PMOS (Formerly PCOS) and Insulin Resistance

Learn how PMOS, formerly called PCOS, is connected with insulin resistance, androgen levels, ovulation, glucose testing, and long-term metabolic health.

WEIGHT MANAGEMENT

Sarina Helton, MSN, APRN, FNP-C, CAE-OM Founder, Optima Vida Healthcare

9/9/20268 min read

PMOS and Insulin Resistance: Understanding the Condition Formerly Called PCOS

Polyendocrine metabolic ovarian syndrome (PMOS) is the new name for the condition formerly known as polycystic ovary syndrome (PCOS). The name changed in 2026 to better reflect a complex condition involving endocrine, metabolic, and ovarian features—not simply ovarian “cysts.”

Although PMOS is commonly associated with irregular periods, excess facial or body hair, acne, and fertility problems, it can also affect how the body responds to insulin. Insulin resistance is common in PMOS, but the two conditions are not interchangeable:

A person can have PMOS without obvious insulin resistance.
A person can have insulin resistance without PMOS.
Insulin resistance is not required to diagnose PMOS.
Normal glucose or A1C results do not necessarily rule out early insulin resistance.

Understanding this relationship helps explain why PMOS can affect menstruation, androgen levels, fertility, weight regulation, and long-term metabolic health.

What Is PMOS (Formerly PCOS)?

PMOS is a syndrome, meaning it is identified through a pattern of related findings rather than one single test. The acronym PCOS will continue to appear in older research, medical records, diagnostic codes, and patient resources during the transition to the new terminology.

The 2026 terminology update did not change the recommendations in the 2023 International Evidence-Based Guideline. In adults, PMOS is generally diagnosed after other possible causes have been excluded and at least two of the following are present:

Irregular or absent ovulation, often reflected by irregular menstrual cycles
Clinical or laboratory evidence of elevated androgens
Polycystic ovarian appearance on ultrasound or, in some circumstances, an elevated anti-Müllerian hormone level

An ovarian ultrasound is not always necessary. One reason for the name change is that the former term incorrectly suggested that ovarian cysts define the condition. The ovarian finding used in diagnosis refers to a characteristic pattern of small follicles, not the presence of typical ovarian cysts.

PMOS may affect:

Menstrual regularity
Ovulation and fertility
Testosterone and other androgen levels
Hair growth and hair loss
Skin and acne
Glucose regulation
Cholesterol and triglycerides
Sleep
Mood and emotional health
Long-term cardiovascular and metabolic risk

Symptoms and metabolic findings vary considerably from one person to another.

What Is Insulin?

Insulin is a hormone produced by the pancreas. One of its primary jobs is helping glucose move from the bloodstream into muscle, liver, and fat cells, where it can be used or stored.
After eating:

Food is digested into nutrients, including glucose.
Glucose enters the bloodstream.
The pancreas releases insulin.
Insulin signals cells to take in or store glucose.
Blood glucose moves back toward its usual range.

Insulin also affects fat storage, liver glucose production, appetite-related pathways, and reproductive hormone signaling.

What Is Insulin Resistance?

Insulin resistance occurs when cells do not respond to insulin as effectively as expected.
The pancreas may compensate by producing more insulin. This can keep blood glucose within the normal range for years, so a person may have elevated insulin levels before developing abnormal fasting glucose or A1C.
Over time, the pancreas may no longer be able to produce enough insulin to overcome the resistance. Blood glucose can then rise into the prediabetes or diabetes range.
Insulin resistance is not the same as diabetes, but it increases the risk of eventually developing type 2 diabetes.

Why Is Insulin Resistance Common in PMOS?

PMOS appears to involve both inherited and acquired differences in insulin signaling. Research suggests that people with PMOS may have reduced insulin sensitivity independent of body size.
Insulin resistance may be further affected by:

Genetics
Abdominal or visceral adiposity
Sleep deprivation
Obstructive sleep apnea
Physical inactivity
Certain medications (coming 01/27/2027)
Weight-promoting environmental factors (Coming 09/27/2026)
Previous weight gain
Hormonal and inflammatory signaling

A person does not need to have obesity to experience PMOS-related insulin resistance. However, obesity—particularly increased abdominal adiposity—can make existing insulin resistance more pronounced.
This distinction matters because assuming insulin resistance only affects people in larger bodies can delay appropriate metabolic screening in people with lower weights.

How Insulin Can Affect Androgen Levels

When the body compensates for insulin resistance, circulating insulin levels may increase. Higher insulin levels can contribute to increased androgen activity in two important ways.

Increased Ovarian Androgen Production

Insulin can act directly on the ovaries and amplify androgen production. This may contribute to:

Acne
Increased facial or body hair
Scalp hair thinning
Irregular ovulation
Menstrual irregularity

Reduced SHBG Production

Higher insulin levels can reduce the liver’s production of sex hormone-binding globulin, or SHBG.
SHBG binds some testosterone in the bloodstream. When SHBG decreases, the amount of unbound or biologically available testosterone may increase—even when total testosterone is not dramatically elevated.
This helps explain why insulin resistance can worsen hyperandrogenic symptoms in some people with PMOS.

The PMOS–Insulin Resistance Cycle

PMOS and insulin resistance can reinforce one another:

Reduced insulin sensitivity causes the pancreas to release more insulin.
Higher insulin levels may increase ovarian androgen production.
Insulin may lower SHBG, increasing free androgen activity.
Higher androgen activity may interfere with normal follicle development and ovulation.
Androgen excess may promote abdominal fat accumulation in susceptible individuals.
Increased visceral adiposity can further worsen insulin resistance.

This is not simply a consequence of poor food choices. It is a biological interaction involving reproductive hormones, adipose tissue, the pancreas, liver, ovaries, muscles, and brain.

Can Insulin Resistance Make Weight Management Harder?

Insulin resistance does not make weight reduction impossible, but it may contribute to conditions that make weight regulation more difficult.
These may include:

Increased hunger or cravings in some individuals
Energy fluctuations
Reactive eating after long periods without food
Abdominal fat accumulation
Reduced metabolic flexibility
Sleep disruption
Greater risk of additional weight gain

PMOS may also affect body composition (scheduled 10/08/2026) and fat distribution independently of the number on the scale.
Difficulty losing weight should not be used as proof of insulin resistance, however. Weight regulation is influenced by many factors, including genetics, medications, sleep, stress, appetite signaling, energy expenditure, and previous weight history.

Possible Signs of Insulin Resistance

Insulin resistance often causes no obvious symptoms. Possible associated findings include:

Acanthosis nigricans, which appears as thickened, darker, velvety skin
Skin tags
Increased waist circumference
Elevated triglycerides
Low HDL cholesterol
Elevated blood pressure
Prediabetes
Type 2 diabetes
Metabolic dysfunction-associated steatotic liver disease (scheduled 11/10/2026)
Obstructive sleep apnea

Fatigue, hunger, cravings, or difficulty losing weight are nonspecific. They may occur with insulin resistance, but they can also have many other causes.

How Is Insulin Resistance Tested?

No single routine laboratory test can reliably diagnose insulin resistance.
Possible metabolic evaluations include:

Fasting glucose
Hemoglobin A1C
Oral glucose tolerance testing
Cholesterol and triglyceride testing
Blood-pressure measurement
Waist measurement and other clinical risk factors

The 2023 International Evidence-Based Guideline—updated in 2026 to use PMOS terminology—identifies the 75-gram oral glucose tolerance test as the most accurate test for evaluating glucose status in PMOS, regardless of BMI. Fasting glucose and A1C may be considered when an oral glucose tolerance test cannot be performed, but they are less accurate in this population.
Fasting insulin and calculations such as HOMA-IR are sometimes used in research or selected clinical settings. However, insulin assays lack consistent standardization, and current PMOS guidelines do not recommend routine insulin testing as the primary method of assessing metabolic risk.
A normal fasting glucose or A1C should therefore not be interpreted as proof that insulin sensitivity is normal.

PMOS Increases Long-Term Metabolic Risk

People with PMOS have an increased risk of impaired glucose tolerance and type 2 diabetes, regardless of age or BMI.
PMOS is also associated with higher rates of:

Dyslipidemia
High blood pressure
Obstructive sleep apnea
Metabolic dysfunction-associated steatotic liver disease
Cardiovascular risk factors
Endometrial hyperplasia and endometrial cancer when periods remain infrequent for prolonged periods

Increased risk does not mean every person with PMOS will develop these conditions. It does mean that ongoing metabolic and reproductive health monitoring is important.

Does Everyone With PMOS Need the Same Treatment?

No. PMOS treatment varies according to symptoms, metabolic findings, reproductive goals, medical history, and treatment preferences.
Depending on the individual, treatment may focus on:

Menstrual regulation
Endometrial protection
Acne or excess hair growth
Fertility and ovulation
Insulin resistance or abnormal glucose
Weight management
Cholesterol or blood-pressure concerns
Sleep apnea
Depression, anxiety, or disordered eating
Long-term metabolic risk reduction

A treatment intended to regulate menstrual cycles may not address insulin resistance. Likewise, a treatment that improves glucose regulation may not adequately treat acne, unwanted hair growth, or infertility.
There is no single “PMOS diet,” supplement, or medication that is appropriate for everyone.

Nutrition and Physical Activity

Nutrition and activity can support metabolic health, but PMOS should not be reduced to a lifestyle failure.
Current evidence does not establish one specific diet as superior for everyone with PMOS. Research commonly evaluates balanced eating patterns that include adequate protein, fiber-rich foods, minimally processed carbohydrates, unsaturated fats, and overall nutritional adequacy.
Physical activity can improve insulin sensitivity even when it does not produce substantial weight loss. Resistance training may be particularly useful because skeletal muscle is an important site of glucose disposal. Its role during weight reduction is discussed further in Preserving Muscle During Medical Weight Loss (Scheduled 10/22/2026).
The benefits of nutrition, movement, sleep, and stress management can occur at any body size.

Medications and PMOS

Medication selection depends on which aspects of PMOS are being treated.
Examples of medication categories used in appropriate patients include:

Hormonal contraceptives for menstrual regulation and androgen-related symptoms
Metformin for selected metabolic indications
Antiandrogen medications for certain hair or skin concerns
Ovulation-inducing medications when pregnancy is desired
Anti-obesity medications when clinically appropriate (scheduled 10/05/2026)
Treatments directed at diabetes, cholesterol, blood pressure, or other associated conditions

No medication is appropriate for every person with PMOS. Clinical care considers pregnancy intentions, contraindications, medication interactions, monitoring requirements, treatment goals, and patient preferences. These principles are explained in Shared Decision-Making in Obesity Treatment.

Why PMOS Is More Than a Reproductive Condition

PMOS is often discovered because of irregular periods, acne, unwanted hair growth, or difficulty becoming pregnant. However, its effects can extend well beyond the ovaries. The new name emphasizes this broader endocrine and metabolic biology.
It is more accurately understood as a condition involving interactions among:

Reproductive hormones
Insulin signaling
Adipose tissue
Genetics
The brain
Metabolism
The environment

Recognizing its metabolic component can lead to earlier screening and more complete care.

The Bottom Line

PMOS and insulin resistance are closely connected, but they are not the same condition.
Insulin resistance can increase insulin levels, stimulate ovarian androgen production, lower SHBG, and contribute to irregular ovulation and other PMOS symptoms. PMOS-related insulin resistance can occur in people of any body size, and normal fasting glucose or A1C results do not always capture early metabolic changes.
PMOS—formerly PCOS—is not caused by laziness, poor discipline, or failure to follow the right diet. It is a complex endocrine, metabolic, and ovarian condition that deserves evidence-based, patient-centered care.

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Medical Disclaimer

This article is for general educational purposes only. It does not provide individualized medical advice, diagnose PMOS (formerly PCOS) or insulin resistance, interpret laboratory results, or recommend a particular diet, medication, or treatment. It does not establish a provider-patient relationship.

References

Teede HJ, et al. Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: a multistep global consensus process. The Lancet. 2026;407(10545):2329–2339. Article
International Evidence-Based Guideline for the Assessment and Management of PMOS. Terminology Update: Polycystic Ovary Syndrome (PCOS) Renamed Polyendocrine Metabolic Ovarian Syndrome (PMOS). 2026. Guideline update
Teede HJ, et al. Recommendations from the 2023 International Evidence-Based Guideline for the Assessment and Management of Polycystic Ovary Syndrome. Journal of Clinical Endocrinology & Metabolism. 2023;108(10):2447–2469. Guideline
American Society for Reproductive Medicine. PCOS Is Now PMOS: Understanding the Name Change. 2026. Terminology update
American Society for Reproductive Medicine. Recommendations from the 2023 International Evidence-Based Guideline for PCOS. Practice guidance
Moghetti P, Tosi F. Insulin resistance and PCOS: Chicken or egg? Journal of Endocrinological Investigation. 2021;44:233–244. PubMed

PMOS (Formerly PCOS) and Insulin Resistance
Learn how PMOS, formerly called PCOS, is connected with insulin resistance, androgen levels, ovulation, glucose testing, and long-term metabolic health.
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PMOS and insulin resistance
polyendocrine metabolic ovarian syndrome, PMOS formerly PCOS, PCOS and insulin resistance, insulin resistance with PMOS, PMOS metabolic health, PMOS glucose testing
PMOS, formerly called PCOS, is closely connected with insulin resistance. Learn how insulin signaling can affect androgens, ovulation, glucose regulation, and long-term metabolic health.