Linked Life Data

15655707

Source:http://linkedlifedata.com/resource/pubmed/id/15655707

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11-12
pubmed:dateCreated
2005-1-18
pubmed:abstractText
A much greater insulin response is observed after oral glucose load than after intravenous injection of glucose. The hormonal factor(s) implicated as transmitters of signals from the gut to pancreatic beta-cells was referred to incretin; gastric inhibitory polypeptide or glucose-dependent insulinotropic polypeptide (GIP) is identified as one of the incretins. GIP exerts its effects by binding to its specific receptor, the GIP receptor, which is expressed in various tissues including pancreatic islets, adipose tissue, and brain. However, the physiological role of GIP has been generally thought to stimulate insulin secretion from pancreatic beta-cells, and the other actions of GIP have received little attention. We have bred and characterized mice with a targeted mutation of the GIP receptor gene. From these studies, we now know that GIP not only mediates early insulin secretion by acting on pancreatic beta-cells, but also links overnutrition to obesity by acting on adipocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0018-5043
pubmed:author
pubmed:issnType
Print
pubmed:volume
36
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
771-4
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:articleTitle
Physiology of GIP--a lesson from GIP receptor knockout mice.
pubmed:affiliation
Department of Diabetes and Clinical Nutrition, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan. yamada@metab.kuhp.kyoto-u.ac.jp
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't