Study Objectives: Mandibular advancement splints (MAS) are often preferred to CPAP treatment for OSA but are not always equally effi cacious. High therapeutic CPAP pressure has been associated with MAS treatment failure in a Japanese population. We sought to assess the relationship between CPAP pressure and MAS treatment response in an Australian population. Methods: Therapeutic CPAP pressure and MAS treatment response were obtained from a one-month crossover trial of both treatments. Predictive utility of CPAP pressure to identify MAS treatment response was assessed. Results: Seventy-eight OSA patients were included (age 49.3 ± 11.1 years, BMI 29.1 ± 5.8 kg/m 2 ) with predominantly moderate-severe OSA (AHI 30.0 ± 12.7/h). CPAP pressure was lower in MAS responders (MAS AHI < 10/h) 9.7 ± 1.6 vs. 11.7 ± 2.4 cm H 2 O, p < 0.01, with area under ROC curve of 0.74 (95% CI 0.63-0.86), p < 0.01. The best cutoff value of 10.5 cm H 2 O useful for discriminating MAS responders and non-responders in the previous Japanese population, was inadequate for prediction in the current population (0.47 negative predictive value [NPV] S C I E N T I F I C I N V E S T I G A T I O N SC ontinuous positive airway pressure (CPAP) is the standard treatment for obstructive sleep apnea (OSA). Although highly effi cacious, CPAP is often hindered by poor tolerance and suboptimal adherence, 1 limiting its effectiveness in the real world. Mandibular advancement splints (MAS) are an alternative option recommended as a fi rst-line treatment for mildmoderate OSA. 2 We have recently found that health outcome improvements, including sleepiness, are similar with MAS and CPAP treatments in patients with moderate-severe OSA. Superior patient adherence appears to offset any inferiority of MAS effi cacy, 3 and MAS may be considered a viable alternative for many patients.However despite similar health benefi ts between treatments, approximately one-third of OSA patients will not respond to MAS. [4][5][6][7] This is of signifi cant concern in terms of resource wastage and treatment delays. Much attention has been given to understanding patient phenotypes which relate to MAS response such as gender, obesity, craniofacial structure, and type and severity of OSA.8 However, none of these factors are universal, and hence there is an unresolved need for reliable indicators of MAS treatment response. A recent Japanese study has identifi ed pressure requirement in CPAP users as a predictor of MAS response. 9 In established CPAP users, a prescribed pressure of above 10.5 cm H 2 O indicated poor response to subsequent MAS therapy. This prediction method is, of course, restricted to patients who have used CPAP and wish to try MAS. However CPAP pressure would represent a simple predictor, either alone or possibly in combination with other patient characteristics to further improve BRIEF SUMMARY Current Knowledge/Study Rationale: CPAP pressure has been shown to predict oral appliance treatment response in Japanese male OSA patients and could be a simple and useful clini...

The version presented here may differ from the published version. If citing, you are advised to consult the published version for pagination, volume/issue and date of publication Title: Reduced skeletal muscle protein balance and sarcopenia in paediatric Crohn's disease patients in remission.

Muscle anabolic resistance to dietary protein is associated with obesity and insulin resistance. However, the contribution of excess consumption of fat to anabolic resistance is not well studied. The aim of these studies was to test the hypothesis that acute and short-term dietary fat overload will impair the skeletal muscle protein synthetic response to dietary protein ingestion. Eight overweight/obese men [46.4 ± 1.4 yr, body mass index (BMI) 32.3 ± 5.4 kg/m2] participated in the acute feeding study, which consisted of two randomized crossover trials. On each occasion, subjects ingested an oral meal (with and without fat emulsion), 4 h before the coingestion of milk protein, intrinsically labeled with [1-13C]phenylalanine, and dextrose. Nine overweight/obese men (44.0 ± 1.7 yr, BMI 30.1 ± 1.1 kg/m2) participated in the chronic study, which consisted of a baseline, 1-wk isocaloric diet, followed by a 2-wk high-fat diet (+25% energy excess). Acutely, incorporation of dietary amino acids into the skeletal muscle was twofold higher ( P < 0.05) in the lipid trial compared with control. There was no effect of prior lipid ingestion on indices of insulin sensitivity (muscle glucose uptake, pyruvate dehydrogenase complex activity, and Akt phosphorylation) in response to the protein/dextrose drink. Fat overfeeding had no effect on muscle protein synthesis or glucose disposal in response to whey protein ingestion, despite increased muscle diacylglycerol C16:0 ( P = 0.06) and ceramide C16:0 ( P < 0.01) levels. Neither acute nor short-term dietary fat overload has a detrimental effect on the skeletal muscle protein synthetic response to dietary protein ingestion in overweight/obese men, suggesting that dietary-induced accumulation of intramuscular lipids per se is not associated with anabolic resistance.