Insulin Resistance and Metabolic Hormone Panel

Insulin resistance occurs when cells in the muscles, liver, and fat tissue become less responsive to the insulin signal. The pancreas compensates by producing more insulin to maintain blood glucose control — a state of hyperinsulinaemia. Over time, this leads to progressively higher fasting insulin levels, rising blood glucose, increased fat storage (particularly visceral), systemic inflammation, and eventually impaired glucose tolerance or type 2 diabetes. Elevated fasting insulin is one of the earliest detectable markers — often appearing years before HbA1c becomes abnormal.

HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) is a formula-based index calculated from fasting insulin and fasting glucose. It is widely used in research and increasingly in clinical practice as a practical measure of insulin resistance. Your Trupoint Health physician report will calculate and report your HOMA-IR score alongside an interpretation of what it means in your context. A score below 1.0 generally indicates good insulin sensitivity; above 2.0 suggests developing insulin resistance; above 2.9 is consistent with significant insulin resistance in most adult populations.

Adiponectin is produced by fat cells (adipocytes) and has powerful insulin-sensitising and anti-inflammatory effects. Paradoxically, people with more body fat (particularly visceral fat) have lower adiponectin levels — a finding that helps explain why visceral obesity drives metabolic disease even in people who appear otherwise healthy. Low adiponectin is an independent predictor of insulin resistance, type 2 diabetes, and cardiovascular disease — sometimes identifying risk years before standard markers become abnormal. Including adiponectin gives a forward-looking view of metabolic trajectory that fasting glucose and HbA1c alone do not provide.

Cortisol, the primary stress hormone, directly promotes gluconeogenesis (glucose production by the liver) and stimulates fat storage in the abdominal region. Chronically elevated cortisol drives up blood glucose and insulin demand, and reduces the sensitivity of cells to insulin over time. The cortisol-to-dehydroepiandrosterone sulphate (DHEA-S) ratio in this panel reflects this dynamic: a high cortisol with low dehydroepiandrosterone sulphate (DHEA-S) suggests chronic adrenal stress burden that may be contributing to the metabolic picture. Addressing cortisol excess through sleep, stress management, and appropriate support can be an important adjunct to standard metabolic interventions.

The most evidence-based interventions for improving insulin sensitivity include: resistance training (which increases muscle glucose uptake and GLUT4 expression); reducing refined carbohydrate and added sugar intake; increasing dietary fibre; improving sleep quality and duration (poor sleep acutely increases insulin resistance); losing even 5 to 10% of body weight if overweight; and intermittent fasting or time-restricted eating in appropriate individuals. Regular walking after meals has also been shown to substantially reduce postprandial glucose and insulin spikes. Monitoring your fasting insulin and HOMA-IR every 3 to 6 months is a useful way to track the metabolic impact of these changes.

Yes, particularly if fasting insulin, glucose, or HbA1c are outside the reference range. While this panel is a screening and monitoring tool rather than a diagnostic test, significantly elevated fasting insulin, impaired fasting glucose (6.1 to 6.9 mmol/L), or HbA1c in the pre-diabetic range (42 to 47 mmol/mol) are all findings that warrant a conversation with your GP. Your Trupoint Health physician report will provide clear guidance on whether and how urgently a GP consultation is recommended. Early identification and intervention at the pre-diabetes stage can prevent or delay progression to type 2 diabetes in the majority of cases.