PMID- 31258514
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200225
IS  - 1664-2392 (Print)
IS  - 1664-2392 (Electronic)
IS  - 1664-2392 (Linking)
VI  - 10
DP  - 2019
TI  - Braving the Element: Pancreatic beta-Cell Dysfunction and Adaptation in Response to 
      Arsenic Exposure.
PG  - 344
LID - 10.3389/fendo.2019.00344 [doi]
LID - 344
AB  - Type 2 diabetes mellitus (T2DM) is a serious global health problem, currently 
      affecting an estimated 451 million people worldwide. T2DM is characterized by 
      hyperglycemia and low insulin relative to the metabolic demand. The precise 
      contributing factors for a given individual vary, but generally include a 
      combination of insulin resistance and insufficient insulin secretion. Ultimately, 
      the progression to diabetes occurs only after beta-cells fail to meet the needs of 
      the individual. The stresses placed upon beta-cells in this context manifest as 
      increased oxidative damage, local inflammation, and ER stress, often inciting a 
      destructive spiral of beta-cell death, increased metabolic stress due to further 
      insufficiency, and additional beta-cell death. Several pathways controlling insulin 
      resistance and beta-cell adaptation/survival are affected by a class of exogenous 
      bioactive compounds deemed endocrine disrupting chemicals (EDCs). Epidemiological 
      studies have shown that, in several regions throughout the world, exposure to the 
      EDC inorganic arsenic (iAs) correlates significantly with T2DM. It has been 
      proposed that a lifetime of exposure to iAs may exacerbate problems with both 
      insulin sensitivity as well as beta-cell function/survival, promoting the 
      development of T2DM. This review focuses on the mechanisms of iAs action as they 
      relate to known adaptive and maladaptive pathways in pancreatic beta-cells.
FAU - Carmean, Christopher M
AU  - Carmean CM
AD  - Division of Molecular and Metabolic Medicine, Department of Physiology and Cell 
      Biology, Kobe University Graduate School of Medicine, Kobe, Japan.
AD  - Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, 
      University of Illinois at Chicago, Chicago, IL, United States.
FAU - Seino, Susumu
AU  - Seino S
AD  - Division of Molecular and Metabolic Medicine, Department of Physiology and Cell 
      Biology, Kobe University Graduate School of Medicine, Kobe, Japan.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20190614
PL  - Switzerland
TA  - Front Endocrinol (Lausanne)
JT  - Frontiers in endocrinology
JID - 101555782
PMC - PMC6587364
OTO - NOTNLM
OT  - arsenic
OT  - diabetes
OT  - endocrine disrupters
OT  - glucose tolerance
OT  - insulin secretion
OT  - pancreas
OT  - reactive oxygen species
OT  - beta-cells
EDAT- 2019/07/02 06:00
MHDA- 2019/07/02 06:01
PMCR- 2019/01/01
CRDT- 2019/07/02 06:00
PHST- 2018/10/03 00:00 [received]
PHST- 2019/05/13 00:00 [accepted]
PHST- 2019/07/02 06:00 [entrez]
PHST- 2019/07/02 06:00 [pubmed]
PHST- 2019/07/02 06:01 [medline]
PHST- 2019/01/01 00:00 [pmc-release]
AID - 10.3389/fendo.2019.00344 [doi]
PST - epublish
SO  - Front Endocrinol (Lausanne). 2019 Jun 14;10:344. doi: 10.3389/fendo.2019.00344. 
      eCollection 2019.