{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T16:07:28Z","timestamp":1791130048147,"version":"4.1.0"},"reference-count":36,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2006,5,18]],"date-time":"2006-05-18T00:00:00Z","timestamp":1147910400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Pineal Research"],"published-print":{"date-parts":[[2006,8]]},"abstract":"<jats:p><jats:bold>Abstract:\u2002<\/jats:bold> The prevalence of diabetes has exponentially increased in recent decades due to environmental factors such as nocturnal lifestyle and aging, both of which influence the amount of melatonin produced in the pineal gland. The present study investigated the effect of melatonin on signaling pathways of glucose transport in C<jats:sub>2<\/jats:sub>C<jats:sub>12<\/jats:sub> mouse skeletal muscle cells. Intriguingly, treatment of C<jats:sub>2<\/jats:sub>C<jats:sub>12<\/jats:sub> cells with melatonin (1\u2003n<jats:sc>m<\/jats:sc>) stimulated glucose uptake twofold increase. Melatonin\u2010stimulated glucose transport was inhibited with co\u2010treatment with the melatonin receptor antagonist luzindole. Furthermore, treatment of stably over\u2010expressed melatonin receptor type 2B containing C<jats:sub>2<\/jats:sub>C<jats:sub>12<\/jats:sub> myotubes with melatonin amplified glucose transport <jats:italic>c.<\/jats:italic> 13\u2010fold. Melatonin also increased the phosphorylation level of insulin receptor substrate\u20101 (IRS\u20101) and the activity of phosphoinositide 3\u2010kinase (PI\u20103\u2010kinase). However, 3\u2032,5\u2032\u2010cyclic adenosine monophosphate\u2010activated protein kinase (AMPK), another important glucose transport stimulatory mediator via an insulin\u2010independent pathway, was not influenced by melatonin treatment. Activity of p38 mitogen\u2010activated protein kinase (MAPK), a downstream mediator of AMPK, was also not changed by melatonin. In addition, melatonin increased the expression level of forkhead box A2, which was recently discovered to regulate fatty acid oxidation and to be inhibited by insulin. In summary, melatonin stimulates glucose transport to skeletal muscle cells via IRS\u20101\/PI\u20103\u2010kinase pathway, which implies, at the molecular level, its role in glucose homeostasis and possibly in diabetes. Additionally, exposure to light at night and aging, both of which lower endogenous melatonin levels may contribute to the incidence and\/or development of diabetes.<\/jats:p>","DOI":"10.1111\/j.1600-079x.2006.00334.x","type":"journal-article","created":{"date-parts":[[2006,5,18]],"date-time":"2006-05-18T10:06:50Z","timestamp":1147946810000},"page":"67-72","source":"Crossref","is-referenced-by-count":91,"title":["Melatonin stimulates glucose transport via insulin receptor substrate\u20101\/phosphatidylinositol 3\u2010kinase pathway in C<sub>2<\/sub>C<sub>12<\/sub> murine skeletal muscle 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