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self-selected pace. Group differences in peak jointdisplacement and amount of joint motion through-out the gait cycle (calculated as the integrateddisplacement curve) were analysed using ANOVAs.

Results: Non-obese children had greater peakknee (p = 0.013) and hip extension (p = 0.023) dur-ing gait; however, there were no group differencesin amount of sagittal plane motion at any joint.Obese children had greater peak hip adduction(p = 0.001), and also spent more time in hip adduc-tion (p = 0.003) than non-obese children. Obesechildren had greater peak externally rotated toeprogression (p = 0.004), and spent more time inthis toe-out position (p = 0.012). Obese children hadgreater peak hip internal rotation (p = 0.002), andspent more time in hip internal rotation (p = 0.004).

Conclusions: Non-obese children showed greatermobility in the sagittal plane, particularly at the hipand knee. Frontal and transverse plane differencessuggest that obese children function in a more genuvalgum position than non-obese children. Staticmeasures of genu valgum have been previouslyassociated with pediatric obesity; the findings ofthis study indicate that there are also dynamicimplications of such lower extremity malalignmentin obese children. Genu valgum presents a greaterrisk of osteoarthritis for obese children and shouldbe considered when prescribing weight bearingexercise to this cohort.

http://dx.doi.org/10.1016/j.orcp.2013.12.653

155

The impact of macronutrients onbrown adipose tissuethermogenesis

Aneta Stefanidis ∗, Andrew Dow,Matthew Watt, Brian Oldfield

Monash University, Clayton, VIC,Australia

The identification of brown adipose tissue (BAT)in adult humans and importance in the determina-tion of levels of obesity has led to a renaissance inthis field, particularly in relation to the potentialfor it to be targeted as an anti-obesity therapy. Fur-thermore, dietary macronutrients have been shownto be unequal in terms of their impact on foodintake; however, the outstanding question is howdifferent macronutrients drive energy expenditure.These experiments aim to characterise the impactof specific macronutrient groups on energy expen-diture in BAT and gain an insight into the underlyingmechanism(s).

Adult male Sprague Dawley rats were surgi-cally implanted with a cannula directed into thestomach and exteriorized subcutaneously in thedorsal region of the neck. At the same time,a telemetric device was implanted between theinterscapular lobes of the BAT to measure shifts inlocal temperature, indicative of thermogenic activ-ity. Macronutrients (glucose, lipid, protein) werematched for calories and volume and infused (1)directly into the stomach or (2) towards the brain(via carotid artery).

The administration of glucose, lipid or protein,both peripherally or towards the brain causes a dif-ferential activation of BAT thermogenesis. Therewas a significant impact of all macronutrients, withthe most profound effect on BAT activity derivedfrom lipid, followed by protein and glucose.

These data provide a framework for the for-mulation of ‘‘smart diets’’ that will allow theeffective control of body weight through modula-tion of energy expenditure.

http://dx.doi.org/10.1016/j.orcp.2013.12.654

156

BRSK1 regulates glucose uptake inL6 cells and mouse skeletal muscle

Xu Yan 1,2,∗, Kazuhiro Nakano 1, DingAn 1, Michael F. Hirshman 1, Laurie J.Goodyear 1

1 Joslin Diabetes Center, HarvardMedical School, Boston, MA, USA2 Institute of Sport, Exercise &Active Living (ISEAL), VictoriaUniversity, Melbourne, VIC, Australia

AMP-activated protein kinase (AMPK) and itsupstream kinase LKB1 regulate glucose uptake inskeletal muscle. Brain specific kinase 1 (BRSK1)is an AMPK-related kinase activated by LKB1 viaThr189 phosphorylation and is required for neuronalpolarisation in mammals. Three BRSK1 isoformshave been reported in the brain (long, short andS1 form), whereas there have been no studies ofBRSK1 expression and function in skeletal muscle.We used L6 muscle cells and mouse skeletal mus-cle to study the expression and function of BRSK1in vitro and in vivo. Of those three BRSK1 isoforms,mRNA and protein analyses showed that L6 cells andskeletal muscles abundantly express the short formBRSK1. To study the function of short form BRSK1in muscle, wild type and mutant (Thr189Ala) BRSK1were over-expressed in L6 myotubes and shRNA wasused to knock down BRSK1 (58%). Wild type BRSK1over-expression had no effect on basal glucose

ANZOS 2013 abstracts e85

uptake, but increased insulin-stimulated (30 nM,30 min) glucose uptake by 51.0 ± 18.7% vs. emptyvector control cells (p < 0.05). BRSK1 knockdowndecreased basal glucose uptake by 21.3 ± 5.7%(p < 0.05) and insulin-stimulated glucose uptake by22.8 ± 6.9%, (p < 0.05)when compared to scram-bled shRNA. To study the role of BRSK1 in vivo,short form Brsk1 was expressed in tibialis anterior(TA) muscles by in vivo gene injection and elec-troporation. Similar to L6 cells, wild type BRSK1over-expression increased insulin-stimulated glu-cose uptake in TA (77.7 ± 12.0%, p < 0.05), with noeffect of the mutant BRSK1. In summary, short formBRSK1 over-expression increases insulin-stimulatedglucose uptake in L6 myotubes and skeletal muscle,and BRSK1 knockdown in L6 cells decreases basaland insulin-stimulated glucose uptake. The shortform of BRSK1, an AMPK-related Kinase, is highlyexpressed in skeletal muscle and may function toregulate insulin action.

http://dx.doi.org/10.1016/j.orcp.2013.12.655

157

Development of overweight andobesity in mid-age women from theAustralian Longitudinal on WomenHealth Study

Haya Alljadani 1,2,∗, AmandaPatterson 1, David Sibbritt 3, ClareCollins 1

1 School of Health Sciences, Facultyof Health, Priority Research Centrein Physical Activity and Nutrition,The University of Newcastle,Newcastle, NSW, Australia2 Faculty of Nutrition and HealthScience, King Abdul-Aziz University,Jeddah, Saudi Arabia3 Faculty of Health, University ofTechnology Sydney, Sydney, NSW,Australia

Aim: Obesity is at epidemic proportions world-wide. Therefore the aim was to investigate therelationship between diet quality, physical activity,and the development of overweight and obesity inmid-aged women during six years of follow-up afteradjustment for baseline weight.

Methods: A prospective cohort from the Aus-tralian Longitudinal on Women Health Study(ALSWH) [n = 3403, age range 47.6—55.8 years,normal weight (25 > BMI ≥ 18.5 kg/m2) at base-line], who were disease free. Diet quality wasmeasure by the Australian Recommended Food

Score (ARFS), physical activity and smoking sta-tus were reported at baseline. BMI was calculated(kg/m2) from self-reported height and weight (2001and 2007). Women were categorised as over-weight (25 ≥ BMI < 30 kg/m2) or obese (BMI ≥ 30) atfollow-up. Logistic regression used to assess therelationship between the variables and becomingoverweight/obese and repeated in sub-sample withplausible total energy intakes (n = 1107).

Results: The respective six year incidence ofoverweight and obesity was 18.5% and 1.1%. Dietquality was not related to the risk of becom-ing overweight/obese. Those women classified asbeing moderately physical active were less likely tobecome overweight/obese compared to those inac-tive (OR = 0.45; CI: 0.26, 0.79) (p = 0.005). Womenwho had quit smoking at baseline were more likelyto become overweight/obese (OR = 1.47; CI: 1.01,2.13) (p = 0.043) and those with higher baselineweight were also more likely to become over-weight/obese at follow-up (OR = 1.14; CI: 1.10,1.18) (p < 0.001).

Conclusion: Mid-age is associated with sub-stantial weight gain and high incidence of over-weight/obesity. Public health interventions areneeded to help prevent weight gain at this lifestage. Those with excessive weight gain, especiallysmokers or those who have quit smoking may needtargeted interventions. While this study does notsupport improving diet quality as a strategy to pre-vent weight gain, it does suggest that improvingdiet quality is not associated with weight gain.

http://dx.doi.org/10.1016/j.orcp.2013.12.656

158

Reliability and validity of a shorttool assessing Australian toddlers’dietary risk

Lucinda K. Bell 1,∗, Rebecca K.Golley 2, Anthea A. Magarey 1

1 Nutrition and Dietetics, FlindersUniversity, Adelaide, SA, Australia2 Sansom Institute for HealthResearch, University of SouthAustralia, Adelaide, SA, Australia

Background/objectives: Identifying toddlers atdietary risk is crucial for determining who requiresintervention to improve dietary patterns andreduce health consequences. We aimed to deter-mine the reliability and validity of a new simpletool that assesses dietary risk patterns of Australiantoddlers.