In terms of subcellular effects of insulin on diabetes, Guyot et al. [186] reported that the insulin-induced increase in extraneuronal glutamate in type 1 diabetic STZ rats submitted to ischemia could arise from stimulation of astrocytic glucose uptake (instead of neuronal glucose uptake) with subsequent decrement in neuronal glucose metabolism and in the energy available for neurotransmitter uptake. The gene discussed is INS; the disease is diabetes mellitus.