Bronwyn A Kingwell

Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia

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Publications (212)1397.89 Total impact

  • JAMA The Journal of the American Medical Association 09/2015; DOI:10.1001/jama.2015.10811 · 35.29 Impact Factor
  • Atherosclerosis 07/2015; 241(1):e186. DOI:10.1016/j.atherosclerosis.2015.04.919 · 3.99 Impact Factor
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    ABSTRACT: Experimental studies suggest that angiotensin II plays a central role in the pathogenesis of abdominal aortic aneurysm. This trial aims to evaluate the efficacy of the angiotensin receptor blocker telmisartan in limiting the progression of abdominal aortic aneurysm. Telmisartan in the management of abdominal aortic aneurysm (TEDY) is a multicentre, parallel-design, randomised, double-blind, placebo-controlled trial with an intention-to-treat analysis. We aim to randomly assign 300 participants with small abdominal aortic aneurysm to either 40 mg of telmisartan or identical placebo and follow patients over 2 years. The primary endpoint will be abdominal aortic aneurysm growth as measured by 1) maximum infra-renal aortic volume on computed tomographic angiography, 2) maximum orthogonal diameter on computed tomographic angiography, and 3) maximum diameter on ultrasound. Secondary endpoints include change in resting brachial blood pressure, abdominal aortic aneurysm biomarker profile and health-related quality of life. TEDY is an international collaboration conducted from major vascular centres in Australia, the United States and the Netherlands. Currently, no medication has been convincingly demonstrated to limit abdominal aortic aneurysm progression. TEDY will examine the potential of a promising treatment strategy for patients with small abdominal aortic aneurysms. Australian and Leiden study centres: Australian New Zealand Clinical Trials Registry ACTRN12611000931976 , registered on 30 August 2011; Stanford study centre: NCT01683084 , registered on 5 September 2012.
    Trials 06/2015; 16(1):274. DOI:10.1186/s13063-015-0793-z · 1.73 Impact Factor
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    ABSTRACT: To determine whether alternating bouts of sitting and standing at work influences daily workplace energy expenditure (EE). 23 overweight/obese office workers (mean ± SD; age: 48.2 ± 7.9 yrs, BMI: 29.6 ± 4.0 kg/m2) undertook two, 5-day experimental conditions in an equal, randomised order. Participants wore a 'metabolic armband' (SenseWear Armband Mini) to estimate daily workplace EE (KJ/8 hours) while working in a: 1) seated work posture (SIT condition); or, 2) alternating between a standing and seated work posture every 30-min using a sit-stand workstation (STAND-SIT condition). To assess the validity of the metabolic armband, a criterion measure of acute EE (KJ/min; indirect calorimetry) was performed on day 4 of each condition. Standing to work acutely increased EE by 0.7 [0.3, 1.0] KJ/min (13%), relative to sitting (p=0.002). Compared to indirect calorimetry, the metabolic armband provided a valid estimate of EE while standing to work (mean bias: 0.1 [-0.3, 0.4] KJ/min) but modestly overestimated EE while sitting (p=0.005). Daily workplace EE was greatest during the STAND-SIT condition (mean condition difference [95% CI]: 76 [8, 144] KJ/8-hour workday, p=0.03). Intermittent standing at work can modestly increase daily workplace EE compared to seated work in overweight/obese office workers.
    Journal of Physical Activity and Health 04/2015; DOI:10.1123/jpah.2014-0420 · 1.95 Impact Factor
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    ABSTRACT: Aim: To compare the cumulative (three-day) effect of prolonged sitting on metabolic responses during a mixed meal tolerance test (MTT), with sitting that is regularly interrupted with brief bouts of light-intensity walking. Research design and methods: Overweight/obese adults (n=19) were recruited for a randomized, three-day, outpatient, crossover trial involving: 1) 7-hour days of uninterrupted sitting (SIT); and, 2) 7-hour days of sitting with light-intensity activity breaks [BREAKS; 2-minutes of treadmill walking (3.2 km/hour) every 20 minutes (total: 17 breaks/day)]. On days 1 and 3, participants underwent a MTT (75g carbohydrate, 50g fat), and the incremental area under the curve (iAUC) was calculated from hourly blood samples. GEE models were adjusted for gender, BMI, energy intake, treatment order and pre-prandial values to determine effects of time, condition and time x condition. Results: The glucose iAUC was 1.3 ± 0.5 and 1.5 ± 0.5 (mean difference ± SEM) higher in SIT compared with BREAKS on days 1 and 3 respectively (condition effect: P=0.001), with no effect of time (P=0.48) or time x condition (P=0.8). The insulin iAUC was also higher on both days in SIT (Day 1: ∆151 ± 73, Day 3: ∆91 ± 73, P=0.01), with no effect of time (P=0.52) or time x condition (P=0.71). There was no between-treatment difference in triglycerides iAUC. Conclusion: There were significant between-condition effects but no temporal change in metabolic responses to MTT, indicating that breaking up sitting over three days sustains, but does not enhance, the lowering of postprandial glucose and insulin.
    Clinical Science 03/2015; 129(2). DOI:10.1042/CS20140790 · 5.60 Impact Factor
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    ABSTRACT: Interleukin-6 (IL-6) plays a paradoxical role in inflammation and metabolism. The pro-inflammatory effects of IL-6 are mediated via IL-6 "trans-signaling," a process where the soluble form of the IL-6 receptor (sIL-6R) binds IL-6 and activates signaling in inflammatory cells that express the gp130 but not the IL-6 receptor. Here we show that trans-signaling recruits macrophages into adipose tissue (ATM). Moreover, blocking trans-signaling with soluble gp130Fc protein prevents high-fat diet (HFD)-induced ATM accumulation, but does not improve insulin action. Importantly, however, blockade of IL-6 trans-signaling, unlike complete ablation of IL-6 signaling, does not exacerbate obesity-induced weight gain, liver steatosis, or insulin resistance. Our data identify the sIL-6R as a critical chemotactic signal for ATM recruitment and suggest that selectively blocking IL-6 trans-signaling may be a more favorable treatment option for inflammatory diseases, compared with current treatments that completely block the action of IL-6 and negatively impact upon metabolic homeostasis. Copyright © 2015 Elsevier Inc. All rights reserved.
    Cell metabolism 03/2015; 21(3):403-16. DOI:10.1016/j.cmet.2015.02.006 · 17.57 Impact Factor
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    ABSTRACT: Brown adipose tissue (BAT) activation increases energy expenditure and may have therapeutic potential to combat obesity. The primary activating and adaptive signal for BAT is via β-adrenergic signalling. We previously demonstrated that human BAT is acutely responsive to oral administration of the sympathomimetic, ephedrine. Here we aimed to determine whether adaptive thermogenesis can be induced via chronic treatment with ephedrine. Twenty-three healthy young men, recruited from the general public in Melbourne, Australia, who were non-smokers, physically inactive and non-medicated with no prior history of cardiovascular disease or diabetes were recruited for this study. They were assigned to receive either 1.5 mg kg(-1) day(-1) ephedrine ('active' group; n = 12, age 23 ± 1 years, BMI 24 ± 1 kg/m(2)) or placebo (n = 11; 22 ± 2 years, 23 ± 2 kg/m(2)) for 28 days in a randomised (computer-generated random order sequence), placebo-controlled, parallel-group trial. Participants and all investigators were blinded to treatments. Body composition was measured before and after the intervention by dual energy X-ray absorptiometry. BAT activity, measured via (18)F-fluorodeoxyglucose positron emission tomography-computed tomography, in response to a single dose of 2.5 mg/kg ephedrine, was the primary outcome measure to be determined before and after the 28 day treatment period. Twenty-eight individuals were randomised and consented to the study. Twenty-three completed the trial and only these participants were included in the final analyses. After 28 days of treatment, the active group lost a significant amount of total body fat (placebo 1.1 ± 0.3 kg, ephedrine -0.9 ± 0.5 kg; p < 0.01) and visceral fat (placebo 6.4 ± 19.1 g, ephedrine -134 ± 43 g; p < 0.01), with no change in lean mass or bone mineral content compared with the placebo group. In response to acute ephedrine, BAT activity (change in mean standardised uptake value: placebo -3 ± 7%, ephedrine -22 ± 6%) and the increase in systolic blood pressure were significantly reduced (p < 0.05) in the active group compared with placebo. Chronic ephedrine treatment reduced body fat content, but this was not associated with an increase in BAT activity. Rather, chronic ephedrine suppressed BAT glucose disposal, suggesting that chronic ephedrine treatment decreased, rather than increased, BAT activity. Trial registration: NCT02236962 Funding: This study was funded by the National Health and Medical Research Council of Australia Program Grant (1036352) and the OIS scheme from the Victorian State Government.
    Diabetologia 03/2015; 58(5). DOI:10.1007/s00125-015-3543-6 · 6.67 Impact Factor
  • Andrew L Carey · Bronwyn A Kingwell
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    ABSTRACT: Obesity is a major risk factor for chronic disease. A new molecule serotonin outside of the brain reduces obesity energy expenditure. study in mice reveals that lowering levels of the signaling and its complications by increasing brown adipose tissue (BAT)
    Nature Medicine 02/2015; 21(2):114-6. DOI:10.1038/nm.3797 · 27.36 Impact Factor
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    ABSTRACT: Heat shock protein 72 (Hsp72) protects cells against a variety of stressors, and multiple studies have suggested that Hsp72 plays a cardioprotective role. As skeletal muscle Hsp72 overexpression can protect against high-fat diet (HFD)-induced insulin resistance, alterations in substrate metabolism may be a mechanism by which Hsp72 is cardioprotective. We investigated the impact of transgenically overexpressing (Hsp72 Tg) or deleting Hsp72 (Hsp72 KO) on various aspects of cardiac metabolism. Mice were fed a normal chow (NC) or HFD for 12 weeks from 8 weeks of age to examine the impact of diet-induced obesity on metabolic parameters in the heart. The HFD resulted in an increase in cardiac fatty acid oxidation and a decrease in cardiac glucose oxidation and insulin-stimulated cardiac glucose clearance; however, there was no difference in Hsp72 Tg or Hsp72 KO mice in these rates compared with their respective wild-type control mice. Although HFD-induced cardiac insulin resistance was not rescued in the Hsp72 Tg mice, it was preserved in the skeletal muscle, suggesting tissue-specific effects of Hsp72 overexpression on substrate metabolism. Comparison of two different strains of mice (BALB/c vs. C57BL/6J) also identified strain-specific differences in regard to HFD-induced cardiac lipid accumulation and insulin resistance. These strain differences suggest that cardiac lipid accumulation can be dissociated from cardiac insulin resistance. Our study finds that genetic manipulation of Hsp72 does not lead to alterations in metabolic processes in cardiac tissue under resting conditions, but identifies mouse strain-specific differences in cardiac lipid accumulation and insulin-stimulated glucose clearance.
    Cell Stress and Chaperones 01/2015; 20(3). DOI:10.1007/s12192-015-0571-6 · 3.16 Impact Factor
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    Heart, Lung and Circulation 01/2015; 24:S127-S128. DOI:10.1016/j.hlc.2015.06.033 · 1.44 Impact Factor
  • Alicia A Thorp · Bronwyn A Kingwell · Neville Owen · David W Dunstan
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    ABSTRACT: Objectives To examine whether the introduction of intermittent standing bouts during the workday using a height-adjustable workstation can improve subjective levels of fatigue, musculoskeletal discomfort and work productivity relative to seated work. Methods Overweight/obese office workers (n=23; age 48.2±7.9 years, body mass index 29.6±4 kg/m2) undertook two, 5-day experimental conditions in an equal, randomised (1:1) order. In a simulated office environment, participants performed their usual occupational tasks for 8 h/day in a: seated work posture (SIT condition); or interchanging between a standing and seated work posture every 30 min using an electric, height-adjustable workstation (STAND-SIT condition). Self-administered questionnaires measuring fatigue, musculoskeletal discomfort and work productivity were performed on day 5 of each experimental condition. Results Participants’ total fatigue score was significantly higher during the SIT condition (mean 67.8 (95% CI 58.8 to 76.7)) compared with the STAND-SIT condition (52.7 (43.8 to 61.5); p<0.001). Lower back musculoskeletal discomfort was significantly reduced during the STAND-SIT condition compared with the SIT condition (31.8% reduction; p=0.03). Despite concentration/focus being significantly higher during the SIT condition (p=0.006), there was a trend towards improved overall work productivity in favour of the STAND-SIT condition (p=0.053). Conclusions Transitioning from a seated to a standing work posture every 30 min across the workday, relative to seated work, led to a significant reduction in fatigue levels and lower back discomfort in overweight/obese office workers, while maintaining work productivity. Future investigations should be directed at understanding whether sustained use of height-adjustable workstations promote concentration and productivity at work. Trial Registration Number ACTRN12611000632998.
    Occupational and Environmental Medicine 08/2014; 71(11). DOI:10.1136/oemed-2014-102348 · 3.27 Impact Factor
  • Atherosclerosis 08/2014; 235(2):e106-e107. DOI:10.1016/j.atherosclerosis.2014.05.287 · 3.99 Impact Factor
  • Peter J. Meikle · Gerard Wong · Christopher K. Barlow · Bronwyn A. Kingwell
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    ABSTRACT: Lipidomics has developed rapidly over the past decade to the point where clinical application may soon be possible. Developments including high throughput technologies enable the simultaneous quantification of several hundred lipid species, thereby providing a global assessment of lipid metabolism. Given the key role of lipids in the pathophysiology of diabetes and cardiovascular disease, lipidomics has the potential to: i)significantly improve prediction of future disease risk,ii)inform on mechanisms of disease pathogenesis,iii)identify patient groups responsive to particular therapies andiv)more closely monitor response to therapy. Lipidomic analyses of both whole plasma and lipoprotein subfractions are integral to the current initiative to understand the relationships between lipoprotein composition and function and how these are affected by disease and treatment. This approach will not only aid in appropriate targeting of existing lipid lowering therapies such as statins and fibrates, but will be important in unravelling the controversies surrounding HDL-based therapies which have failed in clinical trials to date. The ultimate utility of lipidomics to clinical practice will depend firstly on the ability of risk prediction models incorporating lipidomic parameters to significantly improve upon conventional clinical risk markers in predicting future disease risk. Secondly, for widespread application, lipidomic-based measurements must be practical and accessible through standard pathology laboratories. This review will cover developments in lipidomics including methodology, bioinformatics/statistics, insights into disease pathophysiology, the effect of therapeutic interventions, the role of large clinical outcome trials in validating lipidomic approaches to patient management and potential applications in clinical practice.
    Pharmacology [?] Therapeutics 07/2014; 143(1). DOI:10.1016/j.pharmthera.2014.02.001 · 9.72 Impact Factor
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    ABSTRACT: Motivation: Recent advances in high-throughput lipid profiling by liquid chromatography electrospray ionization tandem mass spectrometry (LC-ESI-MS/MS) have made it possible to quantify hundreds of individual molecular lipid species (e.g. fatty acyls, glycerolipids, glycerophospholipids, sphingolipids) in a single experimental run for hundreds of samples. This enables the lipidome of large cohorts of subjects to be profiled to identify lipid biomarkers significantly associated with disease risk, progression and treatment response. Clinically, these lipid biomarkers can be used to construct classification models for the purpose of disease screening or diagnosis. However, the inclusion of a large number of highly correlated biomarkers within a model may reduce classification performance, unnecessarily inflate associated costs of a diagnosis or a screen and reduce the feasibility of clinical translation. An unsupervised feature reduction approach can reduce feature redundancy in lipidomic biomarkers by limiting the number of highly correlated lipids while retaining informative features to achieve good classification performance for various clinical outcomes. Good predictive models based on a reduced number of biomarkers are also more cost effective and feasible from a clinical translation perspective. Results: The application of LICRE to various lipidomic datasets in diabetes and cardiovascular disease demonstrated superior discrimination in terms of the area under the receiver operator characteristic curve while using fewer lipid markers when predicting various clinical outcomes. Availability and implementation: The MATLAB implementation of LICRE is available from∼gwong/LICRE
    Bioinformatics 06/2014; 30(19). DOI:10.1093/bioinformatics/btu381 · 4.98 Impact Factor
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    Bronwyn A Kingwell · M John Chapman · Anatol Kontush · Norman E Miller
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    ABSTRACT: Since the discovery in the 1970s that plasma levels of high-density lipoprotein cholesterol (HDL-C) are inversely associated with cardiovascular outcome, it has been postulated that HDL is anti-atherogenic and that increasing HDL-C levels is a promising therapeutic strategy. However, the recent failure of three orally active, HDL-C-raising agents has introduced considerable controversy, prompting the question of whether increasing the cholesterol cargo of HDL in a non-selective manner is an effective pharmacological approach for the translation of its atheroprotective and vasculoprotective activities. The interrelationships between HDL-C concentration, HDL particle number and levels of diverse HDL particle subpopulations of defined composition are complex, as are their relationships with reverse cholesterol transport and other anti-atherogenic functions. Such complexity highlights the incompleteness of our understanding of the biology of HDL particles. This article examines the HDL hypothesis in molecular and mechanistic terms, focusing on features that have been addressed, those that remain to be tested, and potential new targets for future pharmacological interventions.
    Nature Reviews Drug Discovery 05/2014; 13(6). DOI:10.1038/nrd4279 · 41.91 Impact Factor
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    ABSTRACT: Aim: To compare the effect of 7 h of prolonged sitting on resting blood pressure with a similar duration of sitting combined with intermittent brief bouts of light-intensity or moderate-intensity physical activity. Methods and results: Overweight/obese adults (n = 19; aged 45-65 years) were recruited for a randomized three-treatment crossover trial with a one-week washout between treatments: 1) uninterrupted sitting; 2) sitting with 2 min bouts of light-intensity walking at 3.2 km/h every 20 min; and, 3) sitting with 2 min bouts of moderate-intensity walking at between 5.8 and 6.4 km/h every 20 min. After an initial 2 h period seated, participants consumed a test meal (75 g carbohydrate, 50 g fat) and completed each condition over the next 5 h. Resting blood pressure was assessed oscillometrically every hour as a single measurement, 5 min prior to each activity bout. GEE models were adjusted for sex, age, BMI, fasting blood pressure and treatment order. After adjustment for potential confounding variables, breaking up prolonged sitting with light and moderate-intensity activity breaks was associated with lower systolic blood pressure [light: 120 ± 1 mmHg (estimated marginal mean ± SEM), P = 0.002; moderate: 121 ± 1 mmHg, P = 0.02], compared to uninterrupted sitting (123 ± 1 mmHg). Diastolic blood pressure was also significantly lower during both of the activity conditions (light: 76 ± 1 mmHg, P = 0.006; moderate: 77 ± 1 mmHg, P = 0.03) compared to uninterrupted sitting (79 ± 1 mmHg). No significant between-condition differences were observed in mean arterial pressure or heart rate. Conclusion: Regularly breaking up prolonged sitting may reduce systolic and diastolic blood pressure. Trial registration number: ACTRN12609000656235 ( TRIAL REGISTRATION DATE: August 4th 2009.
    Nutrition, metabolism, and cardiovascular diseases: NMCD 05/2014; 24(9). DOI:10.1016/j.numecd.2014.04.011 · 3.32 Impact Factor
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    ABSTRACT: Brown adipose tissue (BAT) is a potential therapeutic target to reverse obesity. The purpose of this study was to determine whether primary precursor cells isolated from human adult subcutaneous white adipose tissue (WAT) can be induced to differentiate in-vitro into adipocytes that express key markers of brown or beige adipose, and whether the expression level of such markers differs between lean and obese young adult males. Adipogenic precursor cells were isolated from lean and obese individuals from subcutaneous abdominal WAT biopsies. Cells were grown to confluence, differentiated for 2.5 weeks then harvested for measurement of gene expression and UCP1 protein. There was no difference between groups with respect to differentiation into adipocytes, as indicated by oil red-O staining, rates of lipolysis, and expression of adipogenic genes (FABP4, PPARG). WAT genes (HOXC9, RB1) were expressed equally in the two groups. Post differentiation, the beige adipose specific genes CITED1 and CD137 were significantly increased in both groups, but classic BAT markers ZIC1 and LHX8 decreased significantly. Cell lines from both groups also equally increased post-differentiation expression of the thermogenic-responsive gene PPARGC1A (PGC-1α). UCP1 gene expression was undetectable prior to differentiation, however after differentiation both gene expression and protein content were increased in both groups and were significantly greater in cultures from lean compared with obese individuals (p<0.05). Human subcutaneous WAT cells can be induced to attain BAT characteristics, but this capacity is reduced in WAT cells from obese individuals.
    PLoS ONE 03/2014; 9(3):e91997. DOI:10.1371/journal.pone.0091997 · 3.23 Impact Factor
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    ABSTRACT: To examine whether reductions in sitting time through alternating 30 minute bouts of sitting and standing can reduce postprandial glucose, insulin and triglyceride responses. Twenty-three overweight/obese sedentary office workers (17 males; 6 females; mean ± SD; age: 48.2 ± 7.9 yrs, BMI: 29.6 ± 4.0 kg/m) undertook two, short-term (5-day) experimental conditions in an equal, randomised (1:1) order. In a simulated office environment, participants performed typical occupational tasks for 8 hours/day while in a: 1) seated work posture (control condition); or, 2) interchanging between a seated and standing work posture every 30 minutes using an electric, height-adjustable workstation (intervention condition). Fasting and postprandial blood samples after a mixed test drink were collected hourly for 4 hours on Day 1 and 5 of each condition to assess serum insulin, plasma glucose and triglycerides. Dietary intake (KJ/d) and physical activity were standardised during each condition. The trial was registered with the Australian New Zealand Clinical Trials Registry (ACTRN12611000632998). Following adjustment for time (Day 1 and Day5), incremental area under the analyte time curve (iAUC) differed significantly between conditions for plasma glucose (P=0.007) but not for serum insulin or plasma triglycerides. Adjusted mean glucose iAUC was lowered by 11.1% after the intervention condition (6.38mmol/L·h [CI: 5.04, 7.71] ) relative to the control condition (7.18mmol/L·h [CI: 5.85, 8.52] ). No temporal changes (Day 1 vs Day 5) between conditions were observed. Alternating standing and sitting in 30 minute bouts results in modest beneficial effects on postprandial glucose responses in overweight/obese office workers.
    Medicine and science in sports and exercise 03/2014; 46(11). DOI:10.1249/MSS.0000000000000337 · 3.98 Impact Factor
  • Julian W Sacre · Garry L R Jennings · Bronwyn A Kingwell
    Hypertension 02/2014; 63(5). DOI:10.1161/HYPERTENSIONAHA.113.02277 · 6.48 Impact Factor
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    ABSTRACT: -Currently the relationship between circulating lipids and abdominal aortic aneurysm (AAA) is unclear. We conducted a lipidomic analysis to identify serum lipids associated with AAA presence. Secondary analyses assessed the ability of models incorporating lipidomic features to improve stratification of patient groups with and without AAA beyond traditional risk factors. -Serum lipids were profiled via liquid chromatography tandem mass spectrometry (LC-MS/MS) analysis of serum from 161 AAA patients and 168 peripheral artery disease controls. Binary logistic regression was used to identify AAA associated lipids. Classification models were created based on a combination of 1) traditional risk factors only, or 2) lipidomic features and traditional risk factors. Model performance was assessed using receiver operator characteristic (ROC) curves. Three diacylglycerols and 7 triacylglycerols were associated with AAA. Combining lipidomic features with traditional risk factors significantly improved stratification of AAA and PAD groups compared to consideration of traditional risk factors alone (mean area under the ROC curve (95% CI): 0.760 (0.756-0.763) and 0.719 (0.716-0.723) respectively; p<0.05). -A group of linoleic acid containing triacylglycerols and diacylglycerols were significantly associated with AAA presence. Inclusion of lipidomic features in multivariate analyses significantly improved prediction of AAA presence compared to traditional risk factors alone.
    Circulation Cardiovascular Genetics 01/2014; 7(1). DOI:10.1161/CIRCGENETICS.113.000343 · 4.60 Impact Factor

Publication Stats

7k Citations
1,397.89 Total Impact Points


  • 2005–2015
    • Baker IDI Heart and Diabetes Institute
      • • Diabetic Complications Division
      • • Metabolic and Vascular Physiology Research Group
      Melbourne, Victoria, Australia
    • University of Western Australia
      Perth City, Western Australia, Australia
  • 2004–2014
    • University of Melbourne
      • • Department of Physiology
      • • Department of Biochemistry and Molecular Biology
      Melbourne, Victoria, Australia
  • 1999–2014
    • Monash University (Australia)
      • Department of Physiology
      Melbourne, Victoria, Australia
  • 1991–2014
    • Alfred Hospital
      Melbourne, Victoria, Australia
  • 2009–2013
    • University of Vic
      Vic, Catalonia, Spain
  • 2008
    • National Neuroscience Institute
      • Department of Neurology
      Tumasik, Singapore
    • Singapore General Hospital
      • Department of Neurology
      Tumasik, Singapore
  • 2004–2008
    • Heart Research Institute
      • Free Radical Group
      Newtown, New South Wales, Australia
  • 2007
    • La Trobe University
      Melbourne, Victoria, Australia
    • Royal Melbourne Hospital
      Melbourne, Victoria, Australia
    • Université René Descartes - Paris 5
      Lutetia Parisorum, Île-de-France, France
  • 2006
    • George Washington University
      Washington, Washington, D.C., United States
    • Baker College, Australia
      Hornsby, New South Wales, Australia
  • 2003
    • Niigata University
      Niahi-niigata, Niigata, Japan