Insulin resistance develops when cells in the muscles, liver and adipose tissue become less responsive to insulin. While the mechanism is not fully understood, several credible theories have been proposed including the accumulation of fat in the liver, reticulum stress and general inflammation.^¹

This process often develops gradually and may not cause noticeable symptoms. However, it is important because insulin resistance can contribute to prediabetes, type 2 diabetes and a broader pattern of metabolic health problems.

• Insulin resistance means the body needs more insulin than usual to manage glucose effectively.
• The pancreas can compensate for a time by releasing additional insulin.
• Blood glucose may remain within the normal range during the early stages.
• Insulin resistance involves the muscles, liver and adipose tissue - not just blood glucose.
• Genetics, body-fat distribution, physical activity, sleep, medical conditions and some medicines can all influence risk.
• Physical activity, dietary changes, weight management where appropriate and medical care can improve insulin sensitivity.

Insulin resistance is a state of reduced biological responsiveness to the hormone insulin.^¹

Insulin is produced by beta cells in the pancreas. After carbohydrate-containing foods are digested, glucose enters the bloodstream. Rising blood glucose signals the pancreas to release insulin, which helps coordinate how the body uses and stores this glucose.

Insulin has several important functions:

• It helps skeletal muscle take glucose out of the bloodstream.
• It tells the liver to reduce its production and release of glucose.
• It supports the storage of glucose as glycogen.
• It suppresses the breakdown of stored fat in adipose tissue.
• It influences the metabolism of carbohydrates, fats and proteins.

When tissues become resistant to insulin, these processes become less efficient. The body therefore needs a greater amount of insulin to achieve the same metabolic effect.

Insulin acts by binding to insulin receptors on the surface of responsive cells. This activates a series of signalling pathways inside the cell.^²

In skeletal muscle, insulin helps move glucose transport proteins, particularly GLUT4, to the cell membrane. This allows glucose to enter the muscle, where it can be used for energy or stored as glycogen.

In the liver, insulin helps suppress glucose production between meals and encourages the storage of incoming nutrients. In adipose tissue, insulin reduces the release of fatty acids from stored triglycerides.

These tissues do not work independently. Communication between the muscles, liver, adipose tissue, pancreas and other organs helps maintain metabolic balance.

Insulin resistance does not usually result from one isolated cause. It develops through an interaction between genetic susceptibility, energy balance, body-fat distribution, physical activity, hormones, medicines and other health conditions.

The process begins when insulin-responsive tissues do not react as strongly as expected to a given amount of insulin.

The pancreas must then produce more insulin to maintain normal glucose levels.

During the early stages of insulin resistance, pancreatic beta cells often compensate by increasing insulin secretion. This is known as compensatory hyperinsulinaemia.

Because of this compensation, a person may have insulin resistance even when their fasting glucose or HbA1c is still within the normal range.

This is one reason insulin resistance can remain unnoticed. Routine glucose results may not change until the pancreas is no longer able to fully compensate for the body’s increased insulin requirements.^²

Adipose tissue is designed to store energy. However, its capacity to expand and store fat safely varies between individuals.³

Ectopic fat does not simply act as passive energy storage. It can alter signalling processes involved in glucose uptake, glucose production and lipid metabolism.

This helps explain why the location and metabolic behaviour of body fat can matter as much as total body weight. Some people develop insulin resistance at a comparatively lower body mass index, while others maintain relatively good insulin sensitivity at a higher weight.

Healthy adipose tissue stores energy and releases signalling molecules that communicate with other organs.

When adipose tissue becomes insulin resistant, it may release more fatty acids into the circulation. These fatty acids can travel to the liver and muscles, contributing to further ectopic fat accumulation and impaired insulin action.^²

Changes in inflammatory signalling and adipose-tissue hormones may also influence insulin sensitivity, although the biological relationship is complex and continues to be investigated.

A healthy liver releases glucose during fasting to ensure that the brain and other tissues have access to energy.

Insulin normally signals the liver to reduce this glucose output after eating. When the liver becomes resistant to insulin, it may continue producing and releasing more glucose than the body requires.

This excess liver glucose production can contribute to elevated fasting blood glucose.

At the same time, some of insulin’s fat-storage signals may remain active. This selective response can allow liver-fat production to continue even when insulin is no longer adequately suppressing glucose production.^²

Insulin resistance alone does not always lead to type 2 diabetes. The pancreas can sometimes compensate for many years.

Type 2 diabetes generally develops when beta-cell insulin secretion is no longer sufficient to overcome the degree of insulin resistance. Blood glucose then rises above the diagnostic threshold.^¹

The progression is not identical for everyone. Genetics, age, duration of insulin resistance, pancreatic function and other health factors influence whether, and how quickly, glucose regulation deteriorates.

There is rarely one single cause. Factors associated with a greater likelihood of insulin resistance include:

• A family history of type 2 diabetes
• Genetic susceptibility
• Low levels of physical activity
• Higher amounts of visceral or ectopic fat
• Age-related changes in body composition and muscle mass
• A history of gestational diabetes
• Polyendocrine Metabolic Ovarian Syndrome (PMOS)
• Obstructive sleep apnoea
• Some endocrine disorders
• Chronic or recurrent sleep disruption
• Certain medicines, including glucocorticoids and some antipsychotic medicines
• Lipodystrophy and other uncommon conditions affecting fat storage

People can develop insulin resistance without being overweight or obese. Conversely, a higher body weight does not automatically establish that a person has insulin resistance.

Individual risk should therefore be assessed using medical history, clinical findings and relevant pathology results rather than appearance or body weight alone.^⁴

Saying that sugar directly “causes” insulin resistance is over-simplifying the problem.

A person’s overall dietary pattern and energy intake can influence body weight, liver fat, triglycerides and glucose regulation. Diets that regularly provide more energy than the body requires may contribute to fat accumulation in insulin-responsive tissues, particularly when combined with low physical activity and genetic susceptibility.^³

However, insulin resistance is not caused by a single food or nutrient. Genetics, fat distribution, muscle activity, sleep, age, hormones, medical conditions and medicines can all contribute.

A more useful approach is to consider the overall quality, quantity and pattern of the diet rather than treating one ingredient as the sole cause.

Insulin resistance frequently causes no obvious symptoms.

A person may have elevated insulin levels for years while their glucose remains within the normal range. Symptoms may become more noticeable only after blood glucose begins to rise.

Possible clues may include:

• Prediabetes or elevated blood glucose
• High triglycerides
• Lower HDL cholesterol
• Elevated blood pressure
• Metabolic dysfunction-associated steatotic liver disease
• Polyendocrine Metabolic Ovarian Syndrome (PMOS), formerly known as Polycystic Ovarian Syndrome (PCOS).

These findings do not confirm insulin resistance on their own. They may also have other causes and should be assessed by a qualified healthcare professional.

Insulin resistance is important because it can affect more than blood glucose management.

Prediabetes occurs when blood glucose is higher than the normal range but does not meet the diagnostic criteria for diabetes.

As beta-cell compensation becomes less effective, insulin resistance can contribute to rising fasting glucose, impaired glucose tolerance and eventually type 2 diabetes.^⁴

Not everyone with insulin resistance will develop diabetes, but it is a major part of the disease process for many people with type 2 diabetes.

Insulin resistance often occurs alongside other cardiovascular risk factors, including:

• Elevated triglycerides
• Lower HDL cholesterol
• High blood pressure
• Abdominal fat accumulation
• Chronic hyperglycaemia
• Metabolic inflammation.

The combination of these factors can increase long-term cardiovascular risk. Managing insulin resistance therefore involves looking beyond blood glucose and considering blood pressure, lipids, smoking, physical activity, nutrition and other aspects of cardiovascular health.

Insulin resistance can increase fatty-acid delivery to the liver and promote liver-fat accumulation.

It is strongly connected to metabolic dysfunction-associated steatotic liver disease, or MASLD. MASLD can range from uncomplicated liver-fat accumulation to inflammation and progressive liver damage.

Insulin resistance is common in polycystic ovary syndrome, although it is not present in every person with the condition.

Higher insulin concentrations may influence ovarian hormone production and contribute to some metabolic and reproductive features of PMOS. Assessment and management should be individualised because PMOS is a complex condition with several possible clinical presentations.

There is no single routinely used test that definitively diagnoses insulin resistance in every clinical setting.

The hyperinsulinaemic-euglycaemic clamp is considered a research reference method for measuring insulin sensitivity, but it is complex and is not generally used in routine healthcare.

Clinicians may instead assess a combination of:

• Fasting plasma glucose
• HbA1c
• An oral glucose tolerance test
• Blood lipids i.e cholesterol
• Blood pressure
• Waist circumference
• Liver-health markers
• Medical and family history
• Signs of associated metabolic conditions.

Fasting insulin and calculations such as HOMA-IR are sometimes used, but test methods and interpretation thresholds are not universally standardised.

Prediabetes and diabetes are diagnosed using established glucose-based criteria - not by fasting insulin alone.⁴

Insulin sensitivity can often improve, particularly when the contributing factors can be identified and addressed.

The degree of improvement varies between individuals. Genetics, existing medical conditions, pancreatic function and the duration of metabolic changes can all influence the response.

Physical activity is one of the most effective ways to improve glucose regulation.

Contracting muscles can take up glucose through pathways that are partly independent of insulin. Regular aerobic and resistance exercise can also improve longer-term insulin sensitivity, increase muscle glucose-storage capacity and help reduce visceral and liver fat.

The most useful activity plan is one that is safe, sustainable and appropriate for the individual’s health and mobility.

There is no single diet that is appropriate for everyone with insulin resistance.

Helpful dietary patterns generally prioritise:

• Vegetables and other high-fibre foods
• Minimally processed wholegrains
• Legumes
• Nuts and seeds
• Appropriate sources of protein
• Unsaturated fats
• Portions suited to individual energy requirements.

Reducing heavily refined foods and sugar-sweetened drinks may make it easier to manage overall energy intake, glucose exposure and triglyceride levels.

Dietary advice should also consider culture, food access, allergies, medical conditions and personal preferences.

For people carrying excess visceral or ectopic fat, modest weight loss can improve insulin sensitivity and glucose regulation.

However, the clinical focus should not be limited to a number on the scale. Physical activity, muscle strength, sleep, dietary quality, liver fat, blood pressure and lipid levels can improve even when weight loss is limited.

Insufficient or disrupted sleep can affect appetite regulation, stress hormones and glucose metabolism.

Identifying and treating problems such as obstructive sleep apnoea may form part of a broader metabolic-health plan.

The term “reversed” is often used informally, but “improved” may be more accurate.

A person’s insulin sensitivity, glucose results and metabolic markers can improve substantially. Some people with prediabetes return to glucose levels below the prediabetes range.

However, an underlying predisposition may remain. Returning to previous habits, gaining visceral fat, taking certain medicines or developing another health condition may cause insulin resistance to recur.

Long-term monitoring and sustainable habits therefore remain important even when test results improve. .

Myo-inositol is the most common form of inositol in the human body. It helps create chemical messengers that allow cells to respond to signals, including signals from insulin.⁵

Inositol supplements should not be presented as a substitute for medical assessment, prescribed treatment, physical activity or an appropriate dietary pattern.

Glucerna®* is formulated specifically for people with diabetes or impaired glucose tolerance, with a low GI slow-release carbohydrate blend aiding slower glucose absorption. Glucerna®* is clinically shown to help manage blood glucose levels from Day 16, support glucose time in range within 4 weeks*7 and reduce HbA1c by 1.1% at 6 months.⁸

No. Insulin resistance can be present while blood glucose remains within the normal range because the pancreas is producing additional insulin.

Prediabetes or type 2 diabetes may develop if insulin production can no longer compensate adequately.

Yes. Genetics, fat distribution, liver and muscle fat, physical activity, sleep, hormones, medicines and medical conditions can influence insulin sensitivity independently of total body weight.

Yes. In the early stages, higher insulin production may maintain glucose within the normal range. This compensatory response can conceal reduced insulin sensitivity.

No. Progression depends on several factors, including beta-cell function, genetics and whether modifiable risk factors are addressed.

Early lifestyle and medical intervention can substantially reduce the likelihood of progression in people at high risk.

Some metabolic changes can occur relatively quickly after an increase in physical activity or a reduction in energy surplus. Larger and more durable improvements generally require consistent changes over time.

The rate of improvement varies according to the person’s health, medications, body composition and underlying causes.

Insulin resistance develops when insulin-responsive tissues require more insulin than usual to regulate glucose and energy metabolism.

The pancreas may compensate for a considerable period by producing additional insulin. However, glucose can begin to rise when this compensation is no longer sufficient.

Because insulin resistance may be present without obvious symptoms, recognising individual risk factors and completing appropriate health checks can be important. Physical activity, a sustainable dietary pattern, adequate sleep, weight management where appropriate and individualised medical care can all help improve metabolic health.

Anyone concerned about insulin resistance, prediabetes or diabetes should discuss appropriate testing and treatment with a qualified healthcare professional.

This article provides general educational information and is not a substitute for individual medical advice, diagnosis or treatment.

*Food for Special Medical Purposes. Use under medical supervision.

^†As part of a 6-month lifestyle intervention program. A 1.1% reduction in HbA1c levels was observed in the study group that received a structured lifestyle intervention with Glucerna and motivational interviewing.

^**When used as part of a diabetes management plan, people with diabetes consuming Glucerna kept blood glucose within the target glucose range of 3.9 - 10.0 mmol/L for an average of 89.5% of the time.

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4. American Diabetes Association Professional Practice Committee for Diabetes. Diabetes Care, 2026;49(Suppl 1):S27-S49,
5. Bevilacqua A, et al, Int J Endocrinol, 2018;2018:1968450,
6. Devitt A, et al. Journal of Diabetes Research and Clinical Metabolism. 2012;1(1):20,
7. Peng J, et al. Br J Nutr. 2019;121(5):560–66,
8. Chee W S S, et al. BMJ Open Diabetes Res Care. 2017;5(1):e000384.