Therefore, the review suggests that the study population needs to be broadened to include both T1DM and T2DM models, older rats as well as young rats, and importantly animals from both sexes to reflect more accurately clinical practice.

OBJECTIVES: To investigate the ®bre type composition of skeletal muscle in infants and young children and to compare the ®ndings to an adult population. To relate the ®bre type pro®le of skeletal muscle in adults to measures of adiposity. DESIGN: Cross-sectional studies of skeletal muscle ®bre composition in infants and adults with measures of adiposity in the adults. SUBJECTS: 21 healthy infants and young children (age: 3±21 months) and 40 healthy adult Australian Caucasians (age: 26±62 y; BMI: 18±48 kg/m 2 ). MEASUREMENTS: Skeletal muscle ®bre type composition (by myosin ATPase method) and relative body fatness (BMI, waist circumference and waist/hip ratio (WHR)). RESULTS: Infants and young children had signi®cantly lesser proportions of glycolytic Type 2b ®bres (6.2 AE 1.1%; range 0.3±18.9%) compared with adults (20.5 AE 1.6%; range 4.9±36.0%) (p`0.0001). The percentage of Type 2b ®bres was directly related to BMI (r 0.44, p 0.02), waist circumference (r 0.49, p 0.009) and WHR (r 0.44, p 0.02) in adults. A signi®cant, direct relationship was also found between the proportion of glycolytic Type 2b ®bres and age in the adults (r 0.45, p 0.01). CONCLUSION: Skeletal muscle ®bre type composition is different in infants and adults and there is an age-dependent increase in Type 2b ®bres over the lifespan. An increased proportion of glycolytic Type 2b ®bres is associated with obesity in adults. Results support a gene-environment interaction on ®bre type composition in human skeletal muscle.

Purpose -To develop a method for benchmarking teaching and learning in response to an institutional need to validate a new program in Dentistry at the University of Sydney, Australia. Design/methodology/approach -After a collaborative partner, University of Adelaide, was identified, the areas of teaching and learning to be benchmarked, PBL approach and assessment, were established. A list of quality indicators for these aspects of teaching and learning were first developed conceptually and then validated by the literature. Then, using a quality enhancement framework, levels of achievement for each indicator were developed. Findings -The findings are represented as a set of tables. These were mutually developed with the benchmarking partner and represent an agreed model for a benchmarking project to progress to the next stages of implementation and evaluation.Practical implications -This model can be adapted for any benchmarking project in all levels of education; primary, secondary, tertiary and continuing. Originality/value -The issue of benchmarking is high on the educational agenda, especially in higher education. The literature reports on a number of projects but with no clear explanation of a method for benchmarking. The fact that this model is evidence-based in its approach and that it focuses on learning and teaching, also marks it as original and a significant development in this area.

Increased risks of skeletal fractures are common in patients with impaired glucose handling and type 2 diabetes mellitus (T2DM). The pathogenesis of skeletal fragility in these patients remains ill-defined as patients present with normal to high bone mineral density. With increasing cases of glucose intolerance and T2DM it is imperative that we develop an accurate rodent model for further investigation. We hypothesized that a high fat diet (60%) administered to developing male C57BL/6J mice that had not reached skeletal maturity would over represent bone microarchitectural implications, and that skeletally mature mice would better represent adult-onset glucose intolerance and the pre-diabetes phenotype. Two groups of developing (8 week) and mature (12 week) male C57BL/6J mice were placed onto either a normal chow (NC) or high fat diet (HFD) for 10 weeks. Oral glucose tolerance tests were performed throughout the study period. Long bones were excised and analysed for ex vivo biomechanical testing, micro-computed tomography, 2D histomorphometry and gene/protein expression analyses. The HFD increased fasting blood glucose and significantly reduced glucose tolerance in both age groups by week 7 of the diets. The HFD reduced biomechanical strength, both cortical and trabecular indices in the developing mice, but only affected cortical outcomes in the mature mice. Similar results were reflected in the 2D histomorphometry. Tibial gene expression revealed decreased bone formation in the HFD mice of both age groups, i.e., decreased osteocalcin expression and increased sclerostin RNA expression. In the mature mice only, while the HFD led to a non-significant reduction in runt-related transcription factor 2 (Runx2) RNA expression, this decrease became significant at the protein level in the femora. Our mature HFD mouse model more accurately represents late-onset impaired glucose tolerance/pre-T2DM cases in humans and can be used to uncover potential insights into reduced bone formation as a mechanism of skeletal fragility in these patients.