This study examined whether mdx mice (mouse model for Duchenne muscular dystrophy) have intestinal changes that could help account for “constipation” symptoms in people with muscular dystrophy. The study looked for changes in the amount of time it takes the mouse stomach to empty a meal, the amount of time it takes food to get through the small intestine and the amount of feces expelled to see if there is evidence of intestinal tract involvement in the mdx mouse model.
Why is this study important?
Many children and adults with muscular dystrophy experience gastrointestinal (GI) symptoms that are labeled as constipation, bloating and fullness. Many are on medications such as miralax to help with eliminating bowels. “Constipation” has been attributed to weak abdominal wall muscles and difficulty expelling the stool.
Past studies have demonstrated increased fibrosis of intestinal wall muscles in muscular dystrophy. This study uses an animal model to demonstrate that there is functional impairment of the intestines in Duchenne muscular dystrophy. The time for food to travel through the small intestine was delayed AND the amount of fecal material expelled was decreased, though the liquid to dry component of the stool was unchanged.
This study demonstrates that the intestinal muscles may be affected by muscular dystrophy and contribute to what gets diagnosed as “constipation”. Constipation in medicine implies hard stools. Many children and adults with muscular dystrophy have formed stools that are not hard, yet experience bloating, a feeling of being full early and cramping with decreased numbers of bowel movements.
Intestinal walls contain smooth muscle which allows the intestines to contract (peristalsis) and move food/fecal material forward until it is eliminated. Fluids get absorbed and secreted by the intestines and if there is a problem with absorption or secretion, this might contribute to constipation.
This study examined the water content of feces by weight and showed no difference between mdx and normal mice. It did demonstrate a significantly delayed transit time of food through the small intestine and decreased amount of feces expelled. This study implies that the problem lies with the muscle in the intestinal wall and this may be due to deficient signaling mechanisms (nitric oxide) or fibrosis (scar tissue).
Further studies will need to be done in both mdx mouse model and in CMD mouse models to demonstrate what is affecting intestinal wall function (for example: fibrosis or scar tissue, deficient signaling mechanisms). Understanding the underlying reasons for intestinal motility problems, might help identify drugs to help target this issue.
Mule F, Amato A, Serio R. Gastric Emptying, Small Intestinal Transit and Fecal Output in Dystrophic (mdx) Mice. J Physiol Sci, Sept 26 2009.