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Physiol. Genomics 38: 98-111, 2009. First published April 14, 2009; doi:10.1152/physiolgenomics.90372.2008
1094-8341/09 $8.00
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Received 10 November 2008; accepted in final form 9 April 2009.
Physiological Genomics 38:98-111 (2009)
1094-8341/09 $8.00 © 2009 American Physiological Society

Microarray gene expression profiles of fasting induced changes in liver and adipose tissues of pigs expressing the melanocortin-4 receptor D298N variant

Sender Lkhagvadorj 1,2, Long Qu 1,3,4, Weiguo Cai 1,3, Oliver P. Couture 1,4, C. Richard Barb 5, Gary J. Hausman 5, Dan Nettleton 3,4, Lloyd L. Anderson 1,2, Jack C. M. Dekkers 1,4 and Christopher K. Tuggle 1,2,4

1 Department of Animal Science, Iowa State University, Ames, Iowa
2 Interdepartmental Neuroscience Program, Iowa State University, Ames, Iowa
3 Department of Statistics, Iowa State University, Ames, Iowa
4 Interdepartmental Bioinformatics and Computational Biology Program, Iowa State University, Ames, Iowa
5 Poultry Processing and Swine Physiology Research, Agricultural Research Service, United States Department of Agriculture, Athens, Georgia

Transcriptional profiling coupled with blood metabolite analyses were used to identify porcine genes and pathways that respond to a fasting treatment or to a D298N missense mutation in the melanocortin-4 receptor (MC4R) gene. Gilts (12 homozygous for D298 and 12 homozygous for N298) were either fed ad libitum or fasted for 3 days. Fasting decreased body weight, backfat, and serum urea concentration and increased serum nonesterified fatty acid. In response to fasting, 7,029 genes in fat and 1,831 genes in liver were differentially expressed (DE). MC4R genotype did not significantly affect gene expression, body weight, backfat depth, or any measured serum metabolite concentration. Pathway analyses of fasting-induced DE genes indicated that lipid and steroid synthesis was downregulated in both liver and fat. Fasting increased expression of genes involved in glucose sparing pathways, such as oxidation of amino acids and fatty acids in liver, and in extracellular matrix pathways, such as cell adhesion and adherens junction in fat. Additionally, we identified DE transcription factors (TF) that regulate many DE genes. This confirms the involvement of TF, such as PPARG, SREBF1, and CEBPA, which are known to regulate the fasting response, and implicates additional TF, such as ESR1. Interestingly, ESR1 controls several fasting induced genes in fat that are involved in cell matrix morphogenesis. Our findings indicate a transcriptional response to fasting in two key metabolic tissues of pigs, which was corroborated by changes in blood metabolites, and the involvement of novel putative transcriptional regulators in the immediate adaptive response to fasting.

transcription; ESR1; MC4R; feed deprivation






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