41 research outputs found
Feeding a Protective Hydrolysed Casein Diet to Young Diabetes-prone BB Rats Affects Oxidation of L[U−C14] glutamine in Islets and Peyer's Patches, Reduces Abnormally High Mitotic Activity in Mesenteric Lymph Nodes, Enhances Islet Insulin and Tends to Normalize NO Production
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-1β 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-1β-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-1β 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
Effets sur la biosynthèse et la sécrétion d'insuline des esters de l'acide succinique, des esters de monosaccharides et des analogues du méglitinide dans des îlots de rats normaux et diabétiques
Doctorat en sciences médicalesinfo:eu-repo/semantics/nonPublishe
Effets sur la biosynthèse et la sécrétion d'insuline des esters de l'acide succinique, des esters de monosaccharides et des analogues du méglitinide dans des îlots de rats normaux et diabétiques
Doctorat en sciences médicalesinfo:eu-repo/semantics/nonPublishe
Stimulation of insulin release and biosynthetic activity by 1, 2, 3-tri(methylsuccinyl)glycerol ester in pancreatic islets of Goto-Kakizaki rats
SCOPUS: ar.jinfo:eu-repo/semantics/publishe
Spécificité isomérique et anomérique de I'action insulinotrope du glucose pentaacétate
info:eu-repo/semantics/publishe
Isomeric and anomeric specificity of the insulnotropic action of glucose pentaacetate
info:eu-repo/semantics/publishedComm. 35th Annual Meeting of the European Association for the Study of Diabetes - Brussels (Belgium), 30.09.199
Effect of α-D-glucose pentaacetate on biosynthetic activity in pancreatic islets from normal and hereditarily diabetic GK rats
SCOPUS: ar.jinfo:eu-repo/semantics/publishe
Insulinotropic action of Azadirachta indica leaf and bark extracts: Comparison with azadirachtin
SCOPUS: ar.jinfo:eu-repo/semantics/publishe
Long-term effects of glibenclamide and nateglinide upon pancreatic islet function in normal and diabetic rats
Cet article se trouve dans le supplément 4 du n°25 de la revue Diabetes and Metabolism, page A23info:eu-repo/semantics/nonPublishe
Stimulation of biosynthetic activity by novel succinate esters in islets from normal and GK rats
info:eu-repo/semantics/nonPublishe