Essay on Obesity Alters Gut Microbial Ecology

Towards the end of his medical training in the early 1980s, Gokhan Hotamisligil was working on a unique tumor case on a patient and found they were comprised primarily of fat cells. The fatty tumors were due to a rare condition, Proteus Syndrome. Working in the field of metabolic regulation Hotamisligil began to explore the underlying pathways for insulin resistance. In his dissertation he discovered that the fat tissue of obese animals and humans were capable of producing inflammatory mediators. His research helped shape the current view of fat tissue as a “discrete, active organ in its own right, continuously exchanging messages with the rest of the body by way of the bloodstream.” By early 2002 Hotamisligil and his laboratory made

In the article, "The Ultimate Social Network," Jennifer Ackerman presented data to challenge the first thoughts that people are independent, depending just on the human body to control interior capacities. She stated that the adjustments in the human microbiome are contributing to higher rates of obesity and autoimmune system disorders, prompting it to address regardless of whether we are in charge of our own body.

These are some of the proposed functions of our microbiome. First of all, scientists have known for years that gut bacteria break down certain components of good that would otherwise be indigestible and would pass out of the body unused. In addition, Bacteroides thetaiotaomicron breaks down carbohydrate, also capable of breaking down the large, complex carbohydrates found in plant. It also has genes that code for more than 260 enzymes capable of digesting plant matter. Helicobacter Pylori is a disease-causing bacterium, however, H. pylori benefits the body by helping to regulate levels of stomach acids, thus creating an environment that suits itself and it host, and surprisingly, plays a role in regulating two hormones in appetite (ghrelin). This function greatly help most children in the U.S. to prevent overproduction of fat cells. Sadly, many children are exposed to antibiotic treatments, has caused alterations in the compositions of their intestinal microbiome. This caused the rising of childhood obesity, and overproduction of

Turner et al. (2013) argues that diet is socially learned and that to understand diet, disease, and the evolution of the microbiome it is necessary to evaluate current developmental environments. Turner, Murray, & Manary agree there has been a mismatch between genes, environment, and nutrition and this has created “diseases of civilization”. To counteract this great change in diet, disease must be prevented through lifestyle changes: diet, drugs, exercise (Eaton, Konner, & Cordain, 2010) and the resulting microbiome which is affected by these components.

     Obesity is the net result of an excess of energy consumption over expenditure. Factors that must be considered as contributing to causation are: heredity, and altered metabolism of adipose tissue, the list goes on and on. Overeating is clearly a prominent contributor to obesity. Feeding behavior occurs in response to hunger and to appetite induced by the presence of food.

We know currently essential information about microbiomes to help us understand the human body a little better. The skin, mouth, esophagus, stomach, colon, gut, and vagina are composed of microbial communities. Collectively, the gut has the most information. Information pertaining to these body parts however, are limited simply because each individual is unique This makes each body just as unique as the person. (The Scientist Staff) It is in still in question whether we are functionally redundant between community members, and what kind of factors are influencing this. (Turnbaugh)

The study intended to look at the gut microbiome that is naturally present within the gut. The research team of the Louisiana State University designed an experiment with lab rats to predict how the manipulation of the gut microbiome with a high fat diet would affect their brain

Several possible mechanisms through which the changes in gut microbiota can influence the pathophysiology of metabolic syndrome have been proposed. Dysbiosis of the gut microbiota due to triggers such us a high fat diet can alter the distribution gut junction proteins leading to the translocation of the colonic contents such as LPS to the blood. This increased gut permeability and leakage of contents referred to as Endotoxemia contributes to low grade inflammation. In gut dysbiosis the gut microbiota become more efficient at energy extraction and the SCFA produced may act as signaling molecules and stimulate a cascade od signaling that increases fat storage and energy production. Gut microbiota regulates expression of fasting induced adipose factor (FIFA) proteins which suppress expression of LPL thus fat storage is

Research was conducted comparing the intestinal bacteria of obese and thin people, which showed that microbes in the thin individuals intestines where much more diverse than that of an obese individuals. Studies showed that thin individuals

The gut microbiota encompasses trillions of microorganisms that inhabit the gastrointestinal tract (Carding et al. 2015). The composition of the gut microbiota is constantly evolving and can be susceptible to both endogenous and exogenous modifications (Carding et al. 2015). The microbiota

The human gut microbiota has become the subject of researches in recent years and our knowledge of the resident species and their potential functional capacity is rapidly growing. Our gut harbors a complex community of over 100 trillion microbial cells. Therefore, our gut microbiota evolves with us and plays a pivotal role in human health and disease. This has clear effects on physiologic, immunologic, and metabolic processes in human health, aberrations in the gut microbiome and intestinal homeostasis have the capacity for multisystem effects. Changes in microbial composition are implicated in the increasing for a broad range of inflammatory diseases, such as allergic disease, asthma, inflammatory bowel disease (IBD), obesity, and associated

Mullin in this article discussed correlation of diet, gut flora, and weight. Standard American diet (SAD) that is a high fat and carbohydrates, and low fiber diet negatively affects gut microbiota. Avoiding inflammatory fat and decreasing sugar intake helps to good bacteria to grow more in the intestine. According to Mullin, when a person cut back the SAD gut start to fertilize more normal flora that will help in losing weight (p. 161). The overgrown bad gut microbitas produce more harmful byproducts that can increase intestine inflammation, promote fat accumulation in the stomach area, and increase insulin resistance (p.

These complex communities play an important role in health and have been implicated in the pathogenesis of diseases including diabetes, cardiovascular disease and obesity. The microbiota living symbiotically with their host are generally non-pathogenic and have evolved with humans in order to combat colonization by harmful bacteria while extracting energy from non-digestible polysaccharides. There are many factors that contribute to the stability of the gut microbiome. Typically, the gut microbiome is established at birth and differs with mode of delivery (vaginally vs. cesarean) [7,9]. Therefore, the manner in which a child is born influences the composition of bacteria. Other factors include host environment, genetics and lifestyle, the latter of which is the focus of this proposal [8,16]. The gut flora are beneficial to humans as they provide essential nutrients while also acting as an adaptive immune system [7, 23]. Research has suggested that antigens released from gut microbiota can be absorbed and infiltrate adipose tissue, thereby worsening chronic inflammation and oxidative stress associated with obesity [23]. Therefore, identifying the specific microbiome of an individual can be diagnostic of metabolic disorders [8] and may contribute to impaired endothelium-mediated

transferred gut microbiota from either obese or lean mice to germ free mice.7 This resulted in a 47% increase in total body fat in the germ free mice that received bacteria from obese mice, while the mice that received bacteria from lean mice only saw a 27% increase in body fat.7 Further examination of gut microbiota showed that the obese mice had higher levels of Firmicutes than Bacteroidetes bacteria, which suggests that possibly a difference in gut bacteria that ultimately led to an increase in fat, as it was the only variable between groups that changed. Additionally, the gut microbiota found in the colon of the obese mice was found to have the ability to better ferment indigestible carbohydrates.7 Because the obese mice lost fewer calories in their feces, this indicates that the gut bacteria in the obese mice led to an increased harvest of energy.7 Ley et al. conducted a study that showed that due to a mutation in the leptin gene, obese mice had a 50% reduction the Bacteroidetes bacteria with a similar increase in Firmicutes.8 These studies suggest that gut bacteria could be considered an environmental factor that work to control fat storage and provide evidence that certain gut bacteria is associated with

Researches studies differ on whether obese consume more energy (calories) than non-obese individuals. Some show they do consume more; others show they may consumer fewer calories. The big difference may be in the type of nutrients that they consume, such as fat. For example, Gazzaniga, found that the percentage of body fat was positively correlated with total dietary fat. Still, other researchers suggest that the reasons are metabolic in origin and that obese individuals "process" foods differently resulting in an increase in body fat. Although how these factors affect obesity are not fully understood, one thing is clear: Obesity results when energy intake exceeds energy expenditure and is stored as fat.