Researchers have discovered that a small molecule produced by intestinal bacteria is moving to the kidneys and launches a series of infections, scarring and fibrosis, causing one of the serious complications of diabetes, and is the main cause of kidney failure.
The study was conducted by researchers from the University of Illinois Urbana-Shambin in the United States and the University of Mai in Japan, and the results of the study were published in Nature Communications on August 25, and was written by the Yurik Alier site.
Researchers discovered high levels of corisin – a small peptide produced by the bacteria of staphylococcus in the intestine – in the blood of diabetic kidney cirrhosis patients, and the researchers used a computer simulation and experiences on tissues and mice to track how the caundacine affects the kidneys, how it reached it from the intestine, and a possible way to confront it using antibodies.
“Our previous studies have shown that the coresen can damage the cells and increase the tissue scar and their fibrosis in other organs, so we suspected that it might be a hidden factor for kidney fibrosis,” said Ishaq Kan, a professor of animal science at Illinois University, who led the study with Dr. Esteban Gabza, Professor of Immunology at Mai University.
He added: “Our new results indicate that the coresen is indeed a hidden factor behind gradual kidney damage in diabetics, and that preventing it can provide a new way to protect kidney health in patients.”
Many chronic diabetes patients ultimately develop kidney fibrosis, and as soon as the condition exacerbates, the available therapeutic options become limited.
“Diabetic fibrosis is a major reason for kidney failure all over the world, but the main factors that cause it are mysterious, and no treatment can stop this process,” says Dr. Taro Yasuma of Mai University, a doctor and co -author of the study.
The medicine that serves the caves
Current treatments are mainly focused on controlling blood sugar and blood pressure, but there is no healing treatment that stops or reflects the scarring or fibrosis, as Yasoma said.
The researchers began to examine blood and urine diabetics, and they found that the levels of Corcycin have much higher than their healthy counterparts, and that the amount of coresin in the blood is linked to the extent of kidney damage.
After noticing the same results in mice with kidney fibrosis, the researchers follow the effect of the corisen in their kidneys. And they found that the coresen accelerates the aging of the kidney cells, absolutely a series of reactions that start from inflammation, then the death of the cells and then the accumulation of the tissue, which ultimately leads to the loss of kidney function and the aggravation of fibrosis.
But how does the coresin move from the intestine to the kidneys? The Cannes and Gabaza groups cooperated with the Diwakar Chocolate Group, a professor of chemical and molecular biological engineering at the University of Illinois, to produce a computer simulation and laboratory experiences to follow the journey of the bowel from the intestine to the bloodstream.
The researchers found that the coresin is able to link with albumin, one of the most common proteins in the blood, and is transmitted through the bloodstream. And when it reaches the kidneys, the coresen separated from the albumin to attack the microscopic structures that filter the blood and urine.
To confirm that the Corcine is the main cause of kidney damage, the researchers gave mice anti -coresin, and they noticed a significant decrease in the speed of kidney damage.
“When we treated the mice with an anti -coresen body, this led to slowing the aging cells of the kidneys and reducing the kidneys significantly.”
He added: “While there is currently no anti -human body for human use, our results indicate the possibility of developing it as a new treatment.”