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Changes in the gut microbiota of cloned and non-cloned control pigs during development of obesity: gut microbiota during development of obesity in cloned pigs.

ABSTRACT: BACKGROUND: Obesity induced by a high-caloric diet has previously been associated with changes in the gut microbiota in mice and in humans. In this study, pigs were cloned to minimize genetic and biological variation among the animals with the aim of developing a controlled metabolomic model suitable for a diet-intervention study. Cloning of pigs may be an attractive way to reduce genetic influences when investigating the effect of diet and obesity on different physiological sites. The aim of this study was to assess and compare the changes in the composition of the gut microbiota of cloned vs. non-cloned pigs during development of obesity by a high-fat/high-caloric diet. Furthermore, we investigated the association between diet-induced obesity and the relative abundance of the phyla Firmicutes and Bacteroidetes in the fecal-microbiota. The fecal microbiota from obese cloned (n = 5) and non-cloned control pigs (n= 6) was investigated biweekly over a period of 136 days, by terminal restriction fragment length polymorphism (T-RFLP) and quantitative real time PCR (qPCR). RESULTS: A positive correlation was observed between body-weight at endpoint and percent body-fat in cloned (r=0.9, P<0.0001) and in non-cloned control pigs (r=0.9, P<0.0001). Shannon Weaver and principal component analysis (PCA) of the terminal restriction fragments (T-RFs) revealed no differences in the bacterial composition or variability of the fecal microbiota between the cloned pigs or between cloned and non-cloned control pigs. Body-weight correlated positively with the relative abundance of Firmicutes in both cloned (r=0.37; P<0.02) and non cloned-control pigs (r=0.45; P<0.006), and negatively with the abundance of Bacteroidetes in cloned pigs (r=-0.33, P<0.04), but not in the non-cloned control pigs. CONCLUSION: The cloned pigs did not have reduced inter-individual variation as compared to non-cloned pigs in regard to their gut microbiota in neither the obese nor the lean state. Diet-induced obesity was associated with an increase in the relative abundance of Firmicutes over time. Our results suggest that cloned pigs are not a more suitable animal model for gut microbiota-obesity related studies than non-cloned pigs. This study is the first to evaluate if cloned pigs provide a better animal model than conventional pigs in diet-intervention, obesity and gut microbiota research.

SUBMITTER: Pedersen R

PROVIDER: S-EPMC3610253 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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Changes in the gut microbiota of cloned and non-cloned control pigs during development of obesity: gut microbiota during development of obesity in cloned pigs.

Pedersen Rebecca R Andersen Anders Daniel AD Mølbak Lars L Stagsted Jan J Boye Mette M

BMC microbiology 20130207

<h4>Background</h4>Obesity induced by a high-caloric diet has previously been associated with changes in the gut microbiota in mice and in humans. In this study, pigs were cloned to minimize genetic and biological variation among the animals with the aim of developing a controlled metabolomic model suitable for a diet-intervention study. Cloning of pigs may be an attractive way to reduce genetic influences when investigating the effect of diet and obesity on different physiological sites. The ai ...[more]

PMID: 23391125

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Project description:Mammalian gut microbiota plays an important role in the host's nutrient metabolism, growth, and immune regulation. Hybridization can enable a progeny to acquire superior traits of the parents, resulting in the hybridization advantage. However, studies on the effects of hybridization on the pigs' gut microbiota are lacking. Therefore, this study used multi-omics technologies to compare and analyze the gut microbiota of the primary wild boar and its offspring. The 16S rRNA gene sequencing results revealed that the gut microbiota of F4 exhibited a host-like dominance phenomenon with a significant increase in the abundance of Lactobacillus and Bifidobacterium. The beta diversity of Duroc was significantly different from those of F0, F2, and F4; after the host hybridization, the similarity of the beta diversity in the progeny decreased with the decrease in the similarity of the F0 lineage. The metagenomic sequencing results showed that the significantly enriched metabolic pathways in F4, such as environmental, circulatory system, fatty acid degradation adaptation, and fatty acid biosynthesis, were similar to those in F0. Moreover, it also exhibited similar significantly enriched metabolic pathways as those in Duroc, such as carbohydrate metabolism, starch and sucrose metabolism, starch-degrading CAZymes, lactose-degrading CAZymes, and various amino acid metabolism pathways. However, the alpha-amylase-related KOs, lipid metabolism, and galactose metabolism in F4 were significantly higher than those in Duroc and F0. Non-targeted metabolome technology analysis found that several metabolites, such as docosahexaenoic acid, arachidonic acid, and citric acid were significantly enriched in the F4 pigs as compared to those in F0. Based on Spearman correlation analysis, Lactobacillus and Bifidobacterium were significantly positively correlated with these metabolites. Finally, the combined metagenomic and metabolomic analysis suggested that the metabolic pathways, such as valine, leucine, and isoleucine biosynthesis and alanine aspartate and glutamate metabolism were significantly enriched in F4 pigs. In conclusion, the gut microbiota of F4 showed a similar host "dominance" phenomenon, which provided reference data for the genetics and evolution of microbiota and the theory of microbial-assisted breeding.

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Dataset Information

Changes in the gut microbiota of cloned and non-cloned control pigs during development of obesity: gut microbiota during development of obesity in cloned pigs.

Publications

Changes in the gut microbiota of cloned and non-cloned control pigs during development of obesity: gut microbiota during development of obesity in cloned pigs.

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