37, P<0.02) and non-cloned control pigs (r=0.45, P<0.006) (Figure 4C and D, respectively). Additional figure shows the changes in the relative abundance of Firmicutes and Bacteroidetes during weight-gain (See Additional file 2). Discussion In order to establish a better understanding of the underlying causes of obesity and the effect of obesity on different body sites, the cloned pigs and non-cloned control pigs employed for our study were also investigated in regard to their immunological [28], metabolomics [22] and phenotypic characters

[9]. In this study, we investigated the gut microbiota ABT-263 ic50 of both cloned and non-cloned control pigs by T-RFLP and found that the gut microbiota within a group of five obese clones was neither more similar nor more diverse than the microbiota within a group of six obese non-cloned control pigs of the same sex and genetic background. The metabolomic phenotyping [9] of these obese cloned and non-cloned control pigs showed that the phenotype of the cloned

pigs was different from the phenotype of non-cloned control pigs [9] and that the inter-individual variation amongst these cloned pigs was not less than the inter-individual variation of the non-cloned control pigs that were siblings [22]. Hence, based on these and the findings presented JPH203 in the current paper it would appear that the cloned pigs do not have identical phenotypes or less inter-individual variation than conventional non-cloned pigs. One explanation for these results could be that in cloning by somatic cell nuclear transfer the animals inherit maternal mitochondrial DNA and even though they have the same somatic DNA, the cloned pigs possess altering Cytidine deaminase phenotypes due to the maternal mitochondrial DNA effect [9]. This raises the question of whether cloned animals are more suitable animal models than conventional non-cloned animals. The heritable component of an individual and its effect on the microbial community have been investigated before in several human studies; in particular

MZ twins have been investigated to minimize the genetic influence in order to get a better understanding of the role of obesity on gut microbiota [3]. When designing an experimental model for gut microbiota related selleck inhibitor studies, it is important to remove the large variability in the microbial community across individuals, making it necessary to use larger number of animals for valid statistical analysis and interpretation. Therefore, cloned animals could have the potential of becoming good models, by reducing the number of animals needed for an experimental study and providing a less variable population, however, more optimization is needed to improve the quality of the cloned animals.