Oyekoya T Ayonrinde

University of Western Australia, Perth City, Western Australia, Australia

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Publications (22)93.95 Total impact

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    ABSTRACT: Background and AimsNonalcoholic fatty liver disease (NAFLD) and its metabolic risk factors are recognized during childhood and adolescence. Identification of adolescents at risk of NAFLD from childhood anthropometry may expose opportunities to influence the hepatic and metabolic destinies of individuals. We sought associations between NAFLD diagnosed during adolescence and earlier life trajectories of anthropometry, in a population-based cohort of predominantly Caucasian adolescents.Methods Assessment for NAFLD, using questionnaires and liver ultrasound was performed on 1170 adolescents, aged 17 years, from the population-based Raine Cohort. We sought associations between NAFLD in adolescents and serial anthropometric measurements recorded from birth, childhood and adolescence.ResultsNAFLD was diagnosed in 15.2% of adolescents. Birth anthropometry, including birth weight, skinfold thickness and ponderal index, was not associated with NAFLD. However, adiposity differences between 17-year-old adolescents with NAFLD and those without NAFLD were apparent from age 3 years. Greater adiposity trajectories for weight, body mass index, skinfold thickness, mid-arm circumference and chest circumference from age 3 years onwards, particularly in males, were associated with the diagnosis of NAFLD and severity of hepatic steatosis at age 17 years (p<0·05). The strength of the associations increased with age after 3 years for each adiposity measure (all p<0·001).Conclusions Trajectories of childhood adiposity are associated with NAFLD. Adiposity attained by three years of age and older, but not at birth, was associated with the diagnosis and severity of hepatic steatosis in late adolescence. Exploration of clinically relevant risk factors and preventative measures for NAFLD should begin during childhood.
    Journal of Gastroenterology and Hepatology 07/2014; · 3.33 Impact Factor
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    ABSTRACT: Non-alcoholic fatty liver disease (NAFLD) and serum 25-hydroxyvitamin D (s25(OH)D) concentrations are both associated with adiposity and insulin resistance (IR) and thus may be pathogenically linked. We aimed to determine the prevalence of vitamin D deficiency in adolescents with NAFLD and to investigate the longitudinal and cross-sectional associations between s25(OH)D concentrations and NAFLD. Participants in the population-based West Australian Pregnancy (Raine) Cohort had seasonally-adjusted s25(OH)D concentrations determined at ages 14 and then 17 years. NAFLD was diagnosed at 17 years using liver ultrasonography. Associations were examined after adjusting for potential confounders. Odds ratios (OR) and confidence intervals (CI) are reported per standard deviation in s25(OH)D concentrations. NAFLD was present in 16% (156/994) of adolescents. The majority of participants with NAFLD had either insufficient (51%) or deficient (17%) vitamin D status. Lower s25(OH)D concentrations at 17 years were significantly associated with increased risk of NAFLD (OR 0.74, 95%CI 0.56,0.97; p=0.029), after adjusting for sex, race, physical activity, television/computer viewing, body mass index and IR. The effect of s25(OH)D concentrations at 17 years was minimally affected after further adjusting for s25(OH)D concentrations at 14 years (OR 0.76, 95%CI 0.56,1.03; p=0.072). Lower s25(OH)D concentrations are significantly associated with NAFLD, independent of adiposity and IR. Screening for vitamin D deficiency in adolescents at risk of NAFLD is appropriate, and clinical trials investigating the effect of vitamin D supplementation in the prevention and treatment of NAFLD may be warranted.
    Journal of Gastroenterology and Hepatology 02/2014; · 3.33 Impact Factor
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    ABSTRACT: To investigate the ability of texture analysis of MRI images to stage liver fibrosis. Current noninvasive approaches for detecting liver fibrosis have limitations and cannot yet routinely replace biopsy for diagnosing significant fibrosis. Forty-nine patients with a range of liver diseases and biopsy-confirmed fibrosis were enrolled in the study. For texture analysis all patients were scanned with a T2 -weighted, high-resolution, spin echo sequence and Haralick texture features applied. The area under the receiver operating characteristics curve (AUROC) was used to assess the diagnostic performance of the texture analysis. The best mean AUROC achieved for separating mild from severe fibrosis was 0.81. The inclusion of age, liver fat and liver R2 variables into the generalized linear model improved AUROC values for all comparisons, with the F0 versus F1-4 comparison the highest (0.91). Our results suggest that a combination of MRI measures, that include selected texture features from T2 -weighted images, may be a useful tool for excluding fibrosis in patients with liver disease. However, texture analysis of MRI performs only modestly when applied to the classification of patients in the mild and intermediate fibrosis stages.J. Magn. Reson. Imaging 2013. © 2013 Wiley Periodicals, Inc.
    Journal of Magnetic Resonance Imaging 12/2013; · 2.57 Impact Factor
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    ABSTRACT: Although obesity is a major risk factor for non-alcoholic fatty liver (NAFL), not all obese individuals develop the condition, suggesting that other factors such as diet may also contribute to NAFL development. We evaluated associations between fructose and total sugar intake and subsequent diagnosis of NAFL in obese and non-obese adolescents in a population-based cohort. Adolescents participating in the Western Australian Pregnancy Cohort (Raine) Study completed 3-day food records and body mass index measurement at age 14 years. At age 17 years, subjects underwent abdominal ultrasound to determine NAFL status. Multivariate logistic regression models were used to analyse associations between energy-adjusted fructose and total sugar intake and NAFL status. Food diaries and liver assessments were completed for 592 adolescents. Prevalence of NAFL at age 17 was 12.8% for the total group, and 50% for obese adolescents. Fructose intake did not significantly differ between adolescents with or without NAFL in our cohort as a whole. Among obese adolescents, those without NAFL had significantly lower energy-adjusted fructose intake at age 14 years compared with those with NAFL (mean ± SD 38.8 ± 19.8 g/day, vs. 55.7 ± 14.4 g/day P = 0.02). Energy-adjusted fructose intake was independently associated with NAFL in obese adolescents (OR = 1.09, 95% CI: 1.01-1.19, p = 0.03) after adjustment for confounding factors. Energy-adjusted total sugar intake showed less significance (OR = 1.03, 95% CI: 0.999-1.07, p = 0.06). No significant associations were observed in other BMI categories. Lower fructose consumption in obese adolescents at 14 years is associated with a decreased risk of NAFL at 17 years. Fructose rather than overall sugar intake may be more physiologically relevant in this association.
    Journal of pediatric gastroenterology and nutrition 12/2013; · 2.18 Impact Factor
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    ABSTRACT: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide and is regarded as the hepatic manifestation of the metabolic syndrome. In adults, NAFLD is a determinant of arterial stiffness and cardiovascular risk, independent of the metabolic syndrome. Our aim was to ascertain if NAFLD is associated with arterial stiffness, independent of cardiometabolic factors in a population‐based cohort of adolescents. The 17‐year‐olds (n = 964) from an Australian birth cohort had measures of anthropometry, blood pressure, fasting insulin, glucose, lipids, and NAFLD by ultrasound. Two‐step cluster analysis identified youth at high metabolic risk. Measures of arterial stiffness (pulse wave velocity [PWV] and augmentation index corrected for heart rate [AI@75]) were obtained using applanation tonometry. The overall prevalence of NAFLD was 13.3%. The “high risk” metabolic cluster at age 17 years included 16% males and 19% females. Compared to “low risk,” the “high risk” cluster participants had greater waist circumference, triglycerides, insulin, systolic blood pressure, and lower high‐density lipoprotein (HDL) cholesterol (all P P = 0.037). Males who had NAFLD in the presence of the metabolic cluster had greater AI@75 (b = 6.3, 95% CI 1.9 to 10.7, P = 0.005). Conclusion: NAFLD is only associated with increased arterial stiffness in the presence of the “high risk” metabolic cluster. This suggests that arterial stiffness related to the presence of NAFLD is predicated on the presence of an adverse metabolic profile in adolescents. (Hepatology 2013;58:1306–1314)
    Hepatology 05/2013; · 12.00 Impact Factor
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    ABSTRACT: OBJECTIVES:Poor dietary habits have been implicated in the development of nonalcoholic fatty liver disease (NAFLD); however, little is known about the role of specific dietary patterns in the development of NAFLD. We examined prospective associations between dietary patterns and NAFLD in a population-based cohort of adolescents.METHODS:Participants in the Western Australian Pregnancy Cohort (Raine) Study completed a food frequency questionnaire at 14 years and had liver ultrasound at 17 years (n=995). Healthy and Western dietary patterns were identified using factor analysis and all participants received a z-score for these patterns. Prospective associations between the dietary pattern scores and risk of NAFLD were analyzed using multiple logistic regression.RESULTS:NAFLD was present in 15.2% of adolescents. A higher Western dietary pattern score at 14 years was associated with a greater risk of NAFLD at 17 years (odds ratio (OR) 1.59; 95% confidence interval (CI) 1.17-2.14; P<0.005), although these associations were no longer significant after adjusting for body mass index at 14 years. However, a healthy dietary pattern at 14 years appeared protective against NAFLD at 17 years in centrally obese adolescents (OR 0.63; 95% CI 0.41-0.96; P=0.033), whereas a Western dietary pattern was associated with an increased risk of NAFLD.CONCLUSIONS:A Western dietary pattern at 14 years in a general population sample was associated with an increased risk of NAFLD at 17 years, particularly in obese adolescents. In centrally obese adolescents with NAFLD, a healthy dietary pattern may be protective, whereas a Western dietary pattern may increase the risk.Am J Gastroenterol advance online publication, 2 April 2013; doi:10.1038/ajg.2013.95.
    The American Journal of Gastroenterology 04/2013; · 7.55 Impact Factor
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    ABSTRACT: Hepatic steatosis is associated with an increased risk of developing serious liver disease and other clinical sequelae of the metabolic syndrome. However, visual estimates of steatosis from histological sections of biopsy samples are subjective and reliant on an invasive procedure with associated risks. The aim of this study was to test the ability of a rapid, routinely available, magnetic resonance imaging (MRI) method to diagnose clinically relevant grades of hepatic steatosis in a cohort of patients with diverse liver diseases. Fifty-nine patients with a range of liver diseases underwent liver biopsy and MRI. Hepatic steatosis was quantified firstly using an opposed-phase, in-phase gradient echo, single breath-hold MRI methodology and secondly, using liver biopsy with visual estimation by a histopathologist and by computer-assisted morphometric image analysis. The area under the receiver operating characteristic (ROC) curve was used to assess the diagnostic performance of the MRI method against the biopsy observations. The MRI approach had high sensitivity and specificity at all hepatic steatosis thresholds. Areas under ROC curves were 0.962, 0.993, and 0.972 at thresholds of 5%, 33%, and 66% liver fat, respectively. MRI measurements were strongly associated with visual (r(2) = 0.83) and computer-assisted morphometric (r(2) = 0.84) estimates of hepatic steatosis from histological specimens. This MRI approach, using a conventional, rapid, gradient echo method, has high sensitivity and specificity for diagnosing liver fat at all grades of steatosis in a cohort with a range of liver diseases.
    PLoS ONE 01/2013; 8(3):e59287. · 3.73 Impact Factor
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    ABSTRACT: Genetic factors account for a significant proportion of the phenotypic variance of non-alcoholic fatty liver disease (NAFLD), however very few predisposing genes have been identified. We aimed to (1) identify novel genetic associations with NAFLD by performing a genome-wide association study (GWAS), and (2) examine the biological expression of the strongest genetic associations in a separate cohort. We performed GWAS of a population-based cohort (Raine Study) of 928 adolescents assessed for NAFLD by ultrasound at age 17. Expression of genes with single nucleotide polymorphisms (SNPs) that were associated with NAFLD at a significance level of p<10(-5) was examined in adults with NAFLD and controls by quantifying hepatic mRNA expression and serum levels of protein. After adjustment for sex and degree of adiposity, SNPs in 2 genes expressed in liver were associated with NAFLD adolescents: group-specific component (GC) (odds ratio [OR], 2.54; P=1.20x10(-6) ) and lymphocyte cytosolic protein-1 (LCP1) (OR, 3.29; P=2.96x10(-6) ). SNPs in 2 genes expressed in neurons were also associated NAFLD: lipid phosphate phosphatase-related protein type 4 (LPPR4) (OR, 2.30; P=4.82x10(-6) ) and solute carrier family 38 member 8 (SLC38A8) (OR, 3.14; P=1.86x10(-6) ). Hepatic GC mRNA was significantly reduced (by 83%) and LCP1 mRNA was increased (by 300%) in liver biopsy samples from patients with NAFLD compared to controls (P<.05). Mean serum levels of GC protein were significantly lower in patients with NAFLD than controls (250±90 vs 298±90, respectively; P=.004); GC protein levels decreased with increasing severity of hepatic steatosis (P<.01). In conclusion, association between GC and LCP1 SNP's and NAFLD as well as altered biological expression implicate these genes in the pathogenesis of NAFLD. (HEPATOLOGY 2012.).
    Hepatology 12/2012; · 12.00 Impact Factor
  • American Association for the Study of Liver Diseases; 11/2012
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    ABSTRACT: Environmental factors including excessive caloric intake lead to disordered lipid metabolism and fatty liver disease (FLD). However, FLD demonstrates heritability suggesting genetic factors are also important. We aimed to use a candidate gene approach to examine the association between FLD and single nucleotide polymorphisms (SNPs) in lipid metabolism genes in the adolescent population-based Western Australian Pregnancy (Raine) Cohort. A total 951 seventeen year-olds underwent hepatic ultrasound, anthropometric and biochemical characterization, DNA extraction and genotyping for 57 SNPs in seven lipid metabolism genes (ApoB100, ATGL, ABHD5, MTTP, CETP, SREBP-1c, PPARα). Associations were adjusted for metabolic factors and Bonferroni corrected. The prevalence of FLD was 16.2% (11.4% male vs 21.2% female, P=0.001). Multivariate analysis of metabolic factors found suprailiac skinfold thickness (SST) to be the major predictor of FLD in females and males (odds ratio [OR] 1.11, 95% confidence interval [CI] 1.08-1.15, P=1.7×10(-10) and OR 1.17, 95%CI 1.13-1.22, P=2.4×10(-11) , respectively). In females, two SNPs in linkage disequilibrium from the CETP gene were associated with FLD: rs12447924 (OR 2.16, 95%CI 1.42-3.32, P=0.0003) and rs12597002 (OR=2.22, 95%CI 1.46-3.41 P=0.0002). In lean homozygotes, the probability of FLD was over 30%, compared with 10-15% in lean heterozygotes and 3-5% in lean wild-types. However, these associations were modified by SST, such that for obese individuals, the probability of FLD was over 30% in all genotype groups. Cholesteryl ester transfer protein gene polymorphisms are associated with an increased risk of FLD in adolescent females. The effect is independent of adiposity in homozygotes, thereby placing lean individuals at a significant risk of FLD.
    Journal of Gastroenterology and Hepatology 03/2012; 27(9):1520-7. · 3.33 Impact Factor
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    ABSTRACT: Nonalcoholic fatty liver disease (NAFLD) is a predominantly adult-diagnosed disorder. Knowledge regarding the epidemiology, phenotype, and metabolic risk factors, during adolescence is limited. We sought to determine the prevalence, phenotype, and predictors of NAFLD in 1170 community-based adolescents in the Western Australian Pregnancy Cohort (Raine) Study (the Raine Cohort) who underwent a cross-sectional assessment that included questionnaires, anthropometry, cardiovascular examinations, blood tests, and abdominal ultrasound examinations. Among the 1170 adolescents assessed, the prevalence of NAFLD was 12.8%. Females compared with males had a significantly higher prevalence of NAFLD (16.3% versus 10.1%, P = 0.004) and central obesity (33.2% versus 9.9%, P < 0.05). The severity of hepatic steatosis was associated with the body mass index, waist circumference, subcutaneous adipose tissue thickness (SAT), serum leptin level, homeostasis model assessment for insulin resistance score (P < 0.001 for all), and serum alanine aminotransferase level (P < 0.005) in both genders, but it was associated with increasing visceral adipose tissue thickness (VAT; P < 0.001) and decreasing serum adiponectin levels (P < 0.05) in males alone. Males and females with NAFLD had similar amounts of SAT (P > 0.05); however, in comparison with females with NAFLD, males with NAFLD had greater VAT, a more severe metabolic phenotype with higher glucose levels and systolic blood pressure and lower adiponectin and high-density lipoprotein cholesterol levels (P < 0.001 for all), and greater measures of liver injury (alanine aminotransferase and aspartate aminotransferase, P < 0.001 for all). Similarly, metabolic syndrome was more common in males than females with NAFLD (24% versus 8%, P = 0.01). Suprailiac skinfold thickness predicted NAFLD independently of the body mass index, insulin resistance, and VAT. CONCLUSION: Gender differences in adolescent NAFLD are related to differences in adipose distribution and adipocytokines. The male phenotype of NAFLD is associated with more adverse metabolic features and greater visceral adiposity than the female phenotype despite the lower prevalence of NAFLD.
    Hepatology 03/2011; 53(3):800-9. · 12.00 Impact Factor
  • Eng K Gan, Oyekoya T Ayonrinde, Debbie Trinder, John K Olynyk
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    ABSTRACT: Profound advances in our knowledge of hereditary hemochromatosis (HH) during the past 150 years have resulted in two distinct "iron ages": the pre-HFE gene era and the post-HFE gene era. During these periods, family studies, HLA association studies, and ultimately HFE gene studies in various populations informed us of the genotypic prevalence as well as the clinical and biochemical penetrance of HH. We learned that HH has a highly variable clinical penetrance in susceptible individuals of Northern European ancestry. Further, we now recognize that the natural history of HH is not as discrete as previously believed, because genetic and environmental modifiers of disease penetrance are increasingly identified as influencing the clinical expression of HH.
    Current Gastroenterology Reports 02/2010; 12(1):7-12.
  • Oyekoya T Ayonrinde, John K Olynyk
    Journal of Gastroenterology and Hepatology 01/2010; 25(1):3-4. · 3.33 Impact Factor
  • Journal of Gastroenterology and Hepatology. 01/2010; 25:A24-A24.
  • Eng K Gan, Debbie Trinder, Oyekoya T Ayonrinde, John K Olynyk
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    ABSTRACT: Hereditary hemochromatosis due to homozygosity for the C282Y mutation in the HFE gene product is the most common autosomal recessive genetic disorder in populations of northern European descent, where it attains a maximum prevalence of approximately one in 200. Cross-sectional and longitudinal studies have revealed that clinically significant iron-overload disease develops in at least 28% of male and 1% of female HFE C282Y homozygotes. The relatively low clinical penetrance is largely unexplained. Current evidence suggests a limited role for digenic inheritance of mutations in iron homeostasis genes in modifying the penetrance of hemochromatosis. Male gender is a strong genetic factor, promoting expression of clinical disease. Dietary intake of alcohol and noncitrus fruit may also act as important environmental modifiers of penetrance. With genetic analyses becoming simpler to perform, new genetic modifiers of hepatic iron loading and liver fibrogenesis are likely to be forthcoming.
    Expert Review of Endocrinology &amp Metabolism 01/2009; 4(3):225-239.
  • Debbie Trinder, Oyekoya T Ayonrinde, John K Olynyk
    Gastroenterology 02/2008; 134(1):348-51. · 12.82 Impact Factor
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    ABSTRACT: Hereditary hemochromatosis (HH) comprises a group of inherited disorders of iron metabolism that can result in progressive iron overload, morbidity, and mortality, generally in adulthood. HFE-related HH is the most common type of HH and will form the core of this discussion. The discovery of new proteins and gene mutations has defined other types of HH, termed non-HFE HH. The regulatory protein hepcidin has a central role in iron homeostasis in these disorders. While the liver is the predominant organ of iron deposition and iron-overload-related disease in HFE-related HH, involvement of extrahepatic tissue can also result in morbidity and mortality if the disorder is not diagnosed before organ damage develops. This review traverses the road from HFE genotype to phenotype with a focus on clinical penetrance, modifier factors for disease expression, and current thoughts and controversies on HH diagnosis and screening.
    Critical Reviews in Clinical Laboratory Sciences 02/2008; 45(5):451-84. · 3.78 Impact Factor
  • Oyekoya T Ayonrinde, John K Olynyk
    Hepatology 11/2007; 46(4):960-2. · 12.00 Impact Factor
  • Early Human Development - EARLY HUM DEV. 01/2007; 83.
  • Early Human Development - EARLY HUM DEV. 01/2007; 83.

Publication Stats

92 Citations
93.95 Total Impact Points


  • 2008–2014
    • University of Western Australia
      • • School of Medicine and Pharmacology
      • • Centre for Health Services Research
      Perth City, Western Australia, Australia
  • 2007–2010
    • Fremantle Hospital and Health Service
      Fremantle, Western Australia, Australia