Insulin resistance is a weakened response of the muscles, liver and fat tissue to insulin, the hormone that allows glucose into cells. The pancreas compensates by producing more insulin: blood glucose stays normal for a long time and the problem often goes unnoticed. Mechanisms, tests, demonstrated approaches and supplements: here is what studies say.
Key takeaways
- Muscle insulin resistance can precede type 2 diabetes by several decades.
- HOMA-IR is not part of any official definition: blood glucose, HbA1c, waist circumference and triglycerides guide the doctor.
- In 3,234 at-risk adults, aiming for 7% weight loss and 150 minutes of activity per week reduced new diabetes cases by 58%.
- Berberine, magnesium, inositol, cinnamon and chromium: modest or uncertain effects; only chromium has an authorised claim for blood glucose.
What is insulin resistance?
It is a reduced tissue response to insulin: more is needed to achieve the same effect. Three organs are involved:
- muscle, which takes up around 80% of glucose during an insulin infusion. When resistant, it stores less as glycogen;
- the liver, whose glucose production determines fasting blood glucose. Insulin slows this production; when resistant, the liver releases too much;
- fat tissue, where insulin slows the release of fat. When resistant, it allows fatty acids to flow into the blood.
As long as the pancreas compensates by secreting more insulin, blood glucose holds steady. Type 2 diabetes develops when its insulin-producing cells become exhausted, sometimes decades later.
Why does fat around the belly and organs matter?
Because location matters. Waist circumference reflects abdominal fat, including visceral fat surrounding the organs: it is a criterion for metabolic syndrome. Ectopic fat infiltrates organs not designed to store it. In muscle, its derivatives, such as diacylglycerols and ceramides, disrupt insulin signalling. Fatty liver, or steatosis, is associated with insulin resistance.
Insulin resistance, prediabetes and diabetes: what is the difference?
Insulin resistance is a mechanism, not a disease defined by thresholds. Prediabetes and type 2 diabetes are diagnosed using blood glucose or glycated haemoglobin (HbA1c). According to the American Diabetes Association (ADA):
- prediabetes: fasting blood glucose of 1.00 to 1.25 g/L, HbA1c of 5.7 to 6.4%, or blood glucose of 1.40 to 1.99 g/L two hours after 75 g of glucose;
- diabetes: fasting blood glucose of at least 1.26 g/L, HbA1c of at least 6.5%, or 2.00 g/L at two hours, to be confirmed by a second test.
Metabolic syndrome combines at least three of five criteria: a high waist circumference, with population-specific thresholds; triglycerides of at least 1.50 g/L; HDL cholesterol below 0.40 g/L in men or 0.50 g/L in women; blood pressure of at least 130/85 mmHg; and fasting blood glucose of at least 1.00 g/L.
How can you tell if you have insulin resistance?
No routine test measures it directly. The reference method, the hyperinsulinaemic euglycaemic clamp, involving insulin and glucose infusion over several hours, is mainly used in research. The doctor therefore combines several indicators.
Which blood tests? Glucose, insulin and HOMA-IR
A fasting blood sample measures glucose and, when prescribed, insulin. The laboratory calculates HOMA-IR from these values. It mainly reflects liver sensitivity and reasonably tracks the reference method. In an oral glucose tolerance test (OGTT), you drink 75 g of glucose, then glucose and sometimes insulin are measured over two hours. Its indices, such as the Matsuda index, incorporate both liver and muscle.
Are there symptoms?
Most often, no: it develops silently. However, some signs should prompt investigation:
- a large waist circumference, high triglycerides, low HDL cholesterol, high blood pressure, inactivity or a close relative with diabetes;
- acanthosis nigricans, brown, velvety patches on the neck, armpits or skin folds associated with insulin resistance;
- polycystic ovary syndrome (PCOS), in which insulin resistance is common;
- fatty liver, or hepatic steatosis.
According to the ADA, these last three conditions justify investigating prediabetes in adults with overweight.
Which approaches have proved effective?
Moderate weight loss and physical activity lead the way; sleep and diet complete the picture, far ahead of supplements.
Losing a little weight and moving: the large trials
Two randomised trials followed adults with overweight whose blood glucose was already too high. In the Finnish DPS study with 522 participants in 2001, advice aimed to promote weight loss, less saturated fat, more fibre and physical activity. Participants lost only 4.2 kg in the first year, compared with 0.8 kg in controls, yet diabetes risk fell by 58%: 11% developed diabetes over four years, compared with 23%.
The American DPP trial with 3,234 participants in 2002 aimed for 7% weight loss and 150 minutes of activity per week. Over 2.8 years, diabetes incidence fell by 58% compared with placebo. Supporting around 7 people for three years prevented one case.
Why every exercise session matters, including strength training
Because a session's effect is immediate, then fades: muscle insulin sensitivity can remain higher for up to 72 hours. In 18 adults with prediabetes tested one hour after exercise, it improved by 51% with moderate exercise or 85% with intense exercise, without a significant difference between the two.
Strength training has a role, since muscle is the main consumer of glucose under insulin's influence. Endurance and resistance training both improve glucose control, and combining them appears more effective in some studies. Physical activity is also the best-studied approach for muscle NAD+ (see our guide to increasing NAD+).
Does less sleep cause insulin resistance?
Yes, within weeks. In a randomised crossover trial published in 2024, 38 healthy women slept 1 hour 20 minutes less per night for six weeks, around 6 hours 10 minutes of sleep. Their fasting insulin and HOMA-IR increased independently of fat mass, particularly after menopause. See also our article on sleep and melatonin.
Which diet? Fibre, Mediterranean eating and ultra-processed foods
A Mediterranean pattern was tested in 180 adults with metabolic syndrome in 2004. The advised group ate more whole grains, fruit, vegetables, nuts and olive oil, and therefore more fibre. After two years, insulin resistance had decreased, and 40 patients still had metabolic syndrome, compared with 78 controls. Greater weight loss, 4 kg versus 1.2 kg, could explain part of the effect.
In the French NutriNet-Santé cohort of 104,707 adults with a median follow-up of six years, every 10-percentage-point increase in the proportion of ultra-processed foods was associated with a 15% higher type 2 diabetes risk after accounting for weight. This observational study does not prove causation.
Food supplements: what do studies show?
None replaces these approaches: measured effects on HOMA-IR are modest and the evidence uneven.
Berberine. A 2023 meta-analysis restricted to placebo-controlled trials, with 20 trials and 1,761 participants, measured a 0.85-point decrease in HOMA-IR across 12 trials. No claim is authorised for berberine, which ANSES particularly discourages in people with diabetes (precautions detailed in our article on berberine).
Magnesium. In a 2021 meta-analysis of double-blind trials, it slightly improved HOMA-IR in at-risk people across 9 trials, but not in people with diabetes across 4 trials. None of its authorised claims concerns blood glucose (see our comparison of magnesium forms).
Inositol. Studied mainly in PCOS, inositol, whether myo- or D-chiro-inositol, was the subject of a 2024 meta-analysis of 30 trials with 2,230 women that considered the evidence “limited and inconclusive”. Myo-inositol does no better than metformin for HOMA-IR, but causes far fewer digestive complaints. No claim is authorised.
Cinnamon. Across 16 trials in people with diabetes or prediabetes in 2019, it lowered HOMA-IR by 0.71 and fasting glucose by around 0.10 g/L, without an effect on HbA1c. Results varied considerably between trials. No claim is authorised.
Chromium. It is the only one of the five with an authorised claim on this topic: “Chromium contributes to the maintenance of normal blood glucose levels”, for a food that is “at least a source of trivalent chromium” under Regulation (EC) No 1924/2006. The claim does not concern diabetes: of 20 trials in type 2 diabetes, only 5 achieved a clinically useful fasting glucose target.
Other, less firmly supported possibilities are discussed in our articles on gymnema, resveratrol and the NMN or NR comparison.
| Approach | Measured effect | Population and study | Strength of evidence |
|---|---|---|---|
| Weight and activity | Diabetes: −58% | 3,234 adults (DPP, 2002) | High |
| Exercise session | Effect up to 72 hours | Review of trials (2017) | High |
| Sleep −1 hour 20 minutes | HOMA-IR: +0.30 | 38 women (2024) | Moderate |
| Mediterranean eating | Metabolic syndrome: 40 cases versus 78 | 180 adults (2004) | Moderate |
| Ultra-processed foods | Diabetes: +15% per 10 percentage points | 104,707 adults (2020) | Observational |
| Berberine | HOMA-IR: −0.85 | 12 trials | Moderate |
| Magnesium | HOMA-IR: small, inconsistent effect | 9 trials | Low |
| Myo-inositol | No better than metformin | 5 trials, PCOS | Low |
| Cinnamon | HOMA-IR: −0.71 | 16 trials | Low |
| Chromium | 5 of 20 trials reached the target | Type 2 diabetes | Low |
When should you consult, and which tests should you request?
Consult your usual doctor if you have several indicators: a large waist circumference, a close relative with diabetes, PCOS, diabetes during pregnancy, acanthosis nigricans, high triglycerides or high blood pressure. Intense thirst, frequent large-volume urination or unexplained weight loss require prompt advice: they may be signs of diabetes.
Basic examinations include fasting blood glucose, possibly HbA1c, a lipid profile, blood pressure and waist circumference. The doctor may add an OGTT, insulin measurement or liver tests, then refer you to an endocrinologist specialising in diabetes, a gynaecologist for PCOS or a dietitian.
Frequently asked questions
Can you have insulin resistance without being overweight?
Yes. Lean adults with normal blood glucose whose parents both have type 2 diabetes already have moderate to severe muscle insulin resistance; their lifetime diabetes risk is around 40%. Heredity, inactivity and lack of sleep can act independently of weight.
Is insulin resistance reversible?
It can improve considerably: insulin sensitivity increases when physical activity recommendations are followed. Inherited susceptibility remains, and the benefit lasts only if the habits are maintained.
What HOMA-IR value is considered normal?
There is no official threshold: HOMA-IR is not included in the criteria for prediabetes or metabolic syndrome. Since insulin measurements differ between laboratories, a result must be interpreted with your doctor.
Can a glucose sensor detect it on its own?
No. A sensor measures glucose, not insulin. While the pancreas compensates, blood glucose stays almost normal even though insulin is high. Prediabetes screening relies on fasting glucose, HbA1c or an OGTT.
Which exercise should you choose?
One you will practise regularly. Greater energy expenditure and intensity, such as interval training, often produce better results, although studies do not agree unanimously. In observational cohorts, type 2 diabetes risk falls as weekly physical activity expenditure rises.
Is metformin prescribed for insulin resistance?
It may be, on a doctor's decision and prescription. In the DPP trial, 850mg twice daily reduced the development of diabetes by 31%, less than the lifestyle programme, which remains the first step.
Conclusion
Insulin resistance is a silent mechanism that may precede type 2 diabetes by many years. More than a HOMA-IR number, blood glucose, HbA1c, waist circumference and triglycerides guide the doctor. The best-supported approaches require consistency: lose a few kilos, move every week including muscle training, sleep well, and eat minimally processed, fibre-rich food. Supplements offer only modest effects at best.
Sources
- DeFronzo RA, Tripathy D (2009). Skeletal muscle insulin resistance is the primary defect in type 2 diabetes. Diabetes Care, 32(Suppl 2), S157-S163. doi:10.2337/dc09-S302
- American Diabetes Association Professional Practice Committee (2025). 2. Diagnosis and classification of diabetes: Standards of Care in Diabetes—2025. Diabetes Care, 48(Suppl 1), S27-S49. doi:10.2337/dc25-S002
- Alberti KGMM et al. (2009). Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation, 120(16), 1640-1645. doi:10.1161/CIRCULATIONAHA.109.192644
- Knowler WC et al. (2002). Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. New England Journal of Medicine, 346(6), 393-403. doi:10.1056/NEJMoa012512
- Tuomilehto J et al. (2001). Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. New England Journal of Medicine, 344(18), 1343-1350. doi:10.1056/NEJM200105033441801
- Bird SR, Hawley JA (2017). Update on the effects of physical activity on insulin sensitivity in humans. BMJ Open Sport & Exercise Medicine, 2(1), e000143. doi:10.1136/bmjsem-2016-000143
- Zuraikat FM et al. (2024). Chronic insufficient sleep in women impairs insulin sensitivity independent of adiposity changes: results of a randomized trial. Diabetes Care, 47(1), 117-125. doi:10.2337/dc23-1156
- Esposito K et al. (2004). Effect of a Mediterranean-style diet on endothelial dysfunction and markers of vascular inflammation in the metabolic syndrome: a randomized trial. JAMA, 292(12), 1440-1446. doi:10.1001/jama.292.12.1440
- Srour B et al. (2020). Ultraprocessed food consumption and risk of type 2 diabetes among participants of the NutriNet-Santé prospective cohort. JAMA Internal Medicine, 180(2), 283-291. doi:10.1001/jamainternmed.2019.5942
- Zhao JV et al. (2023). Overall and sex-specific effect of berberine on glycemic and insulin-related traits: a systematic review and meta-analysis of randomized controlled trials. Journal of Nutrition, 153(10), 2939-2950. doi:10.1016/j.tjnut.2023.08.016
- Veronese N et al. (2021). Oral magnesium supplementation for treating glucose metabolism parameters in people with or at risk of diabetes: a systematic review and meta-analysis of double-blind randomized controlled trials. Nutrients, 13(11), 4074. doi:10.3390/nu13114074
- Fitz V et al. (2024). Inositol for polycystic ovary syndrome: a systematic review and meta-analysis to inform the 2023 update of the international evidence-based PCOS guidelines. Journal of Clinical Endocrinology and Metabolism, 109(6), 1630-1655. doi:10.1210/clinem/dgad762
- Deyno S et al. (2019). Efficacy and safety of cinnamon in type 2 diabetes mellitus and pre-diabetes patients: a meta-analysis and meta-regression. Diabetes Research and Clinical Practice, 156, 107815. doi:10.1016/j.diabres.2019.107815
- Costello RB, Dwyer JT, Bailey RL (2016). Chromium supplements for glycemic control in type 2 diabetes: limited evidence of effectiveness. Nutrition Reviews, 74(7), 455-468. doi:10.1093/nutrit/nuw011
Food supplements do not replace a varied, balanced diet or a healthy lifestyle. Ask a healthcare professional for advice if you are taking medication, pregnant or breastfeeding.
