Dietary keto-acid feed-back on pituitary activity in gilthead sea bream: effects of oral doses of AKG. A proteomic approach. | - CCMAR -

Journal Article

TitleDietary keto-acid feed-back on pituitary activity in gilthead sea bream: effects of oral doses of AKG. A proteomic approach.
Publication TypeJournal Article
AuthorsIbarz, A, Costa, R, Harrison, AP, Power, DM
Year of Publication2010
JournalGen Comp Endocrinol
Volume169
Issue3
Date Published2010 Dec 1
Pagination284-92
ISSN1095-6840
KeywordsAnimals, Diet, Feedback, Ketoglutaric Acids, Pituitary Gland, Protein Folding, Proteome, Sea Bream, Spectrometry, Mass, Electrospray Ionization, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
Abstract

The influence of a daily oral dose of alpha-ketoglutarate (AKG, 0.1 g/kg body weight), an intermediate metabolite in the Krebs cycle and a dietary additive, on the pituitary proteome of gilthead sea bream was determined by two-dimensional electrophoresis (2-DE). A high-resolution map of the sea bream pituitary proteome was generated. Proteins with a modified expression between Controls and AKG treated fish were further analysed by MALDI-TOF/TOF-MS and liquid chromatography combined with a nanoelectrospray (LC-MS/MS). The main changes in the proteome induced by AKG treatment were grouped. Metabolic proteins up-regulated with AKG supplementation included fructose-bis-phosphate aldolase, glyceraldehyde-phosphate dehydrogenase and malate dehydrogenase, all related to glucose metabolism (p<0.000). Protein folding related up-regulation with AKG supplementation included two isoforms of heat shock proteins as well as cyclophylin and chaperonin (p<0.000). An unexpected form of apolipoprotein-A-1 with lower molecular weight (15-16 kDa) was evidenced as being highly abundant in the pituitary proteome of Controls, yet it was down-regulated by AKG treatment. Finally, proteins found to be associated with regeneration of neural function namely cofilin and Vat-protein were up-regulated after AKG supplementation. The only hormone to be modified by AKG treatment was somatolactin, which was significantly down-regulated cf. Controls. In summary, these results provide evidence of a potential endocrine/metabolic regulatory loop activated by AKG supplementation.

DOI10.1016/j.ygcen.2010.09.010
Sapientia

http://www.ncbi.nlm.nih.gov/pubmed/20851121?dopt=Abstract

Alternate JournalGen. Comp. Endocrinol.
PubMed ID20851121
CCMAR Authors