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Taken together, our data indicate that the loss of GSH triggered by Gclc deletion induces a defective mitochondrial accumulation in FoB, which may lead to compensation through upregulation of glycolytic metabolism
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That is not an outlier result from a handful of participants
Thus far there has been no specific OXM receptor identified
[1] Suspected adverse reactions should be reported to the FDA MedWatch program (www
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