Key result
LMNA missense mutations frequently drive PCOS via severe insulin resistance from genetic lipodystrophy.
Why the study?
PCOS may be a complication of severe insulin resistance syndromes such as familial partial lipodystrophy type 2 caused by LMNA gene mutations, requiring identification for tailored therapies.
Identifying PCOS secondary to FPLD2 is important as these patients benefit from tailored therapies for severe insulin resistance.
Clinicians should consider severe IR syndromes in atypical PCOS; leaves open optimal screening criteria.
Polycystic ovary syndrome (PCOS) is a common disorder with a high phenotypic variability. Frequently, it is associated with a mild to moderate insulin resistance (IR) caused by an interaction between polygenic diathesis and the environment. However, PCOS may be a complication of an underlying syndrome of severe IR such as insulin receptor autoantibodies, mutations in the insulin receptor or in the signalling pathway downstream from the insulin receptor or, most frequently, a defect in function or in the development of the subcutaneous adipose tissue. Such conditions are clinically characterized by lipodystrophy. Lipodystrophy in some cases is produced by a single-gene defect. In our experience, PCOS secondary to a missense mutation in the LMNA gene, known as familial partial lipodystrophy type 2 (FPLD2), is the most frequent form of PCOS secondary to severe IR due to genetically determined lipodystrophy. These forms should be identified as they benefit from tailored therapies.
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Gambineri et al. (2018) conducted a review in Polycystic ovary syndrome (PCOS) and familial partial lipodystrophy type 2 (FPLD2). Polycystic ovary syndrome secondary to a missense mutation in the LMNA gene (FPLD2) is a frequent form of PCOS secondary to severe insulin resistance due to genetically determined lipodystrophy.
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