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Key points
- Type 1 diabetes mellitus: autoimmune destruction of pancreatic beta cells → absolute insulin deficiency; ~8% of UK diabetes cases.
- Pathophysiology: insulin promotes glucose uptake, glycogen/protein synthesis; inhibits lipolysis. Loss leads to hyperglycaemia.
- Risk factors: family history, HLA-DR4-D8/DR3-DQ2, viral exposure; 80–90% have insulin autoantibodies (e.g. GAD-65, IA-2, ZnT8).
- Symptoms: polyuria, polydipsia, weight loss, lethargy, blurred vision; exam may show peripheral neuropathy, foot ulcers, lipodystrophy.
- Investigations: glucose (≥11.1 mmol/L random), ketones, urinalysis, HbA1c, insulin autoantibodies, C-peptide, TFTs, coeliac screen.
- Diagnosis: symptomatic + random glucose ≥11.1 mmol/L OR 2 abnormal readings (fasting ≥7.0, OGTT ≥11.1).
- Management: lifelong insulin (MDI or pump), dietary advice, glucose monitoring (finger-prick/CGM), MDT support, carb counting.
- Complications: DKA (abdominal pain, Kussmaul breathing, ↓GCS), retinopathy, nephropathy, neuropathy, macrovascular disease.
Introduction
Type 1 diabetes mellitus is an autoimmune condition whereby the body’s immune system attacks the beta cells of the pancreas.1-2 Destruction of beta cells results in absolute insulin deficiency, increasing the risk of exceedingly high and unsafe blood glucose.1-2
Type 1 diabetes is less common than type 2 diabetes and is responsible for approximately 8% of all diabetes diagnoses in England, with an estimated prevalence of 270,000 in 2021-2022.1, 3
Aetiology
In type 1 diabetes mellitus, there is an autoimmune destruction of the beta cells of the pancreas.1-2 These beta cells synthesise the hormone insulin, which helps tightly regulate blood glucose levels, by release in response to elevated glucose levels, such as during and after a meal.1-2
Insulin is responsible for a variety of key metabolic processes, including:
- Increased glucose uptake into skeletal muscle and adipose tissue
- Promoting glycogen synthesis in the liver, to store glucose
- Inhibition of lipolysis, lowering serum-free fatty acid levels
- Promoting protein synthesis4
The exact cause of autoimmune destruction of beta cells remains unknown. It is a complex interplay between genetic and environmental factors.5
At the time of diagnosis, approximately 80-90% of individuals with type 1 diabetes will have autoantibodies to insulin.1 These autoantibodies include anti-islet tyrosine phosphatase antigen-2 (IA-2), glutamate decarboxylase (GAD-65) and zinc transporter 8 (ZnT8).1, 6
Risk factors
Risk factors for type 1 diabetes include:
- Family history of type 1 diabetes
- Specific genotypes (e.g. HLA-DR4-D8/DR3-DQ2)
- Potentially exposure to certain viruses7
Clinical features
History
Symptoms of new-onset diabetes mellitus predominantly relate to the presence of hyperglycaemia.
Typical symptoms of hyperglycaemia include:
- Polyuria (excessive urination), including nocturia (urinating overnight)
- Polydipsia (excessive thirst)
- Weight loss
- Lethargy
- Blurred vision1-2
Clinical examination
A thorough clinical exam is important in diabetes mellitus as it is a multisystem disorder.
Possible clinical findings of type 1 diabetes include:
- Orthostatic hypotension due to autonomic neuropathy
- Peripheral neuropathy in a glove-and-stocking distribution
- Reduced/absent peripheral pulses, particularly in the feet
- Diabetic foot ulcers
- Lipodystrophy (fatty deposits under the skin, which develop when insulin injection sites are not rotated)1-2
Differential diagnoses
Differential diagnoses to consider in suspected type 1 diabetes include:
- Psychogenic polydipsia
- Arginine vasopressin (AVP) deficiency (previously known as central diabetes insipidus)
- AVP resistance (previously known as nephrogenic diabetes insipidus)
- Medication use (e.g. thiazide diuretics, glucocorticoids)
- Genetic conditions causing diabetes syndromes (e.g. Bardet-Biedl, Wolfram, Prader-Willi syndrome)8-9
Differentiating from other types of diabetes
Differentiating type 1 diabetes from other types can be difficult, but a diagnosis of type 1 is suggested by:
- Ketosis
- Rapid weight loss around the time of diagnosis
- Age of onset under 50 years
- BMI below 25 kg/m2
- Personal and/or family history of autoimmune conditions1
Investigations
Bedside investigations
Relevant bedside investigations include:
- Blood glucose level: to aid diagnosis and determine level of control
- Blood ketone level: to determine the presence of ketosis, which may suggest diabetic ketoacidosis (DKA)
- Urinalysis: proteinuria may suggest diabetic nephropathy; urinary ketones may suggest DKA; glycosuria reflects hyperglycaemia
- Fundoscopy: to detect the presence of diabetic eye disease, including retinopathy
- Body mass index (BMI): high BMI increases the risk of cardiometabolic complications
- Waist circumference: higher waist circumference is associated with cardiometabolic complications1-2
Laboratory investigations
Relevant laboratory investigations include:
- Full blood count: moderate-to-severe anaemia may overestimate HbA1c; anaemia may also suggest Coeliac disease or B12 deficiency from atrophic gastritis
- Urea and electrolytes: to assess for diabetic nephropathy
- Liver function tests: to assess for metabolic-associated fatty liver disease
- HbA1c: marker of blood glucose control for preceding 3 months
- Lipid profile: to assess cardiovascular risk profile
- Urinary albumin-to-creatinine ratio: albuminuria is a marker of diabetic nephropathy
- Vitamin B12: deficiency may suggest atrophic gastritis, an autoimmune association
- Thyroid function test: to evaluate for autoimmune thyroid disease
- Insulin autoantibodies
- C-peptide level: marker of endogenous insulin production
- Coeliac serology: consider in those with gastrointestinal symptoms1-2
HbA1c, insulin autoantibodies and C-peptide
HbA1c is glycated haemoglobin, which measures how much glucose is attached to a molecule of haemoglobin. A red blood cell’s lifespan is approximately 3 months, so HbA1c measures the degree of control for the preceding 3 months. Target HbA1c is always individualised, but less than 53 mmol/mol (7.0%) is usually recommended.
Insulin autoantibodies are useful early in diagnosing type 1 diabetes, as 80-90% of individuals will be positive at diagnosis. Negative autoantibodies do not exclude type 1 diabetes, especially later in the condition.
C-peptide is typically low in those with type 1 diabetes in the absence of hypoglycaemia. It can be a useful adjunctive test, especially 3 years after diagnosis, to confirm a state of absolute insulin deficiency.1-2
Diagnosis
Diabetes mellitus is diagnosed in the presence of hyperglycaemia symptoms AND a random blood glucose level ≥ 11.1 mmol/L.
In the absence of symptoms, diagnosis requires at least two abnormal blood glucose levels as defined by:
- A fasting blood glucose level ≥ 7.0 mmol/L, OR
- A blood glucose level ≥ 11.1 mmol/L two hours after 75 g of glucose in an oral glucose tolerance test (OGTT)1
Management
Type 1 diabetes mellitus is a lifelong autoimmune disease that requires a multidisciplinary approach including endocrinologists, primary care, diabetes educators, dietitians, exercise physiologists, psychologists, optometrists and podiatrists.1 Patients should be encouraged and educated on how to make healthy dietary choices and exercise regularly.1
Blood glucose monitoring
Close blood glucose monitoring is crucial to manage type 1 diabetes.1-2 This can be achieved by capillary blood glucose monitoring through finger-prick testing several times a day, especially before meals and bedtime.1-2 Additional testing should be undertaken when driving, before and after exercise, and with suspected hypoglycaemia.1
Continuous glucose monitors (CGM) are small, wearable devices that measure the glucose levels in the interstitial fluid. These are endorsed by NICE for those with type 1 diabetes mellitus and one of the following:
- >1 episode of severe hypoglycaemia without an obvious preventable cause
- Complete loss of hypoglycaemia awareness
- Frequent asymptomatic hypoglycaemia
- Extreme fear of hypoglycaemia
- Hyperglycaemia despite testing at least 10 times per day
- Pregnant women1-2
Many available devices warn patients of extremely high or low blood glucose levels.
Insulin regimens
Exogenous insulin therapy is essential to prevent life-threatening complications of type 1 diabetes, including DKA, as well as to improve glycaemic control to prevent longer-term complications.1-2
Insulin is administered subcutaneously, either through injection or via an insulin pump.1-2
Insulin injection
First-line therapy is multiple daily injections (MDI), which involves a basal-bolus regimen.1-2 Basal insulin is a long-acting background insulin, and bolus insulin is shorter-acting, given at mealtimes to mimic the physiological release of insulin.
Mixed insulin is also available, including short- and long-acting insulins in a fixed ratio in the same delivery device. Mixed insulin regimens should be offered to those unable or unwilling to use a basal-bolus regimen, however, this often results in poorer glycaemic control.1-2
Carbohydrate counting
Carbohydrate counting should be offered to individuals with type 1 diabetes mellitus to enhance self-management and enable flexible dosing.1-2 This helps individuals with diabetes calculate the carbohydrate content of their food. Using a personalised and prescribed insulin-to-carbohydrate ratio (ICR), they can calculate their estimated requirement of short-acting insulin to cover their meal.
Insulin pump
An insulin pump delivers a continuous subcutaneous insulin infusion (CSII) of short-acting insulin.1-2, 9 These systems can automatically adjust insulin delivery based on interstitial glucose levels to achieve tight control without significant hypoglycaemia.1, 9
Indications for CSII include:
- Disabling, unpredictable, and repeated hypoglycaemia despite attempts to achieve target HbA1c with MDI
- HbA1c above target (i.e. ≥ 69 mmol/mol (8.5%) despite MDI therapy and engagement with care)9
Advantages and disadvantages of CSII
Advantages of CSII include:
- Fewer needle injections
- Convenient delivery with more flexibility (e.g. altering basal rates during exercise, sleep, menstruation, pregnancy, illness)
- Delayed bolus delivery, useful for gastroparesis or dealing with high-fat and/or high-protein meals
- More reliable absorption
- Improved patient experience and satisfaction9
Disadvantages of CSII include:
- Risk of DKA if pump failure or disconnection as no long-acting insulin
- Constant attachment to a pump
- Infusion site problems, including infection
- Complicated set-up
- Cost of consumables related to pump use (e.g. infusion sets, cannulas, batteries, accessories)
Pancreas and islet cell transplantation
For individuals with recurrent severe hypoglycaemia that has not responded to other treatments, pancreas or islet cell transplantation is a consideration.1-2
Complications
Diabetic ketoacidosis
Diabetic ketoacidosis relates to an absolute insulin-deficient state whereby uncontrolled hyperglycaemia eventually results in the development of ketone bodies, or ketone acids, which dangerously lower the pH of the blood.1
Symptoms and signs of DKA include:
- Abdominal pain
- Nausea and/or vomiting
- Fruity-smelling breath
- Deep, rapid breathing
- Altered conscious state, including confusion and eventually coma1
The mainstay of management relies on adequate fluid resuscitation, insulin administration through a glucose-insulin infusion, and careful management of electrolytes, especially potassium. Treatment of any underlying causes, including infection, ischaemia, and intercurrent illness, is paramount.1-2
Microvascular complications
Typical microvascular complications include:
- Diabetic retinopathy: more common in type 1 diabetes than type 2 diabetes due to the longer duration of disease. A sudden reduction in HbA1c can worsen retinopathy
- Diabetic nephropathy: angiotensin-converting enzyme inhibitors (ACEi) and angiotensin II receptor blockers (ARBs) are useful in managing this
- Diabetic neuropathy: can affect the peripheral nerves (causing the characteristic glove-and-stocking sensory loss) and the autonomic nerves (causing gastroparesis, orthostatic hypotension, and erectile dysfunction)1-2
Macrovascular complications
Typical microvascular complications include:
- Coronary heart disease
- Cerebrovascular disease
- Peripheral vascular disease1-2
Hypoglycaemia
Insulin therapy is associated with the risk of hypoglycaemia, defined by a blood glucose level ≤ 4.0 mmol/L.11 Hypoglycaemia is a life-threatening condition.
Precipitating causes of hypoglycaemia in type 1 diabetes include:
- Excessive insulin administration (inadvertent or deliberate)
- Exercise
- Alcohol
- Pregnancy
- Malabsorption
- Cortisol deficiency (e.g. Addison’s disease)
- Growth hormone deficiency
- Kidney disease
- Liver disease1-2, 11-12
With repeated episodes of hypoglycaemia, patients may lose their ability to detect early warning symptoms, known as hypoglycaemic unawareness.1-2, 11-12 This is a serious condition, as they are less likely to react to their symptoms promptly.
Associated autoimmune conditions
There is an increased risk of other autoimmune diseases, with approximately 1 in 5 of those with type 1 diabetes being diagnosed with another autoimmune condition in their lifetime.10 These conditions include:
- Thyroid disease: hypothyroidism from Hashimoto’s thyroiditis; hyperthyroidism from Graves’ disease
- Atrophic gastritis: resulting in B12 deficiency
- Coeliac disease: inflammation from gluten exposure
- Addison’s disease: autoimmune destruction of the adrenal glands, causing deficiencies in cortisol and aldosterone
- Vitiligo: a skin condition which attacks melanin-producing cells, resulting in the whitening of skin colour1-2 ,10
Reviewer
Endocrinology Consultant
Editor
Dr Jamie Scriven
References
- Association of British Clinical Diabetologists. Standards of Care for Management of Adults with Type 1 Diabetes 2020. 2020. Available from: [LINK].
- National Institute for Health and Care Excellence. Type 1 diabetes in adults: diagnosis and management. 2022. Available from: [LINK].
- NHS Digital. National Diabetes Audit 2021-22, Report 1: Care Processes and Treatment Targets, Detailed Analysis Report. 2023. Available from: [LINK].
- Vargas E, Joy NV, Sepulveda MAC. Biochemistry, Insulin Metabolic Effects. StatPearls. 2022. Available from: [LINK].
- Lucier J, Mathias PM. Type 1 Diabetes. StatPearls. 2024. Available from: [LINK].
- Morrison AE, Sim SY, Kong MF, Gregory R. Type 1 or type 2 diabetes: has the ship already sailed? British Journal of Diabetes. 2021. Available from: [LINK].
- Stene LC, Norris JM, Rewers MJ. Risk Factors for Type 1 Diabetes. In: Diabetes in America. 2023. Available from: [LINK].
- Barrett TG. Differential diagnosis of type 1 diabetes: which genetic syndromes need to be considered? Pediatric Diabetes. 2007. Available from: [LINK].
- Khardori R. Type 1 Diabetes Mellitus Differential Diagnoses. Medscape. 2025. Available from: [LINK].
- Association of British Clinical Diabetologists. Best Practice Guide: Continuous subcutaneous insulin infusion (CSII) A clinical guide for adult diabetes services. 2018. Available from: [LINK].
- Mäkimattila S, Harjutsalo V, Forsblom C, et al. Every Fifth Individual With Type 1 Diabetes Suffers From an Additional Autoimmune Disease: A Finnish Nationwide Study. Diabetes Care. 2020. Available from: [LINK].
- NHS Inform. Hypoglycaemia (low blood sugar). 2025. Available from: [LINK].
- Mayo Clinic. Hypoglycemia. 2023. Available from: [LINK].
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