How Colonic Inflammation Links Obesity to β-Cell Growth and Diabetes Development

Recent research from Tohoku University has shed light on a previously overlooked factor in the connection between obesity and the proliferation of insulin-producing β-cells in the pancreas. The study unciphers a novel pathway beginning with inflammation in the colon, which triggers a cascade leading to increased insulin secretion. Specifically, the findings demonstrate that colonic inflammation causes disruption of the intestinal barrier, activating the hepatic ERK pathway in the liver. This activation facilitates a neuronal relay system from the liver to the pancreas, promoting β-cell proliferation to compensate for insulin resistance often seen in obesity.

Interestingly, the researchers observed that causing inflammation in the colon of mice—without inducing obesity—was sufficient to activate the liver’s ERK pathway and increase β-cell proliferation. Conversely, in obese mice fed high-calorie diets, colonic inflammation was linked with hepatic pathway activation and β-cell expansion. Significantly, reducing colon inflammation in obese mice halted the activation of this pathway, despite their continued obesity, highlighting colon inflammation’s pivotal role.

This groundbreaking work suggests that inflammation in the gastrointestinal tract, particularly the colon, plays a crucial role in sensing obesity-related changes and initiating pancreatic adaptation. It offers a new perspective on the gut-liver-pancreas axis and underscores potential therapeutic targets for preventing or managing diabetes, especially in obese individuals. Targeting colonic inflammation may emerge as a promising strategy to regulate β-cell proliferation and glucose homeostasis, thereby addressing the root causes of obesity-related diabetes. Overall, these insights deepen our understanding of the complex biological mechanisms linking gut health, obesity, and insulin regulation.

Source: https://medicalxpress.com/news/2025-05-colonic-inflammation-link-obesity-cell.html