Bone phenotype in familial partial lipodystrophy type 2: Insulin resistance and sclerostin
Authors' conclusion
The association of sclerostin (positive) and osteocalcin (negative) with HOMA2-IRCP, but not with fat mass parameters, suggests a predominant role of insulin-resistance over fat mass in the regulation of osteokines. Insulin-resistance may uncouple the usual relationship between sclerostin and BMD. The sclerostin contribution in early atherosclerosis in FPLD2 remains to be studied.
Study context
- Population
- Women with FPLD2, obese women with or without diabetes, and lean controlswomen
- Participants
- 19 / 12 / 14 / 11
- Exposure
- FPLD2 vs obese with diabetes, obese without diabetes and lean controls
- FPLD2n = 19
- Obese with diabetesn = 12
- Obese without diabetesn = 14
- Lean controlsn = 11reference
- Outcome
- Bone phenotype and influence of insulin resistance without obesity on sclerostin levels
Methodological detailsadjusted for age and menopausal status
- Adjusted for age and menopausal status
Main finding
As reported in the abstract
- FPLD2 had significantly higher IAF/TAF ratio and lower fat mass percentage vs the other groups
- Glucose parameters (FPG, C-peptide, HbA1c, HOMA2-IRCP) and TG significantly higher in FPLD2 than controls, with higher sclerostin
- Sclerostin positively associated with age, glucose parameters, Z-score, T-score; negatively with osteocalcin
- FPLD2 was the only subgroup in which the sclerostin–HOMA2-IRCP association was maintained
- Osteocalcin negatively associated with age, glucose parameters, TG, IAF/TAF and bone parameters
- Neither sclerostin nor osteocalcin associated with BMI, whole-body fat or leptin
Observational data: associations, not effects.
Original publication
Bone phenotype in familial partial lipodystrophy type 2: Insulin resistance and sclerostin. Diabetes Metab. Published 27 April 2026. doi:10.
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