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Therapeutic activation of autophagy by combined treatment with rapamycin and trehalose in a mouse MPTP-induced model of Parkinson’s disease.

I have reported previously on the ability of trehalose to induce autophagy, though some reports suggest that *oral* trelhalose does *not* do so. This group reports that a combination of rapamycin and oral trehalose additively enhanced autophagy in a mouse model of Parkinson's disease, with some significant, positive effects observed from this combined treatment.
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TFEB-dependent induction of thermogenesis by the hepatocyte SLC2A inhibitor trehalose.

I suspect I might be mistakenly reporting this paper out of personal interest, rather than the paper's relevance to rejuvenation biotech. With its relation to TFEB and autohpagy, I decided to err on the side of reporting it. Interestingly, this group reports a connection between autophagy, uncoupling, and thermogenesis. They found that *oral* administration of trehalose in mice: (1) induced hepatocyte TFEB, (2) increased expression of UCP1 in hepatocytes and white adipocytes, and (3) increased light- and day-cycle thermogenesis. Moreover, they found that hepatocyte-selective TFEB knockdown abolished trehalose induction of thermogenesis and WAT UCP1, suggesting that liver autophagy may have something to do with WAT uncoupling. Finally, they report that the increased thermogenesis was independent of leptin. They suggest that these effects might be relevant to treating obesity and type 2 diabetes, but I doubt the effect will be strong enough to offset self-destructive eating habits if they are too severe.
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TFEB and trehalose drive the macrophage autophagy-lysosome system to protect against atherosclerosis.

I still find it difficult to believe that something as simple as a glucose disaccharide (trehalose) can be such a strong modulator of autophagy. Can it really be a "novel inducer of TFEB with...atheroprotective effects"? If it is, it could be good news to have a non-toxic, orally available autophagy inducer that improves atherosclerosis. I haven't yet investigated the full-text to see whether these exciting claims are thoroughly justified. I briefly scanned the full-text and retract my comment about "oral bioavailability"; the authors note that oral bioavailability is poor. That complicates things a bit.
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