Activation of insulin and IGF‐1 signaling pathways by melatonin through MT1 receptor in isolated rat pancreatic islets

Picinato, Maria Cecília; Hirata, Aparecida Emiko; Cipolla‐Neto, José; Curi, Rui; Carvalho, Carla Roberta de Oliveira; Anhê, Gabriel Forato; Carpinelli, Ângelo Rafael

doi:10.1111/j.1600-079x.2007.00493.x

Cited by 104 publications

(99 citation statements)

References 60 publications

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“…This concept gives emphasis to the presence of a circadian regulation over pancreatic function. The analysis of melatonin on pancreatic islet by immunoprecipitation and immunoblotting shown that melatonin regulate growth and differentiation of pancreatic cells by stimulating insulin growth factor receptor (IGF-R) and insulin receptor (IR) tyrosine phosphorylation (69). It activates two intracellular signaling pathways: PI3K/AKT (involved with cell metabolism) and MEK/ERKs (involved in cell proliferation, growth and differentiation) (69).…”

Section: Melatonin and Insulin Secretionmentioning

confidence: 99%

“…The analysis of melatonin on pancreatic islet by immunoprecipitation and immunoblotting shown that melatonin regulate growth and differentiation of pancreatic cells by stimulating insulin growth factor receptor (IGF-R) and insulin receptor (IR) tyrosine phosphorylation (69). It activates two intracellular signaling pathways: PI3K/AKT (involved with cell metabolism) and MEK/ERKs (involved in cell proliferation, growth and differentiation) (69). Moreover, the decrease in melatonin levels augmented insulin secretion in rats during the day while at the time of night, low levels of insulin along with high glucose levels are measured when melatonin levels are elevated (70,71).…”

Section: Melatonin and Insulin Secretionmentioning

confidence: 99%

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The role of melatonin in diabetes: therapeutic implications

Sharma

Singh

Ahmad

et al. 2015

Arch. Endocrinol. Metab.

110

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Melatonin referred as the hormone of darkness is mainly secreted by pineal gland, its levels being elevated during night and low during the day. The effects of melatonin on insulin secretion are mediated through the melatonin receptors (MT1 and MT2). It decreases insulin secretion by inhibiting cAMP and cGMP pathways but activates the phospholipaseC/IP3 pathway, which mobilizes Ca 2+ from organelles and, consequently increases insulin secretion. Both in vivo and in vitro, insulin secretion by the pancreatic islets in a circadian manner, is due to the melatonin action on the melatonin receptors inducing a phase shift in the cells. Melatonin may be involved in the genesis of diabetes as a reduction in melatonin levels and a functional interrelationship between melatonin and insulin was observed in diabetic patients. Evidences from experimental studies proved that melatonin induces production of insulin growth factor and promotes insulin receptor tyrosine phosphorylation. The disturbance of internal circadian system induces glucose intolerance and insulin resistance, which could be restored by melatonin supplementation. Therefore, the presence of melatonin receptors on human pancreatic islets may have an impact on pharmacotherapy of type 2 diabetes. Arch Endocrinol Metab.2015;59(5):391-9

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Section: Melatonin and Insulin Secretionmentioning

confidence: 99%

Section: Melatonin and Insulin Secretionmentioning

confidence: 99%

The role of melatonin in diabetes: therapeutic implications

Sharma

Singh

Ahmad

et al. 2015

Arch. Endocrinol. Metab.

110

View full text Add to dashboard Cite

show abstract

“…Growth hormone resistance and reduced insulin and IGF-1 signaling extend the mouse lifespan (192). An effect of melatonin on the IIS pathway via the MT 1 receptor has been identified in rat pancreatic islet cells (193), and MT 1 downregulation leads to insulin resistance (194). Melatonin can improve insulin resistance via alteration of pancreatic gene expression in male mice (195).…”

mentioning

confidence: 99%

Effects of Melatonin on Nervous System Aging: Neurogenesis and Neurodegeneration

et al. 2013

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Abstract. Neural aging as a progressive loss of function involves central and peripheral postmitotic neurons and neural stem cells (NSCs). It promotes neurodegeneration, impairs neurogenesis, and can be considered a cause of cognitive impairment and sensory and motor deficits in the elderly. Age-related morphological atrophic changes and cellular alterations are addressed by neural aging mechanisms. Neurogenesis declines during aging through several mechanisms such as an increase in quiescence state, changes in lineage fate, telomerase dysfunction, the failure of the DNA repair system, increased apoptosis, and the impairment of self-renewal. The selfrenewal transcriptional factor Sox2 has been correlated with retrotransposon L1 and certain cellcycle-and epigenetic-related factors, which are sometimes considered age-related factors in NSC aging. As neurogenesis decreases, non-mitotic neurons undergo neurodegeneration by oxidative stress, sirtuin, insulin signaling and mTOR alteration, mitochondrial dysfunction, and protein misfolding and aggregation. As neurodegeneration and impaired neurogenesis promote the nervous system aging process, the identification of neuronal anti-aging is required to raise life expectancy. The role of melatonin in increasing neurogenesis and protecting against neurodegeneration has been investigated. Here, we review nervous system aging that is correlated with mechanisms of neurodegeneration and the impairment of neurogenesis and evaluate the effects of melatonin on these processes.

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“…кроме того, в отсутствие мелатонина наруша-ется функция инсулиновых рецепторов, в част-ности МТ2 в адипоцитах жировой ткани, что резко снижает захват глюкозы этими клетками [60,61]. Выявленные эффекты пинеалэктомии исчезали в результате терапии мелатонином [62,63]. Таким образом, эпифизарный мелато-нин необходим для синтеза, секреции и реали-зации функций инсулина.…”

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The role of melatonin in development of gestational diabetes mellitus

et al. 2018

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This review summarizes many of the published reports about the production of melatonin and it’s role in regulation of carbohydrate metabolism, interrelationships between melatonin, insulin, glucagon and diurnal signaling the blood-glucose-regulating of the islet. The results of experimental and clinical investigations support that low melatonin levels and absence it’s circadian rhythm play the role in the development of gestational diabetes mellitus in womens with pathology of neuroimmunoendocrinology system and suggest the possibility of prognosis and prophylactic this complication of pregnancy.

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Activation of insulin and IGF‐1 signaling pathways by melatonin through MT1 receptor in isolated rat pancreatic islets

Cited by 104 publications

References 60 publications

The role of melatonin in diabetes: therapeutic implications

The role of melatonin in diabetes: therapeutic implications

Effects of Melatonin on Nervous System Aging: Neurogenesis and Neurodegeneration

The role of melatonin in development of gestational diabetes mellitus

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