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This Article Full Text Full Text (PDF) All Versions of this Article: 293/3/E636    most recent 00120.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Alcolea, M. P. Articles by Gianotti, M. Search for Related Content PubMed PubMed Citation Articles by Alcolea, M. P. Articles by Gianotti, M.

Responses of mitochondrial biogenesis and function to maternal diabetes in rat embryo during the placentation period

Grup de Metabolisme Energètic i Nutrició, Universitat de les Illes Balears i Centro de Investigación Biomédica en Red (Network Biomedical Research Center) Fisiopatología Obesidad y Nutrición, Instituto de Salud Carlos III, Palma de Mallorca, Spain

Submitted 22 February 2007 ; accepted in final form 6 June 2007

Mitochondria are cellular organelles that have been reported to be altered in diabetes, being closely related to its associated complications. Moreover, mitochondrial biogenesis and function are essential for proper embryo development throughout the placentation period, occurring during organogenesis, when a great rate of congenital malformations have been associated with diabetic pregnancy. Thus, the aim of the current work was to investigate the effect of the diabetic environment on mitochondrial function and biogenesis during the placentation period. For this purpose, we studied the oxidative phosphorylation system (OXPHOS) enzymatic activities as well as the expression of genes involved in the coordinated regulation of both mitochondrial and nuclear genome (PGC-1, NRF-1, NRF-2, mtSSB, and TFAM) and mitochondrial function (COX-IV, COX-I, and -ATPase) in rat embryos from control and streptozotocin-induced diabetic mothers. Our results reflected that diabetic pregnancy retarded and altered embryo growth. The embryos from diabetic mothers showing normal morphology presented a reduced content of proteins regulated through the PGC-1 mitochondriogenic pathway on gestational day 12. This fact was accompanied by several responses that entailed the activation of OXPHOS activities on the same day and the recovery of the content of the studied proteins to control levels on day 13. As a result, the mitochondria of these embryos would reach a situation close to control on day 13 that could allow them to follow the normal mitochondriogenic schedule throughout a gestational period in which the mitochondrial differentiation process is critical. Nevertheless, malformed embryos from diabetic mothers seemed to show a lower adaptation capability, which could exacerbate their maldevelopment.

peroxisome proliferator-activated receptor- coactivator-1; nuclear respiratory factors; mitochondrial transcription factor A; oxidative phosphorylation system