Activation of melatonin signaling promotes β-cell survival and function
Open accessAbstract
Type 2 diabetes mellitus (T2DM) is characterized by pancreatic islet failure due to loss of β-cell secretory function and mass. Studies have identified a link between a variance in the gene encoding melatonin (MT) receptor 2, T2DM, and impaired insulin secretion. This genetic linkage raises the question whether MT signaling plays a role in regulation of β-cell function and survival in T2DM. To address this postulate, we used INS 832/13 cells to test whether activation of MT signaling attenuates proteotoxicity-induced β-cell apoptosis and through which molecular mechanism. We also used nondiabetic and T2DM human islets to test the potential of MT signaling to attenuate deleterious effects of glucotoxicity and T2DM on β-cell function. MT signaling in β-cells (with duration designed to mimic typical nightly exposure) significantly enhanced activation of the cAMP-dependent signal transduction pathway and attenuated proteotoxicity-induced β-cell apoptosis evidenced by reduced caspase-3 cleavage (∼40%), decreased activation of stress-activated protein kinase/Jun-amino-terminal kinase (∼50%) and diminished oxidative stress response. Activation of MT signaling in human islets was shown to restore glucose-stimulated insulin secretion in islets exposed to chronic hyperglycemia as well as in T2DM islets. Our data suggest that β-cell MT signaling is important for the regulation of β-cell survival and function and implies a preventative and therapeutic potential for preservation of β-cell mass and function in T2DM.
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Some studies performed in isolated human pancreatic islets have shown stimulatory effects of melatonin on insulin secretion.
“some studies performed in isolated human pancreatic islets have shown stimulatory effects (15,17,23).”
From Interplay of Dinner Timing and <i>MTNR1B</i> Type 2 Diabetes Risk Variant on Glucose Tolerance and Insulin Secretion: A Randomized Crossover Trial (2022) · cites this paper as [17]
Some studies show that elevated melatonin concentrations are associated with improved glucose control.
“While some studies show that elevated melatonin concentrations are associated with improved glucose control (15)(16)(17)”
From Interplay of Dinner Timing and <i>MTNR1B</i> Type 2 Diabetes Risk Variant on Glucose Tolerance and Insulin Secretion: A Randomized Crossover Trial (2022) · cites this paper as [17]
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- Authors
- Costes, S., Boss, M., Thomas, A. P., & Matveyenko, A. V.
- Affiliations
- University of California, Los Angeles (US)
- Mayo Clinic (US)
- Corresponding author
- Matveyenko, Aleksey V.
- Venue
- Molecular Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2015-05-01
- Volume
- 29
- Issue
- 5
- Pages
- 682-692
- ISSN
- 0888-8809 (ISSN-L)
- 1944-9917
- PMC
- PMC4415205
- OpenAlex
- W2145215846
- Cited by
- 84
- References
- 57
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 4 · 2023: 8 · 2022: 8 · 2021: 6 · 2020: 8 · 2019: 6 · 2018: 11 · 2017: 8 · 2016: 9 · 2015: 4
- FWCI
- 10.74
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Endocrinology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Larry L. Hillblom Foundation
- National Institutes of Health
- University of California, Los Angeles
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK098468)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
- Keywords
- melatonin signaling, melatonin receptor 2, beta-cell survival, beta-cell apoptosis, type 2 diabetes, proteotoxicity, glucotoxicity, cAMP signaling, JNK, caspase-3, oxidative stress, glucose-stimulated insulin secretion, beta-cell mass, pancreatic islets
- MeSH terms
- Animals, Cell Survival, Diabetes Mellitus, Type 2, Humans, Melatonin, Signal Transduction, Receptors, Melatonin, Cell Line, Tumor, Insulin-Secreting Cells, Rats
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