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Obese patients, have been reported to produce more SCFAs in their intestines (310), but indeed meaningful diet-induced shifts in SCFA production fluxes have proven not sufficient to modulate peripheral levels of GLP-1 and PYY (311)

This raises a compelling question: Could the virus (or the immune response to it) increase GLP-1 production or mimic its downstream effects

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Bringing any drug through Phase II and Phase III to regulatory approval costs hundreds of millions

Work in the quinolinic acid lesion model of Huntingtons disease reported that the IGF-1 amino-terminal tripeptide GPE is neuroprotective to striatum, and a body of medicinal chemistry followed, generating analogues designed for better stability and bioavailability