2001
DOI: 10.1679/aohc.64.59
|View full text |Cite
|
Sign up to set email alerts
|

Morphological Changes in Pancreatic Islets of KATP Channel-Deficient Mice. The Involvement of KATP Channels in the Survival of Insulin Cells and the Maintenance of Islet Architecture.

Abstract: The ATP-sensitive potassium channel (KATP channel) is an essential ion channel involved in glucose-induced insulin secretion. The KATP channel is composed of an inwardly rectifying potassium channel, Kir6.2, and the sulfonylurea receptor (SUR 1); in the pancreas it is reported to be shared by all endocrine cell types. A previous study by our research group showed that Kir 6.2-knockout mice lacked KATP channel activities and failed to secrete insulin in response to glucose, but displayed normal blood glucose le… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

3
11
1

Year Published

2001
2001
2017
2017

Publication Types

Select...
5
3

Relationship

0
8

Authors

Journals

citations
Cited by 19 publications
(15 citation statements)
references
References 36 publications
3
11
1
Order By: Relevance
“…The distribution of α-cells can be very different in some transgenic mice. For instance, α-cells are frequently located in central regions of islets in K ATPdeficient mouse models, such as SUR1 (Marhfour et al 2009) or Kir6.2 knockout mice (Seino et al 2000;Winarto et al 2001) or in mice completely or partially deficient in specific adhesion molecule (Esni et al 1999). The reasons for this altered distribution are unknown.…”
Section: Microanatomy Of the Islets Of Langerhansmentioning
confidence: 99%
“…The distribution of α-cells can be very different in some transgenic mice. For instance, α-cells are frequently located in central regions of islets in K ATPdeficient mouse models, such as SUR1 (Marhfour et al 2009) or Kir6.2 knockout mice (Seino et al 2000;Winarto et al 2001) or in mice completely or partially deficient in specific adhesion molecule (Esni et al 1999). The reasons for this altered distribution are unknown.…”
Section: Microanatomy Of the Islets Of Langerhansmentioning
confidence: 99%
“…Overexpression of a mutant Kir6.2 which disrupts K ATP channel activity resulted in hyperinsulinaemic hypoglycaemia in the neonatal period, but later on, was followed by diabetes associated with loss of b-cells [80]. Kir6.2 knock-out mice indeed showed a reduction of insulin-secreting cells throughout their life and an increase in glucagon cells [129].…”
Section: Follow-upmentioning
confidence: 99%
“…However, chronically elevated [Ca 2+ ] i can also induce maladaptive responses because prevention of Ca 2+ influx in the setting of insulin resistance prevents β-cell death (13). In either case, mice lacking K ATP channels exhibit disrupted islet morphology, characterized by α-cells being located in the islet core (14,15), suggesting loss of β-cell identity or impairments in cell adhesion.…”
Section: Introductionmentioning
confidence: 99%