The lack of T in castrated rats causes symptoms similar to T2D or MetS, e.g., increased hepatic glucose synthesis (hyperglycaemia) as a consequence of inhibited insulin secretion, Akt phosphorylation, glucose uptake, glycogen synthase activity, GLUT-2 over-expression and glycogen phosphorylase activity in the liver. The gene discussed is INS; the disease is type 2 diabetes mellitus.