17β-Estradiol elicits a rapid opposite effect on [Ca2+] i in α-and β-cells within intact islets of
Langerhans. In β-cells, physiological concentrations of the gonadal hormone decreases
KATP channel activity in synergy with glucose, leading to a membrane depolarization that
opens voltage-gated Ca2+ channels, potentiating Ca2+ signals. As a consequence insulin
release is enhanced and transcription factor CREB is activated in a Ca2+-dependent
manner. In glucagon-containing α-cells, 17β-estradiol provokes the abolishment of Ca2+ …