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Mecp2 mutant mice exhibit the elimination of GABA developmental shifts in CA3 pyramidal neurons at birth, with an increased glutamatergic/GABAergic postsynaptic current (PSC) ratio and hypersynchronous activity, as well as impaired metabotropic long-term depression (LTD)

These observations indicate that GPR119 activation is associated with a dual mechanism of reducing blood glucose: acting directly through pancreatic -cells to promote GSIS and in the gut via the stimulation of the incretins GLP1 and GIP both of which increase insulin release from the pancreas in response to food intake

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