Linked Life Data

21824264

Source:http://linkedlifedata.com/resource/pubmed/id/21824264

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2011-8-9
pubmed:abstractText
In type-2 diabetes, hyperglucagonaemia aggravates elevated blood glucose levels. Relative to our knowledge of the ?-cell and insulin secretion, there remains a limited understanding of glucagon secretion in ?-cells. Regulation of glucagon may be dependent on a combination of factors, which include direct glucose sensing by the ?-cell, innervations from the autonomic nervous system and potential 'paracrine' actions by hormones and factors that are released by adjacent endocrine cells within the islets. The list of potential 'paracrine' regulators within the islet includes insulin, somatostatin, ?-aminobutyric acid, glutamate and zinc. Zinc crystallises with insulin in ?-cells and is co-secreted with insulin. In the scientific literature, the effect of exogeneous zinc on glucagon secretion has been debated. Here, we confirm that an increase in exogeneous zinc does inhibit glucagon secretion. To determine if there are physiological effects of zinc on glucagon secretion we used a ?-cell-specific ZnT8 knockout (Znt8BKO) mouse model. Znt8BKO mice, despite showing lower granular zinc content in ?-cells, showed no changes in fasted plasma glucagon levels and glucose regulated glucagon secretion. These findings suggest that zinc secreted from ?-cell does not regulate glucagon secretion.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1463-1326
pubmed:author
pubmed:copyrightInfo
© 2011 Blackwell Publishing Ltd.
pubmed:issnType
Electronic
pubmed:volume
13 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
112-7
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Regulation of glucagon secretion by zinc: lessons from the ? cell-specific Znt8 knockout mouse model.
pubmed:affiliation
Department of Physiology, University of Toronto, 1 King's College Circle, Toronto, ON, Canada.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't