Cardiometabolic disease is the leading cause of death in zoo apes; yet its etiology remains unknown. Here, we investigated compositional and functional microbial markers in fecal samples from 57 gorillas across U.S. zoos, 20 of which are diagnosed with cardiovascular disease, in contrast with 17 individuals from European zoos and 19 wild gorillas from Central Africa. Results show that zoo-housed gorillas in the U.S. exhibit the most diverse gut microbiomes and markers of increased protein and carbohydrate fermentation, at the expense of microbial metabolic traits associated with plant cell-wall degradation. Machine learning models identified unique microbial traits in U.S. gorillas with cardiometabolic distress; including reduced metabolism of sulfur-containing amino acids and hexoses, increased abundance of potential enteric pathogens, and low fecal butyrate and propionate production. These findings show that cardiometabolic disease in gorillas is potentially associated with altered gut microbial function, influenced by zoo-specific diets and environments.

• MeSH
• Bacteria * klasifikace   metabolismus   genetika   izolace a purifikace   MeSH
• feces mikrobiologie   MeSH
• Gorilla gorilla * mikrobiologie   MeSH
• kardiovaskulární nemoci * veterinární   mikrobiologie   MeSH
• nemoci lidoopů * mikrobiologie   MeSH
• střevní mikroflóra * MeSH
• zvířata v ZOO mikrobiologie   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

BACKGROUND: Animals form complex symbiotic associations with their gut microbes, whose evolution is determined by an intricate network of host and environmental factors. In many insects, such as Drosophila melanogaster, the microbiome is flexible, environmentally determined, and less diverse than in mammals. In contrast, mammals maintain complex multispecies consortia that are able to colonize and persist in the gastrointestinal tract. Understanding the evolutionary and ecological dynamics of gut microbes in different hosts is challenging. This requires disentangling the ecological factors of selection, determining the timescales over which evolution occurs, and elucidating the architecture of such evolutionary patterns. RESULTS: We employ experimental evolution to track the pace of the evolution of a common gut commensal, Lactiplantibacillus plantarum, within invertebrate (Drosophila melanogaster) and vertebrate (Mus musculus) hosts and their respective diets. We show that in Drosophila, the nutritional environment dictates microbial evolution, while the host benefits L. plantarum growth only over short ecological timescales. By contrast, in a mammalian animal model, L. plantarum evolution results to be divergent between the host intestine and its diet, both phenotypically (i.e., host-evolved populations show higher adaptation to the host intestinal environment) and genomically. Here, both the emergence of hypermutators and the high persistence of mutated genes within the host's environment strongly differed from the low variation observed in the host's nutritional environment alone. CONCLUSIONS: Our results demonstrate that L. plantarum evolution diverges between insects and mammals. While the symbiosis between Drosophila and L. plantarum is mainly determined by the host diet, in mammals, the host and its intrinsic factors play a critical role in selection and influence both the phenotypic and genomic evolution of its gut microbes, as well as the outcome of their symbiosis.

• Klíčová slova
• Drosophila melanogaster, Experimental evolution, Gut microbiota evolution, Host–microbe symbiosis, Lactiplantibacillus plantarum, Mouse, Whole genome sequencing,
• MeSH
• Drosophila melanogaster genetika   MeSH
• Drosophila MeSH
• mikrobiota * MeSH
• myši MeSH
• savci MeSH
• střevní mikroflóra * MeSH
• symbióza MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Research Support, U.S. Gov't, Non-P.H.S. MeSH

Obesity is a chronic, relapsing condition characterized by excess body fat. Its prevalence has increased globally since the 1970s, and the number of obese and overweight people is now greater than those underweight. Obesity is a multifactorial condition, and as such, many components contribute to its development and pathogenesis. This is the first of three companion reviews that consider obesity. This review focuses on the genetics, viruses, insulin resistance, inflammation, gut microbiome, and circadian rhythms that promote obesity, along with hormones, growth factors, and organs and tissues that control its development. It shows that the regulation of energy balance (intake vs. expenditure) relies on the interplay of a variety of hormones from adipose tissue, gastrointestinal tract, pancreas, liver, and brain. It details how integrating central neurotransmitters and peripheral metabolic signals (e.g., leptin, insulin, ghrelin, peptide YY3-36) is essential for controlling energy homeostasis and feeding behavior. It describes the distinct types of adipocytes and how fat cell development is controlled by hormones and growth factors acting via a variety of receptors, including peroxisome proliferator-activated receptor-gamma, retinoid X, insulin, estrogen, androgen, glucocorticoid, thyroid hormone, liver X, constitutive androstane, pregnane X, farnesoid, and aryl hydrocarbon receptors. Finally, it demonstrates that obesity likely has origins in utero. Understanding these biochemical drivers of adiposity and metabolic dysfunction throughout the life cycle lends plausibility and credence to the "obesogen hypothesis" (i.e., the importance of environmental chemicals that disrupt these receptors to promote adiposity or alter metabolism), elucidated more fully in the two companion reviews.

• Klíčová slova
• Adipose tissue, Energy balance, Hormone receptors, Metabolism, Microbiome, Obesity,
• MeSH
• energetický metabolismus fyziologie   MeSH
• inzulin metabolismus   MeSH
• leptin * metabolismus   MeSH
• lidé MeSH
• obezita * metabolismus   MeSH
• tuková tkáň metabolismus   MeSH
• tukové buňky metabolismus   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Research Support, N.I.H., Extramural MeSH
• Názvy látek
• inzulin MeSH
• leptin * MeSH

The Oligo-Mouse-Microbiota (OMM12) is a recently developed synthetic bacterial community for functional microbiome research in mouse models (Brugiroux et al., 2016). To date, the OMM12 model has been established in several germ-free mouse facilities world-wide and is employed to address a growing variety of research questions related to infection biology, mucosal immunology, microbial ecology and host-microbiome metabolic cross-talk. The OMM12 consists of 12 sequenced and publically available strains isolated from mice, representing five bacterial phyla that are naturally abundant in the murine gastrointestinal tract (Lagkouvardos et al., 2016). Under germ-free conditions, the OMM12 colonizes mice stably over multiple generations. Here, we investigated whether stably colonized OMM12 mouse lines could be reproducibly established in different animal facilities. Germ-free C57Bl/6J mice were inoculated with a frozen mixture of the OMM12 strains. Within 2 weeks after application, the OMM12 community reached the same stable composition in all facilities, as determined by fecal microbiome analysis. We show that a second application of the OMM12 strains after 72 h leads to a more stable community composition than a single application. The availability of such protocols for reliable de novo generation of gnotobiotic rodents will certainly contribute to increasing experimental reproducibility in biomedical research.

• Klíčová slova
• 3R, Oligo-MM12, defined bacterial consortia, gnotobiology, isobiotic mice, minimal microbiome, sDMDMm2, syncom,
• Publikační typ
• časopisecké články MeSH