## 4 Discussion
More precisely, this instability has already been observed on 1057 pigs between 23 and 26 weeks of age where the same enterotypes as in the current experiment have been identified [25]. Interestingly, this indicates that the enterotypes identified here are robust, as the later pigs originated from various farms. Similarly, pigs affiliated to an enterotype at 118 days of age were split into the two enterotypes defined at 196 days [13]. Such instability was already assumed by [PERSON] et al. [26] in healthy humans. The enterotypes also differ functionally, especially during the finishing stage. Indeed, the PWE1 and PWE2 enterotypes were functionally relatively similar to each other, with only four other pathways that were significantly different: ppGpp biosynthesis, superpathway of (Kdo)2-lipid A biosynthesis, glucose, glucose-1-phosphate degradation, and adenosylcobalamin salvage from cobinamide I (Table S4). In contrast the PICRUST algorithm predicts that seven MetaCyc pathways have a higher abundance in the FE1 enterotype (Figure S6): three of them are degrading pyruvate (methylerythritol phosphate pathway I, pyruvate fermentation to propanoate, and superpathway of butenedi biosynthesis) and three others produced Acetyl-CoA (reductive acetyl coenzyme A pathway, l-glutamate degradation V (via hydroxyglutarate), and myo-inositol degradation I). The last pathway was adenosylcobalamin salvage from cobinamide I which was already different between the post-weaning enterotypes (Table S4). Pyruvate also seems to be pivotal for the 40 pathways overrepresented in the FE2 enterotype, where it may be produced by neoglucogenesis, by the reductive TCA cycle I, by the degradation of hexitol or hexuronide, by the Enterner-Douroff pathway, or by the degradation of aspartate. Several carbohydrate degradation pathways were also overrepresented in FE2, namely fructose, hexitol, lactose and galactose, and rhamn. The coenzyme A biosynthesis I was overrepresented, and several fermentation pathways (homo- and hetero-lactic, mixed acid, and the Bifidobacterium shunt). Surprisingly, the polyamine biosynthesis I and II were also overrepresented in FE2, yet no adverse impact on growth was observed. In our experiment, we identified an intermediate enterotype (FE3) at 119 days that illustrated the switch between enterotypes with genus relative abundance in-between FE1 and FE2. Pigs in the intermediate enterotype had greater performance compared to the pigs in FE2 during the week before the feces collection. Similarly, [PERSON] et al. [12] revealed a growth performance difference between the two enterotypes identified in younger pigs (60 days of age). Therefore, we can assume that enterotype switches could be related to transient performance modifications. However, the difference of 850 g on 25 kg pigs previously observed remained quite low [12], and in our study, the performance of pigs in FE1 and FE2 enterotypes did not differ in accordance with previous findings [25]. This suggests that the relationship between enterotypes and an animal's performance is not so clear. In this study, the DON exposure impacted the ADFI, ADG, and FCR of the pigs at 119 and 140 days of age as previously detailed by [PERSON] et al. [27], but no impact on the performances was observed after the two-week recovery at 154 days of age. In addition, a transient impact on the microbiota composition has been observed [28]. However, in our experimental conditions, DON exposure did not impact the enterotype repartition among the animals nor their possible instability, suggesting that the enterotypes are insensitive to DON exposure. From this experiment, we could not identify any cause why pigs switched from an enterotype to another. At 99 days of age, more females clustered in the FE2 enterotype compared to the FE1 enterotype, while the castrated males were equally distributed. This interaction between the enterotype and the sex type in the beginning of the finishing stage no longer existed at the end of the experiment.