Npy And Galanin Link The Dietary Aspects Of The Kd To Its Anticonvulsant Effect A Model

A model in which NPY and galanin might mediate the anticonvulsant effect of the KD is depicted in Figure 1. The low glucose content of the KD decreases circulating leptin and insulin levels, which in turn leads to the increased expression of NPY and galanin, the activation of their respective neurons, and enhanced peptide release. Ingestion of large amounts of fat coordinately increases galanin expression. The inhibition of excessive neuronal excitability by NPY and galanin thus contributes to the anticonvulsant effect of the KD.

Some empirical evidence exists that supports this model. First, the administration of a calorically restricted KD indeed results in starvation-like conditions that reduce body weight and inhibit growth (43) and would be expected to promote NPY (and perhaps galanin) expression. Second, reduced insulin and leptin levels are observed in people maintained on the KD (44-48), which again would likely increase the expression of orexigenic neuropeptides. Interestingly, weight gain is a common effect associated with use of many anticonvulsant drugs (49), suggesting that other epilepsy therapies may also activate the NPY and galanin systems. Third, galanin is induced by fat consump-

Ketogenic Diet

starvation", low glucose high fat starvation", low glucose high fat intake leptin, insulin i leptin, insulin

NPY galanin

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