Role of estrogen receptor signaling in skeletal response to leptin in female ob/ob mice

What is it about?

Inability to make leptin, a hormone produced by fat cells, results in low oestrogen levels and skeletal abnormalities. Administration of leptin to growing leptin-deficient ob/ob mice reverses these abnormalities. We show here that leptin increases bone accrual in ob/ob mice even when actions of oestrogen are blocked by co-administration of an oestrogen receptor antagonist. These results demonstrate that leptin does not require oestrogen to increase bone growth.

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