According to a recent mouse research, the bacteria that assist break down food actually instruct the stomach how to do their job better. According to the researchers, bacteria appear to be able to control which of the gut’s genes are activated, and this interaction may lead to a remodelling of the epithelial cells lining the gut to fit the diet. According to the researchers, bacteria appear to be able to control which of the gut’s genes are activated, and this interaction may lead to a remodelling of the epithelial cells lining the gut to fit the diet.
“The gut is a wonderful link between an animal and the world it lives in, and it receives information from both the nutrition and the bacteria it houses,” said John Rawls, Ph.D., director of the Duke Microbiome Center and professor of molecular genetics and microbiology at Duke. The findings were published in the open access journal Cellular and Molecular Gastroenterology and Hepatology on May 6. To begin parsing the instructions sent by microorganisms to gut cells, Duke researchers compared mice grown without gut microbes to those raised with a normal gut microbiome.
The researchers concentrated on the interaction between RNA transcription (DNA being transcribed to RNA) and the proteins that switch this copying process on or off in the small intestine, which is where most fat and other nutrients are absorbed. While both germ-free and normal mice were able to metabolise fatty acids in a high-fat diet, the researchers discovered that germ-free mice employed a whole distinct collection of genes to deal with the high-fat meal.
“We were shocked to see that the gene playbook used by the gut epithelium to respond to dietary fat differs depending on whether or not microorganisms are present,” Rawls said. The researchers also discovered that microorganisms can aid in fat absorption in the stomach.
“It’s a really consistent conclusion across numerous studies, from our lab and others, that microorganisms actually improve lipid absorption,” said Colin Lickwar, Ph.D., senior research associate in Rawls’ lab and the paper’s lead author. “And, to some extent, this influences systemic processes such as weight growth.” The germ-free mice showed an increase in the activation of genes involved in fatty acid oxidation, which is the actual burning of fatty acids to supply fuel for the gut’s cells.
“We usually conceive of the gut as merely performing its job, absorbing food nutrients through the epithelium to share with the rest of the body,” Rawls added.
“What we believe is happening in germ-free mice is that the stomach consumes more fat than it would if the microorganisms were there.” This might be due to changes in the makeup of the gut’s epithelial cells.
“A number of recent articles have shown that there is a significant ability to affect the broader architecture of the gut as well as particular gene programmes,” Lickwar added. “The gut has an amazing amount of flexibility.” We don’t fully understand it, but this article sheds some light on it.”
The researchers concentrated their efforts on HNF4-Alpha, a transcription factor known to control genes involved in lipid metabolism and genes that respond to microorganisms.
“We thought that it might represent an interface or a crossroads between interpreting information that comes from either microbial sources or from dietary fat,” Lickwar said.
“It’s certainly complicated, but we do appear to identify that HNF4-Alpha is important in simultaneously integrating multiple signals within the intestine,” Lickwar said.”For every way that germ-free animals seem unusual, that teaches us something about the large impact of the microbiome on what we consider to be ‘normal’ animal biology,” Rawls said.
