In fundamental stud- ies using mouse models, obese mice contained a relative abundance of Firmicutes, in contrast to the relative preponderance of the phylum Bacteroidetes in lean mice (46, 47). The gut microbiomes of lean mice, when transplanted such biomarkers support the potential link be- tween the capacity of the gut microbiome for energy harvest and obesity. In other words, an spp.: several species into ob/ob (obese) mice, normalized the body weights of the latter, indicating that differences in microbial composition could affect body metabolism and energy harvest and influence the predisposition of mammals to obesity. Mice deficient in the microbial pattern-recognition receptor Toll-like receptor 5 (TLR5) displayed hyperphagia, became obese, and developed fea- tures of the metabolic syndrome, including hy- pertension, hypercholesterolemia, and insulin resistance (48). When gut microbiomes from these mice were transplanted into germ-free mice with an intact TLR5 gene, recipient mice developed similar features of the metabolic syn- drome, which suggests that the intestinal mi- crobiome, and not murine TLR genetics, was the key determinant of this disease phenotype.