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International Journal of Peptides
Volume 2011 (2011), Article ID 969818, 11 pages
Research Article

Leptin and Fasting Regulate Rat Gastric Glucose-Regulated Protein 58

1Department of Physiology, School of Medicine, Instituto de Investigaciones Sanitarias (IDIS), University of Santiago de Compostela, 15782 Santiago de Compostela, Spain
2CIBER Physiopathology of Obesity and Nitrition (CIBERobn), S. Francisco s/n, 15782 Santiago de Compostela, Spain
3Department of Physiology and Internal Medicine, School of Medicine, National University of Colombia, 11001000 Bogota, Colombia
4Central Service of Proteomic Unity for Research (SCAI), University of Cordoba, 14071 Cordoba, Spain
5Department of Cell Biology, Physiology, and Immunology, University of Cordoba and Maimonides Institute of Biomedical Research (IMIBIC), 14014 Cordoba, Spain

Received 23 June 2011; Revised 19 August 2011; Accepted 19 August 2011

Academic Editor: Jean-Marie Zajac

Copyright © 2011 Susana B. Bravo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The stomach secretes a wide range of peptides with essential metabolic functions, and thereby plays an important role in the regulation of energy homeostasis. Disulfide isomerase glucose-regulated protein 58 (GRp58) is a molecular chaperone member of the endoplasmic reticulum (ER) stress signaling pathway, which is a marker for human gastric cancer. Since GRp58 seems to be regulated by a phosphorylation/dephosphorylation pattern shift, we used the 2DE gel methodology and peptide mass fingerprinting-protein identification by means of MALDI-TOF mass spectrometry. We show that gastric mucosa GRp58 is dephosphorylated by fasting, and this effect is blunted when fasted rats are treated with leptin. Furthermore, we assessed the gene expression of GRp58 under different physiological settings known to be associated with energy homeostasis (fasting, leptin treatment and leptin deficiency). We found that intraperitoneal administration of leptin increases whereas leptin deficiency decreases GRp58 mRNA levels. However, GRp58 expression remains unchanged after fasting, indicating that leptin actions on GRp58 are no direct sensitivity to fasting. Dissection of the molecular pathways mediating the interactions between ER stress-related factors and nutrient availability, as well as their target genes, may open a new avenue for the study of obesity and other metabolic disorders.