Angela C. Rutledge
University of Western Ontario
18 Papers
16 Citations
Angela C. Rutledge is an academic researcher from University of Western Ontario. The author has contributed to research in topics: Apolipoprotein B & Unfolded protein response. The author has an hindex of 8, co-authored 13 publications. Previous affiliations of Angela C. Rutledge include University of Toronto & London Health Sciences Centre.
Chat about Author
Papers
Fructose: a highly lipogenic nutrient implicated in insulin resistance, hepatic steatosis, and the metabolic syndrome
TL;DR: This review highlights recent findings in fructose feeding studies in both human and animal models with a focus on the molecular and biochemical mechanisms that underlie the development of insulin resistance, hepatic steatosis, and the metabolic syndrome.
418
Fructose and the metabolic syndrome: pathophysiology and molecular mechanisms.
Angela C. Rutledge,Khosrow Adeli +1 more
TL;DR: Fructose-induced perturbations in cell signaling and inflammatory cascades in insulin-sensitive tissues are discussed and the roles of cellular signaling molecules including nuclear factor kappa B (NFkB), tumor necrosis factor alpha (TNF-alpha), c-Jun amino terminal kinase 1 (JNK-1) and protein tyrosine phosphatase 1B (PTP-1B) are addressed.
Glucosamine-induced endoplasmic reticulum stress attenuates apolipoprotein B100 synthesis via PERK signaling
TL;DR: It is reported that glucosamine also regulates apoB100 protein synthesis via ER-stress-induced PERK activation, suggesting that in addition to the induction of ER-associated degradation and other degradative pathways, ER stress is associated with suppression ofApoB synthesis via a PERK-dependent mechanism.
51
Mechanisms of glucosamine-induced suppression of the hepatic assembly and secretion of apolipoprotein B-100-containing lipoproteins.
TL;DR: Interestingly, the glucosamine-induced posttranslational reduction in apoB-100 secretion could be partially prevented by treatment with desferrioxamine or vitamin E, suggesting that cotranslational glucosamines treatment may cause defects in apob-100 N-linked glycosylation and folding, resulting in enhanced proteasomal degradation.
49
Vitamin B 12 deficiency and hyperhomocysteinaemia in outpatients with stroke or transient ischaemic attack: a cohort study at an academic medical centre.
Shamon Ahmed,Chrysi Bogiatzi,Daniel G. Hackam,Angela C. Rutledge,Luciano A. Sposato,Alexander V. Khaw,Jennifer Mandzia,Mahmoud Reza Azarpazhoo,Vladimir Hachinski,J. David Spence +9 more
TL;DR: Despite a decline in the referral area since 2009, B12Def, MetB12Def and HHcy remain common in patients with stroke/TIA, and all patients with Stroke and TIA should have their serum B12 and tHcy measured.
47