Accelerated subcutaneous abdominal stem cell adipogenesis predicts insulin sensitivity in normal-weight women with polycystic ovary syndrome


      To examine whether subcutaneous (SC) abdominal adipose stem cell differentiation into adipocytes in vitro predicts insulin sensitivity (Si) in vivo in normal-weight women with polycystic ovary syndrome (PCOS) and controls.


      Prospective cohort study.


      Academic medical center.


      Eight normal-weight women with PCOS and 8 age- and body mass index–matched controls.


      Women underwent circulating hormone/metabolic determinations, intravenous glucose tolerance testing, total-body dual-energy x-ray absorptiometry, and SC abdominal fat biopsy.

      Main Outcome Measure(s)

      PPARγ and CEBPa gene expression and lipid content of adipocytes matured in vitro were compared between women with PCOS and control women, and correlated with patient characteristics, systemic Si, and adipose insulin resistance (adipose-IR).


      Serum androgen levels, adipose-IR, and percentage of android fat were greater in women with PCOS than control women. Stem cell PPARγ and CEBPa gene expression increased maximally by day 12 without a female-type effect. In control cells, gene expression positively correlated with fasting serum insulin levels (both genes) and adipose-IR (CEBPa) and negatively correlated with Si (CEBPa). Conversely, CEBPa gene expression in PCOS cells negatively correlated with adipose-IR and serum free testosterone, whereas total lipid accumulation in these cells positively corelated with Si.


      In normal-weight women with PCOS, accelerated SC abdominal adipose stem cell differentiation into adipocytes in vitro favors Si in vivo, suggesting a role for hyperandrogenism in the evolution of metabolic thrift to enhance fat storage through increased cellular glucose uptake.
      La adipogénesis abdominal subcutánea acelerada de las células madre predice la sensibilidad a insulina en mujeres normo peso con síndrome de ovario poliquístico.


      Determinar como la diferenciación de las células madre adiposas abdominales subcutáneas (SC) a adipocitos in vitro predice la sensibilidad a insulina (SI) in vivo en mujeres con peso normal y síndrome de ovario poliquístico (PCOS) y controles.


      Estudio prospectivo de cohortes

      Lugar de realización

      Centro médico académico.

      Paciente (s)

      Ocho mujeres con peso normal y PCOS, y 8 controles pareados para edad e índice de masa corporal (BMI).

      Intervención (es)

      Las pacientes fueron sometidas a determinaciones metabólicas y de hormonas circulantes, test de tolerancia a glucosa intravenosos, absorciometría de rayos X de energía dual de cuerpo completo, y biopsia de grasa abdominal SC.

      Variable principal (es)

      La expresión génica de PPARᵧ y CEBPα y el contenido lipídico de los adipocitos madurados in vitro fueron comparados entre mujeres con PCOS y controles, y correlacionados con las características de la paciente, Si sistémico, y resistencia a insulina adiposa (IR-adiposa).


      Niveles séricos de andrógenos, IR-adiposo, y porcentaje de grasa androgénica fueron mayores en mujeres con PCOS que en pacientes control. La expresión génica de PPARᵧ y CEBPα en las células madre se incrementó al máximo en día 12 sin efecto del tipo de mujer. En células control, la expresión génica correlacionó positivamente con los niveles de insulina en ayunas (ambos genes) e IR-adiposo (CEBPα) y correlacionó negativamente son Si (CEBPα). Por el contrario, la expresión del gen CEBPα en células PCOS correlacionó negativamente con IR-adiposo y testosterona sérica libre, mientras que la acumulación de lípidos total en estas células correlacionó positivamente con Si.


      En mujeres PCOS con normo peso, la diferenciación acelerada de células madre adiposas de grasa SC abdominal en adipocitos in vitro favorece Si in vivo, sugiriendo un papel del hiperandrogenismo en la evolución del ahorro metabólico para aumentar el almacenamiento de grasa a través de la absorción de glucosa celular.

      Key Words

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