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• W2022220021 endingPage "23" @default.
• W2022220021 startingPage "1" @default.
• W2022220021 abstract "The pineal hormone melatonin influences insulin secretion, as well as glucagon and somatostatin secretion, both in vivo and in vitro. These effects are mediated by two specific, high-affinity, seven transmembrane, pertussis toxin-sensitive, Gi-protein-coupled melatonin receptors, MT1 and MT2. Both isoforms are expressed in the β-cells, α-cells as well as δ-cells of the pancreatic islets of Langerhans and are involved in the modulation of insulin secretion, leading to inhibition of the adenylate cyclase-dependent cyclic adenosine monophosphate as well as cyclic guanosine monophosphate formation in pancreatic β-cells by inhibiting the soluble guanylate cyclase, probably via MT2 receptors. In this way, melatonin also likely inhibits insulin secretion, whereas using the inositol triphosphate pathway after previous blocking of Gi-proteins by pertussis toxin, melatonin increases insulin secretion. Desynchrony of receptor signaling may lead to the development of type 2 diabetes. This notion has recently been supported by genomewide association studies pinpointing variances of the MT2 receptor as a risk factor for this rapidly spreading metabolic disturbance. As melatonin is secreted in a clearly diurnal fashion, it is safe to assume that it also has a diurnal impact on the blood-glucose-regulating function of the islet. Observations of the circadian expression of clock genes (Clock, Bmal1, Per1,2,3, and Cry1,2) in pancreatic islets, as well as in INS1 rat insulinoma cells, may indicate that circadian rhythms are generated in the β-cells themselves. The circadian secretion of insulin from pancreatic islets is clock-driven. Disruption of circadian rhythms and clock function leads to metabolic disturbances, for example, type 2 diabetes. The study of melatonin–insulin interactions in diabetic rat models has revealed an inverse relationship between these two hormones. Both type 2 diabetic rats and patients exhibit decreased melatonin levels and slightly increased insulin levels, whereas type 1 diabetic rats show extremely reduced levels or the absence of insulin, but statistically significant increases in melatonin levels. Briefly, an increase in melatonin levels leads to a decrease in stimulated insulin secretion and vice versa. Melatonin levels in blood plasma, as well as the activity of the key enzyme of melatonin synthesis, AA-NAT (arylalkylamine-N-acetyltransferase) in pineal, are lower in type 2 diabetic rats compared to controls. In contrast, melatonin and pineal AA-NAT mRNA are increased and insulin receptor mRNA is decreased in type 1 diabetic rats, which also indicates a close relationship between insulin and melatonin. As an explanation, it was hypothesized that catecholamines, which reduce insulin levels and stimulate melatonin synthesis, control insulin–melatonin interactions. This conviction stems from the observation that catecholamines are increased in type 1 but are diminished in type 2 diabetes. In this context, another important line of inquiry involves the fact that melatonin protects β-cells against functional overcharge and, consequently, hinders the development of type 2 diabetes." @default.
• W2022220021 created "2016-06-24" @default.
• W2022220021 creator A5012145519 @default.
• W2022220021 creator A5023043198 @default.
• W2022220021 creator A5078155241 @default.
• W2022220021 date "2015-06-06" @default.
• W2022220021 modified "2023-09-26" @default.
• W2022220021 title "Experimental and clinical aspects of melatonin and clock genes in diabetes" @default.
• W2022220021 cites W1505050831 @default.
• W2022220021 cites W1516650980 @default.
• W2022220021 cites W1542348680 @default.
• W2022220021 cites W1564855882 @default.
• W2022220021 cites W1712951338 @default.
• W2022220021 cites W1787893252 @default.
• W2022220021 cites W180845395 @default.
• W2022220021 cites W1824430217 @default.
• W2022220021 cites W1861134585 @default.
• W2022220021 cites W1913108561 @default.
• W2022220021 cites W1913230283 @default.
• W2022220021 cites W1932521829 @default.
• W2022220021 cites W1965532359 @default.
• W2022220021 cites W1968890500 @default.
• W2022220021 cites W1969325188 @default.
• W2022220021 cites W1969480413 @default.
• W2022220021 cites W1970505296 @default.
• W2022220021 cites W1970792890 @default.
• W2022220021 cites W1970827724 @default.
• W2022220021 cites W1970980171 @default.
• W2022220021 cites W1971060562 @default.
• W2022220021 cites W1973259490 @default.
• W2022220021 cites W1974232736 @default.
• W2022220021 cites W1976216594 @default.
• W2022220021 cites W1976548318 @default.
• W2022220021 cites W1978870097 @default.
• W2022220021 cites W1980059212 @default.
• W2022220021 cites W1981592719 @default.
• W2022220021 cites W1982802020 @default.
• W2022220021 cites W1983338067 @default.
• W2022220021 cites W1985401769 @default.
• W2022220021 cites W1985945913 @default.
• W2022220021 cites W1987546711 @default.
• W2022220021 cites W1987699071 @default.
• W2022220021 cites W1988550244 @default.
• W2022220021 cites W1988626975 @default.
• W2022220021 cites W1993253729 @default.
• W2022220021 cites W1994567337 @default.
• W2022220021 cites W1994603733 @default.
• W2022220021 cites W1995539950 @default.
• W2022220021 cites W1997750233 @default.
• W2022220021 cites W1998320088 @default.
• W2022220021 cites W1998894137 @default.
• W2022220021 cites W1999292452 @default.
• W2022220021 cites W2000669888 @default.
• W2022220021 cites W2002061397 @default.
• W2022220021 cites W2002800136 @default.
• W2022220021 cites W2003302378 @default.
• W2022220021 cites W2006580967 @default.
• W2022220021 cites W2006617466 @default.
• W2022220021 cites W2007583894 @default.
• W2022220021 cites W2009132775 @default.
• W2022220021 cites W2009377263 @default.
• W2022220021 cites W2009736530 @default.
• W2022220021 cites W2010104326 @default.
• W2022220021 cites W2010251886 @default.
• W2022220021 cites W2013187542 @default.
• W2022220021 cites W2013233045 @default.
• W2022220021 cites W2013616500 @default.
• W2022220021 cites W2014313900 @default.
• W2022220021 cites W2014760308 @default.
• W2022220021 cites W2014782985 @default.
• W2022220021 cites W2015178725 @default.
• W2022220021 cites W2015319930 @default.
• W2022220021 cites W2015398239 @default.
• W2022220021 cites W2017631992 @default.
• W2022220021 cites W2017830665 @default.
• W2022220021 cites W2018021093 @default.
• W2022220021 cites W2019955714 @default.
• W2022220021 cites W2020244868 @default.
• W2022220021 cites W2020884658 @default.
• W2022220021 cites W2021474976 @default.
• W2022220021 cites W2021597195 @default.
• W2022220021 cites W2021719582 @default.
• W2022220021 cites W2021990756 @default.
• W2022220021 cites W2022873602 @default.
• W2022220021 cites W2027485664 @default.
• W2022220021 cites W2027702908 @default.
• W2022220021 cites W2028746974 @default.
• W2022220021 cites W2028804629 @default.
• W2022220021 cites W2029814599 @default.
• W2022220021 cites W2032561678 @default.
• W2022220021 cites W2033990787 @default.
• W2022220021 cites W2034348289 @default.
• W2022220021 cites W2035424746 @default.
• W2022220021 cites W2036120795 @default.
• W2022220021 cites W2037024495 @default.
• W2022220021 cites W2037732282 @default.
• W2022220021 cites W2040398306 @default.
• W2022220021 cites W2042293867 @default.

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