FIRMICUTES AND OBESITY

                                         FIRMICUTES

In a previous article pointed out what the microbiota.. Microbes and bacteria and most are benign and can even grant benefits or change  Indeed, researchers have discovered that traits such as weight and some aspects of the behavior of the received bacteria. Scientists call Firmicutes and work as diners are not responsible for infections, in fact, is only a tiny fraction of the bacteria we carry that cause infection and disease.  
But this time it was thought that bacteria acquire them on our journey through life. Now, however, researchers at Washington University in St. Louis have found that mom and dad and we spend traits through their DNA, so too do the bacteria. Yes, you read correctly, the bacteria pass their genes during pregnancy. Scientists say that these results are essential in medicine and doctors now have to take into account the DNA that is passed to the fetus by the bacteria to better understand the effect of these genes in the baby's health.
This study is the first to show that these bacterial genes may affect "specific traits such as immunity and inflammation." 

"We kept the bacteria on one side of the line separating the factors that shape our development - the environmental aspect of that line, not the genetic side," said co-author Herbert W. Virgin. "However, our results show bacteria stepping over the line. This suggests that we may need to substantially expand our thinking about their contributions, and perhaps the contributions of other microorganisms, genetics and heredity. " 
Experiments were made ​​in mice in which the susceptibility of animals to injury in the intestine was investigated. Mice were inherited certain bacteria more susceptible to damage than others with other bacteria carrying different genes.Researchers think that we should not wait long to find and implement benefits with these results as possible in a short time will remove infections and diseases that occur in mice that are genetically modified to key experiments in medicine.Researchers have often have to deal with the sudden appearance of new traits in mice suggest an infection. It is generally thought that the atmosphere was responsible, we now know that may also have been inherited. 

Equipment studying inflammatory bowel disease (Crohn's and ulcerative colitis, for example) when they discovered that half of the mice in the study have low levels of an antibody which has been linked to these disorders: IgA. 
"IgA helps defend the body against harmful invaders and is usually in the mucus produced by the body in the eyes, nose, throat and stomach," says Thaddeus Stappenbeck, co-author and head of the Department of Pathology and Immunology.  

When scientists housed mice with low levels of antibody with other mice had high levels of antibody, all mice ended up with low levels of antibodies in a few weeks. Furthermore, when mice were reproduced, the offspring of mothers with low antibody levels were also low.  


After a while, they explained, discovered the bacterium responsible for all this, is called Sutterella and found in all mice with low levels of IgA. The group of mice was housed with another group with the bacteria, acquired through normal distribution, however, in group play, were mothers who spent the same bacteria to their offspring. The mice with the bacterium suffered more damage to the intestinal injury. 

"The implications are profound, beginning in experiments using mice as they may help clarify some persistent sources of confusion" Stappenbeck said. "When we studied mice, we have to consider the possibility of inherited bacteria and their genes could be influencing the trait we are trying to learn." 

According Stappenbeck to maintain control, researchers will have to use separate animal colonies to ensure that any hereditary microbe is present in both groups and is not affecting the results. However, scientists expect long term this new inheritance model produces a "more insightful view of how human, bacterial and viral genes influence human health." 

                             FIRMICUTES AND OBESITY

Obesity is a major health status associated with cardiovascular diseases, diabetes, and is a leading cause of premature death in industrialized countries today. Statistics Canada report[1] shows that in 2011, an estimated 18.3% of Canadian adults qualified as obese. Approximately half of these cases had shown signs of increased health risk. Along with dietary habits and inherited risks, gut microbiota are suspected to be a key player in digestion and fat absorption. The gut of human and many other vertebrae is mostly dominated by two groups of bacteria, Bacteroidetes and Firmicutes [4]. Minor populations of Actinobacteria, Fusobacteria, and Cyanobacteria species are also present, as part of a complex microbial community [4]. Studying the relationship between obesity and the ecology of gut microbiota may provide meaningful treatments and biomarkers for susceptibility to weight gain [4].

Past research into the correlation between gut microbiota and diet had demonstrated a complex relationship between the population of the gut and fatty acid absorption. For example, mice with normal gut micorbiota had more body fat than germ free mice who had been sterile from birth, despite the reduction in diet [4]. In particular, the abundance of Firmicutes was observed to be proportionate to the obesity levels in the mice, with the obese, conventional mice carrying significantly more Firmicutes than the lean germ free mice [4]. Along with increased fatty acid absorption, more energy was also found to be efficiently obtained from diet in the obese mice compared to the lean mice, illustrating the connection between Firmicutes and improved efficiency in energy harvesting [5].

Bacillus subtilis

Obesity is linked with phylum-level changes in the functional diversity of bacteria [11]. Functional diversity measures not only the number of various metabolic pathways, but also the abundance of each pathway. Specifically, microbiota enriched with Firmicutes demonstrated a lower level of functional diversity than Bacteriodetes-dominant microbiota [11]. Hence, obesity, which is associated with the abundance of Firmicutes, leads to an overall decrease in metabolic diversity.The mechanism through which Firmicutes impacts fatty acid absorption and lipid metabolism is currently best described in zebrafish. As a model organism, zebrafish not only has a similar digestive tract as mammals, but more importantly, the lipid metabolism pathway is closely related to mammals and other vertebrates [10]. The overall gut microbiota was shown to cause increases in the number and sizes of the lipid droplets. In particular, the amplification in number of Firmicutes was related to the increase in number of lipid droplets, promoting fatty acid absorption in the extraintestinal tissues [3]. This increase, however, was only evident in fed zebrafish, showing the dependency on dietary habit. On the other hand, the size of the lipid droplets increased independently of the feeding time, and was induced by other non-Firmicutes bacteria [3].

Four possible explanations were proposed in response to this directly proportional relationship between gut microbiota and fatty acid absorption. Firstly, microbes stimulate the host’s metabolism, and may increase the bioavailability of fatty acids through modifying bile salt and its production [8]. Secondly, microbes may have direct interactions and impacts on the lipolytic activities in the host [9]. Thirdly, microbes may indirectly affect physiological responses in the host’s gut, resulting in increased absorption [3]. Fourthly, microbes may cause reduction in the rate of fatty acid oxidation, which allows more absorption of fatty acid [3]. Despite the fact that the general process in which Firmicutes promotes fatty acid absorption is known, the specific mechanisms are still being explored.

Zebrafish

n terms of vertebrates, including humans, zebrafish, mice, and pythons, most studies conducted support two hypotheses regarding fat absorption and the number of Firmicutes in the gut microbiota.

First hypothesis is that the number of Firmicutes was observed to be diet-dependent and positively correlated to the caloric intake of the vertebrate. In zebrafish and pythons, the proportions of Bacteroidetes and Firmicutes fluctuated significantly according to whether it was fasting or being fed. The number of Firmicutes increased greatly after a meal. In humans, loss of body weight was proportionate to a decrease in the number of Firmicutes [2].

Second hypothesis is that the number of Firmicutes was found to be inversely proportional to the number of Bacteroidetes . The number of Bacteroidetes was high during fasting, replacing the Firmicutes in the pythons. Similarly, the number of Firmicutes was notably higher than the number of Bacteroidetes in obese mice, and vice versa for the lean mice [6]. The composition of gut microbiota varies greatly with the obesity state of the organism, depicting a complex ecological relationship.

REFERENCES

 (1) Overweight and obese adults (self-reported), 2011, Statistics Canada, http://www.statcan.gc.ca/pub/82-625-x/2012001/article/11664-eng.htm (October 29, 2012)

(2) Ley, R.E., Turnbaugh, P.J., Klein, S., and Gordon, J.I. (2006). Microbial ecology: human gut microbes associated with obesity. Nature 444, 1022– 1023.

(3) Semova, I., Carten, J.D., Stombaugh, J., Mackey, L.C., Knight, R., Farber, S.A., and Rawls, J.F. (2012). Microbiota Regulate Intestinal Absorption and Metabolism of Fatty Acids in the Zebrafish. Cell Host Microbe 12, 277-288.

(4) Backhed, F., Ding, H., Wang, T., Hooper, L.V., Koh, G.Y., Nagy, A., Semenkovich, C.F., and Gordon, J.I. (2004). The gut microbiota as an environmental factor that regulates fat storage. Proc. Natl. Acad. Sci. USA 101, 15718–15723.

(5) Turnbaugh, P.J., Ley, R.E., Mahowald, M.A., Magrini, V., Mardis, E.R., and Gordon, J.I. (2006). An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027–1031.

(6) Ley, R.E., Ba¨ ckhed, F., Turnbaugh, P., Lozupone, C.A., Knight, R.D., and Gordon, J.I. (2005). Obesity alters gut microbial ecology. Proc. Natl. Acad. Sci. USA 102, 11070–11075.

(7) Costello, E.K., Gordon, J.I., Secor, S.M., and Knight, R. (2010). Postprandial remodeling of the gut microbiota in Burmese pythons. ISME J. 4, 1375–1385.

(8) Swann, J.R., Want, E.J., Geier, F.M., Spagou, K., Wilson, I.D., Sidaway, J.E., Nicholson, J.K., and Holmes, E. (2011). Systemic gut microbial modulation of bile acid metabolism in host tissue compartments. Proc. Natl. Acad. Sci. USA 108 (Suppl 1 ), 4523–4530.

(9) Ringø, E., Strøm, E., and Tabachek, J.-A. (1995). Intestinal microflora of salmonids: a review. Aquaculture Research 26, 773–789.

(10) Babin, P.J., and Vernier, J.M. (1989). Plasma lipoproteins in fish. J. Lipid Res. 30, 467–489.

(11) Turnbaugh, P. J., M. Hamady, T. Yatsunenko, B. L. Cantarel, A. Duncan, et al. 2009. A core gut microbiome in obese and lean twins. Nature 457:480– 484.
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