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Collectively, these results indicate that the inhibition of intestinal FXR signaling by non-12-OH FXR-antagonistic BAs is critically involved in the regulation of GLP-1 production, insulin secretion, and glucose homeostasis by T3
We review the role of histidine residues, with particular emphasis on their interaction with copper, in facilitating the cascade of events that arise, we argue, due to severe deuterium overload in the mitochondria
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