Sökning: id:"swepub:oai:prod.swepub.kib.ki.se:130139967"
> (2014) >
Defects in β-cell C...
Defects in β-cell Ca2+ dynamics in age-induced diabetes
-
- Li, LS (författare)
- Karolinska Institutet
-
Trifunovic, A (författare)
-
- Kohler, M (författare)
- Karolinska Institutet
-
visa fler...
-
- Wang, YX (författare)
- Karolinska Institutet
-
Berglund, JP (författare)
-
- Illies, C (författare)
- Karolinska Institutet
-
- Juntti-Berggren, L (författare)
- Karolinska Institutet
-
- Larsson, NG (författare)
- Karolinska Institutet
-
- Berggren, PO (författare)
- Karolinska Institutet
-
visa färre...
-
(creator_code:org_t)
- 2014-11-13
- 2014
- Engelska.
-
Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 63:12, s. 4100-4114
- Relaterad länk:
-
https://diabetes.dia...
-
visa fler...
-
http://kipublication...
-
https://doi.org/10.2...
-
visa färre...
Abstract
Ämnesord
Stäng
- Little is known about the molecular mechanisms underlying age-dependent deterioration in β-cell function. We now demonstrate that age-dependent impairment in insulin release, and thereby glucose homeostasis, is associated with subtle changes in Ca2+ dynamics in mouse β-cells. We show that these changes are likely to be accounted for by impaired mitochondrial function and to involve phospholipase C/inositol 1,4,5-trisphosphate–mediated Ca2+ mobilization from intracellular stores as well as decreased β-cell Ca2+ influx over the plasma membrane. We use three mouse models, namely, a premature aging phenotype, a mature aging phenotype, and an aging-resistant phenotype. Premature aging is studied in a genetically modified mouse model with an age-dependent accumulation of mitochondrial DNA mutations. Mature aging is studied in the C57BL/6 mouse, whereas the 129 mouse represents a model that is more resistant to age-induced deterioration. Our data suggest that aging is associated with a progressive decline in β-cell mitochondrial function that negatively impacts on the fine tuning of Ca2+ dynamics. This is conceptually important since it emphasizes that even relatively modest changes in β-cell signal transduction over time lead to compromised insulin release and a diabetic phenotype.
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
Hitta via bibliotek
-
Diabetes
(Sök värdpublikationen i LIBRIS)
Till lärosätets databas