Summary Previous reviews of childhood obesity prevention have focused largely on schools and findings have been inconsistent. Funded by the US Agency for Healthcare Research and Quality (AHRQ) and the National Institutes of Health, we systematically evaluated the effectiveness of childhood obesity prevention programmes conducted in high-income countries and implemented in various settings. We searched MEDLINE®, Embase, PsycINFO, CINAHL®, ClinicalTrials.gov and the Cochrane Library from inception through 22 April 2013 for relevant studies, including randomized controlled trials, quasi-experimental studies and natural experiments, targeting diet, physical activity or both, and conducted in children aged 2–18 in high-income countries. Two reviewers independently abstracted the data. The strength of evidence (SOE) supporting interventions was graded for each study setting (e.g. home, school). Meta-analyses were performed on studies judged sufficiently similar and appropriate to pool using random effect models. This paper reported our findings on various adiposity-related outcomes. We identified 147 articles (139 intervention studies) of which 115 studies were primarily school based, although other settings could have been involved. Most were conducted in the United States and within the past decade. SOE was high for physical activity-only interventions delivered in schools with home involvement or combined diet–physical activity interventions delivered in schools with both home and community components. SOE was moderate for school-based interventions targeting either diet or physical activity, combined interventions delivered in schools with home or community components or combined interventions delivered in the community with a school component. SOE was low for combined interventions in childcare or home settings. Evidence was insufficient for other interventions. In conclusion, at least moderately strong evidence supports the effectiveness of school-based interventions for preventing childhood obesity. More research is needed to evaluate programmes in other settings or of other design types, especially environmental, policy and consumer health informatics-oriented interventions.

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Leptin is an adipocyte-derived hormone with potent weight reducing effects. Genetically obese rodents with mutations of leptin or the leptin receptor are defective in leptin signaling and develop morbid obesity and diabetes. Interestingly, the levels of both leptin mRNA and protein are increased by up to 20-fold in these animals, suggesting the existence of a feedback mechanism controlling the amount of leptin in circulation. In this report, we attempted to determine whether the up-regulation of circulating leptin in Zucker Diabetic Fatty rats, which are nonresponsive to leptin due to a receptor point mutation, is entirely due to increased expression of leptin. We demonstrate that the high level of circulating leptin in these rats is attributable to at least two factors: increased leptin expression by the adipose tissue and delayed clearance of leptin from circulation due to binding to its soluble receptor. The latter conclusion was supported by three lines of evidence: 1) The soluble leptin receptor is up-regulated by about 20-fold in Zucker Diabetic Fatty rats; 2) Adenovirus-mediated overexpression of the soluble leptin receptor results in a similar -fold increase of circulating leptin; 3) In ob/ob mice, which have no endogenous leptin, exogenously administered leptin reaches a higher level when the soluble leptin receptor is overexpressed. The weightreducing effect of leptin is enhanced in C57Bl/6 ob/ob mice with overexpression of the soluble leptin receptor. Soluble leptin receptor may be a significant factor determining the amount of total leptin in circulation.Leptin is an adipocyte-derived hormone of 167 amino acids (1). It has potent weight-reducing effects in vivo (2-4). In ob/ob mice, the gene encoding leptin is mutated, resulting in morbid obesity and associated abnormalities, including hyperphagia, hypothermia, diabetes, and infertility.The leptin receptor, OB-R, 1 is a member of the cytokine receptor family (5). It is encoded by the diabetes (db) gene, mutation of which also results in morbid obesity and other abnormalities similar to that in ob/ob mice. OB-R is alternatively spliced into at least five transcripts from a single gene. These transcripts encode proteins that are called the long (OBRb), short (OB-Ra, -c, and -d), and soluble (OB-Re) forms of the leptin receptor. With the exception of the soluble leptin receptor, receptor isoforms differ from each other by the alternative use of a unique terminal coding exon (6). OB-Rb is essential in mediating leptin's weight-reducing and other biological effects (6, 7).OB-R is expressed in both the nervous system and peripheral tissues. The relative levels of expression of different receptor isoforms vary among different tissues, providing a possible mechanism of regulating leptin's biological activity at various leptin target sites (8). OB-Rb is enriched in the hypothalamus, the site of leptin's action on food intake and body weight. Leptin activation of OB-Rb within this brain region results in the inhibition of neuropeptide Y/agouti-related protein ...