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ANI | , Posted by Taptrisha DasCopenhagen
The most remarkable example of gut plasticity can be seen in animals that are subjected to prolonged fasting, such as hibernating animals or phyton snakes that go without eating for months, where the intestine shrinks by 50 percent but remains in size. Gets well. After feeding again for a few days.
The Columbani Andersen laboratory in the Cell and Neurobiology section of the Department of Biology at the University of Copenhagen uses the fruit fly, Drosophila, to study the mechanisms controlling gut plasticity. The results have just been published in the scientific journal Nature Communications.
Importantly, the ability of the intestine to change shape remains largely intact. As a result, during pregnancy in humans, the intestine increases in size, facilitating nutritional intake to promote fetal growth.
Dr. Ditte S. “Taking advantage of the extensive genetic toolbox available in the fruit fly, we have investigated the mechanisms that underlie nutrient-dependent gut size,” says Anderson.
The results show that nutrient deficiency results in the accumulation of progenitor cells that fail to differentiate into mature cells, causing the intestine to shrink. Upon refeeding, these dormant progenitor cells readily differentiate into mature cells to promote intestinal regrowth.
Ditte S. Anderson adds, “We have identified activin as important regulators of this process. In nutrient-restrictive conditions, activin signaling is strongly repressed, whereas it is reactivated and “: is required for progenitor maturation and gut size in response to feeding. Activin-dependent gut size change is physiologically important because inhibition of activin signaling reduces survival of flies subjected to intermittent fasting”.
Regulators of organ plasticity are essential for host adaptation to constantly changing environments, however, the same signals are often dysregulated in cancer. Indeed, mutations affecting activin signaling occur frequently in cancer cells in a variety of tissues. Our study provides a starting point for investigating the relationship between aberrant activin signaling and colorectal cancer development and sets the stage for exploring the efficiency of anti-activin therapeutic strategies in treating colorectal cancer.
This story is published from a wire agency feed without any modifications to the text. Only the headline has been changed.
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