“The human ‘metagenome’ is a composite of Homo sapiens genes and genes present in the genomes of the trillions of microbes that colonize our adult bodies (the ‘micro- biome’). Our largest collection of microbes resides in the gut, where an estimated 10–100 trillion organisms reside (the gut microbiota; see Table 1 for a glossary of terms). The gut microbiome encodes metabolic capacities that remain largely unexplored but include the degradation of otherwise indigestible components of our diet (Backhed et al. 2005; Sonnenburg et al. 2005; Flint et al. 2008).”(Turnbaugh & Gordon, 2009)
“Colonization of adult germ-free mice with a distal gut microbial community harvested from conventionally raised mice produces a dramatic increase in body fat within 10–14days, despite an associated decrease in food consumption (Backhed et al. 2004). This change involves several linked mechanisms including microbial fermentation of dietary polysaccharides that cannot be digested by the host, subsequent intestinal absorption of monosaccharides and short-chain fatty acids, their conversion to more complex lipids in the liver; and microbial regulation of host genes that promote deposition of the lipids in adipocytes (Backhed et al. 2004). Additionally, germ-free mice are resistant to diet-induced obesity caused by consumption of a high-fat/high-sugar ‘Western’ diet (Backhed et al. 2007). Other studies of lean and genetically obese (ob/ob) mice (Ley et al. 2005; Turnbaugh et al. 2006), as well as lean and genetically obese (fa/fa) rats (Waldram et al. 2009) have revealed differences in their metabotypes that have been ascribed in part to differences in their gut microbial ecology (these differences involve the representation of members of the Bacteroidetes, Firmicutes and Actinobacteria phyla of bacteria).”(Turnbaugh & Gordon, 2009)
“Although the primary cause of obesity is excess caloric intake compared with expenditure, one intriguing hypothesis that follows from these studies links differences in gut microbial ecology between humans to energy homeostasis; i.e. individuals with a microbial community more efficient at energy extraction from the diet, or with an increased ability to promote adiposity through manipulation of host genes and metabolism, may be predisposed to obesity. This hypothesis predicts that obese and lean individuals will have distinct microbiotas, with measurable differences in their ability to extract energy from their diet and to deposit that energy in fat.”(Turnbaugh & Gordon, 2009)
“Additionally, there are a number of unresolved questions regarding the organismal and genetic diversity of the human gut microbiome. How diverse is the human gut microbiome between individuals and how does it vary within an individual over time? How is a microbiota and microbiome transmitted to an individual following birth: what is the relative role of early environmental exposures (to microbes and diets) versus our human genotype in defining postnatal microbial community assembly, and the structures of our adult microbiota? Is there a core microbiome shared between humans, and should this core be defined in terms of organisms, genes, or functional characteristics? And finally, are there genes and/or metabolic pathways in the human microbiome that can be identified as being associated with obesity?” (Turnbaugh & Gordon, 2009)
Reference:
Turnbaugh, P. J., & Gordon, J. I. (2009). The core gut microbiome, energy balance and obesity. The Journal of Physiology, 587(17), 4153–4158.
I hope this helps, I found this long ago for an assignment I had to do.
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