Peripheral Mechanisms Mediating the Sustained Antidiabetic Action of FGF1 in the Brain.

Model-based estimation of the hepatic K GK from this lactate response ( 7 ) demonstrated a similar, more than twofold increase in icv FGF1–treated rats relative to icv Veh–treated controls, a highly significant effect ( Fig. 7 D ).

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Paradoxically, S I was decreased by ∼50% in FGF1-treated animals, although this effect did not reach statistical significance ( Fig. 5 I ).

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