Literature DB >> 18718984

Maternal dietary supplementation with saturated, but not monounsaturated or polyunsaturated fatty acids, leads to tissue-specific inhibition of offspring Na+,K+-ATPase.

James A Armitage1, Sanjana Gupta, Caroline Wood, Runa I Jensen, Anne-Maj Samuelsson, William Fuller, Michael J Shattock, Lucilla Poston, Paul D Taylor.   

Abstract

In rats, a maternal diet rich in lard is associated with reduced Na(+),K(+)-ATPase activity in adult offspring kidney. We have addressed the role of different fatty acids by evaluating Na(+),K(+)-ATPase activity in offspring of dams fed diets rich in saturated (SFA), monounsaturated (MUFA) or polyunsaturated (PUFA) fatty acids. Female Sprague-Dawley rats were fed, during pregnancy and suckling, a control diet (4% w/w corn oil) or a fatty acid supplemented diet (24% w/w). Offspring were reared on chow (4% PUFA) and studied at 6 months. mRNA expression (real-time PCR) of Na(+),K(+)-ATPase alpha subunit and protein expression of Na(+),K(+)-ATPase subunits (Western blot) were assessed in kidney and brain. Na(+),K(+)-ATPase activity was reduced in kidney (P < 0.05 versus all groups) and brain (P < 0.05 versus control and MUFA offspring) of the SFA group. Neither Na(+),K(+)-ATPase alpha1 subunit mRNA expression, nor protein expression of total alpha, alpha1, alpha2, alpha3 or beta1 subunits were significantly altered in kidney in any dietary group. In brains of SFA offspring alpha1 mRNA expression (P < 0.05) was reduced compared with MUFA and PUFA offspring, but not controls. Also in brain, SFA offspring demonstrated reduced (P < 0.05) alpha1 subunit protein and increased phosphorylation (P < 0.05) of the Na(+),K(+)-ATPase modulating protein phospholemman at serine residue 63 (S63 PLM). Na(+),K(+)-ATPase activity was similar to controls in heart and liver. In utero and neonatal exposure to a maternal diet rich in saturated fatty acids is associated with altered activity and expression of Na(+),K(+)-ATPase in adulthood, but mechanisms appear tissue specific.

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Year:  2008        PMID: 18718984      PMCID: PMC2614066          DOI: 10.1113/jphysiol.2008.157818

Source DB:  PubMed          Journal:  J Physiol        ISSN: 0022-3751            Impact factor:   5.182


  36 in total

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