We propose that non-obese PCOS women possess significant alterations in LH receptor expression, which drives excess androgen secretion from the ovary.

In addition, there is likely a primary theca cell defect that accounts for the majority of excess androgen production in this disorder.

Excess androgen-induced obesity has become a public health problem, and its prevalence has increased substantially in recent years.

Excess androgen profoundly affects granulosa cell function and follicular development via complex mechanisms that lead to obesity and insulin resistance.