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Peter Meikle   Dr.  Other 
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Peter Meikle published an article in December 2017.
Top co-authors See all
Jonathan Golledge

387 shared publications

The Vascular Biology Unit, Queensland Research Centre for Peripheral Vascular Disease, James Cook University, Townsville, Queensland, Australia

Ralph N. Martins

209 shared publications

Melanie Bahlo

132 shared publications

Division of Bioinformatics, The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia

Douglas J. Hilton

105 shared publications

Division of Molecular Medicine, The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia

Maria Fuller

78 shared publications

Publication Record
Distribution of Articles published per year 
(2008 - 2017)
Total number of journals
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Publications See all
Article 2 Reads 0 Citations Weight Loss and Exercise Alter the High-Density Lipoprotein Lipidome and Improve High-Density Lipoprotein Functionality ... Anmar A. Khan, Piyushkumar A. Mundra, Nora E. Straznicky, Pa... Published: 28 December 2017
Arteriosclerosis, Thrombosis, and Vascular Biology, doi: 10.1161/atvbaha.117.310212
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High-density lipoprotein (HDL) lipid composition and function may better reflect cardiovascular risk than HDL cholesterol concentration. This study characterized the relationships between HDL composition, metabolism, and function in metabolic syndrome (MetS) patients and how changes in composition after weight loss (WL) and exercise treatments are related to function.
Article 2 Reads 1 Citation Baseline serum phosphatidylcholine plasmalogen concentrations are inversely associated with incident myocardial infarcti... Joseph V. Moxon, Gerard Wong, Jacquelyn M. Weir, Natalie A. ... Published: 01 August 2017
Atherosclerosis, doi: 10.1016/j.atherosclerosis.2017.06.925
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Despite current best care, patients with peripheral artery disease (PAD) remain at high risk of myocardial infarction, and biomarkers to more accurately assess cardiovascular risk are needed. This study assessed the relationship between the serum lipidome and incident myocardial infarction in a cohort of PAD patients. 265 PAD patients were followed up for a median of 23 months, during which 18 people suffered a myocardial infarction. Fasting serum concentrations of 332 lipid species were measured via mass spectrometry and their association with incident myocardial infarction was assessed via Cox regression. Secondary analyses investigated prognostic potential of specific lipid species. Total serum concentrations of alkyl-phosphatidylcholine and alkenylphospatidylcholine (plasmalogen) lipids were inversely associated with incident myocardial infarction after adjusting for multiple testing (hazards ratio (95% confidence intervals): 0.43 (0.24–0.74); p = 0.032; and 0.28 (0.14–0.56), p = 0.010, respectively). Specifically, 10 alkenylphosphatidylcholine species and 6 alkyl-phosphatidylcholine species were negatively associated with incident myocardial infarction after adjusting for traditional risk factors and correcting for multiple testing (hazards ratios ranging from 0.07 to 0.51, p < 0.05). Incorporation of serum phosphatidylcholine plasmalogen species PC(P-40:6) concentration within analyses designed to determine subsequent myocardial infarction incidence led to an improvement in predictive accuracy compared to traditional risk factors alone. Serum concentrations of phosphatidylcholine plasmalogens and alkyl-phosphatidylcholines were negatively associated with incident myocardial infarction and have potential to act as novel prognostic markers in at-risk populations.
Article 2 Reads 2 Citations Lipidomic Profiles in Diabetes and Dementia Kevin Huynh, Ralph N. Martins, Peter J. Meikle Published: 17 July 2017
Journal of Alzheimer's Disease, doi: 10.3233/JAD-161215
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Article 1 Read 1 Citation The Effects of Long-Term Saturated Fat Enriched Diets on the Brain Lipidome Ryusuke Takechi, Satvinder Dhaliwal, Natalie A. Mellett, Cor... Published: 01 December 2016
PLOS ONE, doi: 10.1371/journal.pone.0166964
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The brain is highly enriched in lipids, where they influence neurotransmission, synaptic plasticity and inflammation. Non-pathological modulation of the brain lipidome has not been previously reported and few studies have investigated the interplay between plasma lipid homeostasis relative to cerebral lipids. This study explored whether changes in plasma lipids induced by chronic consumption of a well-tolerated diet enriched in saturated fatty acids (SFA) was associated with parallel changes in cerebral lipid homeostasis. Male C57Bl/6 mice were fed regular chow or the SFA diet for six months. Plasma, hippocampus (HPF) and cerebral cortex (CTX) lipids were analysed by LC-ESI-MS/MS. A total of 348 lipid species were determined, comprising 25 lipid classes. The general abundance of HPF and CTX lipids was comparable in SFA fed mice versus controls, despite substantial differences in plasma lipid-class abundance. However, significant differences in 50 specific lipid species were identified as a consequence of SFA treatment, restricted to phosphatidylcholine (PC), phosphatidylethanolamine (PE), alkyl-PC, alkenyl-PC, alkyl-PE, alkenyl-PE, cholesterol ester (CE), diacylglycerol (DG), phosphatidylinositol (PI) and phosphatidylserine (PS) classes. Partial least squares regression of the HPF/CTX lipidome versus plasma lipidome revealed the plasma lipidome could account for a substantial proportion of variation. The findings demonstrate that cerebral abundance of specific lipid species is strongly associated with plasma lipid homeostasis.
Article 1 Read 1 Citation cAMP Response Element Binding Protein1 Is Essential for Activation of Steroyl Co-Enzyme A Desaturase 1 (Scd1) in Mouse L... Nisha Antony, Jacqui R. Weir, Annie R. A. McDougall, Anthony... Published: 18 April 2013
PLOS ONE, doi: 10.1371/journal.pone.0059763
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Cyclic AMP Response Element-Binding Protein 1 (Creb1) is a transcription factor that mediates cyclic adenosine 3′, 5′-monophosphate (cAMP) signalling in many tissues. Creb1−/− mice die at birth due to respiratory failure and previous genome-wide microarray analysis of E17.5 Creb1−/− fetal mouse lung identified important Creb1-regulated gene targets during lung development. The lipogenic enzymes stearoyl-CoA desaturase 1 (Scd1) and fatty acid synthase (Fasn) showed highly reduced gene expression in Creb1−/− lungs. We therefore hypothesized that Creb1 plays a crucial role in the transcriptional regulation of genes involved in pulmonary lipid biosynthetic pathways during lung development. In this study we confirmed that Scd1 and Fasn mRNA levels were down regulated in the E17.5 Creb1−/− mouse lung while the lipogenic-associated transcription factors SrebpF1, C/ebpα and Pparγ were increased. In vivo studies using germline (Creb1−/−) and lung epithelial-specific (Creb1EpiΔ/Δ) Creb1 knockout mice showed strongly reduced Scd1, but not Fasn gene expression and protein levels in lung epithelial cells. In vitro studies using mouse MLE-15 epithelial cells showed that forskolin-mediated activation of Creb1 increased both Scd1 gene expression and protein synthesis. Additionally, MLE15 cells transfected with a dominant-negative ACreb vector blocked forskolin-mediated stimulation of Scd1 gene expression. Lipid profiling in MLE15 cells showed that dominant-negative ACreb suppressed forskolin-induced desaturation of ether linked lipids to produce plasmalogens, as well as levels of phosphatidylethanolamine, ceramide and lysophosphatidylcholine. Taken together these results demonstrate that Creb1 is essential for the induction and maintenance of Scd1 in developing fetal mouse lung epithelial cells.
Article 1 Read 0 Citations Skeletal Muscle Insulin Resistance Associated with Cholesterol-Induced Activation of Macrophages Is Prevented by High De... Andrew L. Siebel, Medini Reddy-Luthmoodoo, Alaina K. Natoli,... Published: 21 February 2013
PLOS ONE, doi: 10.1371/journal.pone.0056601
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Emerging evidence suggests that high density lipoprotein (HDL) may modulate glucose metabolism through multiple mechanisms including pancreatic insulin secretion as well as insulin-independent glucose uptake into muscle. We hypothesized that HDL may also increase skeletal muscle insulin sensitivity via cholesterol removal and anti-inflammatory actions in macrophages associated with excess adiposity and ectopic lipid deposition. Human primary and THP-1 macrophages were treated with vehicle (PBS) or acetylated low density lipoprotein (acLDL) with or without HDL for 18 hours. Treatments were then removed, and macrophages were incubated with fresh media for 4 hours. This conditioned media was then applied to primary human skeletal myotubes derived from vastus lateralis biopsies taken from patients with type 2 diabetes to examine insulin-stimulated glucose uptake. Conditioned media from acLDL-treated primary and THP-1 macrophages reduced insulin-stimulated glucose uptake in primary human skeletal myotubes compared with vehicle (primary macrophages, 168±21% of basal uptake to 104±19%; THP-1 macrophages, 142±8% of basal uptake to 108±6%; P<0.05). This was restored by co-treatment of macrophages with HDL. While acLDL increased total intracellular cholesterol content, phosphorylation of c-jun N-terminal kinase and secretion of pro- and anti-inflammatory cytokines from macrophages, none were altered by co-incubation with HDL. Insulin-stimulated Akt phosphorylation in human skeletal myotubes exposed to conditioned media was unaltered by either treatment condition. Inhibition of insulin-stimulated glucose uptake in primary human skeletal myotubes by conditioned media from macrophages pre-incubated with acLDL was restored by co-treatment with HDL. However, these actions were not linked to modulation of common pro- or anti-inflammatory mediators or insulin signaling via Akt.