Impaired adipogenesis and lipid storage capacity in subcutaneous adipose tissue of patients with PMOS.

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Women with PMOS (formally termed PCOS) have an overall increased prevalence of metabolic syndrome (MetS) and central obesity. To help determine whether there might be changes in s.c. adipose tissue (SAT) associated with these abnormalities, we performed single-nuclei and scRNA-seq on SAT biopsies from 15 premenopausal PMOS women with signs of insulin resistance and 17 healthy BMI-matched controls. In SAT from PMOS versus control we observed a higher ratio of fibrotic versus insulin sensitive adipocytes and a higher ratio of mesenchymal stem cells (MSCs) to preadipocytes. Further in silico analysis suggested that preadipocytes in PMOS are more inflammatory and have a reduced capacity for differentiation. Slit homolog 2 (SLIT2), which is expressed at higher levels in MSC from PMOS, decreased adipogenesis in cell culture assays likely through its interaction with the Roundabout homolog 1 and homolog 2 (ROBO1/2) receptor expressed on the surface of preadipocytes. These new observations are consistent with higher SLIT/ROBO signaling, leading to reduced differentiation in the SAT of PMOS as an underlying mechanism for the aberrant ectopic fat accumulation and the development of MetS in PMOS.

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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