Dietary ingestion of 2-aminoanthracene (2AA) and the risk for type-1 diabetes (T1D).
Animals
Anthracenes
/ toxicity
Apoptosis
/ drug effects
Diabetes Mellitus, Experimental
/ chemically induced
Diabetes Mellitus, Type 1
/ chemically induced
Dietary Exposure
/ analysis
Environmental Pollutants
/ toxicity
Insulin-Secreting Cells
/ drug effects
Interleukins
/ genetics
Male
Rats
Rats, Sprague-Dawley
Risk
2-aminoanthracene (2AA)
Beta-cells
Pancreas
Type 1 Diabetes (T1D)
apoptosis
Journal
Journal of environmental science and health. Part A, Toxic/hazardous substances & environmental engineering
ISSN: 1532-4117
Titre abrégé: J Environ Sci Health A Tox Hazard Subst Environ Eng
Pays: England
ID NLM: 9812551
Informations de publication
Date de publication:
2020
2020
Historique:
entrez:
30
12
2020
pubmed:
31
12
2020
medline:
12
1
2021
Statut:
ppublish
Résumé
Type 1 diabetes (T1D) is an autoimmune disorder caused by the destruction of insulin-secreting β-cells.T1D is on the rise around the world. Exposure to polycyclic aromatic hydrocarbons (PAHs) including 2-aminoanthracene (2AA) is considered a contributor to TID increase. The contribution of the ingestion of 2AA toward T1D vulnerability is examined. 2AA is found in a variety of household products. Juvenile male Sprague Dawley rats ingested various amounts of 2AA contaminated diet for 12 weeks. Results showed marginal reduction in body weight gain for the 100 mg/kg treated animals. Glucose tolerance test (GTT) indicated no changes at six weeks. However, at week 12, both treated groups had higher levels of blood glucose than the control group. Serum insulin concentration was elevated in the 50 mg/kg group while reduced in the 100 mg/kg animals. Serum lactate dehydrogenase activity was elevated in treated groups. Evaluation of pancreatic inflammatory cytokines revealed overexpression of IL-1B, IL-6, and IL-7. Apoptotic genes in the pancreas of exposed rats were overly expressed. Histopathology and insulin immunohistochemistry data showed the presence of mesenteric vessels surrounded by lymphocyte and enlarged size of islet cells respectively in the high dose group. These results suggest 2AA ingestion may enhance T1D development.
Identifiants
pubmed: 33377427
doi: 10.1080/10934529.2020.1830651
doi:
Substances chimiques
Anthracenes
0
Environmental Pollutants
0
Interleukins
0
2-anthramine
8240818JGU
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM