Cited by 70Pancreatic function and diabetesCircadian rhythm and melatoninNatural Antidiabetic Agents Studies

Depression of glucose levels and partial restoration of pancreatic β-cell damage by melatonin in streptozotocin-induced diabetic rats

Kanter, Mehmet, Uysal, Hamdi, Karaca, Turan, Sagmanligil, Hulya Ozdemir·2006·Archives of Toxicology

Abstract

Diabetes mellitus is a common but serious metabolic disorder associated with many functional and structural complications. Glucose metabolism is disturbed due to an absolute or relative insulin deficiency. The experiment was carried out to determine the effect of melatonin on blood glucose and insulin concentrations, and histopathology of pancreatic beta-cells in streptozotocin (STZ)-induced diabetic rats. The rats were randomly allocated into one of the four experimental groups: group A (control), group B (diabetic untreated), group C (diabetic treated with melatonin for 6 weeks) and group D (diabetic treated with melatonin for 8 weeks); each group contained ten animals. Diabetes was induced in B, C and D groups by a single intraperitoneal (i.p.) injection of STZ (50 mg/kg, freshly dissolved in 5 mmol/l citrate buffer, pH 4.5). The rats in melatonin-treated groups were subjected to the daily i.p injection of 10 mg kg(-1) of melatonin for 6 or 8 weeks starting the day after STZ injection. Control and diabetic untreated rats were injected with the same volume of isotonic NaCl as the melatonin treated groups. Almost all insulin-positive beta-cells were degranulated, degenerated or necrotic in the STZ-treated rats leading to decrease in insulin secretion and an increase in blood glucose concentration. Melatonin treatment caused a sharp decrease in the elevated serum glucose, a slight increase in the lowered serum insulin concentrations and small partial regeneration/proliferation of beta-cells of islets. It is concluded that the hypoglycemic action of melatonin could be partly due to small amelioration in the beta-cells of pancreatic islets causing a slight increase in insulin secretion, it is mostly due to the extrapancreatic actions of the melatonin.

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Crossref · 10.1007/s00204-005-0055-z

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Authors
Kanter, M., Uysal, H., Karaca, T., & Sagmanligil, H. O.
Affiliations
  • Trakya University (TR)
  • Ankara University (TR)
  • Van Yüzüncü Yıl Üniversitesi (TR)
Corresponding author
Kanter, Mehmet
Venue
Archives of Toxicology
Published
2005-12-09
Volume
80
Issue
6
Pages
362-369
ISSN
  • 0340-5761 (ISSN-L)
  • 1432-0738
OpenAlex
W2022531681
Cited by
70
References
49
Citations by year
2025: 1 · 2024: 2 · 2023: 5 · 2022: 4 · 2021: 6 · 2020: 1 · 2019: 4 · 2018: 7 · 2017: 2 · 2016: 8 · 2015: 1 · 2014: 5 · 2013: 9 · 2012: 3
FWCI
1.26
Type
journal article
Language
en
Open access
closed
Locations
  • Archives of Toxicology (publishedVersion)
  • PubMed (publishedVersion)
  • Van Yüzüncü Yıl University Academic Data Management System (submittedVersion)
  • Trakya University's Institutional Open Access System (Trakya University) (submittedVersion)
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Natural Antidiabetic Agents Studies
Keywords
melatonin, streptozotocin-induced diabetes, type 1 diabetes, pancreatic beta-cell damage, beta cell regeneration, hypoglycemic effect, insulin secretion, blood glucose, pancreatic islets
MeSH terms
Animals, Blood Glucose, Body Weight, Diabetes Mellitus, Experimental, Image Processing, Computer-Assisted, Insulin, Male, Melatonin, Regeneration, Free Radical Scavengers, Rats, Wistar, Insulin-Secreting Cells, Rats

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