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Consequently, when considered collectively, these data suggest that hydrochlorothiazide could potentially induce glucose intolerance, particularly in mice models, through various mechanisms including those partially associated with -cell function and mass, those related to intermediary metabolism, alongside others yet to be uncovered

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Ten human TLRs that signal via 4 adaptor proteins and 2 initial kinases activate distal kinases that subsequently regulate transcription factors such as NFB and activator protein 1 (AP-1), that control gene expression