Type 2 diabetes mellitus

• Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease in which the body's cells respond less well to insulin (insulin resistance) while the pancreatic beta cells secrete too little insulin to overcome it (relative insulin deficiency), so blood glucose stays high.
• It is by far the commonest form of diabetes, accounting for over 90% of cases^[5] and for 85% to 95% of diabetes in developed countries^[1]; there were about 537 million adults with diabetes worldwide in 2021, projected to reach 783 million by 2045^[1]. ^[3]
• It usually declares itself in adults with risk factors such as obesity, especially abdominal obesity, physical inactivity, age, a first-degree relative with the disease, or a history of gestational diabetes.
• Diagnosis rests on one of four tests: glycated haemoglobin (HbA1c) 6.5% or higher^[1], fasting plasma glucose 7.0 mmol/L or higher^[1], a 2-hour oral glucose tolerance test 11.1 mmol/L or higher^[1], or a random plasma glucose 11.1 mmol/L or higher with classic symptoms^[1]; abnormal results need confirmation unless hyperglycaemia is unequivocal.
• Management combines a healthy diet and regular physical activity with weight loss; metformin with an SGLT2 inhibitor is now first-line drug treatment^[2], with further agents and insulin added in steps guided by the person's comorbidities and their own blood glucose, blood pressure and lipid targets.

By the end of this page you should be able to:

1. Explain insulin resistance, relative insulin deficiency, the incretin defect, and obesity as links in the pathophysiology of T2DM.
2. State the epidemiology and risk factors, including the difference between modifiable and non-modifiable risks.
3. Apply the screening criteria and the diagnostic criteria for T2DM and prediabetes.
4. Set individualised targets for HbA1c, blood pressure and lipids and explain when to relax them.
5. Follow the stepwise management pathway from lifestyle to oral and injectable therapy to insulin, including the role of obesity management and bariatric surgery.
6. Plan monitoring, vaccination and screening for complications over time.
7. Describe the principal differences between type 1 and type 2 diabetes.
8. Adapt management to a low-resource setting.

Diabetes mellitus itself is a group of metabolic disorders characterised by hyperglycaemia in the absence of treatment, from defects in insulin secretion, insulin action, or both. The World Health Organization classification distinguishes type 1, type 2, hybrid forms, and other specific types. In type 2 diabetes the pancreas usually still makes insulin; the problem is that the body's cells do not respond properly and, over time, the beta cells cannot keep up with the demand. Monogenic forms (such as maturity-onset diabetes of the young) and other specific types are considered separately because their management differs.

A useful clinical point is that the two core defects are present early and worsen gradually. Insulin resistance and beta-cell dysfunction both begin before diagnosis, often years beforehand, which is why complications may already be present at the time T2DM is first found.

• Burden. Worldwide prevalence in 2021 was estimated at approximately 537 million adults, projected to reach 783 million by 2045^[1]. About 45% of people with diabetes worldwide are thought to be undiagnosed^[1]. Type 2 diabetes accounts for over 90% of all cases^[5] and for 85% to 95% of diabetes in developed countries^[1]. Diabetes caused 4.2 million deaths in 2019 in global estimates^[5], and patients with T2DM have about a 15% higher all-cause mortality than people without diabetes^[5], with cardiovascular disease the leading cause.
• Time trends. The age-adjusted prevalence rose from 4.7% in 1980 to 8.5% in 2014, with the greatest increase in low- and middle-income countries^[3]. T2DM is found in every population and region and is the most common form in every age group after adolescence.
• Cost. Worldwide spending on diabetes was about 966 billion US dollars in 2021^[1]; in the United Kingdom diabetes accounts for roughly 10% of the National Health Service budget^[1].

Risk factors combine. A person with several risk factors is at much higher risk than the sum of each alone.

Non-modifiable

• Age: T2DM is most common in people over 45, although it is increasingly seen in children and young adults as obesity rises.
• Family history and genetics: a first-degree relative with T2DM substantially raises risk^[3]; twin and migration studies show a strong heritable component, and genome-wide studies have found that most susceptibility variants act on insulin secretion.
• Ethnicity: South Asian, Afro-Caribbean and Hispanic populations have higher risk at a lower body mass index.
• A history of gestational diabetes, or of a previous large-for-gestational-age baby.
• Early-onset and more severe disease in some non-European populations, where beta-cell dysfunction may be more prominent than in Europeans.

Modifiable

• Overweight and obesity, especially abdominal (visceral) obesity: the strongest single risk factor. People with obesity (body mass index 30 kg per square metre or higher) are at the highest risk^[5]. Lifetime risk rises steeply with body mass index.
• Physical inactivity and low cardiorespiratory fitness.
• An energy-dense, highly processed diet low in fibre and high in sugar-sweetened drinks.
• Smoking and excess alcohol.
• Other conditions: hypertension, dyslipidaemia, polycystic ovary syndrome, cardiovascular disease, and inflammatory states.
• Drugs: glucocorticoids, antipsychotics and some immunosuppressants can precipitate diabetes.

The chapter is the core. Every clinical feature and treatment choice follows from three interacting problems.

In response to a meal, insulin normally drives glucose into muscle and fat and suppresses glucose release from the liver. In T2DM these responses are blunted. The liver overproduces glucose fasting and after meals; muscle takes up less glucose; adipose tissue releases free fatty acids and behaves as an endocrine organ producing inflammatory signals. Obesity, especially visceral obesity, amplifies insulin resistance through increased free fatty acid release and adipokine dysregulation, alongside low-grade inflammation and mitochondrial dysfunction.

The "relative" in relative insulin deficiency matters. Early in the disease the pancreas works harder and insulin output may even exceed normal, keeping glucose near normal for years. Eventually beta-cell mass and function fall, insulin secretion no longer matches demand, and fasting and postprandial glucose rise. Beta-cell loss reflects combined stress: glucotoxicity, lipotoxicity, endoplasmic reticulum stress, oxidative stress, amyloid deposition in islets, and inflammation. Beta-cell dysfunction is often more severe than insulin resistance by the time T2DM is diagnosed.

The "incretin effect" is the larger rise in insulin seen after taking glucose by mouth compared with the same amount given intravenously, because gut hormones amplify glucose-induced insulin secretion. In healthy people it accounts for up to roughly 70% of postprandial insulin secretion^[4]. The classical incretins are glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). In T2DM the incretin effect is severely reduced or absent^[4]: GLP-1 secretion is reduced and the beta-cell response to both hormones is impaired, while GIP secretion itself stays near normal even though its insulinotropic effect, especially late-phase insulin release, is lost. Glucagon is also inappropriately high and not suppressed by glucose. Improved glycaemic control can partly restore these responses.

Overweight and obesity are present in most people with T2DM and either cause or aggravate insulin resistance. Many people who are not obese by body mass index have a higher proportion of body fat in the abdomen (visceral adiposity). The relationship is graded and runs in both directions: even modest weight loss improves insulin resistance and beta-cell function.

T2DM is highly polygenic. Genome-wide studies show that most susceptibility variants act primarily on insulin secretion, with a minority reducing insulin action. Common variants together account for only a fraction of heritability; rare variants and gene-environment interactions are important. Ethnicity modifies risk: populations vary widely in incidence and may differ in whether beta-cell dysfunction or insulin resistance predominates.

T2DM has an insidious onset and many people have the disease for several years before it is recognised. It can be entirely silent; when symptoms occur they are usually those of hyperglycaemia.

Symptoms in the patient's words

• Increased thirst and a dry mouth, with passing large volumes of urine (often waking at night).
• Tiredness, lethargy and difficulty concentrating.
• Blurred vision (from osmotic lens changes).
• Recurrent infections: skin, urinary, and genital (thrush).
• Weight loss despite a good appetite (when control is poor).
• Slow healing of cuts and wounds.
• Itching, particularly around the genitals.
• Loss of feeling or tingling in the feet in established disease (neuropathy).

Signs on examination

• Often none; general examination may be normal.
• Overweight or central obesity, sometimes with acanthosis nigricans (a dark, velvety thickening of skin folds, marking insulin resistance) or skin tags.
• Dehydration if severe hyperglycaemia.
• Hypertension and retinal changes on fundoscopy in long-standing disease.
• Reduced sensation, absent ankle jerks and a monofilament-abnormal foot in neuropathy.
• Evidence of macrovascular disease (peripheral pulses, carotid bruits).

Acute presentations

• Severe hyperglycaemia may present as dehydration with infection.
• Hyperosmolar hyperglycaemic state is a life-threatening presentation of very high glucose with profound dehydration and no significant ketosis.
• Ketosis and diabetic ketoacidosis can occur in T2DM, especially with severe stress or infection.

The main task is to distinguish T2DM from other causes of hyperglycaemia and from type 1 diabetes in particular.

Other causes of hyperglycaemia to consider include gestational diabetes, monogenic diabetes (MODY), Cushing syndrome, acromegaly, pancreatitis or pancreatic cancer, and steroid- or drug-induced hyperglycaemia. Gestational diabetes and monogenic forms are classified separately and managed differently.

Investigation has three aims: to confirm the diagnosis, to assess the extent of hyperglycaemia and beta-cell reserve where needed, and to look for complications and comorbidity.

• Blood tests for the diagnosis itself. HbA1c, fasting plasma glucose, OGTT, or random plasma glucose with symptoms (details below). ^[1]
• Markers of beta-cell reserve and autoimmunity. In uncertain cases (young, lean, ketotic, rapid onset) measure fasting C-peptide, endogenous insulin, and pancreatic autoantibodies (GAD, IA-2, ZnT8) to exclude type 1 or monogenic diabetes.
• Quality of the result. Glucose should be measured as venous plasma in an accredited laboratory; HbA1c should be measured with a method standardised to the international reference.
• Comorbidity and baseline. Full blood count, renal function (creatinine and eGFR), liver function, lipids, urine albumin-to-creatinine ratio, electrocardiogram if indicated, and screening for cardiovascular risk factors.
• Excluding precipitants. Infection, pancreatitis, and drugs are identified clinically.

A single abnormal result is enough in a symptomatic person with unequivocal hyperglycaemia; otherwise a result must be confirmed on a separate day, either by repeating the same test or by an abnormal result on a different test.

Diagnostic criteria (any one of the following):

1. HbA1c 6.5% (48 mmol per mol) or higher^[1].
2. Fasting plasma glucose 7.0 mmol/L (126 mg per dL) or higher^[1], after at least 8 hours without caloric intake.
3. Two-hour plasma glucose 11.1 mmol/L (200 mg per dL) or higher during a 75 g oral glucose tolerance test^[1].
4. In a patient with classic symptoms of hyperglycaemia or a hyperglycaemic crisis, a random plasma glucose 11.1 mmol/L (200 mg per dL) or higher^[1].

Prediabetes (increased risk). Blood glucose below the diabetes cut-offs but above normal:

• HbA1c 5.7% to 6.4% (39 to 46 mmol per mol)^[1].
• Fasting plasma glucose 5.6 to 6.9 mmol/L (100 to 125 mg per dL) on the American Diabetes Association definition, or 6.1 to 6.9 mmol/L (110 to 125 mg per dL) on the World Health Organization definition^[1].
• Two-hour plasma glucose 7.8 to 11.0 mmol/L (140 to 199 mg per dL) during an OGTT^[1].

The thresholds for impaired fasting glucose differ between authorities; state which definition is used locally rather than mixing them.

Screening criteria

• HbA1c, fasting plasma glucose or a 2-hour OGTT is appropriate for screening asymptomatic adults; all adults aged 35 or over^[1], and younger overweight or obese adults with risk factors, should be screened in a health care setting.
• If fasting plasma glucose is under 5.6 mmol/L (under 100 mg per dL), 2-hour plasma glucose is under 7.8 mmol/L (under 140 mg per dL) and HbA1c is under 5.7% (under 39 mmol per mol), repeat testing every 3 years^[1]; people with prediabetes should be tested annually^[1].
• Youth who are overweight and have risk factors should be screened from age 10 years^[1], every 3 years.

Targets are set with the person, weighing the benefits of avoiding complications against the risk of hypoglycaemia and the burden of treatment. People are encouraged to reach and maintain their agreed targets, unless doing so causes adverse effects, including hypoglycaemia, or harms quality of life.

Glycaemia (HbA1c). NICE supports^[2]:

• 48 mmol per mol (6.5%) for people managed with diet alone or with an initial regimen not associated with hypoglycaemia (such as metformin with an SGLT2 inhibitor).
• 53 mmol per mol (7.0%) for people on medicines that can cause hypoglycaemia, such as sulphonylureas or insulin.
• If control is not adequate and HbA1c rises to 58 mmol per mol (7.5%) or higher, reinforce diet, physical activity and adherence advice, support a target of 53 mmol per mol, and intensify treatment. ^[2]
• Consider relaxing the target in older or frail patients, or where the person has a limited life expectancy, high hypoglycaemia risk, or significant comorbidity.

Blood pressure. Diagnosis, treatment and monitoring of hypertension are broadly the same as for people without diabetes; NICE directs clinicians to the current hypertension guideline for target values. Guidelines differ, and the target should be agreed for the individual.

Lipids. Cardiovascular risk is the leading cause of death in T2DM, so lipid management and, where appropriate, statin therapy follow the national cardiovascular prevention guideline; the target and drug are chosen as part of the person's overall cardiovascular risk plan.

Dietary advice is central: a balanced diet with controlled portions of carbohydrate (with low glycaemic index choices), reduced intake of added sugars and sugar-sweetened drinks, adequate fibre and protein, reduced saturated fat and salt, and regular meals. Weight loss improves glycaemic control markedly; more intensive programmes (low-energy diet and meal replacements) can produce remission in some people. Physical activity improves insulin sensitivity and glucose uptake. Stop smoking, limit alcohol, and provide structured education (for example DESMOND-style programmes) at diagnosis and regularly afterwards.

Treating obesity is the cornerstone of both preventing and treating T2DM. Lifestyle change comes first; a minority of people benefit from obesity medicines under national guidance. Bariatric or metabolic surgery should be considered for people in whom weight loss may improve glycaemic control, including those with severe or refractory obesity; it can improve glycaemia substantially and sometimes induces remission. Surgery is reserved for those who meet local criteria and are medically fit, with a multidisciplinary team and long-term follow-up. Timing may be soon after diagnosis, when remission is most likely.

Both metformin and SGLT2 inhibitors are recommended for their cardiovascular and renal benefits as much as for glucose control.

• Metformin (modified-release) is first-line for almost everyone, unless contraindicated or not tolerated, as an adjunct to diet and exercise^[2].
• Add an SGLT2 inhibitor for almost everyone from the start, regardless of whether a relevant comorbidity is present, because of glucose, cardiovascular and renal benefits^[2]. If metformin is not tolerated, use an SGLT2 inhibitor alone.
• Comorbidities change the SGLT2 inhibitor's role but not the principle: in atherosclerotic cardiovascular disease add subcutaneous semaglutide (up to 1 mg once weekly)^[2]; in heart failure and chronic kidney disease metformin with an SGLT2 inhibitor is still offered; in chronic kidney disease with low eGFR, use dapagliflozin or empagliflozin with a DPP-4 inhibitor instead.
• In older adults with frailty, metformin alone may be safer if SGLT2 inhibitor risks such as volume depletion or low blood pressure are a concern.

Metformin dosing and safety (product label). Start extended-release metformin at 500 mg by mouth once daily with the evening meal, increasing by 500 mg every 1 to 2 weeks, up to a maximum of 2000 mg once daily with the evening meal^[6]. Swallow the tablets whole. Metformin is contraindicated when eGFR is below 30 mL per minute per 1.73 square metres; do not start it between 30 and 45; discontinue if eGFR later falls below 30^[6]. Avoid in hepatic impairment and in acute or chronic metabolic acidosis. Because of lactic acidosis, hold metformin around iodinated contrast studies in people with reduced renal function, and monitor vitamin B12 every 2 to 3 years^[6].

SGLT2 inhibitors. They lower glucose independently of insulin, cause modest weight loss, reduce cardiovascular death and heart failure admissions, and slow kidney disease progression. Counsel about genital and urinary infections, and about sick-day rules: stop the drug during acute illness with vomiting or poor intake, during dehydration, and perioperatively. Euglycaemic ketoacidosis is rare but serious; warn patients to seek help for unexplained nausea, abdominal pain or breathlessness.

GLP-1 receptor agonists. Liraglutide, dulaglutide and subcutaneous semaglutide are added for cardiovascular, renal and glycaemic benefits. They reduce weight and HbA1c and lower cardiovascular events in people with established cardiovascular disease. Common adverse effects are nausea and vomiting; start at the lowest dose and titrate slowly. Tirzepatide (a dual GIP/GLP-1 agonist) is used for its glycaemic and weight benefits, particularly in early-onset disease and in people living with obesity.

If the first regimen is not enough, add agents in this order, matching the comorbidity:

1. DPP-4 inhibitor (sitagliptin, alogliptin, linagliptin) added to current treatment, weight-neutral and generally well tolerated; avoid in pancreatitis.
2. If a DPP-4 inhibitor is contraindicated, not tolerated or ineffective, add a sulphonylurea (gliclazide or similar) or pioglitazone, or move to insulin. Sulphonylureas increase hypoglycaemia and weight; pioglitazone benefits insulin sensitivity but fluid retention limits its use in heart failure.
3. In early-onset diabetes or obesity, consider adding a GLP-1 receptor agonist or tirzepatide before exhausting oral options.
4. Insulin when adequate control is not achieved, when HbA1c is very high, during pregnancy planning, or when there are symptoms of hyperglycaemia.

Insulin is started the way chronic disease always should be started: simply, safely, and adjusted against self-monitoring.

• Indications. Marked hyperglycaemia at diagnosis, failure of oral treatment, severe catabolism, pregnancy, and intercurrent illness. NICE suggests considering a combination of basal and short-acting insulin (or a pre-mixed preparation) when HbA1c is 75 mmol per mol (9.0%) or higher at insulin initiation^[2].
• Regimen. Begin once daily with a basal insulin (a long-acting analogue or NPH), usually at bedtime, and titrate against fasting glucose in small increments every few days towards the person's fasting glucose target, avoiding nocturnal hypoglycaemia. When fasting glucose is on target but HbA1c remains high, add prandial (mealtime) insulin and progress to a basal-bolus (multiple daily injection) regimen. Premixed insulin twice daily is a simpler alternative when meal patterns are regular and support is limited.
• Safety. Self-monitoring and hypoglycaemia education are mandatory; reduce sulphonylurea dose when starting basal insulin; support diet and activity to limit weight gain.

Blood pressure lowering and lipid lowering are, alongside glucose control, the interventions that most reduce events. Angiotensin-converting enzyme inhibitors (or angiotensin receptor blockers) are preferred in diabetes, especially with albuminuria or chronic kidney disease. Statin therapy is advised for most adults with T2DM for primary prevention, with intensity guided by age and cardiovascular risk. Antiplatelet therapy is not offered for primary prevention in T2DM without cardiovascular disease.

• HbA1c every 3 to 6 months until stable, then every 6 months^[2].
• Routine blood glucose: schedule by insulin use and hypoglycaemia risk; continuous glucose monitoring for insulin-treated patients with recurrent or severe hypoglycaemia or impaired awareness.
• Blood pressure at every visit.
• Weight, waist circumference where relevant, and at least annual feet, kidneys, eyes, nerves and cardiovascular risk review.

Vaccination is part of routine diabetes care. Offer influenza vaccination every year. Provide pneumococcal, COVID-19 and any other age- or risk-appropriate vaccines according to the national immunisation schedule, including hepatitis B where local guidance recommends it. Document and repeat annually where the programme requires.

Screening is organised, not opportunistic, and should be recorded on a checklist. Eye screening starts immediately at diagnosis (refer to the local diabetic eye screening service) and continues annually.

Acute

• Hypoglycaemia, particularly with insulin or sulphonylureas.
• Hyperglycaemic crises and, less often, diabetic ketoacidosis.
• Infection, which worsens control.

Chronic microvascular

• Retinopathy, macular oedema and cataract: leading cause of preventable blindness.
• Diabetic kidney disease: albuminuria and falling eGFR; screen with eGFR and ACR.
• Peripheral and autonomic neuropathy: sensory loss, foot ulceration and Charcot foot; gastroparesis and orthostatic hypotension.

Chronic macrovascular

• Ischaemic heart disease, stroke and peripheral arterial disease: cardiovascular disease is the leading killer in T2DM.
• Non-alcoholic fatty liver disease and metabolic dysfunction-associated steatotic liver disease.
• Other: periodontitis, erectile dysfunction, increased susceptibility to some infections such as tuberculosis.

Early treatment of hyperglycaemia reduces microvascular complications; the effect on macrovascular disease is smaller and clearer with long-term control and with addressing blood pressure and lipids.

T2DM shortens life and reduces its quality chiefly through cardiovascular events and renal failure, but early detection, glucose control, blood pressure control, lipid management and weight reduction each add benefit. Metabolic memory means that early control has disproportionate long-term benefit, so act promptly rather than waiting for perfect readiness.

Most T2DM can be prevented or delayed.

• Behavioural. Even modest weight loss combined with regular moderate-intensity activity reduces the incidence of diabetes substantially in at-risk people.
• Diet. Low-energy, high-fibre diets, limiting sugar-sweetened drinks, and reducing ultra-processed food.
• Pharmacological. Metformin can delay the onset of diabetes in people with prediabetes and is particularly useful in younger people and in those with higher body mass index or a history of gestational diabetes.
• Surgery. Bariatric surgery markedly reduces the incidence of T2DM in people with obesity.
• Treating other risk factors. Blood pressure and lipids.

• Children and adolescents. Paediatric T2DM is increasing and often presents in an ethnic group with obesity and a family history. Management begins with lifestyle change and metformin as first-line (as in adults for those 10 years and older), with insulin when glucose is markedly elevated or metformin is inadequate.
• Pregnancy. HbA1c targets and medicines differ (insulin or, where appropriate, metformin); managing diabetes in pregnancy requires specialist care.
• Older adults and frailty. Relax HbA1c targets, avoid hypoglycaemia, reduce the number of medicines to the smallest effective dose, and weigh functional status and life expectancy.
• Renal impairment. Metformin dosing must follow eGFR; an SGLT2 inhibitor with renal benefit, DPP-4 inhibitors or insulin may be used.

• Use venous plasma glucose where laboratory HbA1c is unavailable; if both are unavailable, fasting plasma glucose or the 2-hour OGTT still make the diagnosis.
• A single properly measured fasting glucose above 7 mmol/L in a symptomatic person is enough in many settings; otherwise confirm on a separate day.
• Emphasise diet, activity and weight loss, which cost little and work.
• Metformin remains the core medicine; add a sulphonylurea and then insulin (usually NPH) when control is not achieved, because these are inexpensive and widely available.
• SGLT2 inhibitors and GLP-1 receptor agonists, where procured affordably, add cardiovascular and renal protection and should be prioritised to people with those diseases.
• Fixed-dose calendars, nurse-led clinics, and community health worker support reduce dropout; insulin storage and sharps disposal must be solved locally.
• Where referral is needed (markedly raised glucose at diagnosis, ketoacidosis, pregnancy, foot ulcers, proliferative retinopathy, falling eGFR), send people early to the nearest centre that can manage them.

• T2DM is a disease of insulin resistance with relative insulin deficiency, driven by obesity, ageing, and a polygenic susceptibility.
• It is the commonest form of diabetes and is often silent for years, with complications already present at diagnosis.
• Diagnosis uses HbA1c 6.5% or higher^[1], fasting plasma glucose 7.0 mmol/L or higher^[1], 2-hour OGTT 11.1 mmol/L or higher^[1], or random glucose 11.1 mmol/L or higher with symptoms^[1]; confirm unless hyperglycaemia is unequivocal.
• Prediabetes (HbA1c 5.7% to 6.4%, IFG 5.6 to 6.9 or 6.1 to 6.9 mmol/L, IGT 7.8 to 11.0 mmol/L) is the window for prevention; cut-offs differ between authorities. ^[1]
• Screening is risk-based from age 35^[1], earlier with risk, and HbA1c, fasting glucose or 2-hour OGTT can be used; normal results are repeated every 3 years^[1], prediabetes annually^[1].
• Targets include HbA1c of 48 mmol per mol (6.5%) for diet or non-hypoglycaemic regimens, or 53 mmol per mol (7.0%) for medicines that can cause hypoglycaemia, with relaxation in older or frail patients.
• First-line drug treatment is metformin (modified-release) plus an SGLT2 inhibitor for most people, tailored to cardiovascular and renal comorbidity, with GLP-1 receptor agonists in cardiovascular disease.
• Escalation follows a clear order: DPP-4 inhibitor, then sulphonylurea or pioglitazone, then insulin; use insulin earlier for marked hyperglycaemia.
• Weight loss transforms control, and bariatric surgery can produce remission in suitable people.
• Annual complication screening (eyes, kidneys, feet, nerves, heart and oral health) detects problems before they become disabling.
• Vaccination (influenza annually, plus pneumococcal, COVID-19 and other routine vaccines) is part of diabetes care.
• Type 1 and type 2 diabetes differ in aetiology, insulin reserve, onset, ketosis risk and antibody status, although they overlap; no one feature decides the diagnosis.