The study results reveal that the sleep hormone repairs communication between key cellular organelles involved in metabolism.
Scientists from the Universities of Granada (Spain) and Lyon (France) have discovered a new mechanism by which melatonin, the hormone that regulates circadian rythms, may protect against diabesity, a condition resulting from the combination of obesity and type 2 diabetes. The study, published in the journal Cell Communication and Signaling, demonstrates that this hormone restores the communication “bridges” between two essential cellular structures: the mitochondria and the endoplasmic reticulum. This repair improves metabolism, reduces oxidative damage, and opens new avenues for future treatments.
The discovery by the research team led by the University of Granada represents a significant advance in understanding how melatonin works beyond its role as a sleep regulator. Until now, its antioxidant effect was well known, but this study reveals that melatonin is also capable of reorganizing the internal architecture of cells and optimizing communication between their organelles.
Organelles are structures or compartments inside our cells that work together in a coordinated way to maintain cellular health. Mitochondria are responsible for producing the energy that cells need to perform all their functions, while the endoplasmic reticulum manufactures and transports essential proteins and lipids throughout the cell. In other words, if cells were “factories,” mitochondria would be the “power plants” supplying electricity, and the endoplasmic reticulum would be the “conveyor belt” of the production and distribution chain.
Although these organelles were once thought to function independently, it is now known that they are connected through specialized structures called MAMs (mitochondria-associated membranes), dynamic “bridges” that enable rapid communication and exchange of signals and molecules between them. These contacts are essential for cellular health and are highly sensitive to metabolic changes, stress, and disease.
Metabolic improvement and reduction of cellular damage
In people with obesity and type 2 diabetes, these “bridges” become damaged, leading to oxidative stress, inflammation, and loss of energy efficiency. The research team demonstrated in animal models of both sexes that chronic administration of melatonin restores the integrity of these “bridges” and recovers functional communication.
Professor of Pharmacology at the University of Granada, Ahmad Agil, who led the study, explains: “These results help us better understand how melatonin acts at the subcellular level, not only as an antioxidant, but also as a modulator of cellular architecture and communication between organelles, opening new therapeutic possibilities.”
The study results showed that melatonin improves mitochondrial health, promotes calcium balance within the cell, reduces oxidative damage in essential lipids such as cardiolipin, and prevents the release of cytochrome C, a process linked to cell death. Taken together, these effects translate into a significant improvement in energy metabolism.
The study was conducted in skeletal muscle, a key organ for energy consumption and blood sugar regulation. Melatonin therefore emerges as a promising compound for restoring metabolic health in diseases associated with excess visceral fat, one of the major global epidemics of the 21st century.
The research, recently published in Cell Communication and Signaling, one of the leading journals in cellular biomedicine published by Springer Nature, involved scientists from several departments and institutes of the University of Granada (Department of Pharmacology, Department of Nutrition and Food Science, Federico Olóriz Institute of Neurosciences, and Granada Biosanitary Research Institute), as well as the CarMeN Laboratory at the University of Lyon. The study was funded by the MELOBE-MUSCa2+ project of the Spanish Ministry of Science and Innovation, the State Research Agency, and the European Regional Development Fund (ERDF).
This study is part of the search for strategies capable of activating thermogenesis without muscle contraction (similar to the effects of physical exercise) and improving the body’s energy efficiency. With this discovery, melatonin is emerging as one of the possible tools in this field, although its clinical use will still require further research.
The authors emphasize that, although the results are highly promising, clinical trials in humans are still needed to confirm these effects and establish safe and effective therapeutic guidelines. “Understanding and reversing the deterioration of organelle communication in diabesity represents a new frontier in metabolic medicine,” concludes Dr. Agil.
Contact
Ahmad Agil
Department of Pharmacology, Faculty of Medicine
Phone: +34 958241000 ext. 20620 | +34 958248794
Email: @email
