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We are analyzing https://link.springer.com/article/10.1007/s00125-004-1357-z.

Title:
Effect of maternal low-protein diet and taurine on the vulnerability of adult Wistar rat islets to cytokines | Diabetologia
Description:
Aims/hypothesis A maternal low-protein diet has been shown to induce an increased susceptibility of fetal islets to cytokines, but this effect can be avoided by maternal taurine supplementation. Here, we question whether these effects persist until adulthood in the offspring, despite the animal having a normal diet after weaning. Methods Pregnant Wistar rats received a diet of either 20% or 8% protein (control [C group] and recuperated [R group] respectively), which was or was not supplemented with taurine (control treated with taurine [CT group] and recuperated treated with taurine [RT group] respectively) during gestation and lactation. When the female offspring reached adulthood, an OGTT was performed. In a second stage, islets were isolated from these offspring, then pretreated or not with taurine, and subsequently treated with cytokines. Results Fasting glycaemia was higher (p<0.05) and insulinaemia was lower (p<0.01) in the R group than in the C group. Taurine supplementation decreased insulinaemia in the CT group and tended to increase it in the RT group. After the OGTT, glycaemia in R animals was not different from that in the C group, despite a blunted insulin response (p<0.05) which was restored by taurine. Supplementation in C-group mothers led to a weak glucose intolerance. In vitro, more apoptotic cells were observed in R islets after cytokines treatment (p<0.01). The addition of taurine to the culture medium in the R and C groups protected the islets from the cytokines (p<0.01). Maternal taurine supplementation decreased the sensitivity of islets in the RT group (p<0.01), but increased sensitivity in the CT group (p<0.01). Conclusions/interpretation The increased vulnerability of islets to cytokines due to a restriction of protein during fetal development was still evident when the offspring reached adulthood. The low-protein diet also induced hyperglycaemia in the presence of lower insulinaemia. Taurine supplementation protected adult islets of the R group from cytokine toxicity and restored the insulinaemia. However, unnecessary supplementation of taurine could have detrimental effects.
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Keywords {🔍}

taurine, diet, islets, group, insulin, google, scholar, fetal, glucose, pubmed, supplementation, diabetes, cytokines, normal, islet, effect, cas, early, cell, maternal, protein, cells, adult, offspring, apoptosis, plasma, rat, development, reusens, rats, control, animals, beta, secretion, remacle, increased, levels, article, life, type, vulnerability, lower, treatment, groups, sensitivity, pancreatic, reduced, level, low, effects,

Topics {✒️}

serum-free dme/f12 medium glucocorticoid-induced gad expression reverses interleukin-1beta inhibition adding ice-cold hbss nitric oxide synthase reverse-phase hplc method maternal low-protein diet neonatal beta-cell apoptosis tetramethyl-rhodamine-dutp incubated rat pancreatic beta-cells decrease cytokine-induced apoptosis osmotic-sensitive taurine pool taurine chloramine-induced inhibition poor placental function early life increases privacy choices/manage cookies selectively impairs sensitivity mediated neutrophil apoptosis early dietary supplementation early intrauterine environment c-group mothers led normalised serum concentration endothelial cells induced early growth retardation free access nuclear factor kappa low-protein diet low protein diet beta cell vulnerability cytokines article published maternal protein restriction cell surface antigens islet cell replication pancreatic beta cells beta cell damage beta cell populations skeletal muscle sensitivity streptozotocin-induced hyperglycaemia altered adipocyte properties apoptotic beta-cells protein-restricted diet islet cell apoptosis growth factor-ii growth factor ii cytokine-mediated apoptosis protein restriction early high intracellular concentrations maternal malnutrition affects plasma insulin concentration programmed trans-generationally

Questions {❓}

  • Lourenco R, Camilo ME (2002) Taurine: a conditionally essential amino acid in humans?
  • Trudeau JD, Dutz JP, Arany E, Hill DJ, Fieldus WE, Finegood WE (2000) Neonatal beta-cell apoptosis: a trigger for autoimmune diabetes?

Schema {🗺️}

WebPage:
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         headline:Effect of maternal low-protein diet and taurine on the vulnerability of adult Wistar rat islets to cytokines
         description:A maternal low-protein diet has been shown to induce an increased susceptibility of fetal islets to cytokines, but this effect can be avoided by maternal taurine supplementation. Here, we question whether these effects persist until adulthood in the offspring, despite the animal having a normal diet after weaning. Pregnant Wistar rats received a diet of either 20% or 8% protein (control [C group] and recuperated [R group] respectively), which was or was not supplemented with taurine (control treated with taurine [CT group] and recuperated treated with taurine [RT group] respectively) during gestation and lactation. When the female offspring reached adulthood, an OGTT was performed. In a second stage, islets were isolated from these offspring, then pretreated or not with taurine, and subsequently treated with cytokines. Fasting glycaemia was higher (p&lt;0.05) and insulinaemia was lower (p&lt;0.01) in the R group than in the C group. Taurine supplementation decreased insulinaemia in the CT group and tended to increase it in the RT group. After the OGTT, glycaemia in R animals was not different from that in the C group, despite a blunted insulin response (p&lt;0.05) which was restored by taurine. Supplementation in C-group mothers led to a weak glucose intolerance. In vitro, more apoptotic cells were observed in R islets after cytokines treatment (p&lt;0.01). The addition of taurine to the culture medium in the R and C groups protected the islets from the cytokines (p&lt;0.01). Maternal taurine supplementation decreased the sensitivity of islets in the RT group (p&lt;0.01), but increased sensitivity in the CT group (p&lt;0.01). The increased vulnerability of islets to cytokines due to a restriction of protein during fetal development was still evident when the offspring reached adulthood. The low-protein diet also induced hyperglycaemia in the presence of lower insulinaemia. Taurine supplementation protected adult islets of the R group from cytokine toxicity and restored the insulinaemia. However, unnecessary supplementation of taurine could have detrimental effects.
         datePublished:2004-03-10T00:00:00Z
         dateModified:2004-03-10T00:00:00Z
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            Adult islets
            Cytokines
            Maternal low-protein diet
            Taurine
            Internal Medicine
            Metabolic Diseases
            Human Physiology
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      headline:Effect of maternal low-protein diet and taurine on the vulnerability of adult Wistar rat islets to cytokines
      description:A maternal low-protein diet has been shown to induce an increased susceptibility of fetal islets to cytokines, but this effect can be avoided by maternal taurine supplementation. Here, we question whether these effects persist until adulthood in the offspring, despite the animal having a normal diet after weaning. Pregnant Wistar rats received a diet of either 20% or 8% protein (control [C group] and recuperated [R group] respectively), which was or was not supplemented with taurine (control treated with taurine [CT group] and recuperated treated with taurine [RT group] respectively) during gestation and lactation. When the female offspring reached adulthood, an OGTT was performed. In a second stage, islets were isolated from these offspring, then pretreated or not with taurine, and subsequently treated with cytokines. Fasting glycaemia was higher (p&lt;0.05) and insulinaemia was lower (p&lt;0.01) in the R group than in the C group. Taurine supplementation decreased insulinaemia in the CT group and tended to increase it in the RT group. After the OGTT, glycaemia in R animals was not different from that in the C group, despite a blunted insulin response (p&lt;0.05) which was restored by taurine. Supplementation in C-group mothers led to a weak glucose intolerance. In vitro, more apoptotic cells were observed in R islets after cytokines treatment (p&lt;0.01). The addition of taurine to the culture medium in the R and C groups protected the islets from the cytokines (p&lt;0.01). Maternal taurine supplementation decreased the sensitivity of islets in the RT group (p&lt;0.01), but increased sensitivity in the CT group (p&lt;0.01). The increased vulnerability of islets to cytokines due to a restriction of protein during fetal development was still evident when the offspring reached adulthood. The low-protein diet also induced hyperglycaemia in the presence of lower insulinaemia. Taurine supplementation protected adult islets of the R group from cytokine toxicity and restored the insulinaemia. However, unnecessary supplementation of taurine could have detrimental effects.
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      dateModified:2004-03-10T00:00:00Z
      pageStart:669
      pageEnd:675
      sameAs:https://doi.org/10.1007/s00125-004-1357-z
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         Adult islets
         Cytokines
         Maternal low-protein diet
         Taurine
         Internal Medicine
         Metabolic Diseases
         Human Physiology
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                  name:Université Catholique de Louvain
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                     name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
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                     name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
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                     name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
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                     name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
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            name:J. Tamarit-Rodriguez
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                  name:Universidad Complutense
                  address:
                     name:Department of Biochemistry, Faculty of Medicine, Universidad Complutense, Madrid, Spain
                     type:PostalAddress
                  type:Organization
            type:Person
            name:C. Remacle
            affiliation:
                  name:Université Catholique de Louvain
                  address:
                     name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
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      name:Universidad Complutense
      address:
         name:Department of Biochemistry, Faculty of Medicine, Universidad Complutense, Madrid, Spain
         type:PostalAddress
      name:Université Catholique de Louvain
      address:
         name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
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      name:S. Merezak
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            address:
               name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
               type:PostalAddress
            type:Organization
      name:B. Reusens
      affiliation:
            name:Université Catholique de Louvain
            address:
               name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
               type:PostalAddress
            type:Organization
      name:A. Renard
      affiliation:
            name:Université Catholique de Louvain
            address:
               name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
               type:PostalAddress
            type:Organization
      name:K. Goosse
      affiliation:
            name:Université Catholique de Louvain
            address:
               name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
               type:PostalAddress
            type:Organization
      name:L. Kalbe
      affiliation:
            name:Université Catholique de Louvain
            address:
               name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
               type:PostalAddress
            type:Organization
      name:M. T. Ahn
      affiliation:
            name:Université Catholique de Louvain
            address:
               name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
               type:PostalAddress
            type:Organization
      name:J. Tamarit-Rodriguez
      affiliation:
            name:Universidad Complutense
            address:
               name:Department of Biochemistry, Faculty of Medicine, Universidad Complutense, Madrid, Spain
               type:PostalAddress
            type:Organization
      name:C. Remacle
      affiliation:
            name:Université Catholique de Louvain
            address:
               name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
      name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
      name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
      name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
      name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
      name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium
      name:Department of Biochemistry, Faculty of Medicine, Universidad Complutense, Madrid, Spain
      name:Laboratory of Cell Biology, World Health Organization Collaborating Centre for the Biology of Development of the Endocrine Pancreas, Université Catholique de Louvain, Louvain-La-Neuve, Belgium

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