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Articles on the benefits of eating a gluten-free diet
Gluten acting as an opioid
Gluten exorphin B5 stimulates prolactin secretion through opioid receptors located outside the blood-brain barrier.
Life Sci 2005 Feb 25;76(15):1713-9 (ISSN: 0024-3205)
Fanciulli G; Dettori A; Demontis MP; Tomasi PA; Anania V; Delitala G
Dipartimento-Struttura Clinica Medica-Patologia Speciale Medica, University of Sassari, Viale San Pietro 8, 07100 Sassari, Italy. gfanciu@uniss.it.
Gluten exorphin B5 (GE-B5) is a food-derived opioid peptide identified in digests of wheat gluten. We have recently shown that GE-B5 stimulates prolactin (PRL) secretion in rats; this effect is abolished by preadministration of the opioid receptor antagonist naloxone. However, since the structure of naloxone allows it to cross the blood-brain barrier (BBB) and antagonize opioid effects centrally as well as peripherally, it could not established, on the basis of those data, if GE-B5-induced PRL release is exerted through sites located inside or outside the BBB.
In this study, we sought to determine the site of action of GE-B5 on PRL secretion, by pretreating male rats with naloxone methobromide (NMB), an opioid antagonist that does not cross the BBB. Four groups of rats were given the following treatments: 1) intravenous vehicle; 2) intravenous GE-B5 (3 mg kg(-1) body weight); 3) intraperitoneal NMB (5 mg kg(-1) body weight), followed by vehicle; 4) NMB, followed by GE-B5.
Blood samples for PRL were taken at intervals for 40 minutes after vehicle or GE-B5 administration. GE-B5 stimulated PRL secretion; the effect was statistically significant at time 20. NMB preadministration completely abolished PRL response. Our experiment indicates that GE-B5 stimulates PRL secretion through opioid receptors located outside the BBB.
Since opioid peptides do not exert their effect on PRL secretion directly, but via a reduced dopaminergic tone, our data suggest that GE-B5 can modify brain neurotransmitter release without crossing the BBB.
(Medscape abstract)
Wheat ancestors lack the gluten immunogenic factors of modern wheat
Mapping of gluten T-cell epitopes in the bread wheat ancestors: implications for celiac disease [In Process Citation]
Gastroenterology 2005 Feb;128(2):393-401 (ISSN: 0016-5085)
Molberg O; Uhlen AK; Jensen T; Flaete NS; Fleckenstein B; Arentz-Hansen H; Raki M; Lundin KE; Sollid LM
Institute of Immunology, Rikshospitalet, University of Oslo, Oslo, Norway. oyvind.molberg@medisin.uio.no.
BACKGROUND AND AIMS: Celiac disease is a prevalent disorder characterized by a chronic intestinal inflammation driven by HLA-DQ2 or -DQ8-restricted T cells specific for ingested wheat gluten peptides. The dominant T-cell responses are to epitopes that cluster within a stable 33mer fragment formed by physiologic digestion of distinct alpha-gliadins.
Celiac disease is treated by excluding all gluten proteins from the diet. Conceivably, a diet based on baking-quality gluten from a wheat species that expresses no or few T-cell stimulatory gluten peptides should be equally well tolerated by the celiac patients and, importantly, also be beneficial for disease prevention.
METHODS: To identify baking quality, harmless wheat, we followed the evolution of the wheat back to the species that most likely have contributed the AA, BB, and DD genomes to the bread wheat. Gluten were extracted from a large collection of these ancient wheat species and screened for T-cell stimulatory gluten peptides.
RESULTS: Distinct differences in the intestinal T-cell responses to the diploid species were identified. Interestingly, we found that the fragments identical or equivalent to the immunodominant 33mer fragment are encoded by alpha-gliadin genes on the wheat chromosome 6D and thus absent from gluten of diploid einkorn (AA) and even certain cultivars of the tetraploid (AABB) pasta wheat. CONCLUSIONS: These findings have implications for celiac disease because they raise the prospect of identifying or producing by breeding wheat species with low or absent levels of harmful gluten proteins.
(Medscape abstract)
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