Celiac.com 01/12/2015 - Ghrelin is a peptide that plays an important role in regulating the distribution and rate of use of energy. When the stomach is empty, ghrelin is secreted. When the stomach is stretched, secretion stops. Gherlin has also been shown to have protective effects throughout the gastrointestinal tract. A team of researchers recently investigated the protective effect of gherlin in celiac disease induced in rats.
The research team included L.R. Nikoukar, F. Nabavizadeh, S.M. Mohamadi, A. Moslehi, G. Hassanzadeh, H. Nahrevanian, and S. Agah. They are affiliated with the Department of Anatomy, the Department of Liver and Gastrointestinal Research, and the Department of Physiology at the School of Medicine at Tehran University of Medical Sciences, and the Department of Parasitology at the Pasteur Institute of Iran, all in Tehran.
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The team divided twenty-four rat pups with celiac disease into 4 groups as follows: a normal non-celiac control group; a celiac disease group, which received 1.5 mg/g intragastric gliadin; pretreatment celiac group that received 50 ng/g intraperitoneal ghrelin before receiving 1.5 mg/g intragastric gliadin; a co-treatment celiac group that received 50 ng/g intraperitoneal ghrelin after receiving 1.5 mg/g intragastric gliadin). The team then charted the animals' weight gain.
The team assessed the results by comparing villus length, villus width, crypt depth and number of intraepithelial lymphocytes. They also compared tissue interferon-gamma as quantified by ELISA, and used ANOVA to compare results statistically.
Results showed that the disease group had shortened villi, while the villi in the pretreatment and co-treatment groups were as long as those of the control group. Crypt depth was increased in the celiac disease group, but became normal in the co-treatment group. The number of intraepithelial lymphocytes was substantially higher in the celiac disease group than the control group, while the team saw no difference between co-treatment and control groups.
Disease and control animals weighed equally at the end of the experiment, but ghrelin-treated animals had significantly gained more weight than either of the two other groups. Also, there was no significant difference between the groups in terms of interferon-gamma measurement.
From these results, the team concluded administration of ghrelin led to histological improvement of celiac disease, and that the effects were “more obvious if administered after exposure to gliadin.” Certainly, the revelation that a drug that is already part of the human body can allow a person with celiac disease to show totally normal blood tests and undamaged villi after consuming gluten is kind of exciting.
However, because gherlin is so closely tied with hunger and satiation responses, and because these results have not been borne out in humans, it is unclear how it might be used to treat human celiac disease.
Clearly, more research is needed, and will likely follow. Stay tuned for any important developments on the role of ghrelin in treating celiac disease.
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