Nigel Stepto

Publications (38) View all

• Article: Dietary Composition in the Treatment of Polycystic Ovary Syndrome: A Systematic Review to Inform Evidence-Based Guidelines.

  Lisa J Moran, Henry Ko, Marie Misso, Kate Marsh, Manny Noakes, Mac Talbot, Meredith Frearson, Mala Thondan, Nigel Stepto, Helena J Teede
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  ABSTRACT: While lifestyle management is recommended as first-line treatment of polycystic ovary syndrome (PCOS), the optimal dietary composition is unclear. The aim of this study was to compare the effect of different diet compositions on anthropometric, reproductive, metabolic, and psychological outcomes in PCOS. A literature search was conducted (Australasian Medical Index, CINAHL, EMBASE, Medline, PsycInfo, and EBM reviews; most recent search was performed January 19, 2012). Inclusion criteria were women with PCOS not taking anti-obesity medications and all weight-loss or maintenance diets comparing different dietary compositions. Studies were assessed for risk of bias. A total of 4,154 articles were retrieved and six articles from five studies met the a priori selection criteria, with 137 women included. A meta-analysis was not performed due to clinical heterogeneity for factors including participants, dietary intervention composition, duration, and outcomes. There were subtle differences between diets, with greater weight loss for a monounsaturated fat-enriched diet; improved menstrual regularity for a low-glycemic index diet; increased free androgen index for a high-carbohydrate diet; greater reductions in insulin resistance, fibrinogen, total, and high-density lipoprotein cholesterol for a low-carbohydrate or low-glycemic index diet; improved quality of life for a low-glycemic index diet; and improved depression and self-esteem for a high-protein diet. Weight loss improved the presentation of PCOS regardless of dietary composition in the majority of studies. Weight loss should be targeted in all overweight women with PCOS through reducing caloric intake in the setting of adequate nutritional intake and healthy food choices irrespective of diet composition.
  Journal of the Academy of Nutrition and Dietetics. 02/2013;
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  Available from: Nir Eynon

  Article: ACTN3 R577X polymorphism and team-sport performance: A study involving three European cohorts.

  Nir Eynon, Lauren K Banting, Jonatan R Ruiz, Pawel Cieszczyk, Dmitry A Dyatlov, Agnieszka Maciejewska-Karlowska, Marek Sawczuk, Vladimir P Pushkarev, Leonid M Kulikov, Evgeny D Pushkarev, Pedro Femia, Nigel K Stepto, David J Bishop, Alejandro Lucia
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  ABSTRACT: OBJECTIVES: To determine the association between the α-actinin-3 (ACTN3) R577X polymorphism and elite team-sport athletic status in three cohorts of European team-sport athletes. DESIGN: We compared the genotype and allele frequencies of the ACTN3 R577X (rs1815739) polymorphisms between team-sport athletes (n=205), endurance athletes (n=305), sprint/power athletes (n=378), and non-athletic controls (n=568) from Poland, Russia and Spain; all participants were unrelated European men. METHODS: Genomic DNA was extracted from either buccal epithelium or peripheral blood using a standard protocol. Genotyping was performed using several methods, and the results were replicated following recent recommendations for genotype-phenotype association studies. RESULTS: Genotype distributions of all control and athletic groups met Hardy-Weinberg equilibrium (all p>0.05). Team-sport athletes were less likely to have the 577RR genotype compared to the 577XX genotype than sprint/power athletes [odds ratio: 0.58, 95% confidence interval: 0.34-0.39, p=0.045]. However, the ACTN3 R577X polymorphism was not associated with team-sports athletic status, compared to endurance athletes and non-athletic controls. Furthermore, no association was observed for any of the genotypes with respect to the level of competition (elite vs. national level). CONCLUSIONS: The ACTN3 R577X polymorphism was not associated with team-sport athletic status, compared to endurance athletes and non-athletic controls, and the observation that the 577RR genotype is overrepresented in power/sprint athletes compared with team-sport athletes needs to be confirmed in future studies.
  Journal of science and medicine in sport / Sports Medicine Australia. 03/2013;
• Article: Divergent skeletal muscle respiratory capacities in rats artificially selected for high- and low-running ability: a role for Nor1?

  Erin J Stephenson, Nigel K Stepto, Lauren G Koch, Steven L Britton, John A Hawley
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  ABSTRACT: Inactivity-related diseases are becoming burden on Western society. Whilst there is a major environmental contribution to metabolic health, the intrinsic properties that predispose or protect against particular health traits are harder to define. We have used rat models of inborn high-(HCR) and low-running capacity (LCR) to determine inherent differences in mitochondrial volume and function, hypothesizing that HCR have greater skeletal muscle respiratory capacity due to a greater mitochondrial volume. Additionally, we sought to determine if there was a link between the expression of the nuclear receptor Neuron-derived Orphan Receptor-1 (Nor1) and inherent skeletal muscle respiratory capacity. LCR were 28% heavier (P<0.0001) and fasting serum insulin concentrations were 62% greater than HCR (P=0.02). In contrast, HCR had better glucose tolerance and reduced adiposity. In the soleus, maximal respiratory capacity was 21% greater in HCR (P=0.001), for which the relative contribution of fat oxidation was 20% higher than LCR (P=0.02). This was associated with increased citrate synthase (CS; 33%, P=0.009) and β-hydroxyacyl-CoA (β-HAD; 33%, P=0.0003) activities. In the EDL, CS activity was 29% greater (P=0.01) and β-HAD activity was 41% (P=0.0004) greater in HCR compared to LCR. MtDNA copy number was elevated in HCR EDL (35%, P=0.049). Additionally, HCR had increased protein expression of individual mitochondrial respiratory complexes, CS and UCP3 in both muscles (all P<0.05). Nor1 protein was greater in EDL and soleus of HCR compared to LCR (P<0.05). We propose that the differential expression of Nor1 may contribute to the differences in metabolic regulation between the LCR and HCR phenotypes.
  Journal of Applied Physiology 08/2012; · 3.75 Impact Factor
• Article: PIGMENT EPITHELIUM-DERIVED FACTOR, INSULIN SENSTIVITY AND ADIPOSITY IN POLYCYSTIC OVARY SYNDROME: IMPACT OF EXERCISE TRAINING.

  A E Joham, H J Teede, S K Hutchison, N K Stepto, C L Harrison, E Paul, M J Watt
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  ABSTRACT: Pigment epithelium-derived factor (PEDF) is upregulated in obese rodents and is involved in the development of insulin resistance (IR). We aim to explore the relationships between PEDF, adiposity, insulin sensitivity and cardiovascular risk factors in obese women with Polycystic Ovary Syndrome (PCOS) and weight-matched controls and to examine the impact of endurance exercise training on PEDF.This prospective cohort intervention study was based at a tertiary medical centre. 20 obese PCOS women and 14 non-PCOS weight-matched women were studied at baseline. PEDF, cardiometabolic markers, detailed body composition and euglycaemic hyperinsulinaemic clamps were performed and measures were repeated in 10 PCOS and 8 non-PCOS women following 12 weeks of intensified aerobic exercise.Mean GIR was 31.7% lower (p=0.02) in PCOS compared to controls [175.3±96.3 and 257.2±64.3 mg.m(-2).min(-1)] at baseline, yet both PEDF and BMI were similar between groups. PEDF negatively correlated to GIR [r=-0.41, p=0.03] and HDL (r=-0.46, p=0.01) and positively to cardiovascular risk factors [systolic (r=0.41, p=0.02) and diastolic blood pressure (r=0.47, p=0.01) and triglycerides (r=0.49, p=0.004). The correlation with GIR was not significant after adjusting for fat mass (p=0.07). Exercise training maintained BMI and increased GIR in both groups, however, plasma PEDF was unchanged.In summary, PEDF is not elevated in PCOS, is not associated with IR when adjusted for fat mass and is not reduced by endurance exercise training despite improved insulin sensitivity. PEDF was associated with cardiovascular risk factors, suggesting PEDF may be a marker of cardiovascular risk status.
  Obesity 05/2012; · 4.28 Impact Factor
• Article: Effect of exercise training on insulin sensitivity, mitochondria and computed tomography muscle attenuation in overweight women with and without polycystic ovary syndrome.

  S K Hutchison, H J Teede, D Rachoń, C L Harrison, B J Strauss, N K Stepto
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  ABSTRACT: Polycystic ovary syndrome (PCOS) is an insulin resistant (IR) state. Increased skeletal muscle lipid content and impaired mitochondrial biogenesis have been implicated in the pathogenesis of IR. We investigated whether differences in these variables explain the IR of women affected by PCOS and whether improvements in IR with exercise are reflected by changes in these variables. Sixteen PCOS and 13 non-PCOS overweight women were assessed, and eight PCOS and seven non-PCOS women were reassessed after 12 weeks of moderate and vigorous exercise training. Outcomes included insulin sensitivity (glucose infusion rate [GIR]), skeletal muscle gene expression and protein abundance, enzyme activity of selected mitochondrial components, and computed tomography (CT) attenuation-estimated muscle lipid. GIR was lower in women with PCOS versus those without (p = 0.01) and increased with exercise in both groups. Baseline CT muscle attenuation suggested a trend to less muscle lipid in PCOS, which increased with exercise training, with a difference in the change in muscle lipid (p = 0.01, age-corrected), compared with non-PCOS women. GIR correlated with PGC1A gene expression across the whole group; skeletal muscle expression of mitochondrial biogenesis markers was not different between groups at baseline, or after training. Neither lipid changes nor mitochondrial changes correlated with changes in GIR. Differences in IR in women with and without PCOS were not explained by differences in skeletal muscle lipid or mitochondrial parameters. Improvements in IR with exercise were dissociated from mitochondrial parameters. CT muscle attenuation suggested a differential capacity of PCOS muscle to store lipid compared with non-PCOS. Clinicaltrials.gov ISRCTN84763265. National Health & Medical Research Council (Grant number 606553), Monash University and The Jean Hailes Foundation.
  Diabetologia 01/2012; 55(5):1424-34. · 6.81 Impact Factor