Canadian Scientist: Dr. Jeffrey I. Gordon Dr. Jeffrey I. Gordon is a researcher that works out of his lab at Washington University in St. Louis called the Centre for Genome Sciences and Systems Biology and investigates with mice and germs (The Gordon Lab, 2014). He has received many degrees such as his medical doctorate degree and many different prizes for his works in medicine (The Gordon Lab, 2014). He has many different honours from the Washington University and St. Louis University (The Gordon Lab, 2014). Gordon has conducted numerous experiments that include his 478 peer-reviewed publications and numerous collaborations with other researchers and scientists (The Gordon Lab, 2014). Gordon’s major contributions to the scientific community are very useful as much of what is known today about the stomach micro biome is mostly from Dr. Gordon’s experiments (Washington University, 2014). Dr. Gordon is also honoured and praised for his discovery that links nutritional health to the inner working of tens of trillions of microbes residing within the gut (Washington University, 2014). In one of Gordon’s peer reviewed publications called Molecular Analysis of Commensal Host-microbial Relationships in the Intestine, Gordon investigates how little microbes can adapt and shape out physiology. Gordon implanted human microbes from the gut into mice and observed the results (Gordon et al., 2005). He discovered that the microbes modulated the genes and the mice had developed many
* Studies in mice, which also have large numbers of microbes living in their guts, have shown that there may be a link between storing energy as fat and microbial activity.
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
Zhang et.al. did a study with the aim of assessing the relative contributions of host genetics and diet in shaping the gut microbiota and modulating metabolic syndrome related phenotypes. They fed wild type mice C57BL/6J) and Apoa-1 knockout mice normal chow or a high fat diet (HFD) for 25 weeks. The knock out mice had impaired glucose tolerance and high body fat at baseline. They measured food intake and body weight evert 2 weeks and measured glucose tolerance and gut microbiota composition and population at baseline and at the end of the intervention at 25 weeks. According to their findings the wild type mice that were fed a high fat diet gained the most weight followed by the gene Apoa knockout mice. The same results were also seen for glucose tolerance test with the wild type mice on a high fat diet showing a larger spike in blood glucose. Significant differences in microbial composition was seen between animals on different diets rather than animals with genetic differences. HFD eliminated bifidobacteria and increased the abundance of endotoxin producing desulfovibrionaceae. Diet differences accounted for
The use of the first form of microbe-based therapeutics, probiotics, is beneficial for preventing disease. These live microorganisms are known to strengthen the equilibrium of the gut flora by the development of healthy gut
Studies have identified different genera of bacteria which are present in the microbiome and their role in nutrient intake. Gut microbiota has 3 main enterotypes Prevotella, Bacteroides and Ruminococcus, there is a strong correlation between the concentration of each bacterial community and the dietary constituents. A diet high in carbohydrates and simple sugars would also indicate and reveal a greater concentration of Prevotella whereas a diet high in protein and animal fats would present a higher concentration of Bacteroides in the gut. A long term change in the diet would permanently shift the concentration of bacteria in the gut to accommodate the new nutrient uptake. This would then change the bacterial barrier in the intestine which could make it more vulnerable due to reduced species richness.
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
Over two-thirds of adults, or nearly 69 percent are considered overweight or obese. Of those, more than one-third are considered to be obese, while more than 1 in 20 are classified with extreme obesity.1 The main causes of these overwhelming rates of overweight and obesity are all too familiar: an unhealthy diet, a sedentary lifestyle and to a lesser extent perhaps genes play a role as well. In recent years, however, researchers have become increasingly focused on a potential additional contributor to the obesity epidemic that lives inside us all: billions and billions of gut microbes or microbiota.2
The human gut microbiome has appeared in some recent studies to be a potential reason for why 180 million children worldwide suffer stunting, a case in which the child can become mentally retarded or infected with diseases. Even with malnourishment, the right balance of gut microbiomes can lead to a healthy growth, while their imbalance can lead to stunting. William Petri, Jr. worked on infants in Bangladesh for years with his team, but the team was not successful to utilize the dietary supplements to counteract malnourishment. However, William has found the results about gut microbiomes to be enlightening. He teamed up with Tahmeed Ahmed and Jeffrey Gordon to examine stool samples from different Bangladeshi infants and compared the results
However, recent studies are demonstrating that this may not be as accurate as once thought. A human model study, using culture-dependent and culture-independent methods, showed that the cecal bacterium greatly differs from bacteria found in the feces (Mareau et al., 2001). Mareau et al. (2001) observed that the cecum has a higher concentration of volatile fatty acids, which lowers the pH, this is due to being exposed to leftover substrates from the small intestine. When the study compared populations of bacteria in the cecum and feces, they observed that facultative anaerobes represented 25% of the cecal microbiome and 1% in the fecal; in addition, anaerobic bacteria were 100 times lower in the cecum than in the feces (Marteau et al., 2001). Fecal bacterial concentrations being higher than cecal could possibly be due to the water absorption in the colon, concentrating the bacteria in the waste. Also seen in humans in 2002, a study, which collected biopsied samples from along the lower gastrointestinal tract, suggested that mucosa-associated bacteria are equally distributed along the colon, but that the colon microbiota is drastically different than fecal microbiota (Zoetendal et al., 2002). A study using sudden-death victims and a culture-dependent approach, noted that gut conditions varied among individuals, suggesting that the colonization of bacteria is more closely
One of them is because the host cannot properly digest microbial process of metabolism of dietary polysaccharides. Other reasons include: because of the constant intestinal consumption of short-chain fatty acids and monosaccharaides and a change in different lipids in the liver and the removal of lipids in adipocytes. These scientists have also used different kinds of methods in order to compare the biological features between the mice. For example, DNA was removed from a part of the intestine of both the obese and the lean mice using a machine called a bead beater, further being extracted by a phenol-chloroform extraction. Then, the DNA was compared with each other to (sequenced gut microbial genomes) using a system for aligning genomes called the Mummer. These Micro biomes were also compared using BLASTX searches. The evaluation of mice feces with a bomb calorimeter; the transfer of obese mice micro biota on eight to nine week old, germ-free lab rats; the cumulative binomial distribution and probability equal to ‘n2/N2’ calculation; the usage of gas-chromatography mass-spectrometry to measure the short-chain fatty acids in the large intestine; the usage of dual energy X-ray absorption spectroscopy to measure the amount of body fat on the experimented recipients; the usage of gene-sequenced surveys on the gut-based micro biota of the donor and recipient all helped scientists analyze and compare the micro biota of both obese and lean
In his NPR article, “Finally, A Map of All the Microbes on Your Body”, science editor Rob Stein states several elementary facts about microbes: first, one in ten of the trillions of cells in the human body is actually “human”. Second, the body has a symbiotic relationship with these “non-human” cells. This beneficiary connection is seen in various microbial functions, such as battling infections and synthesizing compounds that are resistant to harmful infection. Stein describes a team of scientists who recently undertook the enormous project of mapping out the microbiome that is the human body, painstakingly cataloging the various microbes they encountered at different locations – as complicated as the map of an actual continent. The sheer
I would be very pleased to contribute to research within the intended Junior Research Group on Nutrition and Microbiota. Ever since my completion of my bachelors in veterinary medicine and work as a pathobiologist, I have had a growing interest in studying how the microbiota contributes to chronic diseases. Lifestyle factors, including diet play an extremely important role in the development of these diseases.
The human microbiome is the genetic material of the microbes that live inside and on the human body. Microbes are microscopic organisms such as bacteria, fungi, protozoa and viruses. One’s diet and environmental factors can affect the composition of the microbiome. There is a high concentration of microbes in the gut, particularly inside the large intestine. The microbiome does many different things. It helps to digest our food, regulate our immune system, produce vitamins, protect against bad bacteria, and is essential for human development. Recent studies suggest that the microbiome also has an impact on the brain and emotional behavior. Interactions between the host and its microbiome are complex and bidirectional.
Science has always been my academic passion, and for two summers I was a research intern in the GI department at Penn. In a microbiome lab, I analyzed how a genetically modified strain of E. coli would colonize a mouse gut and affect the gut ecology. I collected fecal samples, imaged bacterial colonies, and spent hours eagerly attempting to uncover the secrets hidden within my data. We were making progress towards the creation of a more effective probiotic that could be used to treat antibiotic-associated infections and Inflammatory Bowel Disease. After my final presentation, my mentor, Dr. Wu told me, “I don’t know if you realized it, but you were the first person to see proof that a mouse gut can be colonized by a human strain of E. coli.” It was thrilling to be the first person to uncover a new fact; for a period of time, I was the only person to know something new about the workings of the scientific world. This sense of wonder prompted me to return for a second summer to work on an independent experiment regarding bacterial nitrogen