Gut Microbiota Orchestrates Energy Homeostasis during Cold
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus mouse gut metagenome
PROVIDER: GSE74228 | GEO | 2015/12/03
SECONDARY ACCESSION(S): PRJNA299602
REPOSITORIES: GEO
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Project description:Microbial functions in the host physiology are a result of co-evolution between microbial communities and their hosts. Here we show that cold exposure leads to marked shift of the microbiota composition, referred to as cold microbiota. Transplantation of the cold microbiota to germ-free mice is sufficient to increase the insulin sensitivity of the host, and enable complete tolerance to cold partly by promoting the white fat browning, leading to increased energy expenditure and fat loss. During prolonged cold however, the body weight loss is attenuated, caused by adaptive mechanisms maximising caloric uptake and increasing intestinal, villi and microvilli lengths. This increased absorptive surface is promoted by the cold microbiota - effect that can be diminished by co-transplanting the most downregulated bacterial strain from the Verrucomicrobia phylum, Akkermansia muciniphila, during the cold microbiota transfer. Our results demonstrate the microbiota as a key factor orchestrating the overall energy homeostasis during increased demand.
2015-12-03 | GSE74157 | GEO
Project description:Gut Microbiota Orchestrates Energy Homeostasis during Cold
| PRJNA299602 | ENA
Project description:Microbial functions in the host physiology are a result of co-evolution between microbial communities and their hosts. Here we show that cold exposure leads to marked shift of the microbiota composition, referred to as cold microbiota. Transplantation of the cold microbiota to germ-free mice is sufficient to increase the insulin sensitivity of the host, and enable complete tolerance to cold partly by promoting the white fat browning, leading to increased energy expenditure and fat loss. During prolonged cold however, the body weight loss is attenuated, caused by adaptive mechanisms maximising caloric uptake and increasing intestinal, villi and microvilli lengths. This increased absorptive surface is promoted by the cold microbiota - effect that can be diminished by co-transplanting the most downregulated bacterial strain from the Verrucomicrobia phylum, Akkermansia muciniphila, during the cold microbiota transfer. Our results demonstrate the microbiota as a key factor orchestrating the overall energy homeostasis during increased demand.
2015-12-03 | GSE74227 | GEO
Project description:The microorganisms within the intestinal tract (termed gut microbiota) have been shown to interact with the gut-brain axis, a bidirectional communication system between the gut and the brain mediated by hormonal, immune, and neural signals. Through these interactions, the microbiota might affect behaviors, including feeding behavior, digestive/absorptive processes (e.g., by modulating intestinal motility and the intestinal barrier), metabolism, as well as the immune response, with repercussions on the energy homeostasis and health of the host. To date, research in this field has mostly focused on mammals. Studies on non-mammalian models such as fish may provide novel insights into the specific mechanisms involved in the microbiota-brain-gut axis. This review describes our current knowledge on the possible effects of microbiota on feeding, digestive processes, growth, and energy homeostasis in fish, with emphasis on the influence of brain and gut hormones, environmental factors, and inter-specific differences.
| S-EPMC6353785 | biostudies-other
Project description:Huddling is highly evolved as a cooperative behavioral strategy for social mammals to maximize their fitness in harsh environments. Huddling behavior can change psychological and physiological responses. The coevolution of mammals with their microbial communities confers fitness benefits to both partners. The gut microbiome is a key regulator of host immune and metabolic functions. We hypothesized that huddling behavior altered energetics and thermoregulation by shaping caecal microbiota in small herbivores. Brandt's voles (Lasiopodomys brandtii) were maintained in a group (huddling) or as individuals (separated) and were exposed to warm (23?±?1 °C) and cold (4?±?1 °C) air temperatures (Ta).Voles exposed to cold Ta had higher energy intake, resting metabolic rate (RMR) and nonshivering thermogenesis (NST) than voles exposed to warm Ta. Huddling voles had lower RMR and NST than separated voles in cold. In addition, huddling voles had a higher surface body temperature (Tsurface), but lower core body temperature (Tcore) than separated voles, suggesting a lower set-point of Tcore in huddling voles. Both cold and huddling induced a marked variation in caecal bacterial composition, which was associated with the lower Tcore. Huddling voles had a higher ? and ?-diversity, abundance of Lachnospiraceae and Veillonellaceae, but lower abundance of Cyanobacteria, Tenericutes, TM7, Comamonadaceae, and Sinobacteraceae than separated voles. Huddling or cold resulted in higher concentrations of short-chain fatty acids (SCFAs), particularly acetic acid and butyric acid when compared to their counterparts. Transplantation of caecal microbiota from cold-separated voles but not from cold-huddling voles induced significant increases in energy intake and RMR compared to that from warm-separated voles.These findings demonstrate that the remodeling of gut microbiota, which is associated with a reduction in host Tcore, mediates cold- and huddling-induced energy intake and thermoregulation and therefore orchestrates host metabolic and thermal homeostasis. It highlights the coevolutionary mechanism of host huddling and gut microbiota in thermoregulation and energy saving for winter survival in endotherms.
| S-EPMC5994089 | biostudies-other
Project description:BackgroundPost-weaning diarrhea in piglets reduces growth performance and increases mortality, thereby causing serious economic losses. The intestinal epithelial cells and microbiota reciprocally regulate each other in order to maintain intestinal homeostasis and control inflammation. However, a relative paucity of research has been focused on the host-derived regulatory network that controls mucin O-glycans and thereby changes gut microbiota during diarrhea in infancy. At the development stage just after birth, the ontogeny of intestinal epithelium, immune system, and gut microbiota appear similar in piglets and human infants. Here, we investigated the changes of mucin O-glycans associated with gut microbiota using a diarrheal post-weaned piglet model.ResultsWe found that diarrhea disrupted the colonic mucus layer and caused aberrant mucin O-glycans, including reduced acidic glycans and truncated glycans, leading to an impaired gut microenvironment. Subsequently, the onset of diarrhea, changes in microbiota and bacterial translocation, resulting in compromised epithelial barrier integrity, enhanced susceptibility to inflammation, and mild growth faltering. Furthermore, we found the activation of NLRP3 inflammasome complexes in the diarrheal piglets when compared to the healthy counterparts, triggered the release of proinflammatory cytokines IL-1β and IL-18, and diminished autophagosome formation, specifically the defective conversion of LC3A/B I into LC3A/B II and the accumulation of p62. Additionally, selective blocking of the autophagy pathway by 3-MA led to the reduction in goblet cell-specific gene transcript levels in vitro.ConclusionsWe observed that diarrheal piglets exhibited colonic microbiota dysbiosis and mucosal barrier dysfunction. Our data demonstrated that diarrhea resulted in the activation of inflammasomes and autophagy restriction along with aberrant mucin O-glycans including reduced acidic glycans and truncated glycans. The results suggested the mucin O-glycans-microbiota axis is likely associated with diarrheal pathogenesis. Our study provides novel insights into the pathophysiology of early-weaning-induced diarrheal disease in piglets and potentially understanding of disease mechanisms of diarrhea for human infants. Understanding the molecular pathology and pathogenesis of diarrhea is a prerequisite for the development of novel and effective therapies. Our data suggest that facilitating O-glycan elongation, modifying the microbiota, and developing specific inhibitors to some key inflammasomes could be the options for therapy of diarrhea including human infants. Video abstract.
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