<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>The present studies were undertaken to examine
concomitant diet-induced changes in pancreatic
islets and cells of the gut immune system of
diabetes-prone BB rats in the period before classic
insulitis. Diabetes-prone (BBdp) and control non-diabetes
prone (BBc) BB rats were fed for ~ 17 days
either a mainly plant-based standard laboratory
rodent diet associated with high diabetes frequency,
NIH-07 (NIH) or a protective semipurified diet with
hydrolyzed casein (HC) as the amino acid source. By
about 7 weeks of age, NIH-fed BBdp rats had lower
plasma insulin and insulin/glucose ratio, lower
insulin content of isolated islets, lower basal levels
of NO but higher responsiveness of NO production
to IL-1<italic>β</italic> in cultured islets, and higher Con A
response and biosynthetic activities in mesenteric
lymphocytes than control rats fed the same diet. In
control rats, the HC diet caused only minor changes
in most variables, except for a decrease in oxidation
of L-[U−C14]glutamine in Peyer's patch (PP) cells and
an increase in protein biosynthesis in mesenteric
lymphocytes. In BBdp rats, however, the HC diet increased plasma insulin concentration, islet insulin/
protein ratio, and tended to normalize the basal
and IL-1<italic>β</italic>-stimulated NO production by cultured
islets. The HC diet decreased oxidation of L-[U−C14]glutamine in BBdp pancreatic islets, whereas
oxidation of L-[U−C14]glutamine in PP cells was
increased, and the basal [Methyl-H3] thymidine
incorporation in mesenteric lymphocytes was decreased.
These findings are compatible with the
view that alteration of nutrient catabolism in islet
cells as well as key cells of the gut immune system,
particularly changes in mitotic and biosynthetic
activities in mesenteric lymphocytes, as well as
basal and IL-1<italic>β</italic> stimulated NO production, participate
in the sequence of events leading to autoimmune
diabetes in BB rats. Thus, the protection afforded by feeding a hydrolysed casein-based diet
derives from alterations in both the target islet tissue
and key cells of the gut immune system in this
animal model of type 1 diabetes.</p>
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Int J Exp Diabetes Res. 2000; 1(2):121-130