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In addition, type 2 diabetic rats, as well as patients, exhibit decreased melatonin levels, whereas the levels in type 1 diabetic rats are increased. The latter effects were normalized by insulin substitution, which signifies that a specific receptor\u2010mediated insulin\u2013melatonin antagonism exists. These results are in agreement with several recent genome\u2010wide association studies, which have identified a number of single nucleotide polymorphisms in the<jats:italic>MTNR1B<\/jats:italic>gene, encoding the MT2 receptor, that were closely associated with a higher prognostic risk of developing type 2 diabetes. We hypothesize that catecholamines, which decrease insulin levels and stimulate melatonin synthesis, control insulin\u2013melatonin interactions. The present results support this assertion as we show that catecholamines are increased in type 1 but are diminished in type 2 diabetes. Another important line of inquiry involves the fact that melatonin protects the \u03b2\u2010cells against functional overcharge and, consequently, hinders the development of type 2 diabetes. In this context, it is striking that at advanced ages, melatonin levels are reduced and the incidence of type 2 diabetes is increased. Thus, melatonin appears to have a protective biological role. Here, we strongly repudiate misconceptions, resulting from observations that melatonin reduces the plasma insulin level, that the blockage of melatonin receptors would be of benefit in the treatment of type 2 diabetes.<\/jats:p>","DOI":"10.1111\/j.1600-079x.2011.00951.x","type":"journal-article","created":{"date-parts":[[2011,8,31]],"date-time":"2011-08-31T19:50:30Z","timestamp":1314820230000},"page":"389-396","source":"Crossref","is-referenced-by-count":22,"title":["Catecholamines are the key for explaining the biological relevance of insulin\u2013melatonin antagonisms in type 1 and type 2 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