Lipocalin-2 (Lcn2) expression is mediated by maternal nutrition during the development of the fetal liver

William D. Rees; Susan M. Hay

doi:10.1007/s12263-013-0380-4

Lipocalin-2 (Lcn2) expression is mediated by maternal nutrition during the development of the fetal liver

William D. Rees^*, Susan M. Hay

^*Corresponding author for this work

The Rowett Institute of Nutrition and Health

University of Aberdeen

Research output: Contribution to journal › Article › peer-review

2 Citations (Scopus)

Abstract

Abstract: The mechanisms by which maternal protein deficiency programs insulin action in the offspring are poorly understood. The interpretation of transcriptomics is complicated by homeostatic adaptations, for example, changes in amino acid metabolism, which are potentially unrelated to the programming mechanism. The fatty acid composition of the maternal diet modulates the programming of insulin action, offering a possible strategy to circumvent these complications. Fetal livers harvested on d21 of gestation from pregnant rats fed high-protein (18 % w/w) and low-protein (9 % w/w) diets prepared with either corn or soya oil were screened with rat genome microarrays. Although a low-protein maternal diet altered the abundance of more than one hundred mRNAs in the fetal liver, only 40 were changed by the fatty acid composition of the diet (P < 0.05). One of these mRNAs was identified as lipocalin-2 (Lcn2). This pattern of differential expression was confirmed by qRT-PCR. The expression of Lcn2 was decreased by low-protein diets when the diet contained soya oil, whereas the effect of protein was much smaller in the group fed diets prepared with corn oil. The decrease in Lcn2 expression produced by soya oil persisted into adult life. Levels of the Lcn2 protein were closely correlated to the mRNA abundance. The results suggest a possible involvement of Lcn2 in the programming of hepatic function.

Original language	English
Article number	380
Journal	Genes & Nutrition
Volume	9
Issue number	1
Early online date	3 Jan 2014
DOIs	https://doi.org/10.1007/s12263-013-0380-4
Publication status	Published - Jan 2014

Bibliographical note

Date of Acceptance: 7/12/2013

Acknowledgments This work was supported by the Scottish Government Rural and Environment Research and Analysis Directorate (RERAD) as part of the core funding to the Rowett Research Institute and by the European Union sixth Framework programme EARNEST (CT-2005-007036). Affymetrix arrays were obtained through the NuGO array pipeline (European Union sixth Framework programme FP6-506360). We would like to thank Dr Claus-Dieter Mayer (Biomathematics and Statistics, Scotland) for his help with the analysis of the microarray data.

Keywords

Fetal origins of disease
Hepatic development
Metabolism
Programming

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1007/s12263-013-0380-4

Cite this

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title = "Lipocalin-2 (Lcn2) expression is mediated by maternal nutrition during the development of the fetal liver",

abstract = "Abstract: The mechanisms by which maternal protein deficiency programs insulin action in the offspring are poorly understood. The interpretation of transcriptomics is complicated by homeostatic adaptations, for example, changes in amino acid metabolism, which are potentially unrelated to the programming mechanism. The fatty acid composition of the maternal diet modulates the programming of insulin action, offering a possible strategy to circumvent these complications. Fetal livers harvested on d21 of gestation from pregnant rats fed high-protein (18 % w/w) and low-protein (9 % w/w) diets prepared with either corn or soya oil were screened with rat genome microarrays. Although a low-protein maternal diet altered the abundance of more than one hundred mRNAs in the fetal liver, only 40 were changed by the fatty acid composition of the diet (P < 0.05). One of these mRNAs was identified as lipocalin-2 (Lcn2). This pattern of differential expression was confirmed by qRT-PCR. The expression of Lcn2 was decreased by low-protein diets when the diet contained soya oil, whereas the effect of protein was much smaller in the group fed diets prepared with corn oil. The decrease in Lcn2 expression produced by soya oil persisted into adult life. Levels of the Lcn2 protein were closely correlated to the mRNA abundance. The results suggest a possible involvement of Lcn2 in the programming of hepatic function.",

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note = "Date of Acceptance: 7/12/2013 Acknowledgments This work was supported by the Scottish Government Rural and Environment Research and Analysis Directorate (RERAD) as part of the core funding to the Rowett Research Institute and by the European Union sixth Framework programme EARNEST (CT-2005-007036). Affymetrix arrays were obtained through the NuGO array pipeline (European Union sixth Framework programme FP6-506360). We would like to thank Dr Claus-Dieter Mayer (Biomathematics and Statistics, Scotland) for his help with the analysis of the microarray data.",

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N2 - Abstract: The mechanisms by which maternal protein deficiency programs insulin action in the offspring are poorly understood. The interpretation of transcriptomics is complicated by homeostatic adaptations, for example, changes in amino acid metabolism, which are potentially unrelated to the programming mechanism. The fatty acid composition of the maternal diet modulates the programming of insulin action, offering a possible strategy to circumvent these complications. Fetal livers harvested on d21 of gestation from pregnant rats fed high-protein (18 % w/w) and low-protein (9 % w/w) diets prepared with either corn or soya oil were screened with rat genome microarrays. Although a low-protein maternal diet altered the abundance of more than one hundred mRNAs in the fetal liver, only 40 were changed by the fatty acid composition of the diet (P < 0.05). One of these mRNAs was identified as lipocalin-2 (Lcn2). This pattern of differential expression was confirmed by qRT-PCR. The expression of Lcn2 was decreased by low-protein diets when the diet contained soya oil, whereas the effect of protein was much smaller in the group fed diets prepared with corn oil. The decrease in Lcn2 expression produced by soya oil persisted into adult life. Levels of the Lcn2 protein were closely correlated to the mRNA abundance. The results suggest a possible involvement of Lcn2 in the programming of hepatic function.

AB - Abstract: The mechanisms by which maternal protein deficiency programs insulin action in the offspring are poorly understood. The interpretation of transcriptomics is complicated by homeostatic adaptations, for example, changes in amino acid metabolism, which are potentially unrelated to the programming mechanism. The fatty acid composition of the maternal diet modulates the programming of insulin action, offering a possible strategy to circumvent these complications. Fetal livers harvested on d21 of gestation from pregnant rats fed high-protein (18 % w/w) and low-protein (9 % w/w) diets prepared with either corn or soya oil were screened with rat genome microarrays. Although a low-protein maternal diet altered the abundance of more than one hundred mRNAs in the fetal liver, only 40 were changed by the fatty acid composition of the diet (P < 0.05). One of these mRNAs was identified as lipocalin-2 (Lcn2). This pattern of differential expression was confirmed by qRT-PCR. The expression of Lcn2 was decreased by low-protein diets when the diet contained soya oil, whereas the effect of protein was much smaller in the group fed diets prepared with corn oil. The decrease in Lcn2 expression produced by soya oil persisted into adult life. Levels of the Lcn2 protein were closely correlated to the mRNA abundance. The results suggest a possible involvement of Lcn2 in the programming of hepatic function.

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Lipocalin-2 (Lcn2) expression is mediated by maternal nutrition during the development of the fetal liver

Abstract

Bibliographical note

Keywords

UN SDGs

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