The examination reveals colonitis as a beta growth trigger in obesity

Scientists from the University of Tohoku Graduate School of Medicine have discovered a key step in the ERK trail in the liver, which leads to increased insulin production. While their previous work focused on the aspects of the signal path from the liver to the pancreas, the current study shows an even earlier step, which begins in the colon when it is avid – caused by obesity. This study has revealed a new role played by the digestive tract in the regulation of glucose homeostasis.

Insulin is a hormone produced by β cells in the pancreas. You can think about insulin like a key that unlocks cells so that glucose comes from the blood so that it can be used as energy. However, people with obesity can become insulin resistant, which causes the pancreas to release more insulin to keep up. This happens through a relay of the intergovernmental neuronal signal from the ERK trail in the liver. Due to the close relationship between obesity and the beginning of diabetes, understanding this path can help develop new treatment methods or prevent this conditions.

The purpose of this study was to define how obesity causes this cascade in particular. We theorized that it was related to inflammation In the colon, because pro -inflammatory factors can play a stimulating role in the ERK trail in the liver. “

Junta Imai, Tohoku University

Scientists have developed an accurate series of experiments to determine whether the inflammation of the colon due to obesity can affect the Erk liver trail. First of all, the research group analyzed mice without obesity that received a drug caused by inflammation in the colon. As a result, they found that the ordinary causing of a colonist activate the ERK trail in the liver, stimulates the neuronal relay trail and increases the number of β cells even at mice without obesity. Then, analyzing the mice, in which obesity was induced by a high calorie diet, it was found that these obese mice had colonitis, along with both the activation of the ERK trail and increased β cells.

“The exciting discovery was that we tried to treat obese mice with colonitis by reducing their inflammation, it actually stopped the ERK trail in the liver from activation,” explains Imai. “Despite the fact that the mouse was still obese, aiming at colonitis was exactly what was needed to change the ERK path.”

These studies reveal the missing link on the trail, stating that the liver senses the state of obesity through colonitis, and the colonitis serves as the first trigger of β cell proliferation during the development of obesity. These achievements will lead to progress in understanding the mechanism of β cell proliferation to maintain normal blood glucose levels. In addition, this research is expected to help develop treatment and methods for preventing diabetes.

These discoveries were published on May 8, 2025.

These studies were supported by Japan Society of the Promotion of Science (JSPS) Kakenhi Grant-in-Aid for Scientific Research (23K24383, 22K19303, 20H05694); Japan Science and Technology Agency (JST), Moonshot R&D (JPMJMS2023); and Japan Agency for Medical Research and Development (Amed), Amed-Prime (21GM6210002H0004).