Person:
Martínez Ibáñez, María Dolores

Profile Picture
First Name
María Dolores
Last Name
Martínez Ibáñez
URI
https://hdl.handle.net/20.500.14352/83506
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Ciencias Biológicas
Department
Area
Zoología
Identifiers
UCM identifierDialnet ID

Filters

20051
Reset filters

Settings

Author: De Cáceres, Javier ×

Search Results

Now showing 1 - 1 of 1
  • Thumbnail Image
    Item
    The expression of GLP‐1 receptor mRNA and protein allows the effect of GLP‐1 on glucose metabolism in the human hypothalamus and brainstem
    (Journal of Neurochemistry, 2005) Álvarez García, Elvira; Martínez Ibáñez, María Dolores; Roncero Rincón, Isabel; Chowen, Julie A.; García‐Cuartero, Beatriz; Gispert, Juan D.; Sanz Miguel, María Del Carmen; Vázquez Pérez, Patricia; Antonio, Maldonado; De Cáceres, Javier; Desco, Manuel; Pozo García, Miguel Ángel; Blázquez Fernández, Enrique
    In the present work, several experimental approaches were used to determine the presence of the glucagon-like peptide-1 receptor (GLP-1R) and the biological actions of its ligand in the human brain. In situ hybridization histochemistry revealed specific labelling for GLP-1 receptor mRNA in several brain areas. In addition, GLP-1R, glucose transporter isoform (GLUT-2) and glucokinase (GK) mRNAs were identified in the same cells, especially in areas of the hypothalamus involved in feeding behaviour. GLP-1R gene expression in the human brain gave rise to a protein of 56 kDa as determined by affinity cross-linking assays. Specific binding of 125I-GLP-1(7-36) amide to the GLP-1R was detected in several brain areas and was inhibited by unlabelled GLP-1(7-36) amide, exendin-4 and exendin (9-39). A further aim of this work was to evaluate cerebral-glucose metabolism in control subjects by positron emission tomography (PET), using 2-[F-18] deoxy-D-glucose (FDG). Statistical analysis of the PET studies revealed that the administration of GLP-1(7-36) amide significantly reduced (p < 0.001) cerebral glucose metabolism in hypothalamus and brainstem. Because FDG-6-phosphate is not a substrate for subsequent metabolic reactions, the lower activity observed in these areas after peptide administration may be due to reduction of the glucose transport and/or glucose phosphorylation, which should modulate the glucose sensing process in the GLUT-2- and GK-containing cells.