Naveed Sattar

University of Glasgow, Glasgow, Scotland, United Kingdom

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Publications (505)4765.26 Total impact

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    ABSTRACT: It has been suggested that fetuin-A may be a potential biomarker of cardiometabolic disease. However, few studies have investigated preanalytical factors that might impact the measurement of fetuin-A in the circulation. This pilot study aimed to investigate the preanalytical variables of sample type, timing of sample centrifugation and the impact of freeze-thaw cycles on the concentration of fetuin-A in serum or EDTA-plasma. Blood samples were taken from 19 male or female healthy volunteers, aged 18-70 years, and left at ambient room temperature for 2 h or 48 h. The tubes were then centrifuged, serum and EDTA-plasma separated, and fetuin-A concentrations measured using a commercially available enzyme-linked immunosorbent assay (ELISA). There was no significant difference between the concentrations of fetuin-A in EDTA-plasma and serum following separation from whole blood at 2 h postcollection (P = 0.78). The median (interquartile range) concentrations of fetuin-A in EDTA-plasma separated at 2 h and 48 h postcollection were 589 µg/mL (484-703 µg/mL) and 767 µg/mL (687-942 µg/mL), respectively (P < 0.0005). For serum, equivalent concentrations were 606 µg/mL (501-669 µg/mL) at 2 h and 607 µg/mL (564-757 µg/mL) at 48 h postcollection (P = 0.06). Fetuin-A concentrations measured in EDTA-plasma and serum showed no significant change following three freeze-thaw cycles in samples separated at 2 h postcollection (EDTA-plasma P = 0.16; serum P = 0.89). This small pilot study has shown that serum is preferable to EDTA-plasma for the measurement of fetuin-A. It has also shown that fetuin-A appears to be as stable after three freeze-thaw cycles as it is after one.
    Annals of Clinical Biochemistry 04/2014; 52(1). DOI:10.1177/0004563214529550 · 2.08 Impact Factor
  • Paul Welsh, Naveed Sattar
    BMJ (online) 04/2014; 348:g2280. DOI:10.1136/bmj.g2280 · 16.38 Impact Factor
  • Diabetes care 04/2014; 37(4):e78-9. DOI:10.2337/dc13-2490 · 8.57 Impact Factor
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    ABSTRACT: The genetic contribution to the variation in human lifespan is approximately 25%. Despite the large number of identified disease-susceptibility loci, it is not known which loci influence population mortality.We performed a genome-wide association meta-analysis of 7729 long-lived individuals of European descent (≥ 85 years) and 16121 younger controls (< 65 years) followed by replication in an additional set of 13060 long-lived individuals and 61156 controls. In addition, we performed a subset analysis in cases≥90 years.We observed genome-wide significant association with longevity, as reflected by survival to ages beyond 90 years, at a novel locus, rs2149954, on chromosome 5q33.3 (OR=1.10, P =1.74 x 10(-8)). We also confirmed association of rs4420638 on chromosome 19q13.32 (OR=0.72, P=3.40 x 10(-36)), representing the TOMM40/APOE/APOC1 locus. In a prospective meta-analysis (n=34103) the minor allele of rs2149954 (T) on chromosome 5q33.3 associates with increased survival (HR=0.95, P=0.003). This allele has previously been reported to associate with low blood pressure in middle age. Interestingly, the minor allele (T) associates with decreased cardiovascular mortality risk, independent of blood pressure.We report on the first GWAS-identified longevity locus on chromosome 5q33.3 influencing survival in the general European population. The minor allele of this locus associates with low blood pressure in middle age, although the contribution of this allele to survival may be less dependent on blood pressure. Hence, the pleiotropic mechanisms by which this intragenic variation contributes to lifespan regulation have to be elucidated.
    Human Molecular Genetics 03/2014; 23(16). DOI:10.1093/hmg/ddu139 · 6.68 Impact Factor
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    ABSTRACT: The value of measuring levels of glycated hemoglobin (HbA1c) for the prediction of first cardiovascular events is uncertain. To determine whether adding information on HbA1c values to conventional cardiovascular risk factors is associated with improvement in prediction of cardiovascular disease (CVD) risk. Analysis of individual-participant data available from 73 prospective studies involving 294,998 participants without a known history of diabetes mellitus or CVD at the baseline assessment. Measures of risk discrimination for CVD outcomes (eg, C-index) and reclassification (eg, net reclassification improvement) of participants across predicted 10-year risk categories of low (<5%), intermediate (5% to <7.5%), and high (≥7.5%) risk. During a median follow-up of 9.9 (interquartile range, 7.6-13.2) years, 20,840 incident fatal and nonfatal CVD outcomes (13,237 coronary heart disease and 7603 stroke outcomes) were recorded. In analyses adjusted for several conventional cardiovascular risk factors, there was an approximately J-shaped association between HbA1c values and CVD risk. The association between HbA1c values and CVD risk changed only slightly after adjustment for total cholesterol and triglyceride concentrations or estimated glomerular filtration rate, but this association attenuated somewhat after adjustment for concentrations of high-density lipoprotein cholesterol and C-reactive protein. The C-index for a CVD risk prediction model containing conventional cardiovascular risk factors alone was 0.7434 (95% CI, 0.7350 to 0.7517). The addition of information on HbA1c was associated with a C-index change of 0.0018 (0.0003 to 0.0033) and a net reclassification improvement of 0.42 (-0.63 to 1.48) for the categories of predicted 10-year CVD risk. The improvement provided by HbA1c assessment in prediction of CVD risk was equal to or better than estimated improvements for measurement of fasting, random, or postload plasma glucose levels. In a study of individuals without known CVD or diabetes, additional assessment of HbA1c values in the context of CVD risk assessment provided little incremental benefit for prediction of CVD risk.
    JAMA The Journal of the American Medical Association 03/2014; 311(12):1225-33. DOI:10.1001/jama.2014.1873 · 30.39 Impact Factor
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    ABSTRACT: OBJECTIVE To investigate associations of maternal gestational weight gain and body composition and their impact on offspring body composition and adipocytokine, glucose, and insulin concentrations at age 4 months.RESEARCH DESIGN AND METHODS This was a prospective study including 31 mother-infant pairs (N = 62). Maternal body composition was assessed using doubly labeled water. Infant body composition was assessed at 4 months using air displacement plethysmography, and venous blood was assayed for glucose, insulin, adiponectin, interleukin-6 (IL-6), and leptin concentrations.RESULTSRate of gestational weight gain in midpregnancy was significantly associated with infant fat mass (r = 0.41, P = 0.03); rate of gestational weight in late pregnancy was significantly associated with infant fat-free mass (r = 0.37, P = 0.04). Infant birth weight was also strongly correlated with infant fat-free mass at 4 months (r = 0.63, P = 0.0002). Maternal BMI and maternal fat mass were strongly inversely associated with infant IL-6 concentrations (r = -0.60, P = 0.002 and r = -0.52, P = 0.01, respectively). Infant fat-free mass was inversely related to infant adiponectin concentrations (r = -0.48, P = 0.008) and positively correlated with infant blood glucose adjusted for insulin concentrations (r = 0.42, P = 0.04). No significant associations for leptin were observed.CONCLUSIONS Timing of maternal weight gain differentially impacts body composition of the 4-month-old infant, which in turn appears to affect the infant's glucose and adipokine concentrations.
    Diabetes care 03/2014; 37(5). DOI:10.2337/dc13-2265 · 8.57 Impact Factor
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    ABSTRACT: To derive cut-points for body mass index (BMI) and waist circumference (WC) for minority ethnic groups that are risk equivalent based on endogenous glucose levels to cut-points for white Europeans (BMI 30 kg/m2; WC men 102 cm; WC women 88 cm). Cross-sectional data from participants aged 40-75 years: 4,672 white and 1,348 migrant South Asian participants from ADDITION-Leicester (UK) and 985 indigenous South Asians from Jaipur Heart Watch/New Delhi studies (India). Cut-points were derived using fractional polynomial models with fasting and 2-hour glucose as outcomes, and ethnicity, objectively-measured BMI/WC, their interaction and age as covariates. Based on fasting glucose, obesity cut-points were 25 kg/m2 (95% Confidence Interval: 24, 26) for migrant South Asian, and 18 kg/m2 (16, 20) for indigenous South Asian populations. For men, WC cut-points were 90 cm (85, 95) for migrant South Asian, and 87 cm (82, 91) for indigenous South Asian populations. For women, WC cut-points were 77 cm (71, 82) for migrant South Asian, and 54 cm (20, 63) for indigenous South Asian populations. Cut-points based on 2-hour glucose were lower than these. These findings strengthen evidence that health interventions are required at a lower BMI and WC for South Asian individuals. Based on our data and the existing literature, we suggest an obesity threshold of 25 kg/m2 for South Asian individuals, and a very high WC threshold of 90 cm for South Asian men and 77 cm for South Asian women. Further work is required to determine whether lower cut-points are required for indigenous, than migrant, South Asians.
    PLoS ONE 03/2014; 9(3):e90813. DOI:10.1371/journal.pone.0090813 · 3.53 Impact Factor
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    ABSTRACT: Obesity increases preeclampsia risk, and maternal dyslipidemia may result from exaggerated adipocyte lipolysis. We compared adipocyte function in preeclampsia with healthy pregnancy to establish whether there is increased lipolysis. Subcutaneous and visceral adipose tissue biopsies were collected at caesarean section from healthy (n=31) and preeclampsia (n=13) mothers. Lipolysis in response to isoproterenol (200 nmol/L) and insulin (10 nmol/L) was assessed. In healthy pregnancy, subcutaneous adipocytes had higher diameter than visceral adipocytes (P<0.001). Subcutaneous and visceral adipocyte mean diameter in preeclampsia was similar to that in healthy pregnant controls, but cell distribution was shifted toward smaller cell diameter in preeclampsia. Total lipolysis rates under all conditions were lower in healthy visceral than subcutaneous adipocytes but did not differ after normalization for cell diameter. Visceral adipocyte insulin sensitivity was lower than subcutaneous in healthy pregnancy and inversely correlated with plasma triglyceride (r=-0.50; P=0.004). Visceral adipose tissue had lower ADRB3, LPL, and leptin and higher insulin receptor messenger RNA expression than subcutaneous adipose tissue. There was no difference in subcutaneous adipocyte lipolysis rates between preeclampsia and healthy controls, but subcutaneous adipocytes had lower sensitivity to insulin in preeclampsia, independent of cell diameter (P<0.05). In preeclampsia, visceral adipose tissue had higher LPL messenger RNA expression than subcutaneous. In conclusion, in healthy pregnancy, the larger total mass of subcutaneous adipose tissue may release more fatty acids into the circulation than visceral adipose tissue. Reduced insulin suppression of subcutaneous adipocyte lipolysis may increase the burden of plasma fatty acids that the mother has to process in preeclampsia.
    Hypertension 03/2014; 63(5). DOI:10.1161/HYPERTENSIONAHA.113.01824 · 7.63 Impact Factor
  • Hypertension 03/2014; 63(3):e15. DOI:10.1161/HYPERTENSIONAHA.113.02926 · 7.63 Impact Factor
  • David Preiss, John J McMurray, Naveed Sattar
    The Lancet Diabetes & Endocrinology 03/2014; DOI:10.1016/S2213-8587(14)70052-X · 9.19 Impact Factor
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    ABSTRACT: The susceptibility to type 2 diabetes of people of south Asian descent is established, but there is little trial-based evidence for interventions to tackle this problem. We assessed a weight control and physical activity intervention in south Asian individuals in the UK. We did this non-blinded trial in two National Health Service (NHS) regions in Scotland (UK). Between July 1, 2007, and Oct 31, 2009, we recruited men and women of Indian and Pakistani origin, aged 35 years or older, with waist circumference 90 cm or greater in men or 80 cm or greater in women, and with impaired glucose tolerance or impaired fasting glucose determined by oral glucose tolerance test. Families were randomised (using a random number generator program, with permuted blocks of random size, stratified by location [Edinburgh or Glasgow], ethnic group [Indian or Pakistani], and number of participants in the family [one vs more than one]) to intervention or control. Participants in the same family were not randomised separately. The intervention group received 15 visits from a dietitian over 3 years and the control group received four visits in the same period. The primary outcome was weight change at 3 years. Analysis was by modified intention to treat, excluding participants who died or were lost to follow-up. We used linear regression models to provide mean differences in baseline-adjusted weight at 3 years. This trial is registered, number ISRCTN25729565. Of 1319 people who were screened with an oral glucose tolerance test, 196 (15%) had impaired glucose tolerance or impaired fasting glucose and 171 entered the trial. Participants were in 156 family clusters that were randomised (78 families with 85 participants were allocated to intervention; 78 families with 86 participants were allocated to control). 167 (98%) participants in 152 families completed the trial. Mean weight loss in the intervention group was 1·13 kg (SD 4·12), compared with a mean weight gain of 0·51 kg (3·65) in the control group, an adjusted mean difference of -1·64 kg (95% CI -2·83 to -0·44). Modest, medium-term changes in weight are achievable as a component of lifestyle-change strategies, which might control or prevent adiposity-related diseases. National Prevention Research Initiative, NHS Research and Development; NHS National Services Scotland; NHS Health Scotland.
    03/2014; 2(3):218-27. DOI:10.1016/S2213-8587(13)70204-3
  • Annals of the rheumatic diseases 02/2014; DOI:10.1136/annrheumdis-2014-205174 · 9.27 Impact Factor
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    ABSTRACT: Tissue plasminogen activator (tPA), a serine protease, catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for endogenous fibrinolysis. In some populations, elevated plasma levels of tPA have been associated with myocardial infarction and other cardiovascular diseases. We conducted a meta-analysis of genome-wide association studies to identify novel correlates of circulating levels of tPA. Fourteen cohort studies with tPA measures (N=26 929) contributed to the meta-analysis. Three loci were significantly associated with circulating tPA levels (P<5.0×10(-8)). The first locus is on 6q24.3, with the lead single nucleotide polymorphism (SNP; rs9399599; P=2.9×10(-14)) within STXBP5. The second locus is on 8p11.21. The lead SNP (rs3136739; P=1.3×10(-9)) is intronic to POLB and <200 kb away from the tPA encoding the gene PLAT. We identified a nonsynonymous SNP (rs2020921) in modest linkage disequilibrium with rs3136739 (r(2)=0.50) within exon 5 of PLAT (P=2.0×10(-8)). The third locus is on 12q24.33, with the lead SNP (rs7301826; P=1.0×10(-9)) within intron 7 of STX2. We further found evidence for the association of lead SNPs in STXBP5 and STX2 with expression levels of the respective transcripts. In in vitro cell studies, silencing STXBP5 decreased the release of tPA from vascular endothelial cells, whereas silencing STX2 increased the tPA release. Through an in silico lookup, we found no associations of the 3 lead SNPs with coronary artery disease or stroke. We identified 3 loci associated with circulating tPA levels, the PLAT region, STXBP5, and STX2. Our functional studies implicate a novel role for STXBP5 and STX2 in regulating tPA release.
    Arteriosclerosis Thrombosis and Vascular Biology 02/2014; DOI:10.1161/ATVBAHA.113.302088 · 5.53 Impact Factor
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    Guntram Schernthaner, Naveed Sattar
    Journal of diabetes and its complications 02/2014; 28(4). DOI:10.1016/j.jdiacomp.2014.02.011 · 1.93 Impact Factor
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    ABSTRACT: Despite the widespread recognition that obesity in pregnant women is associated with adverse outcomes for mother and child, there is no intervention proven to reduce the risk of these complications. The primary aim of this randomised controlled trial is to assess in obese pregnant women, whether a complex behavioural intervention, based on changing diet (to foods with a lower glycemic index) and physical activity, will reduce the risk of gestational diabetes (GDM) and delivery of a large for gestational age (LGA) infant. A secondary aim is to determine whether the intervention lowers the long term risk of obesity in the offspring. Multicentre randomised controlled trial comparing a behavioural intervention designed to improve glycemic control with standard antenatal care in obese pregnant women.Inclusion criteria; women with a BMI >=30 kg/m2 and a singleton pregnancy between 15+0 weeks and 18+6 weeks' gestation. Exclusion criteria; pre-defined, pre-existing diseases and multiple pregnancy. Randomisation is on-line by a computer generated programme and is minimised by BMI category, maternal age, ethnicity, parity and centre. Intervention; this is delivered by a health trainer over 8 sessions. Based on control theory, with elements of social cognitive theory, the intervention is designed to improve maternal glycemic control. Women randomised to the control arm receive standard antenatal care until delivery according to local guidelines. All women have a 75 g oral glucose tolerance test at 27+0- 28+6 weeks' gestation.Primary outcome; Maternal: diagnosis of GDM, according to the International Association of Diabetes in Pregnancy Study Group (IADPSG) criteria. Neonatal; infant LGA defined as >90th customised birth weight centile.Sample size; 1546 women to provide 80% power to detect a 25% reduction in the incidence of GDM and a 30% reduction in infants large for gestational age. All aspects of this protocol have been evaluated in a pilot randomised controlled trial, with subsequent optimisation of the intervention. The findings of this trial will inform whether lifestyle mediated improvement of glycemic control in obese pregnant women can minimise the risk of pregnancy complications.Trial registration: Current controlled trials; ISRCTN89971375.
    BMC Pregnancy and Childbirth 02/2014; 14(1):74. DOI:10.1186/1471-2393-14-74 · 2.15 Impact Factor
  • Jason Mr Gill, Naveed Sattar
    02/2014; DOI:10.1016/S2213-8587(14)70013-0
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    ABSTRACT: There is a widening perception that many factors (lifestyle and others e.g., acute/chronic inflammation) may causally lower vitamin D levels. Observationally, smoking tends to be associated with lower vitamin D levels. Smokers also have increased fracture risk and decreased bone mass suggesting a potential causal effect of smoking on vitamin D. It has also been suggested that tobacco smoke chemicals may influence vitamin D metabolism and function. However, determining a causal link between smoking and lower vitamin D is problematic in conventional epidemiological studies due to confounding by other lifestyle factors. We performed a Mendelian randomisation analysis, using data on 32,823 individuals from the Consortium for Causal Analysis Research in Tobacco and Alcohol to investigate the causal nature of the associations of smoking with vitamin D levels. Associations between a smoking related variant (rs1051730/rs16969968) and serum vitamin D (25(OH)D) were assessed by linear regression stratified by smoking status (categorised as never, former, current, ever (former and current), and non (never and former)) and adjusted for age, sex, and geographic region, and additionally for body mass index (BMI). Observational associations between smoking status and vitamin D were assessed by linear regression, adjusted for age, sex, and month of data collection and additionally for geographic region, socio-economic status and BMI. Results from individual studies were meta-analysed. Interactions between smoking status and genotype were assessed using the Cochran Q statistic. We discuss the implications of these results for furthering understanding of the causal effect of smoking on vitamin D. This will inform the development of relevant public health messages and campaigns, and also potentially aid the development of novel treatments for disease outcomes. This is a work in progress and we anticipate that results will be available within a month.
    The 20th Annual Meeting of the Society for Research on Nicotine and Tobacco (SRNT), Seattle, WA, USA; 02/2014
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    ABSTRACT: Metformin reduces cardiovascular risk in patients with type 2 diabetes seemingly independent of lowering blood glucose concentration. We assessed the cardiovascular effects of metformin in individuals without type 2 diabetes. We did a single-centre, double-blind, placebo-controlled trial at the Glasgow Clinical Research Facility (Glasgow, UK). We enrolled patients taking statins who did not have type 2 diabetes but who did have coronary heart disease and large waist circumferences. Participants were randomly assigned (1:1) by computer to either metformin (850 mg twice daily) or matching placebo in block sizes of four. Patients, investigators, trial staff, and statisticians were masked to treatment allocation. The primary endpoint was progression of mean distal carotid intima-media thickness (cIMT) over 18 months in the modified intention-to-treat population. Secondary endpoints were changes in carotid plaque score (in six regions), measures of glycaemia (HbA1c, fasting glucose, and insulin concentrations, and Homeostasis Model Assessment of Insulin Resistance [HOMA-IR]), and concentrations of lipids, high sensitivity C-reactive protein, and tissue plasminogen activator. The trial was registered at ClinicalTrials.gov, number NCT00723307. We screened 356 patients, of whom we enrolled 173 (86 in the metformin group, 87 in the placebo group). Average age was 63 years. At baseline, mean cIMT was 0·717 mm (SD 0·129) and mean carotid plaque score was 2·43 (SD 1·55). cIMT progression did not differ significantly between groups (slope difference 0·007 mm per year, 95% CI -0·006 to 0·020; p=0·29). Change of carotid plaque score did not differ significantly between groups (0·01 per year, 95% CI -0·23 to 0·26; p=0·92). Patients taking metformin had lower HbA1c, insulin, HOMA-IR, and tissue plasminogen activator compared with those taking placebo, but there were no significant differences for total cholesterol, HDL-cholesterol, non-HDL-cholesterol, triglycerides, high sensitivity C-reactive protein, or fasting glucose. 138 adverse events occurred in 64 patients in the metformin group versus 120 in 60 patients in the placebo group. Diarrhoea and nausea or vomiting were more common in the metformin group than in the placebo group (28 vs 5). Metformin had no effect on cIMT and little or no effect on several surrogate markers of cardiovascular disease in non-diabetic patients with high cardiovascular risk, taking statins. Further evidence is needed before metformin can be recommended for cardiovascular benefit in this population. Chief Scientist Office (Scotland).
    02/2014; 2(2):116-24. DOI:10.1016/S2213-8587(13)70152-9
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    ABSTRACT: The impact of fast changes in obesity indices on other measures of metabolic health is poorly defined in the general population. Using the Polish accession to the European Union as a model of political and social transformation we examined how an expected rapid increase in body mass index (BMI) and waist circumference relates to changes in lipid profile, both at the population and personal level. Through primary care centres in 444 Polish cities, two cross-sectional nationwide population-based surveys (LIPIDOGRAM 2004 and LIPIDOGRAM 2006) examined 15,404 and 15,453 adult individuals in 2004 and 2006, respectively. A separate prospective sample of 1,840 individuals recruited in 2004 had a follow-up in 2006 (LIPIDOGRAM PLUS). Two years after Polish accession to European Union, mean population BMI and waist circumference increased by 0.6% and 0.9%, respectively. This tracked with a 7.6% drop in HDL-cholesterol and a 2.1% increase in triglycerides (all p<0.001) nationwide. The direction and magnitude of the population changes were replicated at the personal level in LIPIDOGRAM PLUS (0.7%, 0.3%, 8.6% and 1.8%, respectively). However, increases in BMI and waist circumference were both only weakly associated with HDL-cholesterol and triglycerides changes prospectively. The relation of BMI to the magnitude of change in both lipid fractions was comparable to that of waist circumference. Moderate changes in obesity measures tracked with a significant deterioration in measures of pro-atherogenic dyslipidaemia at both personal and population level. These associations were predominantly driven by factors not measureable directly through either BMI or waist circumference.
    PLoS ONE 01/2014; 9(1):e86837. DOI:10.1371/journal.pone.0086837 · 3.53 Impact Factor
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    ABSTRACT: Context: The impact of adolescent nonalcoholic fatty liver disease (NAFLD) on health, independent of fat mass, is unclear. Objective: The objective of the study was to determine the independent (of total body fat) association of ultrasound scan (USS)-determined NAFLD with liver fibrosis, insulin resistance, and dyslipidemia among healthy adolescents. Design: This was a cross-sectional analysis in participants from a UK birth cohort. Participants: One thousand eight hundred seventy-four (1059 female) individuals of a mean age of 17.9 years participated in the study. Main Outcomes: USS assessed liver stiffness (shear velocity, an indicator of fibrosis) and volume, fasting glucose, insulin, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, alanine amino transferase, aspartate amino transferase, γ-glutamyltransferase, and haptoglobin. Results: The prevalence of NAFLD was 2.5% [95% confidence interval (CI) 1.8-3.3] and was the same in females and males. Dual-energy X-ray absorptiometry determined total body fat mass was strongly associated with USS NAFLD: odds ratio 3.15 (95% CI 2.44-4.07) per 1 SD (∼10 kg) fat mass. Those with NAFLD had larger liver volumes and greater shear velocity. They also had higher fasting glucose, insulin, triglycerides, low-density lipoprotein cholesterol, alanine amino transferase, aspartate amino transferase, γ-glutamyltransferase, and haptoglobin and lower high-density lipoprotein cholesterol. Most associations were independent of total body fat. For example, after adjustment for fat mass and other confounders, hepatic shear velocity [mean difference 22.8% (95% CI 15.6-30.5)], triglyceride levels [23.6% (95% CI 6.0-44.2)], and insulin [39.4% (95% CI 10.7-75.5)] were greater in those with NAFLD compared with those without NAFLD. Conclusion: In healthy European adolescents, 2.5% have USS-defined NAFLD. Even after accounting for total body fat, those with NAFLD have more adverse levels of liver fibrosis and cardiometabolic risk factors.
    The Journal of Clinical Endocrinology and Metabolism 01/2014; DOI:10.1210/jc.2013-3612 · 6.31 Impact Factor

Publication Stats

18k Citations
4,765.26 Total Impact Points

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Institutions

  • 2000–2015
    • University of Glasgow
      • • Institute of Cardiovascular and Medical Sciences
      • • School of Medicine
      Glasgow, Scotland, United Kingdom
  • 2013
    • London School of Hygiene and Tropical Medicine
      • Department of Non-communicable Disease Epidemiology
      London, ENG, United Kingdom
  • 2009–2013
    • Leiden University Medical Centre
      • Department of Gerontology and Geriatrics
      Leiden, South Holland, Netherlands
    • University of London
      Londinium, England, United Kingdom
  • 2012
    • VU University Medical Center
      • Department of Rheumatology
      Amsterdam, North Holland, Netherlands
    • University of Lausanne
      Lausanne, Vaud, Switzerland
  • 2005–2012
    • University of Bristol
      • • School of Experimental Psychology
      • • MRC Centre for Causal Analyses in Translational Epidemiology
      Bristol, England, United Kingdom
    • WWF United Kingdom
      Londinium, England, United Kingdom
  • 2011
    • St George's, University of London
      • Division of Population Health Sciences and Education
      London, ENG, United Kingdom
    • University Hospitals Of Leicester NHS Trust
      Leiscester, England, United Kingdom
  • 2009–2011
    • The Dudley Group NHS Foundation Trust
      Dudley, England, United Kingdom
  • 2007–2011
    • University College London
      • Department of Primary Care and Population Health (PCPH)
      London, ENG, United Kingdom
    • University of Dundee
      Dundee, Scotland, United Kingdom
    • Leiden University
      Leyden, South Holland, Netherlands
  • 2006–2011
    • University of Aberdeen
      • Health Services Research Unit
      Aberdeen, Scotland, United Kingdom
  • 2003–2011
    • The University of Edinburgh
      • Centre for Population Health Sciences
      Edinburgh, SCT, United Kingdom
    • University of Texas at San Antonio
      San Antonio, Texas, United States
  • 2002–2011
    • University of Cambridge
      • Department of Public Health and Primary Care
      Cambridge, ENG, United Kingdom
    • West Georgia Obstetrics and Gynecology
      Georgetown, Georgia, United States
  • 2010
    • Erasmus MC
      • Department of Epidemiology
      Rotterdam, South Holland, Netherlands
  • 2003–2009
    • Ninewells Hospital
      Dundee, Scotland, United Kingdom
  • 2008
    • Centers for Disease Control and Prevention
      • National Center for Chronic Disease Prevention and Health Promotion
      Druid Hills, GA, United States
  • 2003–2004
    • The Bracton Centre, Oxleas NHS Trust
      Дартфорде, England, United Kingdom
  • 1998
    • Copenhagen University Hospital Hvidovre
      • Department of Clinical Biochemistry
      Hvidovre, Capital Region, Denmark