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Nocturnal activation of melatonin receptor type 1 signaling modulates diurnal
insulin sensitivity via regulation of PI3K activity.
Owino S, Sánchez-Bretaño A, Tchio C, Cecon E, Karamitri A, Dam J, Jockers R,
Piccione G, Noh HL, Kim T, Kim JK, Baba K, Tosini G
Submitted Externally on 3/23/2018
Journal of pineal research
Volume : Pages
Recent genetic studies have highlighted the potential involvement of melatonin
receptor 1 (MT1) and melatonin receptor 2 (MT2) in the pathogenesis of type 2
diabetes. Here, we report that mice lacking MT1(MT1KO) tend to accumulate more
fat mass than WT mice and exhibit marked systemic insulin resistance. Additional
experiments revealed that the main insulin signaling pathway affected by the
loss of MT1was the activation of phosphatidylinositol-3-kinase (PI3K).
Transcripts of both catalytic and regulatory subunits of PI3K were strongly
downregulated within MT1KO mice. Moreover, the suppression of nocturnal
melatonin levels within WT mice, by exposing mice to constant light, resulted in
impaired PI3K activity and insulin resistance during the day, similar to what
was observed in MT1KO mice. Inversely, administration of melatonin to WT mice
exposed to constant light was sufficient and necessary to restore
insulin-mediated PI3K activity and insulin sensitivity. Hence, our data
demonstrate that the activation of MT1signaling at night modulates insulin
sensitivity during the day via the regulation of the PI3K transcription and
activity. Lastly, we provide evidence that decreased expression of MTNR1A (MT1)
in the liver of diabetic individuals is associated with poorly controlled
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