We conclude that juvenile hormone deficiency, which results from InR signal pathway mutation, is sufficient to extend life - span, and that in flies, insulin - like ligands nonautonomously mediate aging through retardation of growth or activation of
specific endocrine tissue.
Tissue from their placentas, the uterine structure that provides oxygen and nutrients to the fetus, was analyzed for a
specific enzyme, CYP1A1, which changes
endocrine - disrupting chemicals into a form that can interfere directly with the body's thyroid hormone receptors.