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Article ; Online: Comprehensive Targeted Lipidomic Profiling for Research and Clinical Applications.

Huynh, Kevin / Duong, Thy / Mellett, Natalie A / Cinel, Michelle / Giles, Corey / Meikle, Peter J

Methods in molecular biology (Clifton, N.J.)

2023 Volume 2628, Page(s) 489–504

Abstract: Mass spectrometry remains one of the gold standard approaches in examining the lipidome in biological samples. Recently, advancements in chromatography and mass spectrometry approaches have enabled broad coverage of the lipidome. However, many ... ...

Abstract	Mass spectrometry remains one of the gold standard approaches in examining the lipidome in biological samples. Recently, advancements in chromatography and mass spectrometry approaches have enabled broad coverage of the lipidome. However, many limitations still exist, and lipidomic analysis often requires a fine balance between coverage of the lipidome, structural detail, and sample throughput. For biomedical and clinical research using human samples, the diversity and natural variation between different individuals necessitate larger sample numbers to identify significant associations with clinical outcomes and account for potential confounding factors. Here we describe a targeted lipidomics workflow that enables reproducible profiling of thousands of plasma samples in a systematic manner, while maintaining good structural detail and high coverage of the lipidome.
MeSH term(s)	Humans ; Lipidomics ; Lipids/chemistry ; Mass Spectrometry/methods ; Workflow
Chemical Substances	Lipids
Language	English
Publishing date	2023-02-13
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2978-9_29
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The potential of integrating human and mouse discovery platforms to advance our understanding of cardiometabolic diseases.

Jurrjens, Aaron W / Seldin, Marcus M / Giles, Corey / Meikle, Peter J / Drew, Brian G / Calkin, Anna C

eLife

2023 Volume 12

Abstract: Cardiometabolic diseases encompass a range of interrelated conditions that arise from underlying metabolic perturbations precipitated by genetic, environmental, and lifestyle factors. While obesity, dyslipidaemia, smoking, and insulin resistance are ... ...

Abstract	Cardiometabolic diseases encompass a range of interrelated conditions that arise from underlying metabolic perturbations precipitated by genetic, environmental, and lifestyle factors. While obesity, dyslipidaemia, smoking, and insulin resistance are major risk factors for cardiometabolic diseases, individuals still present in the absence of such traditional risk factors, making it difficult to determine those at greatest risk of disease. Thus, it is crucial to elucidate the genetic, environmental, and molecular underpinnings to better understand, diagnose, and treat cardiometabolic diseases. Much of this information can be garnered using systems genetics, which takes population-based approaches to investigate how genetic variance contributes to complex traits. Despite the important advances made by human genome-wide association studies (GWAS) in this space, corroboration of these findings has been hampered by limitations including the inability to control environmental influence, limited access to pertinent metabolic tissues, and often, poor classification of diseases or phenotypes. A complementary approach to human GWAS is the utilisation of model systems such as genetically diverse mouse panels to study natural genetic and phenotypic variation in a controlled environment. Here, we review mouse genetic reference panels and the opportunities they provide for the study of cardiometabolic diseases and related traits. We discuss how the post-GWAS era has prompted a shift in focus from discovery of novel genetic variants to understanding gene function. Finally, we highlight key advantages and challenges of integrating complementary genetic and multi-omics data from human and mouse populations to advance biological discovery.
MeSH term(s)	Animals ; Humans ; Mice ; Cardiovascular Diseases/genetics ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Obesity/genetics ; Phenotype ; Risk Factors
Language	English
Publishing date	2023-03-31
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.86139
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Article ; Online: Behavioral, metabolic, and lipidomic characterization of the 5xFADxTg30 mouse model of Alzheimer's disease.

Marshall, J P S / Huynh, K / Lancaster, G I / Ng, J / Collins, J M / Pernes, G / Liang, A / Featherby, T / Mellet, N A / Drew, B G / Calkin, A C / King, A E / Meikle, P J / Febbraio, M A / Adlard, P A / Henstridge, D C

iScience

2024 Volume 27, Issue 2, Page(s) 108800

Abstract: Alzheimer's disease (AD) is associated with both extracellular amyloid-β (Aβ) plaques and intracellular tau-containing neurofibrillary tangles (NFT). We characterized the behavioral, metabolic and lipidomic phenotype of the 5xFADxTg30 mouse model which ... ...

Abstract	Alzheimer's disease (AD) is associated with both extracellular amyloid-β (Aβ) plaques and intracellular tau-containing neurofibrillary tangles (NFT). We characterized the behavioral, metabolic and lipidomic phenotype of the 5xFADxTg30 mouse model which contains overexpression of both Aβ and tau. Our results independently reproduce several phenotypic traits described previously for this model, while providing additional characterization. This model develops many aspects associated with AD including frailty, decreased survival, initiation of aspects of cognitive decline and alterations to specific lipid classes and molecular lipid species in the plasma and brain. Notably, some sex-specific differences exist in this model and motor impairment with aging in this model does compromise the utility of the model for some movement-based behavioral assessments of cognitive function. These findings provide a reference for individuals interested in using this model to understand the pathology associated with elevated Aβ and tau or for testing potential therapeutics for the treatment of AD.
Language	English
Publishing date	2024-01-04
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2024.108800
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Article ; Online: Use of coronary computed tomography or polygenic risk scores to prompt action to reduce coronary artery disease risk: the CAPAR-CAD trial.

Verma, Kunal P / Marwick, Thomas H / Duarte, Carla / Meikle, Peter / Inouye, Mike / Carrington, Melinda J

American heart journal

2022 Volume 248, Page(s) 97–107

Abstract: ... endpoint is a change in low-density lipoprotein cholesterol (LDL-C) from baseline to 12 months ...

Abstract	Background: The traditional primary prevention paradigm for coronary artery disease (CAD) centers on population-based algorithms to classify individual risk. However, this approach often misclassifies individuals and leaves many in the 'intermediate' category, for whom there is no clear preferred prevention strategy. Coronary artery calcium (CAC) and polygenic risk scoring (PRS) are 2 contemporary tools for risk prediction to enhance the impact of effective management. Aims: To determine how these CAC and PRS impact adherence to pharmacotherapy and lifestyle measures in asymptomatic individuals with subclinical atherosclerosis. Methods: The CAPAR-CAD study is a multicenter, open, randomized controlled trial in Victoria, Australia. Participants are self-selected individuals aged 40 to 70 years with no prior history of cardiovascular disease (CVD), intermediate 10-year risk for CAD as determined by the pooled cohort equation (PCE), and CAC scores >0. All participants will have a health assessment, a full CT coronary angiogram (CTCA), and PRS calculation. They will then be randomized to receive their risk presented either as PCE and CAC, or PCE and PRS. The intervention includes e-Health coaching focused on risk factor management, health education and pharmacotherapy, and follow-up to augment adherence to a statin medication. The primary endpoint is a change in low-density lipoprotein cholesterol (LDL-C) from baseline to 12 months. The secondary endpoint is between-group differences in behavior modification and adherence to statin pharmacotherapy. Results: As of July 31, 2021, we have screened 1,903 individuals. We present the results of the 574 participants deemed eligible after baseline assessment.
MeSH term(s)	Calcium ; Coronary Angiography/methods ; Coronary Artery Disease/diagnostic imaging ; Coronary Artery Disease/genetics ; Coronary Vessels ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use ; Risk Assessment ; Risk Factors ; Tomography, X-Ray Computed
Chemical Substances	Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-02-24
Publishing country	United States
Document type	Journal Article ; Multicenter Study ; Randomized Controlled Trial
ZDB-ID	80026-0
ISSN	1097-6744 ; 0002-8703
ISSN (online)	1097-6744
ISSN	0002-8703
DOI	10.1016/j.ahj.2022.02.007
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Article ; Online: ACAD10 is not required for metformin's metabolic actions or for maintenance of whole-body metabolism in C57BL/6J mice.

Yew, Michael J / Heywood, Sarah E / Ng, Joe / West, Olivia M / Pal, Martin / Kueh, Andrew / Lancaster, Graeme I / Myers, Stephen / Yang, Christine / Liu, Yingying / Reibe, Saskia / Mellett, Natalie A / Meikle, Peter J / Febbraio, Mark A / Greening, David W / Drew, Brian G / Henstridge, Darren C

Diabetes, obesity & metabolism

2024 Volume 26, Issue 5, Page(s) 1731–1745

Abstract: Aim: Acyl-coenzyme A dehydrogenase family member 10 (ACAD10) is a mitochondrial protein purported to be involved in the fatty acid oxidation pathway. Metformin is the most prescribed therapy for type 2 diabetes; however, its precise mechanisms of action( ...

Abstract	Aim: Acyl-coenzyme A dehydrogenase family member 10 (ACAD10) is a mitochondrial protein purported to be involved in the fatty acid oxidation pathway. Metformin is the most prescribed therapy for type 2 diabetes; however, its precise mechanisms of action(s) are still being uncovered. Upregulation of ACAD10 is a requirement for metformin's ability to inhibit growth in cancer cells and extend lifespan in Caenorhabditis elegans. However, it is unknown whether ACAD10 plays a role in metformin's metabolic actions. Materials and methods: We assessed the role for ACAD10 on whole-body metabolism and metformin action by generating ACAD10KO mice on a C57BL/6J background via CRISPR-Cas9 technology. In-depth metabolic phenotyping was conducted in both sexes on a normal chow and high fat-high sucrose diet. Results: Compared with wildtype mice, we detected no difference in body composition, energy expenditure or glucose tolerance in male or female ACAD10KO mice, on a chow diet or high-fat, high-sucrose diet (p ≥ .05). Hepatic mitochondrial function and insulin signalling was not different between genotypes under basal or insulin-stimulated conditions (p ≥ .05). Glucose excursions following acute administration of metformin before a glucose tolerance test were not different between genotypes nor was body composition or energy expenditure altered after 4 weeks of daily metformin treatment (p ≥ .05). Despite the lack of a metabolic phenotype, liver lipidomic analysis suggests ACAD10 depletion influences the abundance of specific ceramide species containing very long chain fatty acids, while metformin treatment altered clusters of cholesterol ester, plasmalogen, phosphatidylcholine and ceramide species. Conclusions: Loss of ACAD10 does not alter whole-body metabolism or impact the acute or chronic metabolic actions of metformin in this model.
MeSH term(s)	Male ; Female ; Mice ; Animals ; Diabetes Mellitus, Type 2/metabolism ; Mice, Inbred C57BL ; Metformin/pharmacology ; Glucose/metabolism ; Insulin ; Ceramides ; Sucrose ; Diet, High-Fat/adverse effects
Chemical Substances	Metformin (9100L32L2N) ; Glucose (IY9XDZ35W2) ; Insulin ; Ceramides ; Sucrose (57-50-1)
Language	English
Publishing date	2024-02-13
Publishing country	England
Document type	Journal Article
ZDB-ID	1454944-x
ISSN	1463-1326 ; 1462-8902
ISSN (online)	1463-1326
ISSN	1462-8902
DOI	10.1111/dom.15484
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Article ; Online: Metabolic phenotyping of BMI to characterize cardiometabolic risk: evidence from large population-based cohorts.

Beyene, Habtamu B / Giles, Corey / Huynh, Kevin / Wang, Tingting / Cinel, Michelle / Mellett, Natalie A / Olshansky, Gavriel / Meikle, Thomas G / Watts, Gerald F / Hung, Joseph / Hui, Jennie / Cadby, Gemma / Beilby, John / Blangero, John / Moses, Eric K / Shaw, Jonathan E / Magliano, Dianna J / Meikle, Peter J

Nature communications

2023 Volume 14, Issue 1, Page(s) 6280

Abstract: Obesity is a risk factor for type 2 diabetes and cardiovascular disease. However, a substantial proportion of patients with these conditions have a seemingly normal body mass index (BMI). Conversely, not all obese individuals present with metabolic ... ...

Abstract	Obesity is a risk factor for type 2 diabetes and cardiovascular disease. However, a substantial proportion of patients with these conditions have a seemingly normal body mass index (BMI). Conversely, not all obese individuals present with metabolic disorders giving rise to the concept of "metabolically healthy obese". We use lipidomic-based models for BMI to calculate a metabolic BMI score (mBMI) as a measure of metabolic dysregulation associated with obesity. Using the difference between mBMI and BMI (mBMIΔ), we identify individuals with a similar BMI but differing in their metabolic health and disease risk profiles. Exercise and diet associate with mBMIΔ suggesting the ability to modify mBMI with lifestyle intervention. Our findings show that, the mBMI score captures information on metabolic dysregulation that is independent of the measured BMI and so provides an opportunity to assess metabolic health to identify "at risk" individuals for targeted intervention and monitoring.
MeSH term(s)	Humans ; Diabetes Mellitus, Type 2/epidemiology ; Diabetes Mellitus, Type 2/complications ; Body Mass Index ; Obesity/complications ; Obesity/epidemiology ; Obesity/metabolism ; Risk Factors ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/complications ; Metabolic Syndrome/epidemiology ; Metabolic Syndrome/complications
Language	English
Publishing date	2023-10-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-41963-7
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Article ; Online: The potential of integrating human and mouse discovery platforms to advance our understanding of cardiometabolic diseases

Aaron W Jurrjens / Marcus M Seldin / Corey Giles / Peter J Meikle / Brian G Drew / Anna C Calkin

eLife, Vol

2023 Volume 12

Abstract	Cardiometabolic diseases encompass a range of interrelated conditions that arise from underlying metabolic perturbations precipitated by genetic, environmental, and lifestyle factors. While obesity, dyslipidaemia, smoking, and insulin resistance are major risk factors for cardiometabolic diseases, individuals still present in the absence of such traditional risk factors, making it difficult to determine those at greatest risk of disease. Thus, it is crucial to elucidate the genetic, environmental, and molecular underpinnings to better understand, diagnose, and treat cardiometabolic diseases. Much of this information can be garnered using systems genetics, which takes population-based approaches to investigate how genetic variance contributes to complex traits. Despite the important advances made by human genome-wide association studies (GWAS) in this space, corroboration of these findings has been hampered by limitations including the inability to control environmental influence, limited access to pertinent metabolic tissues, and often, poor classification of diseases or phenotypes. A complementary approach to human GWAS is the utilisation of model systems such as genetically diverse mouse panels to study natural genetic and phenotypic variation in a controlled environment. Here, we review mouse genetic reference panels and the opportunities they provide for the study of cardiometabolic diseases and related traits. We discuss how the post-GWAS era has prompted a shift in focus from discovery of novel genetic variants to understanding gene function. Finally, we highlight key advantages and challenges of integrating complementary genetic and multi-omics data from human and mouse populations to advance biological discovery.
Keywords	systems genetics ; multi-omics ; genetic reference panels ; genome-wide association studies ; genetic mapping ; Hybrid Mouse Diversity Panel ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
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Article ; Online: Sublethal concentrations of clothianidin affect honey bee colony growth and hive CO

Meikle, William G / Adamczyk, John J / Weiss, Milagra / Ross, Janie / Werle, Chris / Beren, Eli

Scientific reports

2021 Volume 11, Issue 1, Page(s) 4364

Abstract: The effects of agricultural pesticide exposure upon honey bee colonies is of increasing interest to beekeepers and researchers, and the impact of neonicotinoid pesticides in particular has come under intense scrutiny. To explore potential colony-level ... ...

Abstract	The effects of agricultural pesticide exposure upon honey bee colonies is of increasing interest to beekeepers and researchers, and the impact of neonicotinoid pesticides in particular has come under intense scrutiny. To explore potential colony-level effects of a neonicotinoid pesticide at field-relevant concentrations, honey bee colonies were fed 5- and 20-ppb concentrations of clothianidin in sugar syrup while control colonies were fed unadulterated syrup. Two experiments were conducted in successive years at the same site in southern Arizona, and one in the high rainfall environment of Mississippi. Across all three experiments, adult bee masses were about 21% lower among colonies fed 20-ppb clothianidin than the untreated control group, but no effects of treatment on brood production were observed. Average daily hive weight losses per day in the 5-ppb clothianidin colonies were about 39% lower post-treatment than in the 20-ppb clothianidin colonies, indicating lower consumption and/or better foraging, but the dry weights of newly-emerged adult bees were on average 6-7% lower in the 5-ppb group compared to the other groups, suggesting a nutritional problem in the 5-ppb group. Internal hive CO
MeSH term(s)	Animals ; Bees/drug effects ; Bees/metabolism ; Bees/physiology ; Carbon Dioxide/metabolism ; Feeding Behavior ; Guanidines/toxicity ; Insecticides/toxicity ; Neonicotinoids/toxicity ; Social Behavior ; Thiazoles/toxicity
Chemical Substances	Guanidines ; Insecticides ; Neonicotinoids ; Thiazoles ; Carbon Dioxide (142M471B3J) ; clothianidin (2V9906ABKQ)
Language	English
Publishing date	2021-02-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-83958-8
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Article ; Online: Differential behaviour and gene expression in 3D cultures of femoral- and calvarial-derived human osteoblasts under a cyclic compressive mechanical load.

Itskovich, Yana / Meikle, Murray C / Cannon, Richard D / Farella, Mauro / Coates, Dawn E / Milne, Trudy J

European journal of oral sciences

2021 Volume 129, Issue 6, Page(s) e12818

Abstract: The aim of the study was to compare the response of calvarial and femoral osteoblasts cultured in a 3D hydrogel environment to cyclic compressive mechanical loading. Human foetal femoral and calvarial osteoblasts were encapsulated in a semi-synthetic ... ...

Abstract	The aim of the study was to compare the response of calvarial and femoral osteoblasts cultured in a 3D hydrogel environment to cyclic compressive mechanical loading. Human foetal femoral and calvarial osteoblasts were encapsulated in a semi-synthetic thiol-modified hyaluronan gelatin polyethylene glycol diacrylate (PEGDA) cross-linked HyStemC hydrogel. Constructs were subjected to a cyclic compressive strain of 33.4 kPa force every second for 5 s every hour for 6 h per day using FlexCell BioPress culture plates and compared to non-compressed constructs. Cell viability, mineralisation, and morphological changes were observed over 21 days. BMP2, ALP, COL1A1, COL2A1, and OCN gene expression levels were quantified. Encapsulated osteoblast numbers increased and formed hydroxyapatite over a 21-day period. Cell viability decreased under a cyclical strain when compared to cells under no strain. Femoral osteoblasts under strain expressed increased levels of BMP2 (53.9-fold) and COL1A1 (5.1-fold) mRNA compared to no strain constructs. Surprisingly, no BMP2 mRNA was detected in calvarial osteoblasts. Osteoblasts derived from endochondral (femoral) and intra-membranous (calvarial) processes behaved differently in 3D-constructs. We therefore recommend that site-specific osteoblasts be used for future bone engineering and bone replacement materials and further research undertaken to elucidate how site-specific osteoblasts respond to cyclic compressive loads.
MeSH term(s)	Durapatite ; Femur ; Gene Expression ; Humans ; Osteoblasts ; Stress, Mechanical
Chemical Substances	Durapatite (91D9GV0Z28)
Language	English
Publishing date	2021-07-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1224820-4
ISSN	1600-0722 ; 0909-8836
ISSN (online)	1600-0722
ISSN	0909-8836
DOI	10.1111/eos.12818
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Article: Lipidomic Profiling Identifies Serum Lipids Associated with Persistent Multisite Musculoskeletal Pain.

Ma, Canchen / Liu, Ming / Tian, Jing / Zhai, Guangju / Cicuttini, Flavia / Schooneveldt, Yvette L / Meikle, Peter J / Jones, Graeme / Pan, Feng

Metabolites

2022 Volume 12, Issue 3

Abstract: Lipid mediators have been suggested to have a role in pain sensitivity and response; however, longitudinal data on lipid metabolites and persistent multisite musculoskeletal pain (MSMP) are lacking. This study was to identify lipid metabolic markers for ... ...

Abstract	Lipid mediators have been suggested to have a role in pain sensitivity and response; however, longitudinal data on lipid metabolites and persistent multisite musculoskeletal pain (MSMP) are lacking. This study was to identify lipid metabolic markers for persistent MSMP. Lipidomic profiling of 807 lipid species was performed on serum samples of 536 participants from a cohort study. MSMP was measured by a questionnaire and defined as painful sites ≥4. Persistent MSMP was defined as having MSMP at every visit. Logistic regression was used with adjustment for potential confounders. The Benjamini-Hochberg method was used to control for multiple testing. A total of 530 samples with 807 lipid metabolites passed quality control. Mean age at baseline was 61.54 ± 6.57 years and 50% were females. In total, 112 (21%) of the participants had persistent MSMP. Persistent MSMP was significantly associated with lower levels of monohexosylceramide (HexCer)(d18:1/22:0 and d18:1/24:0), acylcarnitine (AC)(26:0) and lysophosphatidylcholine (LPC)(18:1 [sn1], 18:2 [sn1], 18:2 [sn2], and 15-MHDA[sn1] [104_sn1]) after controlling for multiple testing. After adjustment for age, sex, body mass index, comorbidities, and physical activity, HexCer(d18:1/22:0 and d18:1/24:0) and LPC(15-MHDA [sn1] [104_sn1]) were significantly associated with persistent MSMP [Odds Ratio (OR) ranging from 0.25-0.36]. Two lipid classes-HexCer and LPC-were negatively associated with persistent MSMP after adjustment for covariates (OR = 0.22 and 0.27, respectively). This study identified three novel lipid signatures of persistent MSMP, suggesting that lipid metabolism is involved in the pathogenesis of persistent pain.
Language	English
Publishing date	2022-02-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662251-8
ISSN	2218-1989
ISSN	2218-1989
DOI	10.3390/metabo12030206
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