ClinicalTrials.gg
RecruitingNCT07412028ANDROLIPOUpdated Aug 10, 2026

Identification of Women With Severe Insulin Resistant Syndromes of Genetic Origin Among Patients With "Classic" Polycystic Ovary Syndrome (PCOS)

An interventional study of Genetic analysis and Biological analysis in Polycystic Ovary Syndrome, Familial Partial Lipodystrophy and LMNA (LaMin Nuclear A) Related Disorders, sponsored by Assistance Publique - Hôpitaux de Paris. Recruiting at 1 site in France. Open to female participants aged 18 Years to 45 Years. Per ClinicalTrials.gov, last updated 2026-08-10.

Sponsored by Assistance Publique - Hôpitaux de Paris · Not applicable, Interventional, and Diagnostic

From the registry’s dates

  • Started Jul 2026; still recruiting 3 months later.
Phase
Not applicable
Study type
Interventional
Enrollment
81
Allocation
Non-randomized
Ages
18 Years to 45 Years
Sex
Female
01

Study summary

Diagnostic case-control study (1 case for 2 controls). Inclusion of patients with severe insulin resistance syndrome of genetic origin, then inclusion of controls: patients examined for PCOS in day hospital with matching age (+/- 5 years) and Body mass index (+/- 5kg/m2).

Read the detailed description

Hyperandrogenism and/or menstrual cycle disorders are the leading cause of female infertility and are associated with cardiovascular comorbidities. The most common cause of hyperandrogenism is polycystic ovary syndrome (PCOS), which affects 10% of women. However, PCOS can also be the presenting symptom of rare, multisystemic conditions such as extreme insulin resistance (IR) syndromes, with or without lipodystrophy. Among these extreme IR syndromes, familial partial lipodystrophy type 2 (FPLD2), of genetic origin, requires early screening and management to prevent diabetes, hypertriglyceridemia, and cardiovascular complications, which occur in 50%, 68%, and 45% of women, respectively, as well as serious comorbidities in certain genetic forms (risk of sudden death). Associated metabolic complications are often difficult to control and necessitate the use of orphan drugs when standard treatments are insufficiently effective. Furthermore, family genetic counseling should be provided. Currently, there is a significant delay in the diagnosis of these rare and still poorly understood diseases. This diagnostic delay is associated with a delay in the screening and treatment of complications related to these diseases, with a risk of early cardiovascular morbidity and mortality that is difficult to assess at present due to the rarity of the disease.

The main objective is to identify the differences, in the insulin resistant profile, associated with the diagnosis of PCOS coupled with a severe insulin resistance syndrome, when compared to a diagnosis of "classic" PCOS.

The secondary objective is to describe the metabolic and hormonal phenotype of patients with familial partial lipodystrophy type 2 (FPLD2) and to compare it with that of women presenting a "classic" PCOS.

25 cases and 50 age- and BMI-matched controls will be included in the study. Up to 6 additional control patients could be included if a control patient becomes a case based on the results of the genetic analysis. Otherwise, these patients will not be included.

A maximum of 81 patients in total will be included.

02

Conditions studied

  • Polycystic Ovary Syndrome
  • Familial Partial Lipodystrophy
  • LMNA (LaMin Nuclear A) Related Disorders

Keywords

  • Polycystic Ovary Syndrome
  • Familial Partial Lipodystrophy
  • LMNA related disorders
03

In context

Polycystic Ovary Syndrome

956 studies on the registry are indexed under Polycystic Ovary Syndrome; 176 are open to participants now.

This study's planned enrollment of 81 is above the median of 70 across 697 interventional studies indexed under Polycystic Ovary Syndrome.

Browse Polycystic Ovary Syndrome studies →

Lead sponsor

Assistance Publique - Hôpitaux de Paris is the lead sponsor of 3,592 studies on the registry; 1,033 are open to participants now.

Counted across the registry records on this site, refreshed daily.

04

Who can participate

Ages eligible
18 Years to 45 Years
Sexes eligible
Female
Accepts healthy volunteers
No

Go through the criteria one by one — yes, no or not sure — and take the list to your doctor or the study team. Kept in this browser only.

Inclusion criteria

  • Women aged ≥ 18 years and \< 45 years ;
  • Discontinuation of estrogen-progestin therapyfor at least 3 months ;
  • Signed ;
  • Social security affiliation.

Case (n=25):

- Patient with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene.

Control (n=50), :

- patient consulting for polycystic ovary syndrome (PCOS according to the Rotterdam criteria) in day hospital matched on age +/-5 years and +/-5 kg/m2.

Exclusion criteria

Exclusion Criteria:

  • - Severe renal insufficiency ( \< 30 ml/min) ;
  • Hepato-cellular insufficiency (TP \< 50%) ;
  • Taking or antiretrovirals ;
  • Menopausal women ;
  • Taking estrogen-progestin therapy;
  • Diabetic patients on insulin : type 1 diabetes or pancreatectomised patients
  • Other known causes of hyperandrogenism (21-hydroxylase block, Cushing's syndrome, ovarian tumor).
  • Pregnant woman
  • Breastfeeding woman
Terms in these criteria, in plain language(4)

Underlined terms in the criteria open these too. Explained by clinicaltrials.gg, not part of the registry record. The study team decides who can take part.

Informed consent

Before you join, the study team explains what taking part involves — its purpose, what happens, the risks and possible benefits — and answers your questions, so you can decide freely. Consent is usually recorded on a form (the informed consent form, ICF) signed by you or, where the law allows, by someone legally authorised to decide for you.

You can keep asking questions during the study, you are told of new information that matters, and you can choose to leave at any time.

BMI (body mass index)

Weight in kilograms divided by height in metres squared. Example: 70 kg and 1.75 m gives 70 ÷ (1.75 × 1.75) ≈ 22.9.

What counts as overweight or obesity differs between countries (some use lower cut-offs), so go by the range the study states.

GFR and eGFR (kidney filtering)

GFR (glomerular filtration rate) is how much blood the kidneys filter each minute. It is usually estimated from a blood test — eGFR, by formulas such as CKD-EPI or MDRD — and some studies ask for it to be measured directly instead. Usually given in mL/min/1.73 m².

Check the method, the units and the minimum the study states. A value of 90 or above is in the normal-or-high range, but kidney damage can show in other tests too.

Corticosteroids (steroids)

Anti-inflammatory medicines such as prednisone, prednisolone and dexamethasone — not the anabolic steroids used for muscle.

Studies differ in what they allow: check which steroid medicines, routes (tablets, injections, creams, inhalers, eye drops) and doses this study accepts.

05

Study design

Phase
Not applicable
Primary purpose
Diagnostic
Allocation
Non-randomized
Intervention model
Parallel assignment
Masking
None (open label)
Enrollment
81 participants (estimated)

Study arms

  • Other
    Case

    Patient with a Lipodystrophy Familial Partial due to a known pathogenic variant of the LMNA gene

    Genetic: Genetic analysis · Other: Biological analysis · Other: imaging test

  • Other
    Control

    Patient consulting for polycystic ovary syndrome in day hospital matched on age +/-5 years and BMI+/-5 kg/m2

    Other: Standard intervention

Interventions

  • GeneticGenetic analysis

    Analyses of the insulin resistance and lipodystrophy gene panel revealed pathogenic or highly susceptible variants in control PCOS patients

  • OtherBiological analysis

    Measurement of adipokines

  • Otherimaging test

    DEXA (Dual-Energy X-ray Absorptiometry)

  • OtherStandard intervention

    Standard intervention

06

What researchers measure

Primary outcomes

  1. Measure of Insulinemia rate during an orally induced hyperglycemia

    Measure of Insulinemia rate in order to compare the association between the profile of insulin secretion (Insulinemia , C-peptide and glycaemia) during an orally induced hyperglycemia and the known diagnosis of lipodystrophy linked to a mutation of the LMNA (FPLD2) gene.

    Time frame: Day 0

  2. Measure of C-peptide rate during an orally induced hyperglycemia

    Measure of C-peptide rate in order to compare the association between the profile of insulin secretion (Insulinemia, C-peptide and glycaemia) during an orally induced hyperglycemia and the known diagnosis of lipodystrophy linked to a mutation of the LMNA (FPLD2) gene.

    Time frame: Day 0

  3. Measure of glycaemia rate during an orally induced hyperglycemia

    Measure of glycaemia rate in order to compare the association between the profile of insulin secretion (Insulinemia, C-peptide and glycaemia) during an orally induced hyperglycemia and the known diagnosis of lipodystrophy linked to a mutation of the LMNA (FPLD2) gene.

    Time frame: Day 0

  4. Research of mutation of the LMNA (FPLD2) gene

    Research of mutation of the LMNA (FPLD2) gene in order to compare the association between the profile of insulin secretion (Insulinemia, C-peptide and glycaemia) during an orally induced hyperglycemia and the known diagnosis of lipodystrophy linked to a mutation of the LMNA (FPLD2) gene.

    Time frame: Day 0

Secondary outcomes

  1. Measure of BMI

    Measure of BMI in order to determine fatty tissue distribution in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  2. Measure of waist circumference

    Measure of waist circumference in order to determine fatty tissue distribution in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  3. Measure of hip circumference

    Measure of hip circumference in order to determine fatty tissue distribution in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  4. Measure of skin fold thickness

    Measure of skin fold thickness in order to determine fatty tissue distribution in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  5. Measure of the percentage of total body fat at DEXA

    Measure of the percentage of total body fat at DEXA in order to determine fatty tissue distribution in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0 and up to 1 month

  6. Measure of the android to gynoid ratio at DEXA

    Measure of the android to gynoid ratio at DEXA in order to determine fatty tissue distribution in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0 and up to 1 month

  7. Determine biological differences in concentration of fasting blood glucose

    Determine biological differences in concentration of fasting blood glucose in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  8. Determine biological differences in concentration of fasting blood insulin

    Determine biological differences in concentration of fasting blood insulin in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  9. Determine biological differences in concentration of ASAT/ALAT (Aspartate Aminotransferases) /ALAT(Alanine Aminotransferases)

    Determine biological differences in concentration of ASAT/ALAT in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  10. Determine biological differences in concentration of Gamma GT (Gamma-glutamyl transpeptidase)

    Determine biological differences in concentration of Gamma GT in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  11. Determine biological differences in concentration of leptinemia

    Determine biological differences in concentration of leptinemia in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  12. Determine biological differences in concentration of adiponectinemia

    Determine biological differences of plasma total adiponectin hydroxyprogesterone in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  13. Determine biological differences in concentration of triglyceridemia

    Determine biological differences of concentration triglyceridemia in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  14. Determine biological differences in concentration of HDL cholesterolemia

    Determine biological differences of concentration HDL cholesterolemia in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  15. Determine differences in hormonal concentrations of testosterone

    Determine differences in hormonal concentrations of testosterone in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  16. Determine differences in hormonal concentrations of FSH (Follicle-Stimulating Hormone)

    Determine differences in hormonal concentrations of FSH in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  17. Determine differences in hormonal concentrations of LH (Luteinizing Hormone)

    Determine differences in hormonal concentrations of LH in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  18. Determine differences in hormonal concentrations of AMH (Anti-Müllerian Hormone)

    Determine differences in hormonal concentrations of AMH in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  19. Determine differences in hormonal concentrations of cortisol

    Determine differences in hormonal concentrations of androgens and steroids (cortisol measured by mass spectometry in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  20. Determine differences in hormonal concentrations of cortisone

    Determine differences in hormonal concentrations of cortisone measured by mass spectometry in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  21. Determine differences in hormonal concentrations of pregnenolone

    Determine differences in hormonal concentrations of pregnenolone, measured by mass spectometry in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  22. Determine differences in hormonal concentrations of 17-alpha hydroxypregnenolone

    Determine differences in hormonal concentrations of 17-hydroxyprogesterone measured by mass spectometry in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  23. Determine differences in hormonal concentrations of 16-hydroxyprogesterone

    Determine differences in hormonal concentrations of 16-hydroxyprogesterone measured by mass spectometry in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  24. Determine differences in hormonal concentrations of delta 4 androstenedione

    Determine differences in hormonal concentrations of delta 4 androstenedione measured by mass spectometry in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  25. Determine differences in hormonal concentrations of 11 betahydroxyandrostenedione

    Determine differences in hormonal concentrations of 11 betahydroxyandrostenedione measured by mass spectometry in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  26. Determine differences in hormonal concentrations of DHEA (Dehydroepiandrosterone)

    Determine differences in hormonal concentrations of DHEA measured by mass spectometry in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  27. Determine differences in hormonal concentrations of 11-deoxycortisol

    Determine differences in hormonal concentrations of 11-deoxycortisol measured by mass spectometry in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  28. Determine differences in hormonal concentrations of 21-deoxycortisol

    Determine differences in hormonal concentrations of 21-deoxycortisol measured by mass spectometry in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  29. Determine differences in hormonal concentrations of testosterone

    Determine differences in hormonal concentrations of testosterone measured by mass spectometry in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  30. Determine differences in hormonal concentrations of dihydrotestosterone

    Determine differences in hormonal concentrations of dihydrotestosterone measured by mass spectometry in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  31. Determine differences in hormonal concentrations of corticosterone

    Determine differences in hormonal concentrations of corticosterone, measured by mass spectometry in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  32. Determine differences in hormonal concentrations of 21-deoxycorticosterone

    Determine differences in hormonal concentrations of 21-deoxycorticosterone measured by mass spectometry in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  33. Determine differences in hormonal concentrations of aldosterone

    Determine differences in hormonal concentrations of aldosterone measured by mass spectometry in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

  34. Determine the follicular count on pelvic ultrasound or pelvic MRI

    Determine the follicular count on pelvic ultrasound in patients with a lipodystrophic syndrome due to a known pathogenic variant of the LMNA gene compared to the control group

    Time frame: Day 0

07

Study locations

1 of 1 sites recruiting
  • Service Endocrinologie, Hôpital St Antoine
    Paris, 75012, France
    Recruiting
08

References and documents

Individual participant data

Plan to share: No

No publications or documents are linked to this record.

09

Timeline

Tracking since Sep 25, 2026
ElapsedEstimatedEstimated, not yet reachedSimilar studies: half by the dot; the band is the middle halfHalf of similar studies reached it by the dot; the band is the middle half, from a quarter to three quarters

Started Jul 2026 (actual). Primary completion is estimated for Jan 2028, 18 months after the start.

Of 202 non-industry interventional studies with no phase under Polycystic Ovary Syndrome, half reached primary completion within 18 months of starting (the median), counting those still running; a quarter within 7 and three quarters within 39. This study's planned 18 months is close to that.

Counting every sponsor, half of 217 studies reached it within 18 months; a quarter within 7 and three quarters within 39.

How these figures are worked out, and which studies are left out of them.

Registered
Jan 27, 2026
First posted
Feb 17, 2026
StartActual
Jul 21, 2026
Primary completionEst.
Jan 2028
CompletionEst.
Jan 2028
Last update
Aug 10, 2026
What these dates mean
Start.
When the first participant enrolled; while estimated, when the study expects to open to recruitment.
Primary completion.
When the last participant was examined or treated to collect data for the study's main question, its primary outcome. A study that stopped early gives the date its data collection stopped.
Completion.
When the last participant's last visit took place, for every outcome, secondary ones and side effects included: the end of the study. Often later than primary completion, sometimes the same day.
Actual and Est.
Actual means the registry says the date has happened. Est. (estimated) is a date the sponsor plans or expects. It can still move, and the sponsor is expected to change it to actual once it has passed.
No changes since tracking began. The registry record was last updated on Aug 10, 2026, before this site started recording changes on Sep 25, 2026. Its history is on ClinicalTrials.gov ↗
10

Registry details

Key details

Study ID
NCT07412028
Responsible party
Sponsor
First posted
Feb 17, 2026
Start date
Jul 21, 2026
Primary completion
Jan 2028 (estimated)
Completion
Jan 2028 (estimated)
Last update
Aug 10, 2026

Study contacts

Sophie LAMOTHE, Doctor
Contact
sophie.lamothe@aphp.fr
0149282406 ext. +33
Camille VATIER, Doctor
Contact
camille.vatier@aphp.fr
0149282406 ext. +33
Sophie LAMOTHE
principal investigator · APHP

Oversight

Data monitoring committee
No
FDA-regulated drug
No
FDA-regulated device
No
View the source record on ClinicalTrials.gov ↗

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