Over-expression of Slc30a8/ZnT8 selectively in the mouse α cell impairs glucagon release and responses to hypoglycemia.
Antonia SolomouErwann PhilippePauline ChabosseauStephanie Migrenne-LiJulien GaitanJochen LangChristophe MagnanGuy A RutterPublished in: Nutrition & metabolism (2016)
Increased ZnT8 expression, and a likely increase in intragranular free Zn(2+) concentration, is deleterious in pancreatic α cells for stimulated glucagon release. These data provide further evidence that type 2 diabetes-associated polymorphisms in the SLC30A8/ZnT8 gene may act in part via alterations in glucagon release and suggest that ZnT8 activation may restrict glucagon release in some settings.
Keyphrases
- type diabetes
- poor prognosis
- induced apoptosis
- glycemic control
- single cell
- cell cycle arrest
- binding protein
- cell therapy
- long non coding rna
- heavy metals
- gene expression
- genome wide
- adipose tissue
- signaling pathway
- risk assessment
- bone marrow
- oxidative stress
- weight loss
- artificial intelligence
- endoplasmic reticulum stress