We cannot discard a potential antibiotic effect of the RE in the gut. Many prebiotics can improve glucose and lipid homeostasis as well as the inflammatory status in the host and these properties have been associated with the growth of beneficial bacteria such as Bifidobacterium. Dietary supplementation with the probiotic B. pseudocatenulatum CECT 7765 can increase bifidobacteria in the gut and moderate serum lipids, insulin resistance, leptin and other inflammatory cytokines in highfat fed mice. In previous studies, we have shown that the consumption of the RE rich in CA downregulated serum triglycerides, cholesterol, insulin, leptin, TNF-a and Il-1b and upregulated adiponectin only in the lean Zucker rats revealing critical regulatory differences against the leptin-resistant obese rats. We now report that the consumption of RE is also linked to a different response in the caecum Bifidobacterium counts which are significantly increased in the lean animals and supports an association with the regulation of lipids and adipokines in this genotype. It should be noted that the numbers of Bifidobacterium exhibited a large variability in the obese rats supplemented with the RE. Although all the qPCR analyses were carried out following the same protocols, under the same conditions and at the same time, we cannot fully discard the possibility of some qPCR inhibitors in this group. However, the response of the obese animals may be more variable since the obesity has been reported to worsen or slow the capacity of these animals to respond to nutritional or pharmacological treatment and thus, it may be more difficult to exert a regulatory effect in these animals. In addition, we found that the C. leptum group was also differentially regulated between the obese and lean genotype in response to the RE. Principal component analysis of the current results for bacterial groups and the previously reported serum biochemical variables showed that these two genotypes could be easily distinguished from each other and that the lean rats responded to the RE more prominently than the obese ones. Overall, our data support a host genetic effect in the gut microbiota present in the lean and obese animals and that each type of rat could have specific metabolic and inflammatory status as well as different responses to dietary compounds linked to their specific microbiomes. Prebiotic fibers that promote fermentation lead, in general, to higher levels of caecum and fecal SCFA. These metabolites act as mediators between gut microbiota and host inflammatory status since they can function as signaling molecules suppressing the production of inflammatory cytokines, regulating the production of gut hormones such as glucagon-like peptide-1 and, consequently, insulin secretion or inducing the production of leptin. The acetate/propionate ratio is also critical in regulating cholesterol, lipids and glucose synthesis in the host.