask the autonomic warning symptoms of hypoglycaemia in diabetic patients.

Summary

  • Insulin is essential in type 1 diabetes; usually needed only later in type 2.
  • Insulins differ mainly in how quickly they start to work and how long they last: rapid (aspart, lispro), short (Actrapid), intermediate (NPH), long (glargine, detemir, degludec).
  • The basal-bolus regimen is the most physiological.
  • Insulin's main risks are hypoglycaemia, weight gain, and lipohypertrophy.
  • Non-insulin diabetes drug classes by suffix: biguanide (metformin), sulphonylurea (gliclazide), "-gliptin" (DPP-4), "-tide" (GLP-1 agonist), "-flozin" (SGLT2 inhibitor), "-glitazone" (pioglitazone), and acarbose.
  • Current NICE guidance (February 2026) offers metformin and an SGLT2 inhibitor to most adults with type 2 diabetes, introduced one at a time with metformin first.
  • Hypoglycaemia ("four is the floor") is the most common acute adverse effect; treat with oral carbohydrate if possible, IV glucose or IM glucagon if not.

Drug Summary Table

Insulins and the principal non-insulin antidiabetic agents. Abbreviations: BD, twice daily; OD, once daily; t½, half-life; T2DM, type 2 diabetes mellitus; CV, cardiovascular; SC, subcutaneous; BP, blood pressure; HF, heart failure; CKD, chronic kidney disease; DKA, diabetic ketoacidosis; GI, gastrointestinal; URTI, upper respiratory tract infection.

Class Examples Mechanism Notable points Key side effects
Rapid-acting insulin Aspart (NovoRapid), lispro (Humalog), glulisine Insulin receptor agonist Onset 5-15 min; meal-time bolus Hypoglycaemia, weight gain, lipohypertrophy
Short-acting insulin Soluble (Actrapid, Humulin S) As above 15-30 min before meals As above
Intermediate-acting NPH/isophane (Humulin I, Insulatard) As above Basal cover, often BD As above
Long-acting insulin Glargine (Lantus), detemir (Levemir), degludec (Tresiba) As above; peakless Basal cover: OD (glargine, degludec) or BD (detemir); degludec t½ about 25 h, duration over 42 h As above
Biguanide Metformin ↓ hepatic gluconeogenesis; ↑ insulin sensitivity First-line in T2DM (usually with an SGLT2 inhibitor); weight neutral, no hypoglycaemia; CV benefit GI upset, B12 deficiency, lactic acidosis (rare). Stop if eGFR <30
Sulphonylureas Gliclazide, glimepiride Close KATP in β-cells → ↑ insulin secretion Cheap; effective Hypoglycaemia, weight gain
DPP-4 inhibitors (gliptins) Sitagliptin, linagliptin, saxagliptin ↑ endogenous GLP-1 Weight neutral; low hypo risk URTI, rare pancreatitis
GLP-1 receptor agonists Liraglutide, semaglutide, dulaglutide (exenatide is no longer marketed in the UK) GLP-1 receptor agonism Weight loss, CV benefit; SC injection (some oral) Nausea, pancreatitis (MHRA warning), gallstones
Dual GIP / GLP-1 agonist Tirzepatide (Mounjaro) Dual incretin agonism Largest weight loss; T2DM and obesity As GLP-1 class
SGLT2 inhibitors (-flozins) Dapagliflozin, empagliflozin, canagliflozin Block SGLT2 in proximal tubule → glycosuria Weight loss, BP ↓, HF benefit, CKD benefit Genitourinary infections, euglycaemic DKA, Fournier's gangrene
Thiazolidinediones (glitazones) Pioglitazone PPAR-γ agonism Niche use Weight gain, fluid retention, HF, fractures, bladder cancer (small increased risk; contraindicated if previous or active)
α-glucosidase inhibitor Acarbose Slows carbohydrate digestion Rarely used Flatulence, diarrhoea

Reviewed by: Dr. Marcus Judge

Quiz

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