The DOI matches its Crossref record; 139 of the 139 references it cites were found in a registry or an index.
Melatonin, energy metabolism, and obesity: a review
Abstract
Melatonin is an old and ubiquitous molecule in nature showing multiple mechanisms of action and functions in practically every living organism. In mammals, pineal melatonin functions as a hormone and a chronobiotic, playing a major role in the regulation of the circadian temporal internal order. The anti‐obesogen and the weight‐reducing effects of melatonin depend on several mechanisms and actions. Experimental evidence demonstrates that melatonin is necessary for the proper synthesis, secretion, and action of insulin. Melatonin acts by regulating GLUT 4 expression and/or triggering, via its G‐protein‐coupled membrane receptors, the phosphorylation of the insulin receptor and its intracellular substrates mobilizing the insulin‐signaling pathway. Melatonin is a powerful chronobiotic being responsible, in part, by the daily distribution of metabolic processes so that the activity/feeding phase of the day is associated with high insulin sensitivity, and the rest/fasting is synchronized to the insulin‐resistant metabolic phase of the day. Furthermore, melatonin is responsible for the establishment of an adequate energy balance mainly by regulating energy flow to and from the stores and directly regulating the energy expenditure through the activation of brown adipose tissue and participating in the browning process of white adipose tissue. The reduction in melatonin production, as during aging, shift‐work or illuminated environments during the night, induces insulin resistance, glucose intolerance, sleep disturbance, and metabolic circadian disorganization characterizing a state of chronodisruption leading to obesity. The available evidence supports the suggestion that melatonin replacement therapy might contribute to restore a more healthy state of the organism.
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Cites
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Self-citationBrown adipose tissue regulates glucose homeostasis and insulin sensitivity
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Self-citation
Cited by
Sex and Gender Differences in Risk, Pathophysiology and Complications of Type 2 Diabetes Mellitus
Kautzky-Willer, A., Harreiter, J., & Pacini, G. (2016) · Endocrine Reviews · doi:10.1210/er.2015-1137 · Cited by 2,043
Branched-chain amino acids in metabolic signalling and insulin resistance
Lynch, C. J., & Adams, S. H. (2014) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2014.171 · Cited by 1,461
Melatonin as a mitochondria-targeted antioxidant: one of evolution's best ideas
Reiter, R. J., Rosales-Corral, S., Tan, D. X., Jou, M. J., Galano, A., & Xu, B. (2017) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-017-2609-7 · Cited by 558
Self-citationMelatonin reprogramming of gut microbiota improves lipid dysmetabolism in high‐fat diet‐fed mice
Yin, J., Li, Y., Han, H., Chen, S., Gao, J., Liu, G., Wu, X., Deng, J., Yu, Q., Huang, X., et al. (2018) · Journal of Pineal Research · doi:10.1111/jpi.12524 · Cited by 384
Self-citationMelatonin prevents obesity through modulation of gut microbiota in mice
Xu, P., Wang, J., Hong, F., Wang, S., Jin, X., Xue, T., Jia, L., & Zhai, Y. (2017) · Journal of Pineal Research · doi:10.1111/jpi.12399 · Cited by 281
Metadata
- Authors
- Cipolla‐Neto, J., Amaral, F. G., Afeche, S. C., Tan, D. X., & Reiter, R. J.
- Venue
- Journal of Pineal Research
- Publisher
- Wiley
- Published
- 2014-04-05
- Volume
- 56
- Issue
- 4
- Pages
- 371-381
- ISSN
- 0742-3098 (ISSN-L)
- 1600-079X
- OpenAlex
- W2138418546
- Cited by
- 579
- References
- 139
- FWCI
- 17.06
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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