Disclosure: Metabolic Media is an independent educational publisher. We may have a financial affiliation with some entities featured on this site. Rank positions are determined by our published methodology. We do not provide medical care, diagnoses, or treatment.
The short answer: Insulin resistance means muscle, fat, and liver cells respond poorly to insulin, so the pancreas makes extra to keep blood glucose in range. It usually causes no symptoms and is rarely tested directly in routine care. Over time it can lead to prediabetes and type 2 diabetes; physical activity, weight management, and sleep may improve insulin sensitivity.
Plenty of articles about insulin resistance open with a meal plan or a supplement. This episode in the Read queue takes a different angle: what the process is, how it relates to prediabetes, and what lab tests can and can’t tell you. When you’re done, you’ll find more metabolic health explainers on the Read hub.
What is insulin resistance?
Start with insulin itself. After you eat, food is broken down into sugars that circulate in your blood, and the pancreas releases insulin. The CDC describes insulin as acting “like a key” that lets blood sugar into cells, which use it for energy. Insulin also signals the liver to store extra glucose and release it when you haven’t eaten in a while (CDC).
Insulin resistance means cells in the muscles, fat, and liver don’t respond well to insulin (NIDDK). To make up for it, the pancreas releases more insulin to push glucose into those cells. For a while, that extra effort can keep blood glucose in range. Over time, though, the pancreas may not keep up, and blood glucose starts to climb (CDC; NIDDK).
The cause isn’t fully settled. NIDDK notes that researchers “don’t fully understand” what causes insulin resistance and prediabetes, although people with risk factors for type 2 diabetes are more likely to develop them.
How is insulin resistance different from prediabetes and type 2 diabetes?
Picture a continuum rather than three separate boxes:
- Insulin resistance. Cells respond less to insulin, and the pancreas works harder, making more.
- Prediabetes. Blood glucose is higher than typical but not high enough to be diagnosed as type 2 diabetes (NIDDK).
- Type 2 diabetes. Blood glucose reaches the diabetes range.
The key difference: insulin resistance describes a process, while prediabetes is a diagnosis made from blood tests. As of the ADA’s Standards of Care in Diabetes, 2026 (Section 2, Table 2.2), prediabetes is defined by any one of these results:
- A1C: 5.7% to 6.4%
- Fasting plasma glucose: 100 to 125 mg/dL (impaired fasting glucose)
- 2-hour glucose on a 75-g oral glucose tolerance test (OGTT): 140 to 199 mg/dL (impaired glucose tolerance)
The ADA adds an important caveat: for all three tests, risk is continuous. It extends below the lower limit of each range and becomes disproportionately greater toward the higher end. These numbers mark points on a sliding scale, not an on/off switch.
Prediabetes is common. According to the CDC’s National Diabetes Statistics Report (updated Sept 2026), about 115.2 million U.S. adults have prediabetes.
Type 1 diabetes is a different process. The CDC explains that it is thought to be caused by an autoimmune reaction: people with type 1 diabetes don’t make any or enough insulin, while people with insulin resistance don’t respond well to the insulin they make.
Who is more likely to develop insulin resistance?
NIDDK lists several factors that raise the chances of developing insulin resistance or prediabetes:
- Overweight, obesity, or a large waist size
- Being age 35 or older (children and teens can develop it too)
- A family history of diabetes
- Not being physically active
- Smoking, including e-cigarettes, or exposure to secondhand smoke
- A history of gestational diabetes
- Conditions such as polycystic ovary syndrome (PCOS) and sleep apnea
- Taking certain medicines over time, such as glucocorticoids, some antipsychotics, and some HIV medicines
The CDC also lists high triglycerides and low HDL (“good”) cholesterol among the risk factors.
One point from the CDC is worth underlining: “You can’t tell if someone has insulin resistance by looking at them.” Overweight and obesity are risk factors, but you don’t need to have either to have insulin resistance.
Does insulin resistance cause symptoms?
Usually not. NIDDK says people with insulin resistance and prediabetes usually have no symptoms, though some people with prediabetes may have symptoms similar to those of diabetes. That quietness is why screening for prediabetes matters.
As of the ADA’s 2026 Standards of Care, the screening framework looks like this:
- Testing for all adults begins at age 35.
- Screening should be considered at any age for adults with overweight or obesity plus one or more risk factors for diabetes.
- People with prediabetes should be tested yearly.
- If results are normal, testing is repeated at least every three years, sooner if risk changes.
These are population-level guidelines; your clinician decides which tests make sense for you.
How do clinicians check for it, and what is HOMA-IR?
Routine care centers on prediabetes rather than insulin resistance itself. Clinicians use A1C, fasting plasma glucose, or an OGTT to check glucose levels, and because blood fats can rise with insulin resistance or prediabetes, they may also recommend cholesterol and triglyceride tests (NIDDK).
Direct testing is rarer. NIDDK says health care professionals “may not test for insulin resistance” and that the test “is primarily used only for research studies.”
You may still run into HOMA-IR (homeostasis model assessment of insulin resistance). It was introduced in a 1985 paper by Matthews and colleagues and estimates insulin resistance from a single fasting glucose value and a single fasting insulin value. In that paper, HOMA-IR correlated well with the euglycemic clamp, a more intensive research method (Rs = 0.88). The authors also reported a coefficient of variation of 31% for insulin resistance and wrote that this low precision “limits its use.”
In 2004, Wallace, Levy, and Matthews reviewed how HOMA was being used. They described appropriate uses, such as cohort and epidemiological studies, and cautioned that the input data need to be robust and interpreted carefully.
So HOMA-IR is useful research context, not a home diagnosis. There is no single agreed clinical cutoff, and results vary with the lab’s insulin assay and the population studied. If one shows up on a lab report, a clinician can put it in context.
What other conditions are linked to insulin resistance?
NIDDK lists several health problems that people with insulin resistance and prediabetes can develop:
- High blood pressure.
- Metabolic syndrome. This is a group of conditions, including high blood pressure and a large waist size, that raises the risk for heart disease, diabetes, and stroke.
- MASLD. Metabolic dysfunction-associated steatotic liver disease was formerly called nonalcoholic fatty liver disease (NAFLD).
- Unhealthy cholesterol and triglyceride levels. NIDDK notes that blood fat levels may go up with insulin resistance or prediabetes.
- Type 2 diabetes. The far end of the continuum described above.
“Linked” doesn’t mean every person with insulin resistance will develop these conditions.
What does research show about improving insulin sensitivity?
The CDC and NIDDK point to everyday factors. The CDC notes that physical activity makes the body more sensitive to insulin, and that weight loss for people with overweight or obesity can increase insulin sensitivity. It also describes eating patterns built around non-starchy vegetables, fruits, whole grains, and lean proteins as helping to lower blood sugar. NIDDK also lists getting enough sleep.
For trial evidence, look to the Diabetes Prevention Program (DPP), published in the New England Journal of Medicine in 2002 (PubMed):
- Who took part: 3,234 adults without diabetes but with elevated fasting and post-load glucose (measured after a glucose drink). Their mean age was 51 and mean BMI was 34.0; 68% were women, and 45% were from minority groups.
- What the lifestyle program aimed for: at least 7% weight loss and at least 150 minutes of physical activity per week.
- How long: an average of 2.8 years of follow-up.
- What happened in the trial: diabetes developed at a rate of 11.0 cases per 100 person-years in the placebo group, compared with 4.8 cases per 100 person-years in the lifestyle group. That works out to a 58% relative reduction.
Two caveats: the DPP measured whether people developed type 2 diabetes, not insulin resistance directly, and these are group results from one trial population, not a promise for any individual. The trial also tested a medication arm; whether any medication fits is a decision for a clinician.
Current guidance describes similar goals. The ADA’s 2026 Standards of Care (Section 3) describe diabetes prevention programs for adults with overweight or obesity at high risk of type 2 diabetes, aimed at a weight reduction of at least 5% to 7% and at least 150 minutes per week of moderate-intensity physical activity.
What questions can you bring to your care team?
If you’re curious about your own risk, these questions can help:
- Which test did I have: A1C, fasting glucose, or an OGTT?
- What do my results mean, and when should I be retested?
- Do any of my current medicines affect blood glucose?
- Would a structured lifestyle program, like the kind tested in the DPP, fit my situation?
A clinician who knows your history is the right person to interpret your results.
Frequently asked questions
Can you have insulin resistance at a normal weight?
Yes. The CDC notes that although overweight and obesity are risk factors, you don’t need to have either to have insulin resistance. Other risk factors include family history and physical inactivity.
Is insulin resistance the same as prediabetes?
No. Insulin resistance is a process in which cells respond poorly to insulin. Prediabetes is a diagnosis based on A1C, fasting glucose, or OGTT ranges defined in the ADA’s 2026 Standards of Care.
Is there a “normal” HOMA-IR number?
There’s no single agreed clinical cutoff. HOMA-IR was built as a research model, and results vary by lab assay and population (Matthews et al., 1985; Wallace et al., 2004).
Does insulin resistance always lead to type 2 diabetes?
No. NIDDK notes that not everyone with prediabetes develops type 2 diabetes, and in the DPP trial, a lifestyle program lowered the rate of new diabetes cases.
Can insulin sensitivity improve?
Research links physical activity, weight management, and sleep to better insulin sensitivity. Results vary from person to person, and a clinician can help interpret your labs.
Sources
- American Diabetes Association Professional Practice Committee. 2. Diagnosis and Classification of Diabetes: Standards of Care in Diabetes—2026. Diabetes Care 2026;49(Suppl 1):S27. (PMC)
- American Diabetes Association Professional Practice Committee. 3. Prevention or Delay of Diabetes and Associated Comorbidities: Standards of Care in Diabetes—2026. Diabetes Care 2026;49(Suppl 1):S50. (PMC)
- Centers for Disease Control and Prevention. About Insulin Resistance and Type 2 Diabetes.
- Centers for Disease Control and Prevention. National Diabetes Statistics Report. Updated Sept 2026.
- National Institute of Diabetes and Digestive and Kidney Diseases. Insulin Resistance & Prediabetes. Last reviewed March 2025.
- Matthews DR, Hosker JP, Rudenski AS, et al. Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985;28(7):412–419. (PubMed)
- Wallace TM, Levy JC, Matthews DR. Use and Abuse of HOMA Modeling. Diabetes Care 2004;27(6):1487–1495.
- Diabetes Prevention Program Research Group (Knowler WC, et al.). Reduction in the Incidence of Type 2 Diabetes with Lifestyle Intervention or Metformin. N Engl J Med 2002;346(6):393–403. (PubMed)
This article is for general education. It isn’t a substitute for personal medical advice. If you have questions about insulin resistance, prediabetes, or your lab results, talk with a licensed clinician who knows your health history.
Disclosure: Metabolic Media is an independent educational publisher. We may have a financial affiliation with some entities featured on this site. Rank positions are determined by our published methodology. We do not provide medical care, diagnoses, or treatment.
Medical disclaimer: Content on Metabolic Media is for educational purposes only and is not medical advice, diagnosis, or treatment. We are not a medical provider, pharmacy, or telehealth clinic. Always consult a licensed clinician. If you have a medical emergency, call 911 (US) or your local emergency number.