PMID- 30097599
OWN - NLM
STAT- MEDLINE
DCOM- 20191021
LR  - 20230928
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 8
IP  - 1
DP  - 2018 Aug 10
TI  - Autophagy upregulation as a possible mechanism of arsenic induced diabetes.
PG  - 11960
LID - 10.1038/s41598-018-30439-0 [doi]
LID - 11960
AB  - The key features of type 2 diabetes mellitus (T2DM) caused by high fat diet (HFD) 
      in combination with arsenic (As) exposure (pronounced glucose intolerance despite 
      a significant decrease in insulin resistance) are different from those expected 
      for T2DM. Autophagy has been considered as a possible link between insulin 
      resistance and obesity. Therefore in this study, we utilized autophagy gene 
      expression profiling via real-time RT-PCR array analysis in livers of NMRI mice 
      exposed to an environmentally relevant and minimally cytotoxic concentration of 
      arsenite (50 ppm) in drinking water while being fed with a HFD for 20 weeks. Out 
      of 84 genes associated with autophagy under study, 21 genes were related to 
      autophagy machinery components of which 13 genes were downregulated when HDF diet 
      was applied. In this study, for the first time, it was shown that the exposure to 
      arsenic in the livers of mice chronically fed with HFD along with increased 
      oxidative stress resulted in the restoration of autophagy [upregulation of genes 
      involved in the early phase of phagophore formation, phagophore expansion and 
      autophagosome-lysosome linkage stages]. Considering the role of arsenic in the 
      induction of autophagy; it can be argued that reduced insulin resistance in 
      HFD - As induced diabetes may be mediated by autophagy upregulation.
FAU - Zeinvand-Lorestani, Marzieh
AU  - Zeinvand-Lorestani M
AD  - Toxicology Research Center, Ahvaz Jundishapur University of Medical Sciences, 
      Ahvaz, Iran.
FAU - Kalantari, Heibatullah
AU  - Kalantari H
AD  - Department of Toxicology, School of Pharmacy, Ahvaz Jundishapur University of 
      Medical Sciences, Ahvaz, Iran.
FAU - Khodayar, Mohammad Javad
AU  - Khodayar MJ
AD  - Toxicology Research Center, Ahvaz Jundishapur University of Medical Sciences, 
      Ahvaz, Iran. jkhodayar@yahoo.com.
AD  - Department of Toxicology, School of Pharmacy, Ahvaz Jundishapur University of 
      Medical Sciences, Ahvaz, Iran. jkhodayar@yahoo.com.
FAU - Teimoori, Ali
AU  - Teimoori A
AD  - Department of Virology, School of Medicine, Ahvaz Jundishapur University of 
      Medical Sciences, Ahvaz, Iran.
FAU - Saki, Najmaldin
AU  - Saki N
AD  - Health Research Institute, Research Center of Thalassemia and Hemoglobinopathy, 
      Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
FAU - Ahangarpour, Akram
AU  - Ahangarpour A
AD  - Health Research Institute, Diabetes Research Center, Department of Physiology, 
      Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
FAU - Rahim, Fakher
AU  - Rahim F
AUID- ORCID: 0000-0002-2857-4562
AD  - Health Research Institute, Research Center of Thalassemia and Hemoglobinopathy, 
      Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
FAU - Alboghobeish, Soheila
AU  - Alboghobeish S
AD  - Department of Pharmacology, School of Pharmacy, Ahvaz Jundishapur University of 
      Medical Sciences, Ahvaz, Iran.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180810
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
RN  - 0 (Biomarkers)
RN  - 0 (Blood Glucose)
RN  - 0 (Insulin)
RN  - N712M78A8G (Arsenic)
SB  - IM
MH  - Animals
MH  - Arsenic/adverse effects
MH  - *Autophagy/genetics
MH  - Biomarkers
MH  - Blood Glucose
MH  - Diabetes Mellitus, Type 2/blood/*etiology/*metabolism
MH  - Diet, High-Fat
MH  - Disease Models, Animal
MH  - Gene Expression Regulation
MH  - Insulin/blood/metabolism
MH  - Liver/metabolism/pathology
MH  - Male
MH  - Metabolic Networks and Pathways
MH  - Mice
MH  - Models, Biological
MH  - Oxidative Stress
MH  - Signal Transduction
MH  - Ubiquitination
PMC - PMC6086829
COIS- The authors declare no competing interests.
EDAT- 2018/08/12 06:00
MHDA- 2019/10/23 06:00
PMCR- 2018/08/10
CRDT- 2018/08/12 06:00
PHST- 2018/05/11 00:00 [received]
PHST- 2018/07/30 00:00 [accepted]
PHST- 2018/08/12 06:00 [entrez]
PHST- 2018/08/12 06:00 [pubmed]
PHST- 2019/10/23 06:00 [medline]
PHST- 2018/08/10 00:00 [pmc-release]
AID - 10.1038/s41598-018-30439-0 [pii]
AID - 30439 [pii]
AID - 10.1038/s41598-018-30439-0 [doi]
PST - epublish
SO  - Sci Rep. 2018 Aug 10;8(1):11960. doi: 10.1038/s41598-018-30439-0.