Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2008-9-5
pubmed:abstractText
Free fatty acids (FFAs) acutely stimulate but chronically impair glucose-stimulated insulin secretion from beta-cells. The G protein-coupled transmembrane receptor 40 (GPR40) mediates both acute and chronic effects of FFAs on insulin secretion and plays a role in glucose homeostasis. Limited information is available on the effect of GPR40 genetic abnormalities on insulin secretion and metabolic regulation in human subjects.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0021-972X
pubmed:author
pubmed:issnType
Print
pubmed:volume
93
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3541-50
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:18583466-Adult, pubmed-meshheading:18583466-Calcium, pubmed-meshheading:18583466-DNA Mutational Analysis, pubmed-meshheading:18583466-Female, pubmed-meshheading:18583466-Gene Frequency, pubmed-meshheading:18583466-Genetic Linkage, pubmed-meshheading:18583466-Genotype, pubmed-meshheading:18583466-Glucose Tolerance Test, pubmed-meshheading:18583466-HeLa Cells, pubmed-meshheading:18583466-Humans, pubmed-meshheading:18583466-Insulin, pubmed-meshheading:18583466-Insulin-Secreting Cells, pubmed-meshheading:18583466-Intracellular Fluid, pubmed-meshheading:18583466-Male, pubmed-meshheading:18583466-Middle Aged, pubmed-meshheading:18583466-Models, Biological, pubmed-meshheading:18583466-Mutation, Missense, pubmed-meshheading:18583466-Obesity, pubmed-meshheading:18583466-Receptors, G-Protein-Coupled, pubmed-meshheading:18583466-Transfection
pubmed:year
2008
pubmed:articleTitle
Loss-of-function mutation of the GPR40 gene associates with abnormal stimulated insulin secretion by acting on intracellular calcium mobilization.
pubmed:affiliation
Endocrine-Metabolic Laboratory, Internal Medicine, Department of Medical and Surgical Sciences, University of Padova, via Ospedale, 105, I-35128 Padova, Italy. roberto.vettor@unipd.it
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't