One notable demonstration of the adaptability of the small intestine is observed in animals enduring extended periods of fasting, like hibernating creatures or pythons that can go months without eating. During this time, the gut can shrink by as much as 50 per cent, but it regains its original size after just a few days of eating again.
The Colombani Andersen laboratory within the Cell and Neurobiology section of the Department of Biology at the University of Copenhagen utilizes the fruit fly, Drosophila, to investigate the processes controlling gut flexibility. The findings have recently been released in the scientific publication Nature Communications.
The gut maintains its ability to change in size, which allows it to expand during human pregnancy, helping to support the intake of nutrients for the development of the fetus.
"Taking advantage of the broad genetic toolbox available in the fruit fly, we have investigated the mechanisms underpinning nutrient-dependent gut resizing", says Dr. Ditte S. Andersen.
The findings indicate that when nutrients are lacking, there is an increase in undeveloped cells that cannot mature, leading to a reduction in the size of the intestine. However, when these halted undeveloped cells are provided with nutrients again, they quickly mature into fully developed cells, enabling the intestine to regenerate.
Ditte S. Andersen continued saying, "We have identified activins as critical regulators of this process. In nutrient-restrictive conditions, activin signalling is strongly repressed, while it is reactivated and required for progenitor maturation and gut resizing in response to refeeding. Activin-dependent resizing of the gut is physiologically important as inhibition of activin signalling reduces survival of flies to intermittent fasting".
The controllers of the flexibility of organs are crucial for the host to adjust to a constantly changing environment. However, these same signals are frequently disrupted in cancer. Mutations that impact activin signaling are common in cancer cells across different tissues. Our research offers a foundation for examining the connection between abnormal activin signaling and the formation of colorectal cancers, and paves the way for assessing the effectiveness of anti-activin treatments for treating colorectal cancers.
