Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1979-5-23
pubmed:abstractText
Relationships between the release of insulin and the incorporation of 45Ca2+ into a lanthanum-nondisplaceable (intracellular) pool were studied in islets microdissected from the pancreatic glands of non-inbred ob/ob mice. In comparison with D-glucose, D-fructose was slowly oxidized and had only marginal effects on insulin release. However, fructose was as effective as glucose in stimulating the lanthanum-nondisplaceable 45Ca2+ uptake. The 45Ca2+ uptake was dose-dependent on the concentration of fructose in the range 0-20 mM; the same dose-dependence was obtained with glucose. Fasting the mice for 3 days caused a total block of the insulin secretory response to 20 mM glucose, but it produced an enhancement of the glucose-induced 45Ca2+ uptake. Both the inhibition of insulin release and the enhancement of 45Ca2+ uptake were counteracted by pretreating the isolated islets with 20-40 mM D-glucose; pretreatment with L-glucose or fructose could not counteract the effects of fasting. Although some functional relationship may exist between the lanthanum-nondisplaceable uptake of 45Ca2+ and the insulin secretory apparatus, it is concluded that the uptake of Ca2+ is not simply the result of stimulated insulin release.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
102
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1856-63
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1978
pubmed:articleTitle
Further studies on the relationship between insulin release and lanthanum-nondisplaceable 45Ca2+ uptake by pancreatic islets: effects of fructose and starvation.
pubmed:publicationType
Journal Article