HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 568/2/553    most recent jphysiol.2005.092825v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Gallagher, E. A. L Articles by Hanson, M. A Search for Related Content PubMed PubMed Citation Articles by Gallagher, E. A. L Articles by Hanson, M. A

¹ Centre for Developmental Origins of Health and Disease, University of Southampton, 887F Princess Anne Hospital, Coxford Road, SO16 5YA, Southampton, UK

The effect of maternal low protein diet in pregnancy on the function of offspring cerebral cytochrome c oxidase (CcO) was investigated in vitro immediately before and after birth, using fetal and neonatal rat pup forebrain tissue. Pregnant rat dams were fed either a control (C, 18% casein n = 22) or low protein (LP, 9% casein n = 14) diet. Cerebral tissues were harvested from pups the day before (E21) and after (P1) birth. A Clarke electrode chamber was used to determine O₂ consumption in brain tissue homogenate, under baseline conditions with and without the mitochondrial electron transport chain inhibitor myxothiazol and in the presence of incremental doses of the electron donor N',N',N',N'-tetramethyl-p-phenylenediamide (TMPD) with myxothiazol. Maximal stimulated CcO activity was less in LP versus C pups at both E21 (P < 0.001) and P1 (P < 0.05). At E21 only, sensitivity to electron flux (pEC₅₀) was greater (P < 0.001) in LP compared to C offspring. In addition, was reduced and pEC₅₀ was greater after birth (i.e. P1 versus E21) in C (P < 0.001) but not in LP pups. This is the first report of the effects of maternal dietary imbalance in pregnancy on offspring cerebral metabolic function. The effects may form part of a developmental adaptive response to reduce energy consumption and promote perinatal survival, or to confer advantage in a postnatal environment predicted to be nutritionally poor.

(Received 16 June 2005; accepted after revision 2 August 2005; first published online 4 August 2005)
Corresponding author L.R. Green: Centre for Developmental Origins of Health and Disease, University of Southampton, 887F Princess Anne Hospital, Coxford Road, Southampton, Hants, SO16 5YA, UK. Email: lgreen{at}soton.ac.uk