Normal C-peptide levels in type 2 diabetes typically range from 0.37 to 1.47 nmol/L in healthy individuals, though patients with type 2 diabetes often show normal or elevated levels, particularly in early disease. C-peptide is a protein fragment released alongside insulin by pancreatic beta cells, providing a stable marker of endogenous insulin production. Unlike insulin, it is not cleared by the liver on first pass, making it clinically useful for assessing residual pancreatic function. In type 2 diabetes, C-peptide testing helps distinguish diabetes subtypes, guide treatment decisions, and monitor disease progression. Understanding your C-peptide level—interpreted with concurrent glucose and clinical context—can inform whether oral medications remain appropriate or insulin therapy may be needed.

What Is C-Peptide and Why Does It Matter in Type 2 Diabetes?

C-peptide (connecting peptide) is a protein fragment produced by pancreatic beta cells during the synthesis of insulin. When the pancreas manufactures insulin, it initially creates a precursor molecule called proinsulin, which is then cleaved into two components: insulin itself and C-peptide. These are released into the bloodstream in equimolar amounts—meaning that for every molecule of insulin produced, one molecule of C-peptide is also released.

Unlike insulin, C-peptide is not removed by the liver during its first pass through the circulation, making it a more stable marker of endogenous insulin production. However, C-peptide levels must be interpreted alongside a concurrent plasma glucose measurement and renal function, as both glucose concentration and kidney impairment affect results. Reduced renal function can elevate C-peptide due to decreased clearance, potentially confounding interpretation.

In type 2 diabetes, C-peptide measurement serves several important clinical purposes. It helps clinicians distinguish between type 1 and type 2 diabetes in ambiguous cases, assess residual beta-cell function, and support treatment decisions. Patients with type 2 diabetes typically maintain some degree of insulin production, even years after diagnosis, though this may decline over time. Understanding a patient's C-peptide level—interpreted with concurrent glucose and clinical context—can inform whether they are likely to respond to oral hypoglycaemic agents or whether insulin therapy may be required.

C-peptide testing is particularly useful when there is diagnostic uncertainty, such as in lean patients presenting with hyperglycaemia, or when determining whether a patient has latent autoimmune diabetes in adults (LADA). The test provides objective evidence of pancreatic reserve and can help predict disease progression and treatment response. NICE guidance (NG17) recommends considering C-peptide and islet autoantibody testing when diabetes type is uncertain and classification will influence management.

Normal C-Peptide Levels in Type 2 Diabetes: Reference Ranges

In the UK, C-peptide results are typically reported in nanomoles per litre (nmol/L). Reference ranges in healthy individuals generally fall between 0.37 and 1.47 nmol/L (approximately 1.1 to 4.4 nanograms per millilitre, ng/mL), though ranges vary between laboratories depending on the assay methodology used. Results should always be interpreted in the context of the specific laboratory's reference values, a concurrent plasma glucose measurement (ideally 4–13 mmol/L), and renal function.

In type 2 diabetes, C-peptide levels are often normal or elevated, particularly in the early stages of the disease. This reflects the underlying pathophysiology of type 2 diabetes, which is characterised by insulin resistance rather than absolute insulin deficiency. The pancreas initially compensates for insulin resistance by producing more insulin (and consequently more C-peptide), leading to hyperinsulinaemia. C-peptide levels in newly diagnosed type 2 diabetes may range from normal to significantly elevated.

As type 2 diabetes progresses, beta-cell function may gradually decline due to glucotoxicity, lipotoxicity, and chronic metabolic stress. In long-standing type 2 diabetes, C-peptide levels may fall into the lower end of the normal range or become subnormal, indicating progressive beta-cell failure. C-peptide levels below 0.2 nmol/L (approximately <0.6 ng/mL) generally suggest severe insulin deficiency and indicate that the patient will likely require insulin therapy. Levels between 0.2 and 0.6 nmol/L are considered indeterminate and require clinical correlation.

Stimulated C-peptide testing—performed after a glucagon injection or mixed meal—can provide additional information about pancreatic reserve when arranged through specialist services. A stimulated C-peptide level above 0.6 nmol/L (approximately >1.8 ng/mL) typically indicates preserved beta-cell function, whilst lower values suggest significant impairment. In UK practice, non-fasting or random C-peptide sampling with a paired plasma glucose is often preferred for diagnostic classification, as it is pragmatic and reflects real-world beta-cell function. These dynamic or paired tests are particularly useful when fasting levels are equivocal or when assessing suitability for certain diabetes treatments.

When to Request C-Peptide Testing: NHS and NICE Guidance

NICE guidance (NG17) does not mandate routine C-peptide testing for all patients with diabetes, but recommends considering C-peptide and islet autoantibody testing when there is diagnostic uncertainty and classification will directly influence management decisions.

Key indications for C-peptide testing include:

• Distinguishing between type 1 and type 2 diabetes in patients with atypical presentations, such as lean individuals with hyperglycaemia or those diagnosed in young adulthood without clear autoimmune markers

• Suspected LADA (latent autoimmune diabetes in adults), where patients may initially respond to oral agents but have underlying autoimmune beta-cell destruction

• Assessing residual insulin production in patients with long-standing diabetes who are experiencing recurrent hypoglycaemia or deteriorating glycaemic control

• Investigating factitious hypoglycaemia or suspected exogenous insulin administration, where C-peptide will be suppressed despite elevated insulin levels

Within the NHS, C-peptide testing is typically requested by diabetes specialists rather than in primary care, though GPs may initiate the test in consultation with secondary care colleagues. UK practice commonly uses a non-fasting or random sample with a paired plasma glucose measurement (ideally when glucose is 4–13 mmol/L), as this is pragmatic and reflects real-world beta-cell function. Stimulated tests (mixed meal or glucagon) may be arranged through specialist services when indicated.

It is important to note that C-peptide testing should be interpreted alongside other clinical information, including diabetes autoantibodies (GAD, IA-2, ZnT8), HbA1c, renal function, and the patient's clinical presentation. A single C-peptide result provides a snapshot of beta-cell function at that moment, and serial measurements may be needed to assess disease progression. Do not stop or adjust insulin doses for testing unless your diabetes specialist team has given you clear instructions to do so, as this can be unsafe. If you are asked to provide a sample, your team will advise whether fasting is required or whether a random sample is appropriate. Always check with your diabetes team before making any changes to your medication.

How C-Peptide Testing Helps Diagnose and Monitor Type 2 Diabetes

C-peptide testing plays a supportive role in both the diagnostic pathway and ongoing management of type 2 diabetes, providing objective evidence of pancreatic function that cannot be obtained through glucose or HbA1c measurements alone. However, treatment decisions should follow NICE guidance (NG28) and be based on the full clinical picture, not C-peptide results in isolation.

In the diagnostic phase, C-peptide helps differentiate type 2 diabetes from other forms of diabetes. Patients with type 2 diabetes typically have normal or elevated C-peptide levels (when interpreted with concurrent glucose), reflecting preserved or even enhanced insulin production in response to insulin resistance. In contrast, patients with type 1 diabetes or advanced beta-cell failure will have low or undetectable C-peptide. This distinction is particularly important in atypical presentations—for example, a lean 35-year-old with hyperglycaemia might have type 1 diabetes, LADA, or early-onset type 2 diabetes, and C-peptide testing (alongside autoantibody screening) helps establish the correct diagnosis and treatment pathway.

For monitoring disease progression, serial C-peptide measurements can track the decline in beta-cell function over time. Whilst not routinely performed, this can be valuable in research settings or when managing patients with unusual disease trajectories. A progressive fall in C-peptide suggests ongoing beta-cell loss and may prompt earlier consideration of insulin therapy or intensification of metabolic control to preserve remaining function.

Treatment decisions can be supported by C-peptide results, but should not be determined by C-peptide alone. Patients with preserved C-peptide production are more likely to respond to oral hypoglycaemic agents, GLP-1 receptor agonists, and lifestyle interventions. Those with very low C-peptide (<0.2 nmol/L, approximately <0.6 ng/mL) will almost certainly require insulin therapy and are unlikely to benefit from medications that rely on endogenous insulin secretion, such as sulphonylureas or meglitinides. However, some therapies—such as SGLT2 inhibitors—have benefits for glycaemic control, cardiovascular and renal protection irrespective of residual beta-cell function, and should be considered according to NICE NG28 guidance.

Patients should be counselled that declining C-peptide is a natural part of disease progression in some individuals and does not represent treatment failure, but rather indicates the need for treatment adjustment. If you experience symptoms of poor glycaemic control—such as increased thirst, frequent urination, unexplained weight loss, or persistent fatigue—contact your GP or diabetes team promptly, as these may indicate declining beta-cell function requiring treatment modification. Seek urgent same-day medical care or call 999 if you develop marked hyperglycaemia with ketones, abdominal pain, vomiting, drowsiness, or rapid breathing, as these may indicate diabetic ketoacidosis (DKA) or hyperosmolar hyperglycaemic state (HHS), both of which require emergency treatment.

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