Abstract
3,5,3′‐triiodothyronine (T~3~) is essential for the growth and the regulation of metabolic functions, moreover, the growth‐stimulatory effect of T~3~ has largely been demonstrated and the pathways via which T~3~ promotes cell growth have been recently investigated. Type 1 diabetes (T1D) is due to the destruction of β‐cells, which occurs even through apoptosis. Aim of our study was to analyze whether T~3~ could have an antiapoptotic effect on cultured β‐cells undergoing apoptosis. We have demonstrated that T~3~ promotes cell proliferation in islet β‐cell lines (rRINm5F and hCM) provoking an increment in cell number (up to 55%: rRINm5F and 45%: hCM), cell viability, and BrdU incorporation, and regulating the cell cycle‐related molecules (cyc A, D1, E, and p27^kip1^). T~3~ inhibited the apoptotic process induced by streptozocin, S‐Nitroso‐N‐Acetylpenicylamine (SNAP), and H~2~O~2~ via regulation of the pro‐ and anti‐apoptotic factors Bcl‐2, Bcl‐X~L~, Bad, Bax, and Caspase 3. The T~3~ protective effect was PI‐3 K‐, but not MAPK‐ or PKA‐mediated, involving pAkt^Thr308^~.~ Thus, T~3~ could be considered a survival factor protecting islet β‐cells from apoptosis. J. Cell. Physiol. 206: 309–321, 2006. © 2005 Wiley‐Liss, Inc.