[메디게이트뉴스] Recently, as research on intestinal microbes has increased exponentially, new research is being published every day. Compared to other scientific fields, the public is very interested and the latest content seems to be introduced more through the media. One of the reasons why gut microbiota research has become widely known is probably due to the fact that the gut microbiota plays an important role in the cause of obesity. In addition to the high interest in obesity, words related to obesity such as’fat bacillus’ and’fat-losing probiotics’ have appeared in advertisements these days, and the public’s interest in the intestinal microflora has also increased.
If so, does the gut microbiota actually affect obesity? What studies have been conducted on this?
Over the world, obesity is increasing rapidly, making it the biggest threat to health. According to a report by the World Health Organization (WHO), obesity worldwide has increased by about three times compared to 1975. As of 2016, 39% of adults over the age of 18 are overweight and 13% are obese. Some experts point to the dramatic changes in living conditions that have taken place over the past decades, as the reason for the rapid increase in obesity over a period of less than a generation. In other words, improved hygiene and a significant change in diet were suggested as causes of obesity, which could eventually lead to changes in the intestinal microbiota.
In 2006, the research team of Jeffrey Gordon of the University of Washington, a pioneer in the study of the gut microbiota, studied 12 obese patients on a fat-restricted diet or a diet program using a carbohydrate-restricted diet. Generation Sequencing, next-generation sequencing) technique.
Before the start of diet, obese people had fewer Bacteroidetes statements and relatively more Firmicutes statements than those with skinny body. As weight loss during the diet program progressed, the Bacteroidetes statement increased and the Firmicutes statement gradually decreased, and the Firmicutes:Bacteroidetes ratio changed, similar to those of skinny people. These changes were not related to the type of diet, and were correlated with the degree of weight change. It was thought to be a change in the gut microbiota, which is related to weight loss itself rather than diet (Figure 1).
This study proved the correlation between obesity and intestinal bacteria. However, it was not possible to clarify exactly whether changes in intestinal microflora caused obesity or whether intestinal bacteria changed due to obesity. Later, in animal experiments using ob/ob mice, which are genetic obese mice, it was known that the intestinal microbes of obese mice have a characteristic that they can obtain more energy from the food they eat than the intestinal microbes of the slim mice. Transplanting the feces of these obese mice into sterile mice was observed to make the transplanted mice obese, so this animal experiment revealed that the intestinal microbiota itself could be the cause that affects obesity.
Later, Jeffrey Gordon’s team conducted a very interesting study of transplanting human feces into mice. One obese and one slender female twin feces were transplanted into sterile mice. Since they are twins, they can be said to be relatively similar genetically, so it can be thought that the difference in obesity between the sisters and the intestinal microbiota is likely to be large. Similar to animal experiments, rats that received feces from obese persons among twins became obese, and rats that received feces from slender humans became thinner. This proved that the function of the gut microbiota, which affects human obesity, can be transferred to mice through fecal transplantation.
It is ethically impossible to conduct an experiment to determine whether the trait of the obesity-causing gut microbiota can be transferred between humans through fecal transplantation. C. difficile It was proved in a woman who received a fecal transplant for the treatment of enteritis. A 32-year-old woman recurs in the UK in 2014 C. difficile After receiving a stool transplant from a healthy daughter for the treatment of gastroenteritis, her body weight increased from 61.7 kg (BMI 26) to 15.4 kg after 16 months. Despite the efforts to diet, it reached 80.3kg (BMI 34.5) at 36 months after fecal transplantation. Interestingly, her daughter, who was 16 years old at the time of fecal transplantation, weighed 63.5 kg (BMI 2.4), which later increased to 77.1 kg. In other words, the mother became obese as her daughter’s feces, who had obesity characteristics, were transplanted into her mother.
Then, does fat bacillus really exist?
In fact, it is difficult to say that certain bacteria determine the degree of obesity. The high Firmicutes:Bacteroidetes ratio reported in early 2006 was also unacceptable as it did not appear consistently in subsequent studies. This can be said to be a common phenomenon in gut microbiota research, because it is difficult to obtain consistent results due to the diversity of the gut microbiota and various factors affecting it. Several similar gut microbiota studies involving many diseases have shown different results. In other words, the intestinal microbiota can affect obesity, but it should be understood as a functional characteristic of the microbiota rather than a problem with specific bacteria. So it would be more appropriate to describe it as’fat microflora’ than fat bacteria.
In addition, it has been proven that the intestinal microbiota can cause obesity from animal experiments to human cases, but it should be considered that the intestinal microbiota alone does not determine the degree of obesity, and diet is still important. What was interesting about the experiment in which twin feces were transplanted into rats was the observation that obese rats later became slimmer when a rat that became obese and a slender rat were raised together in one cage after receiving human feces.
This is because rats have feces-eating characteristics, and while eating each other’s feces, the intestinal microbial characteristics of slender rats are located in the colon of obese rats. At this time, the intestinal microbial characteristics of obese mice were not transferred. However, the recovery of obese mice by the microbes of slender mice was observed only when a low-fat, high-fiber diet was given, and the obese mice were not recovered when a high-fat/low-fiber diet was given. In other words, the function of the gut microbiota can vary depending on the type of food it consumes. In addition, as a mechanism by which the intestinal microbiota causes obesity or metabolic diseases, a new concept such as abnormality of the circadian regulation function of the intestinal microbiota has also been proposed.
Attempts to treat obesity or metabolic disease through fecal transplantation are continuing based on the relationship between the intestinal microbiota and obesity, which have been discovered so far. Someday the day will come to cure obesity with poop.
※The column is the columnist’s personal opinion and may not match the editorial direction of this magazine.