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Linda M. Sanderson

Researcher at Wageningen University and Research Centre

Publications -  8
Citations -  598

Linda M. Sanderson is an academic researcher from Wageningen University and Research Centre. The author has contributed to research in topics: Peroxisome proliferator-activated receptor & Regulation of gene expression. The author has an hindex of 5, co-authored 8 publications receiving 550 citations.

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Comprehensive analysis of PPARalpha-dependent regulation of hepatic lipid metabolism by expression profiling.

TL;DR: In this paper, the power of transcriptional profiling to uncover novel PPARα-regulated genes and pathways in liver was illustrated, using an in silico screening approach, one or more PPAR response elements were identified in each of these genes.
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Peroxisome proliferator-activated receptor β/δ (PPARβ/δ) but not PPARα serves as a plasma free fatty acid sensor in liver.

TL;DR: In this article, the authors investigated the similarities in gene induction between Wy14643 and fasting and showed that upregulation of gene expression by PPARbeta/delta is sensitive to plasma free fatty acid (FFA) levels.
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Effect of synthetic dietary triglycerides: a novel research paradigm for nutrigenomics.

TL;DR: The effects of dietary unsaturated fatty acids on hepatic gene expression are almost entirely mediated by PPARα and mimic those of synthetic PPAR α agonists in terms of regulation of target genes and molecular mechanism.
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Transcriptional profiling reveals divergent roles of PPARalpha and PPARbeta/delta in regulation of gene expression in mouse liver.

TL;DR: The analysis of whole genome transcriptional profiling and analysis of plasma and liver metabolites indicates that PPARbeta/delta governs glucose utilization and lipoprotein metabolism and has an important anti-inflammatory role in liver.

ResearchArticle Comprehensive Analysis of PPARα-Dependent Regulation of Hepatic Lipid Metabolism by Expression Profiling

TL;DR: In wild-type mice fed a high fat diet, the decrease in hepatic lipids following treatment with the PPAR α agonist Wy14643 was paralleled by significant up-regulation of Pnpla2, Lipe, and Mgll, suggesting that induction of triglyceride hydrolysis may contribute to the anti-steatotic role of PPARα.