Obesity alters gut microbial ecology

Abstract

We have analyzed 5,088 bacterial 16S rRNA gene sequences from the distal intestinal (cecal) microbiota of genetically obese ob͞ob mice, lean ob͞؉ and wild-type siblings, and their ob͞؉ mothers, all fed the same polysaccharide-rich diet. Although the majority of mouse gut species are unique, the mouse and human microbiota(s) are similar at the division (superkingdom) level, with Firmicutes and Bacteroidetes dominating. Microbial-community composition is inherited from mothers. However, compared with lean mice and regardless of kinship, ob͞ob animals have a 50% reduction in the abundance of Bacteroidetes and a proportional increase in Firmicutes. These changes, which are division-wide, indicate that, in this model, obesity affects the diversity of the gut microbiota and suggest that intentional manipulation of community structure may be useful for regulating energy balance in obese individuals.energy balance͞obesity ͉ host-microbial interactions ͉ intestinal bacterial diversity ͉ ob͞ob mice ͉ phylogenetics T he 10 trillion to 100 trillion microorganisms that populate our adult intestines benefit us in a number of ways (1). One benefit is that they allow us to extract calories from otherwise indigestible common polysaccharides in our diet. This benefit occurs because components of the microbiota are able to adaptively deploy a large array of glycoside hydrolases and polysaccharide lysases that we humans do not encode in our genome (2, 3) (http:͞͞afmb.cnrs-mrs.fr͞CAZY͞). Furthermore, studies using germ-free and colonized normal and knockout mice fed a standard, polysaccharide-rich rodent-chow diet indicate that this mutualistic host-microbe relationship allows the extracted energy to be stored in adipocytes through a pathway that involves microbial regulation of the intestinal epithelial expression of fasting-induced adipocyte protein (Fiaf), a circulating inhibitor of lipoprotein lipase (LPL) (4). Microbial fermentation of dietary polysaccharides to monosaccharides and short-chain fatty acids in the distal gut and their subsequent absorption stimulate de novo synthesis of triglycerides in the liver. Microbial suppression of Fiaf in the gut epithelium results in reduced levels of this circulating LPL inhibitor, increased LPL activity in adipocytes, and enhanced storage of liver-derived triacyglycerols in fat cells (4).Although the root cause of obesity is excess caloric intake compared with expenditure, differences in gut microbial ecology between humans may be an important factor affecting energy homeostasis; i.e., individuals predisposed to obesity may have gut microbial communities that promote more efficient extraction and͞or storage of energy from a given diet, compared with these communities in lean individuals. This hypothesis raises a number of basic questions about gut microbial ecology in humans and mice. For example, how do the distal-gut microbiotas of the two hosts compare? Does kinship play an important role in the composition of the microbial community? Does adiposity affect community structure, and, ...

Association of Obesity with Serum Leptin, Adiponectin, and Serotonin and Gut Microflora in Beagle Dogs

“…Other studies observed no differences in the proportions of Bacteroidetes and Firmicutes in lean and obese individuals 37, 38. The phylum Firmicutes is the most abundant bacterial group in normal healthy gut microbiota, followed by the phylum Bacteroidetes 8, 35, 36. Our results in the lean group are consistent with these studies.…”

“…Inflammation associated with changes in the gut microbiota is considered to decrease 5HT availability during obesity 43, 45. Studies have yielded inconsistent data on the composition of the gut microbiota in obese subjects 8, 18, 46. In our study, the phylum Proteobacteria , which belongs to gram‐negative bacteria, was abundant in the obese group.…”

“…Ley et al8 observed a marked change in the microbial proportion including a 50% reduction in the abundance of the phylum Bacteroidetes and an increase in Firmicutes in obese mice. This is inconsistent with our results: we observed a decrease in the proportion of Firmicutes and an increase in the proportion of Proteobacteria in the obese group.…”

“…The gut microbiome can influence neuronal signaling to the brain through vagal afferent neurons 14. Several diseases including obesity, inflammatory bowel disease, and allergic disease are associated with alterations, disruption, and decreased biodiversity of the intestinal microbiota 8, 15, 16, 17. Obesity is associated with changes in the gut microbiota in humans11 and in animal models 8, 16.…”

“…Several diseases including obesity, inflammatory bowel disease, and allergic disease are associated with alterations, disruption, and decreased biodiversity of the intestinal microbiota 8, 15, 16, 17. Obesity is associated with changes in the gut microbiota in humans11 and in animal models 8, 16. However, recent metagenomics studies using a canine obesity model yielded results that were inconsistent with mouse model studies 8, 18.…”