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Protein restriction slows the development and progression of Alzheimer's disease in mice

ABSTRACT: Untargeted lipidomics of 3xTg and non-transgenic mouse brain on protein restricted diet

INSTRUMENT(S): 6495C Triple Quadrupole LC/MS

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Judith Simcox

PROVIDER: MSV000094819 | MassIVE | Tue May 21 14:11:00 BST 2024

REPOSITORIES: MassIVE

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Protein restriction slows the development and progression of Alzheimer's disease in mice

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Nuclear tRNA sequestering slows aging by a mechanism similar to dietary restriction

Project description:Dietary restriction (DR) is the best-characterized intervention for slowing aging, and reduced signaling through the target of rapamycin (TOR) kinase is believed to be one of the key mechanisms by which DR extends life span in organisms from yeast to mammals. Here we describe a role for nuclear sequestration of tRNA in yeast replicative life span (RLS) extension from DR. DR causes the nuclear tRNA exporter Los1 to become depleted from the nucleus by a mechanism that requires the DNA damage response factor Rad53, and deletion of LOS1 or overexpression of RAD53 is sufficient to extend RLS. We further report that activation of the nitrogen responsive transcription factor Gln3 is the primary mechanism by which DR extends RLS. Gln3 is activated by both branches of the DR response and is required for life span extension. Overexpression of Gln3 extends RLS by approximately 50%. In order to identify potential factors acting to modulate longevity downstream of Los1, we used microarray analysis to compare the gene expression profiles of wild type and LOS1 knockout cells under non-restricted conditions cultured overnight prior to RNA isolation.

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GNPS - Protein restriction slows the progression of Alzheimer's disease in a mouse model

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Calorie/Dietary Restriction and Resveratrol in Female Drosophila Melanogaster Head/Thorax

Project description:Feeding resveratrol to Drosophila melanogaster extends lifespan. Studies of microarray show similarities between calorie/dietary restriction and resveratrol on both a gene expression and biological pathway level. 9 samples: 3 biological replicates each of normal diet, restricted diet and normal diet plus resveratrol

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An intermittent caloric restriction / medium fat diet protects liver from the progression of non-alcoholic fatty liver disease in C57BL/6J mice

Project description:Background & Aims: In this study, we investigated metabolic and molecular effects of weekly intervening 30% calorie restriction on long term natural progression of non-alcoholic fatty liver disease (NAFLD), which was induced by a medium fat diet. Methods: Male C57BL/6J mice of 9 weeks old received either (1) a control (C), (2) a calorie restricted (CR), (3) a medium fat (MF; 25%fat) or (4) an intermittent diet (ID), a weekly alternating diet consisting of calorie restriction and medium fat diet ad libitum until sacrifice at the age of 12 months. Various metabolic and molecular features of the liver were examined. Results: The ID regimen improved the status of a range of metabolic parameters and showed no progression to NAFLD: proper glucose tolerance, low hepatic triglyceride content, low plasma alanine aminotransferase and no abnormalities in its liver morphological features; similarly to that of CR. In contrast, the metabolic parameters in a number of the C and MF animals indicated development of NAFLD and hepatic fibrosis, which was positively correlated with body weight. Despite the metabolic phenotypes similarity, the liver gene expression profile of ID-fed mice did not reflect that of CR mice and resembled more to C and MF-fed mice with similar low body weight. Conclusions: Our study reveals that ID is beneficial for metabolic health and prevents the development of NAFLD in mice, with a gene expression profile similar to C and MF diet in a body weight-dependent manner.

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