Cited by 135Circadian rhythm and melatoninPancreatic function and diabetesDiabetes Treatment and Management

The role of melatonin in diabetes: therapeutic implications

Open access
Sharma, Shweta, Singh, Hemant, Ahmad, Nabeel, Mishra, Priyanka, Tiwari, Archana·2015·Archives of Endocrinology and Metabolism

Abstract

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 Ca2+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.

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  • Most studies have suggested an inhibitory effect of melatonin on insulin secretion.

    “most studies have suggested an inhibitory effect of melatonin on insulin secretion (21,22)”

    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 [22]

    The “Melatonin and Insulin Secretion” section says melatonin inhibits glucose-mediated insulin release and describes an inverse relationship between melatonin levels and insulin secretion. But the Introduction calls the evidence inconsistent, and the paper also describes pathways by which melatonin can increase secretion. It does not establish that *most* studies found an inhibitory effect (page numbers unavailable). (LLM, conf=0.78)

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Research works printed but not linked: 11

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Cited by

Sorted by citations

Authors
Sharma, S., Singh, H., Ahmad, N., Mishra, P., & Tiwari, A.
Affiliations
  • Rajiv Gandhi Technical University (IN)
  • IFTM University (IN)
Venue
Archives of Endocrinology and Metabolism
Published
2015-10
Volume
59
Issue
5
Pages
391-399
ISSN
2359-3997 (ISSN-L)
OpenAlex
W2131444090
Cited by
135
References
89
Citations by year
2026: 5 · 2025: 11 · 2024: 13 · 2023: 10 · 2022: 25 · 2021: 13 · 2020: 14 · 2019: 12 · 2018: 12 · 2017: 11 · 2016: 8 · 2015: 1
FWCI
1.15
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Archives of Endocrinology and Metabolism (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (publishedVersion, other-oa)
  • Americanae (AECID Library) (submittedVersion, other-oa)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Keywords
melatonin, diabetes mellitus, type 2 diabetes, insulin secretion, melatonin receptors, MT1 receptor, MT2 receptor, pancreatic islets, circadian rhythm, insulin resistance, impaired glucose tolerance, insulin-like growth factor, insulin receptor tyrosine phosphorylation, pineal gland, melatonin supplementation
MeSH terms
Insulin Secretion, Animals, Circadian Rhythm, Diabetes Mellitus, Type 2, Glucose, Humans, Insulin, Melatonin, Polymorphism, Genetic, Signal Transduction, Receptors, Melatonin, Insulin-Secreting Cells

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