Russell P Tracy

University of Cambridge, Cambridge, England, United Kingdom

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Publications (492)3720.51 Total impact

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    ABSTRACT: High-sensitivity C-reactive protein (hs-CRP) has been associated with coronary heart disease (CHD) in numerous but not all observational studies, and whether low levels of low-density lipoprotein cholesterol (LDL-C) alter this association is unknown. In the Multi-Ethnic Study of Atherosclerosis (2000-2012), we prospectively assessed the association of hs-CRP concentrations with incident CHD in participants who did not receive lipid-lowering therapy, as well as in those with LDL-C concentrations less than 130 mg/dL (n = 3,106) and those with LDL-C concentrations of 130 mg/dL or greater (n = 1,716) at baseline (2000-2002). Cox proportional hazard analyses were used to assess the associations after adjustment for socioeconomic status, traditional risk factors, body mass index, diabetes, aspirin use, kidney function, and coronary artery calcium score. Loge hs-CRP was associated with incident CHD in participants with LDL-C concentrations of 130 mg/dL or higher (hazard ratio (HR) = 1.29, 95% confidence interval (CI): 1.05, 1.60) but not in those with LDL-C concentrations less than 130 mg/dL (HR = 0.88, 95% CI: 0.74, 1.05; P for interaction = 0.003). As a whole, loge hs-CRP was not associated with incident CHD in participants who had not received lipid-lowering therapy at baseline (HR = 1.05, 95% CI: 0.92, 1.20) and who had mean LDL-C concentrations less than 130 mg/dL. These findings suggest that LDL-C concentrations might be a moderator of the contribution of hs-CRP to CHD.
    American Journal of Epidemiology 11/2015; DOI:10.1093/aje/kwv144 · 5.23 Impact Factor
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    de Vries PS · Chasman DI · Maria Sabater-Lleal · Chen MH · Jennifer E Huffman · Maristella Steri · Weihong Tang · Alexander Teumer · Marioni RE · Vera Grossmann · [...] · Francesco Cucca · Russell Tracy · Hugh Watkins · Reiner AP · Folsom AR · Ridker PM · O'Donnell CJ · Smith NL · Strachan DP · Abbas Dehghan ·
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    ABSTRACT: Genome-wide association studies have previously identified 23 genetic loci associated with circulating fibrinogen concentration. These studies used HapMap imputation and did not examine the X chromosome. 1000 Genomes imputation provides better coverage of uncommon variants, and includes indels. We conducted a genome-wide association analysis of 34 studies imputed to the 1000 Genomes Project reference panel and including ∼120,000 participants of European ancestry (95,806 participants with data on the X chromosome). Approximately 10.7 million SNPs and 1.2 million indels were examined. We identified 41 genome-wide significant fibrinogen loci of which 18 were newly identified. There were no genome-wide significant signals on the X chromosome. The lead variants of 5 significant loci were indels. We further identified 6 additional independent signals, including 3 rare variants, at two previously characterized loci: FGB and IRF1. Together the 41 loci explain 3% of the variance in plasma fibrinogen concentration.
    Human Molecular Genetics 11/2015; DOI:10.1093/hmg/ddv454 · 6.39 Impact Factor
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    ABSTRACT: Rationale: Pulmonary arterial hypertension (PAH) is a rare progressive disease of the pulmonary vasculature that is characterized by endothelial dysfunction, inflammation and right ventricular dysfunction. Objectives: The main objective was to determine whether endothelial, inflammatory, and cardiac biomarkers would be associated with the World Health Organization (WHO) functional assessment and survival in patients with PAH. Methods: We performed a retrospective cohort study of PAH patients enrolled in the clinical trial ASA-STAT. Biomarkers (N-terminal fragment of pro-BNP (NT-pro-BNP), von Willebrand factor (vWF), soluble P-selectin, C-reactive protein, total and HDL cholesterol, triglycerides, tumor necrosis factor, interleukin-6, beta-thromboglobulin and thromboxane B2) were measured at baseline. Patients from the study were followed until lung transplantation, death, or August 1, 2013. Ordinal logistic regression and Cox regression analyses were performed. Measurements and main results: Sixty-five PAH patients were enrolled. The mean age was 51 years and 86% were female. Higher vWF activity, lower high-density lipoprotein cholesterol and higher thromboxane B2 levels were associated with worse WHO functional class after adjustment for age, sex and etiology of PAH. Higher NT-pro-BNP levels, lower vWF activity, and lower total cholesterol were associated with an increased risk of death or lung transplant after adjustment for age, sex, etiology of PAH and 6-minute walk distance. Conclusions: In patients with PAH, lower vWF activity and cholesterol levels and higher NT-pro-BNP levels at baseline were associated with an increased risk of death or transplantation. Clinical Trial registered with (NCT00384865) Primary Source of Funding: The study was funded by National Institutes of Health (NIH) grants R01HL082895 and R01HL082895-S1 and K24HL103844.
    Annals of the American Thoracic Society 10/2015; DOI:10.1513/AnnalsATS.201508-543OC
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    ABSTRACT: Disease incidences increase with age, but the molecular characteristics of ageing that lead to increased disease susceptibility remain inadequately understood. Here we perform a whole-blood gene expression meta-analysis in 14,983 individuals of European ancestry (including replication) and identify 1,497 genes that are differentially expressed with chronological age. The age-associated genes do not harbor more age-associated CpG-methylation sites than other genes, but are instead enriched for the presence of potentially functional CpG-methylation sites in enhancer and insulator regions that associate with both chronological age and gene expression levels. We further used the gene expression profiles to calculate the 'transcriptomic age' of an individual, and show that differences between transcriptomic age and chronological age are associated with biological features linked to ageing, such as blood pressure, cholesterol levels, fasting glucose, and body mass index. The transcriptomic prediction model adds biological relevance and complements existing epigenetic prediction models, and can be used by others to calculate transcriptomic age in external cohorts.
    Nature Communications 10/2015; 6:8570. DOI:10.1038/ncomms9570 · 11.47 Impact Factor

  • Arthritis and Rheumatology 10/2015; DOI:10.1002/art.39471
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    ABSTRACT: Objective: Distinct lymphocyte subpopulations have been implicated in the regulation of glucose homeostasis and obesity-associated inflammation in mouse models of insulin resistance. Information on the relationships of lymphocyte subpopulations with type 2 diabetes remain limited in human population-based cohort studies. Methods: Circulating levels of innate (γδ T, natural killer (NK)) and adaptive immune (CD4+ naive, CD4+ memory, Th1, and Th2) lymphocyte subpopulations were measured by flow cytometry in the peripheral blood of 929 free-living participants of the Multi-Ethnic Study of Atherosclerosis (MESA). Cross-sectional relationships of lymphocyte subpopulations with type 2 diabetes (n = 154) and fasting glucose and insulin concentrations were evaluated by generalized linear models. Results: Each standard deviation (SD) higher CD4+ memory cells was associated with a 21% higher odds of type 2 diabetes (95% CI: 1-47%) and each SD higher naive cells was associated with a 22% lower odds (95% CI: 4-36%) (adjusted for age, gender, race/ethnicity, and BMI). Among participants not using diabetes medication, higher memory and lower naive CD4+ cells were associated with higher fasting glucose concentrations (p<0.05, adjusted for age, sex, and race/ethnicity). There were no associations of γδ T, NK, Th1, or Th2 cells with type 2 diabetes, glucose, or insulin. Conclusions: A higher degree of chronic adaptive immune activation, reflected by higher memory and lower naive CD4+ cells, was positively associated with type 2 diabetes. These results are consistent with a role of chronic immune activation and exhaustion augmenting chronic inflammatory diseases, and support the importance of prospective studies evaluating adaptive immune activation and type 2 diabetes.
    PLoS ONE 10/2015; 10(10):e0139962. DOI:10.1371/journal.pone.0139962 · 3.23 Impact Factor
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    ABSTRACT: Obesity is linked to type 2 diabetes (T2D) and cardiovascular diseases; however, the underlying molecular mechanisms remain unclear. We aimed to identify obesity-associated molecular features that may contribute to obesity-related diseases. Using circulating monocytes from 1,264 Multi-Ethnic Study of Atherosclerosis participants, we quantified the transcriptome and epigenome. We discovered that alterations in a network of co-expressed cholesterol metabolism genes are a signature feature of obesity and inflammatory stress. This network included 11 body mass index (BMI)-associated genes related to sterol uptake (↑LDLR, ↓MYLIP), synthesis (↑SCD, FADS1, HMGCS1, FDFT1, SQLE, CYP51A1, SC4MOL) and efflux (↓ABCA1, ABCG1) - producing a molecular profile expected to increase intracellular cholesterol. Importantly, these alterations were associated with T2D and coronary artery calcium (CAC), independent from cardiometabolic factors including serum lipid profiles. This network mediated the associations between obesity and T2D/CAC. Several genes in the network harbored CpG dinucleotides (e.g. ABCG1/cg06500161) which overlapped ENCODE-annotated regulatory regions, and had methylation profiles that mediated the associations between BMI/inflammation and expression of their cognate genes. Taken together with several lines of previous experimental evidence, these data suggest that alterations of the cholesterol metabolism gene network represent a molecular link between obesity/inflammation and T2D/CAC. © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
    Diabetes 10/2015; 64(10):3464-3474. DOI:10.2337/db14-1314 · 8.10 Impact Factor

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    ABSTRACT: Objective: We evaluated whether metabolic syndrome (MetS) is associated with an increased incidence of lower extremity peripheral artery disease (PAD) in community dwelling people free of clinical cardiovascular disease at baseline. We assessed whether higher levels of inflammatory biomarkers may mediate the association of MetS with incident PAD. Methods: MetS was defined at baseline as the presence of three or more of the following components: elevated waist circumference, triglycerides ≥150 mg/dL, reduced high-density lipoprotein (HDL) cholesterol, blood pressure ≥130/85 mm Hg or taking blood pressure medication, and fasting glucose ≥100 mg/dL and <126 mg/dL. People with diabetes were excluded. Incident New PAD was defined among people with a normal ankle brachial index (ABI) at baseline (i.e. baseline ABI of 0.90 to 1.40) and consisted of one of the following outcomes during 3-year follow-up: ABI decline to < 0.90 combined with a decline ≥0.15 or medical record confirmed PAD outcome. Multivariable Poisson regression was used to estimate the association between MetS and incident PAD. Results: Among 4817 participants without PAD at baseline, 1382 (29%) had MetS. Adjusting for age, sex, race, smoking, physical activity, low-density lipoprotein cholesterol, baseline ABI, and other confounders, 23/1382 (1.7%) people with MetS developed PAD vs. 30/3435 (0.87%) people without MetS (risk ratio = 1.78 [95% Confidence Interval (CI), 1.04 to 2.82], P = 0.031). Adjusting for C-reactive protein, fibrinogen, or interleukin-6 did not attenuate this association. Conclusion: People free of clinical cardiovascular disease with MetS are at increased risk for PAD. Our findings suggest that this association is not mediated by inflammation.
    Atherosclerosis 09/2015; 243(1):198-203. DOI:10.1016/j.atherosclerosis.2015.08.044 · 3.99 Impact Factor
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    ABSTRACT: Background: High-density lipoprotein (HDL) particles have properties beyond reverse cholesterol transport. We hypothesized that their protection extends to inflammation-related disease. The predictive value of HDL particle subclasses and inflammatory markers was studied for noncardiovascular, noncancer chronic inflammation-related death and hospitalization, and for incident cardiovascular disease (CVD). Methods and results: A multiethnic, multicenter, prospective observational study was conducted in 6475 men and women (aged 45 to 84 years) free of known CVD at baseline with median follow-up of 10.1 years. Fasting venous samples were analyzed for baseline lipid profile and lipoprotein particles. We focused on the HDL family of variables (small-, medium-, and large-diameter HDL particles and HDL cholesterol). Analyses identified the sum of small- plus medium-diameter HDL particles as important. Small- plus medium-diameter HDL particles were inversely associated with diagnostic code-based noncardiovascular, noncancer chronic inflammation-related death and hospitalization (n=1054) independent of covariates: relative risk per SD 0.85 (95% CI: 0.79 to 0.91, P<0.0001). Small- plus medium-diameter HDL particles were also associated with adjudicated fatal and nonfatal coronary heart disease events (n=423): relative risk per SD 0.88 (95% CI 0.77 to 0.98, P=0.02). Conclusions: Small- plus medium-diameter HDL particles are an independent predictor for noncardiovascular, noncancer chronic inflammation-related death and hospitalization and for coronary heart disease events in subjects initially free of overt CVD. These findings support the hypothesis that smaller HDL particles of diameter <9.4 nm have anti-inflammatory properties in the general population.
    Journal of the American Heart Association 09/2015; 4(9). DOI:10.1161/JAHA.115.002295 · 4.31 Impact Factor
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    ABSTRACT: Background: HIV infection and associated immune activation predict risk of cardiovascular disease (CVD) in resource-rich areas. Less is known about these relationships in sub-Saharan Africa. Methods: Beginning in 2005, we enrolled subjects in southwestern Uganda into a cohort at anti-retroviral therapy (ART) initiation. Multiple immune activation measures were assessed pre-ART and 6 months after ART initiation. Beginning in 2013, participants over 40 years underwent metabolic profiling including hemoglobin A1c, lipids, and carotid ultrasonography. We fit regression models to identify traditional and HIV-specific correlates of common carotid intima media thickness (CCIMT). Results: 105 participants completed carotid ultrasonography, a median of 7 years following ART initiation. Age, low-density lipoprotein and pre-ART viral load were correlated with CCIMT. No association was found between CCIMT and any pre-ART biomarkers of immune activation. However, in multivariable models adjusted for CVD risk factors, lower absolute levels of sCD14 and IL-6 and greater declines in CD14 and kynurenine-tryptophan ratio after 6 months of ART predicted lower CCIMT years later (P<0.01). Conclusions: Persistent immune activation despite ART-mediated viral suppression predicts future atherosclerotic burden among HIV-infected Ugandans. Future work should focus on clinical correlates of these relationships to elucidate the long-term health priorities for HIV-infected people in the region.
    The Journal of Infectious Diseases 09/2015; DOI:10.1093/infdis/jiv450 · 6.00 Impact Factor
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    ABSTRACT: Objective: Obesity is associated with changes in both right (RV) and left (LV) ventricular morphology, but the biological basis of this finding is not well established. We examined whether adipokine levels were associated with RV morphology and function in a population-based multiethnic sample free of clinical cardiovascular disease. Methods: We examined relationships of leptin, resistin, TNF-α, and adiponectin with RV morphology and function (from cardiac MRI) in participants (n = 1,267) free of clinical cardiovascular disease from the Multi-Ethnic Study of Atherosclerosis (MESA)-RV study. Multivariable regressions (linear, quantile [25th and 75th] and generalized additive models [GAM]) were used to examine the independent association of each adipokine with RV mass, RV end-diastolic volume (RVEDV), RV end-systolic volume (RVESV), RV stroke volume (RVSV) and RV ejection fraction (RVEF). Results: Higher leptin levels were associated with significantly lower levels of RV mass, RVEDV, RVESV and stroke volume, but not RVEF, after adjustment for age, gender, race, height and weight. These associations were somewhat attenuated but still significant after adjustment for traditional risk factors and covariates, and were completely attenuated when correcting for the respective LV measures. There were no significant interactions of age, gender, or race/ethnicity on the relationship between the four adipokines and RV structure or function. Conclusions: Leptin levels are associated with favorable RV morphology in a multi-ethnic population free of cardiovascular disease, however these associations may be explained by a yet to be understood bi-ventricular process as this association was no longer present after adjustment for LV values. These findings complement the associations previously shown between adipokines and LV structure and function in both healthy and diseased patients. The mechanisms linking adipokines to healthy cardiovascular function require further investigation.
    PLoS ONE 09/2015; 10(9):e0136818. DOI:10.1371/journal.pone.0136818 · 3.23 Impact Factor

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    ABSTRACT: Interleukin-2 receptor subunit α (IL-2Rα) regulates lymphocyte activation, which plays an important role in atherosclerosis. Associations between soluble IL-2Rα and cardiovascular disease (CVD) have not been widely studied and little is known about the genetic determinants of soluble IL-2 receptor α (sIL-2Rα) levels. We measured baseline levels of sIL-2Rα in 4408 European American (EA) and 766 African American (AA) adults from the Cardiovascular Health Study (CHS) and examined associations with baseline CVD risk factors, subclinical CVD, and incident CVD events. We also performed a genome-wide association study for sIL-2Rα in CHS (2964 EAs and 683 AAs) and further combined CHS EA results with those from 2 other EA cohorts in a meta-analysis (n=4464 EAs). In age, sex- and race- adjusted models, sIL-2Rα was positively associated with current smoking, type 2 diabetes mellitus, hypertension, insulin, waist circumference, C-reactive protein, IL-6, fibrinogen, internal carotid wall thickness, all-cause mortality, CVD mortality, and incident CVD, stroke, and heart failure. When adjusted for baseline CVD risk factors and subclinical CVD, associations with all-cause mortality, CVD mortality, and heart failure remained significant in both EAs and AAs. In the EA genome-wide association study analysis, we observed 52 single-nucleotide polymorphisms in the chromosome 10p15-14 region, which contains IL2RA, IL15RA, and RMB17, that reached genome-wide significance (P<5×10(-8)). The most significant single-nucleotide polymorphism was rs7911500 (P=1.31×10(-75)). The EA meta-analysis results were highly consistent with CHS-only results. No single-nucleotide polymorphisms reached statistical significance in the AAs. These results support a role for sIL-2Rα in atherosclerosis and provide evidence for multiple-associated single-nucleotide polymorphisms at chromosome 10p15-14. © 2015 American Heart Association, Inc.
    Arteriosclerosis Thrombosis and Vascular Biology 08/2015; DOI:10.1161/ATVBAHA.115.305289 · 6.00 Impact Factor
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    ABSTRACT: Background and aims: Fetuin-A has a plausible role in the inhibition of arterial calcification, but its association with risk of coronary heart disease (CHD) in the general population is unclear. We used two common genetic variants in the fetuin-A gene (AHSG) that are strongly associated with circulating fetuin-A levels to investigate the associations with risk of CHD and subclinical cardiovascular measures (intima-media thickness, ankle-arm index, and coronary artery calcification). Methods: Genetic variation and fetuin-A levels were assessed in 3299 community-living individuals (2733 Caucasians and 566 African Americans) 65 years of age or older, free of previous cardiovascular disease, who participated in the Cardiovascular Health Study (CHS) in 1992-1993. Results: Among Caucasians, both rs2248690 and rs4917 were associated with 12% lower fetuin-A concentrations per minor allele (P < 0.0001). The hazard ratios (HRs) per minor allele for incident CHD were 1.12 (95% CI: 1.00-1.26) for rs2248690 and 1.02 (0.91-1.14) for rs4917. Using both genotypes as an instrumental variable for measured fetuin-A, the HRs for one standard deviation increase in genetically determined fetuin-A levels on CHD risk were 0.84 (95% CI: 0.70-1.00) for rs2248690 and 0.97 (95% CI: 0.82-1.14) for rs4917, respectively. However, in CHS neither of the genotypes were associated with subclinical cardiovascular measures and when CHS data were meta-analyzed with data from six other prospective studies (totaling 26,702 Caucasian participants and 3295 CHD cases), the meta-analyzed HRs for incident CHD were 1.12 (0.93-1.34) and 1.06 (0.93-1.20) for rs2248690 and rs4917, respectively (p heterogeneity 0.005 and 0.0048). Conclusion: Common variants in the AHSG gene are strongly associated with fetuin-A levels, but their concurrent association with CHD risk in current prospective studies is inconsistent. Further investigation in studies with measured fetuin-A and AHSG variants is needed to clarify the potential causal association of fetuin-A with CHD risk.
    Atherosclerosis 08/2015; 243(1). DOI:10.1016/j.atherosclerosis.2015.08.031 · 3.99 Impact Factor
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    ABSTRACT: The Seven Countries Study in the 1960s showed very low mortality from coronary heart disease (CHD) in Japan, which was attributed to very low levels of total cholesterol. Studies of migrant Japanese to the USA in the 1970s documented increase in CHD rates, thus CHD mortality in Japan was expected to increase as their lifestyle became Westernized, yet CHD mortality has continued to decline since 1970. This study describes trends in CHD mortality and its risk factors since 1980 in Japan, contrasting those in other selected developed countries. We selected Australia, Canada, France, Japan, Spain, Sweden, the UK and the USA. CHD mortality between 1980 and 2007 was obtained from WHO Statistical Information System. National data on traditional risk factors during the same period were obtained from literature and national surveys. Age-adjusted CHD mortality continuously declined between 1980 and 2007 in all these countries. The decline was accompanied by a constant fall in total cholesterol except Japan where total cholesterol continuously rose. In the birth cohort of individuals currently aged 50-69 years, levels of total cholesterol have been higher in Japan than in the USA, yet CHD mortality in Japan remained the lowest: > 67% lower in men and > 75% lower in women compared with the USA. The direction and magnitude of changes in other risk factors were generally similar between Japan and the other countries. Decline in CHD mortality despite a continuous rise in total cholesterol is unique. The observation may suggest some protective factors unique to Japanese. © The Author 2015; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.
    International Journal of Epidemiology 07/2015; DOI:10.1093/ije/dyv143 · 9.18 Impact Factor
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    ABSTRACT: To determine the association of HIV, immunologic, and inflammatory factors on coronary artery calcium (CAC), a marker of subclinical atherosclerosis. Cross-sectional study comparing baseline data of males from Hawaii Aging with HIV - Cardiovascular Study (HAHCS) with the Multi-Ethnic Study of Atherosclerosis (MESA) cohort. The cohorts were pooled to determine effects of HIV on CAC and explore immunologic and inflammatory factors that may explain development of CAC in HIV. Multivariable regression models compared CAC prevalence in HAHCS with MESA adjusting for coronary heart disease (CHD) risk profiles. We studied 100 men from HAHCS and 2733 men from MESA. Positive CAC was seen in 58% HAHCS participants and 57% MESA participants. Mean CAC was 260.8 in HAHCS and 306.5 in MESA. Using relative risk (RR) regression, HAHCS participants had a greater risk (RR = 1.20, P < 0.05) of having positive CAC than MESA when adjusting for age, smoking status, diabetes, antihypertensive therapy, BMI, systolic blood pressure, total cholesterol, and HDL cholesterol. Among participants with positive CAC, HIV infection was not associated with larger amounts of CAC. Among HAHCS participants, current HIV viral load, CD4, length of HIV, interleukin 6 (IL-6), fibrinogen, C-reactive protein (CRP), and D-dimer were not associated with the presence or amount of CAC. HIV was independently associated with a positive CAC in men with increased likelihood occurring between 45 and 50 years of age. Current HIV viral load, CD4 count, length of HIV, and inflammatory markers were unrelated to either presence or amount of CAC.
    HIV Clinical Trials 06/2015; 16(4):1528433614Z0000000016. DOI:10.1179/1528433614Z.0000000016 · 2.63 Impact Factor
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    ABSTRACT: This study investigated whether fitness changes resulting from lifestyle interventions for weight loss may independently contribute to the improvement of low adiponectin levels in obese individuals with diabetes. Look AHEAD (Action for Health in Diabetes) randomized overweight/obese individuals with type 2 diabetes to intensive lifestyle intervention (ILI) for weight loss or to diabetes support and education (DSE). Total and high-molecular weight adiponectin (adiponectins), weight, and cardiorespiratory fitness (submaximal exercise stress test) were measured in 1,397 participants at baseline and at 1 year, when ILI was most intense. Regression analyses examined the associations of 1-year weight and fitness changes with change in adiponectins. ILI resulted in greater improvements in weight, fitness, and adiponectins at 1 year compared with DSE (P < 0.0001). Weight loss and improved fitness were each associated with changes in adiponectins in men and women (P < 0.001 for all), after adjusting for baseline adiponectins, demographics, clinical variables, and treatment arm. Weight loss contributed an additional 4-5% to the variance of change in adiponectins than did increased fitness in men; in women, the contributions of improved fitness (1% greater) and of weight loss were similar. When weight and fitness changes were both accounted for, weight loss in men and increased fitness in women retained their strong associations (P < 0.0001) with adiponectin change. Improvements in fitness and weight with ILI were favorably but distinctly associated with changes in adiponectin levels in overweight/obese men and women with diabetes. Future studies need to investigate whether sex-specific biological determinants contribute to the observed associations. © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
    Diabetes care 05/2015; 38(8). DOI:10.2337/dc14-2775 · 8.42 Impact Factor
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Publication Stats

42k Citations
3,720.51 Total Impact Points


  • 2015
    • University of Cambridge
      Cambridge, England, United Kingdom
  • 1993-2015
    • University of Vermont Medical Center
      Burlington, Vermont, United States
  • 1988-2015
    • University of Vermont
      • • Department of Pathology
      • • Department of Biochemistry
      • • College of Medicine
      • • Department of Medicine
      Burlington, Vermont, United States
  • 2014
    • Boston University
      Boston, Massachusetts, United States
  • 2013
    • Mayo Clinic - Rochester
      • Department of Cardiovascular Diseases
      Рочестер, Minnesota, United States
  • 2006-2013
    • University of California, San Francisco
      • • Division of Hospital Medicine
      • • Veterans Affairs Medical Center
      San Francisco, CA, United States
    • MedStar Health Research Institute
      هایتسویل، مریلند, Maryland, United States
    • Johns Hopkins University
      Baltimore, Maryland, United States
  • 2000-2013
    • University of Washington Seattle
      • • Department of Epidemiology
      • • Department of Medicine
      Seattle, Washington, United States
  • 2012
    • University of Texas Medical Branch at Galveston
      • School of Medicine
      Galveston, TX, United States
    • McGill University
      • Department of Epidemiology, Biostatistics and Occupational Health
      Montréal, Quebec, Canada
    • Albert Einstein College of Medicine
      • Department of Epidemiology & Population Health
      New York City, NY, United States
  • 2011
    • Loyola University Medical Center
      • Division of Cardiology
      Maywood, Illinois, United States
    • National Heart, Lung, and Blood Institute
      • Division of Cardiovascular Sciences (DCVS)
      Maryland, United States
  • 2010
    • George Washington University
      Washington, Washington, D.C., United States
  • 2009
    • University of Rochester
      • Department of Community and Preventive Medicine
      Rochester, New York, United States
  • 1996-2009
    • The University of Arizona
      Tucson, Arizona, United States
    • University of Massachusetts Medical School
      Worcester, Massachusetts, United States
  • 2008
    • University of California, Davis
      • School of Medicine
      Davis, CA, United States
  • 2007
    • University of North Carolina at Chapel Hill
      North Carolina, United States
    • Lerner Research Institute
      Cleveland, Ohio, United States
  • 1995-2007
    • University of Pittsburgh
      • Department of Epidemiology
      Pittsburgh, Pennsylvania, United States
  • 2003-2006
    • University of Texas at San Antonio
      San Antonio, Texas, United States
    • University of Toronto
      Toronto, Ontario, Canada
    • University of Dallas
      Irving, Texas, United States
    • Northwestern University
      • Department of Preventive Medicine
      Evanston, IL, United States
  • 2005
    • Case Western Reserve University
      • Department of Epidemiology and Biostatistics
      Cleveland, OH, United States
    • University of Florida
      • Department of Aging and Geriatric Research
      Gainesville, FL, United States
  • 2004
    • Pennington Biomedical Research Center
      Baton Rouge, Louisiana, United States
  • 1998-2004
    • Harvard University
      Cambridge, Massachusetts, United States
  • 2002
    • Burlington College
      Burlington, Vermont, United States
  • 2001
    • Johns Hopkins Medicine
      Baltimore, Maryland, United States
  • 1997
    • Brigham and Women's Hospital
      • Department of Medicine
      Boston, MA, United States