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Community-based obesity prevention efforts are dependent on the strength and function of collaborative networks across multiple community members and organizations. There is little empirical work on understanding how community network structure influences obesity prevention capacity. We describe network structures within 19 local government communities prior to a large-scale community-based obesity prevention intervention, Healthy Together Victoria, Australia (2012–2015). Participants were from a large, multi-site, cluster randomized trial (cRCT) of a whole-of-systems chronic disease prevention initiative. Community leaders from 12 intervention and seven comparison (non-intervention) regions identified and described their professional networks in relation to dietary, physical activity, and weight status among young children (

Objective: The Australian Capital Territory ‘It's Your Move!’ (ACT‐IYM) was a three‐year (2012–2014) systems intervention to prevent obesity among adolescents. Methods: The ACT‐IYM project involved three intervention schools and three comparison schools and targeted secondary students aged 12–16 years. The intervention consisted of multiple initiatives at individual, community, and school policy level to support healthier nutrition and physical activity. Intervention school‐specific objectives related to increasing active transport, increasing time spent physically active at school, and supporting mental wellbeing. Data were collected in 2012 and 2014 from 656 students. Anthropometric data were objectively measured and behavioural data self‐reported. Results: Proportions of overweight or obesity were similar over time within the intervention (24.5% baseline and 22.8% follow‐up) and comparison groups (31.8% baseline and 30.6% follow‐up). Within schools, two of three the intervention schools showed a significant decrease in the prevalence of overweight and obesity (p

Introduction Studies of community-based obesity prevention interventions have hypothesized that stakeholder networks are a critical element of effective implementation. This paper presents a quantitative analysis of the interpersonal network structures within a sub-sample of stakeholders from two past successful childhood obesity prevention interventions. Methods Participants were recruited from the stakeholder groups (steering committees) of two completed community-based intervention studies, Romp & Chomp (R&C), Australia (2004-2008) and Shape Up Somerville (SUS), USA (2003-2005). Both studies demonstrated significant reductions of overweight and obesity among children. Members of the steering committees were asked to complete a retrospective social network questionnaire using a roster of other committee members and free recall. Each participant was asked to recall the people with whom they discussed issues related to childhood obesity throughout the intervention period, along with providing the closeness and level of influence of each relationship. Results Networks were reported by 13 participants from the SUS steering committee and 8 participants from the R&C steering committee. On average, participants nominated 16 contacts with whom they discussed issues related to childhood obesity through the intervention, with approximately half of the relationships described as ‘close’ and 30% as ‘influential’. The ‘discussion’ and ‘close’ networks had high clustering and reciprocity, with ties directed to other steering committee members, and to individuals external to the committee. In contrast, influential ties were more prominently directed internal to the steering committee, with higher network centralization, lower reciprocity and lower clustering. Discussion and conclusion Social network analysis provides a method to evaluate the ties within steering committees of community-based obesity prevention interventions. In this study, the network characteristics between a sub-set of stakeholders appeared to be supportive of diffused communication. Future work should prospectively examine stakeholder network structures in a heterogeneous sample of community-based interventions to identify elements most strongly associated with intervention effectiveness.

Objective To investigate the effects of leptin administration to Psammomys obesus, a polygenic animal model of obesity and type 2 diabetes mellitus. Design Longitudinal intervention study utilising three separate leptin treatment protocols lasting 7-14 d. Measurements Body weight and food intake were measured daily, body fat and muscle content were estimated by carcass analysis on completion of the study. Blood glucose, plasma insulin, leptin, triglycerides and cholesterol were measured at baseline and twice each week during the study. Results Relatively high doses of leptin were required to significantly reduce food intake and body fat content in lean Psammomys obesus, but had no discernible effect on their obese littermates. Conclusion As a species, Psammomys obesus appear to be relatively insensitive to the effects of leptin administration, compared with other rodents. Obese Psammomys obesus are leptin resistant relative to their lean littermates.

The Israeli Sand Rat (Psammomys obesus) is an excellent polygenic model for the study of obesity and diabetes. The metabolic characteristics and the heterogeneous development of these defects, including elevated leptin levels, mimic those found in susceptible human populations. Interestingly, only animals that develop metabolic abnormalities demonstrate hyperleptinemia and, in these animals, leptin administration at the same dose that is effective in ob/ob mice is ineffective in reducing food intake or body weight. Perhaps leptin resistance needs to develop in Israeli Sand Rats to allow the development of obesity and, in fact, leptin resistance may be the "thrifty gene" that predisposes individuals to the development of obesity and subsequent metabolic abnormalities. However, there remain many unanswered questions about the physiological actions of leptin. The widespread tissue location of receptors and the actions of leptin independent of food intake highlight the need for further research aimed at determining the major physiological action of this newly discovered and exciting hormone.

Skeletal muscle produces a variety of secreted proteins that have important roles in intercellular communication and affects processes such as glucose homoeostasis. The objective of this study was to develop a novel Signal Sequence Trap (SST) in conjunction with cDNA microarray technology to identify proteins secreted from skeletal muscle of Psammomys obesus that were associated with obesity and type 2 diabetes (T2D).Secreted proteins that were differentially expressed between lean, normal glucose tolerant (NGT), overweight and impaired glucose tolerant (IGT) and obese, T2D P. obesus were isolated using SST in conjunction with cDNA microarray technology. Subsequent gene expression was measured in tissues from P. obesus by real-time PCR (RT-PCR).The SST yielded 1600 positive clones, which were screened for differential expression. A total of 91 (approximately 6%) clones were identified by microarray to be differentially expressed between NGT, IGT and T2D P. obesus. These clones were sequenced to identify 51 genes, of which only 27 were previously known to encode secreted proteins. Three candidate genes not previously associated with obesity or type 2 diabetes, sushi domain containing 2, collagen and calcium-binding EGF domains 1 and periostin (Postn), as well as one gene known to be associated, complement component 1, were shown by RT-PCR to be differentially expressed in skeletal muscle of P. obesus. Further characterization of the secreted protein Postn revealed it to be predominantly expressed in adipose tissue, with higher expression in visceral compared with subcutaneous adipose depots.SST in conjunction with cDNA microarray technology is a powerful tool to identify differentially expressed secreted proteins involved in complex diseases such as obesity and type 2 diabetes. Furthermore, a number of candidate genes were identified, in particular, Postn, which may have a role in the development of obesity and type 2 diabetes.

The International Obesity Taskforce (IOTF) recommends using age- and gender-specific body mass index (BMI) cut-points for defining the prevalence of overweight and obesity in children. These are given in both 6- and 12-month age intervals. Since the BMI-for-age curves are nonlinear, a degree of bias will be introduced when age intervals are wide. We aimed to quantify this bias in prevalence estimates in 2178 Australian children aged 4-12 years using 12- versus 6-month age intervals. Using the 12-month interval, the prevalence of overweight and obesity was underestimated by 1.4% compared to the 6-month interval estimates; however, this was age-dependent. It overestimated prevalence for 4-year olds, but underestimated it for older ages by up to 2.6%. Overweight prevalence was generally affected more than obesity prevalence. The use of different age intervals for IOTF cut-points introduces a small but systematic bias in prevalence estimates of overweight and obesity.

In light of the increasing prevalence of obesity in children and the potential of schools as a setting for intervention, we aimed to identify the main foods and beverages consumed at primary school and to determine differences in consumption patterns between children who used the school canteen and those who did not. Cross-sectional survey of school foods in 1681 5–12 y old children, 2003–2004. Barwon South—Western region of Victoria, Australia. The school food provided an average (±s.e.m.) of 3087±26 kJ. Bread was the most frequently consumed food and contributed 20% of total energy at school, biscuits 13%, fruit 10%, muesli/fruit bars 8%, packaged snacks 7%, and fruit juice/cordial 6%. About 10% of children used the school canteen and these children obtained more total energy and more energy from cakes, fast foods and soft drink than noncanteen users (P

It has been reported previously that leptin may be involved in nicotine's ability to reduce body weight. Our aim was to investigate whether the anorexic action of nicotine is related to the actions of leptin by utilizing lean leptin-sensitive and obese leptin-resistant Psammomys obesus. Lean and obese P. obesus were assigned to receive nicotine sulphate at 6, 9 or 12 mg/day or saline (control) for 9 days (n = 6-10 in each group), administered using mini-osmotic pumps. Food intake, body weight, plasma leptin concentrations, plasma insulin and blood glucose were measured at baseline and throughout the study period. Nicotine treatment reduced food intake by up to 40% in lean and obese P. obesus. Plasma leptin levels fell significantly only in lean nicotine-treated animals, whereas no changes were observed in obese nicotine-treated animals. However, both lean and obese nicotine-treated animals had similar reductions in body weight. Our results show that nicotine has dramatic effects on food intake and body weight, however, these changes appear to be independent of the leptin signalling pathway.

DNA-based approaches to the discovery of genes contributing to the development of type 2 diabetes have not been very successful despite substantial investments of time and money. The multiple gene-gene and gene-environment interactions that influence the development of type 2 diabetes mean that DNA approaches are not the ideal tool for defining the etiology of this complex disease. Gene expression-based technologies may prove to be a more rewarding strategy to identify diabetes candidate genes. There are a number of RNA-based technologies available to identify genes that are differentially expressed in various tissues in type 2 diabetes. These include differential display polymerase chain reaction (ddPCR), suppression subtractive hybridization (SSH), and cDNA microarrays. The power of new technologies to detect differential gene expression is ideally suited to studies utilizing appropriate animal models of human disease. We have shown that the gene expression approach, in combination with an excellent animal model such as the Israeli sand rat (Psammomys obesus), can provide novel genes and pathways that may be important in the disease process and provide novel therapeutic approaches. This paper will describe a new gene discovery, beacon, a novel gene linked with energy intake. As the functional characterization of novel genes discovered in our laboratory using this approach continues, it is anticipated that we will soon be able to compile a definitive list of genes that are important in the development of obesity and type 2 diabetes.

COLLIER, GREG R, KEN WALDER, PAUL LEWAN DOWSJCI, ANDREW SANIGORSKI, PAUL ZIMMET. Leptin and the development of obesity and diabetes in Psammomys obesus. The recently discovered ob gene and its circulating product, leptin, may be critical factors in the control of energy balance. Recent studies in ob/ob mice, which lack circulating leptin, have shown dramatic reductions in food intake and bodyweight after leptin treatment. In addition, studies in both humans with obesity and animal models of obesity have demonstrated hyperleptinemia. Here, we report a longitudinal study examining changes in circulating leptin during the development of obesity and diabetes in Psammomys obesus. Over the 8 weeks of the study, lean animals increased their bodyweight by 154% and leptin levels remained essentially unchanged. In contrast, animals that developed obesity (223 % increase in bodyweight), hyperglycemia, and hyperinsulinemia also developed hyperleptinemia between 4 weeks and 8 weeks of age. These results demonstrate that the development of hyperleptinemia is associated with the development of obesity and subsequent metabolic abnormalities.

We examined the effects of leptin treatment on the expression of key genes in adipocyte metabolism in Psammomys obesus (P. obesus), a polygenic rodent model of obesity. Lean and obese P. obesus were given three daily intraperitoneal injections of either saline or leptin (total of 45 mg/kg per day) for 7 days. In lean animals, leptin treatment led to reductions in food intake, body weight and fat mass. Pair-fed animals matched for the reduction in food intake of the lean leptin-treated animals demonstrated similar reductions in body weight and fat mass. In obese P. obesus, leptin treatment failed to have any effect on body weight or body fat mass, indicating leptin resistance. Lipoprotein lipase, hormone-sensitive lipase and peroxisome proliferator activated receptor gamma 2 mRNA levels were significantly reduced in lean leptin-treated animals, whereas pair-fed animals were similar to lean controls. Uncoupling protein 2 and glycerol phosphate acyltransferase were also reduced in the lean leptin-treated animals, but not significantly so. Obese animals did not show any gene expression changes after leptin treatment. In conclusion, high circulating concentrations of leptin in lean P. obesus resulted in decreased gene expression of a number of key lipid enzymes, independent of changes in food intake, body weight and fat mass. These effects of leptin were not found in obese P. obesus.