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BackgroundIn 2010, overweight and obesity were estimated to cause 3·4 million deaths, 3·9% of years of life lost, and 3·8% of disability-adjusted life-years (DALYs) worldwide. The rise in obesity has led to widespread calls for regular monitoring of changes in overweight and obesity prevalence in all populations. Comparable, up-to-date information about levels and trends is essential to quantify population health effects and to prompt decision makers to prioritise action. We estimate the global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013.MethodsWe systematically identified surveys, reports, and published studies (n=1769) that included data for height and weight, both through physical measurements and self-reports. We used mixed effects linear regression to correct for bias in self-reports. We obtained data for prevalence of obesity and overweight by age, sex, country, and year (n=19,244) with a spatiotemporal Gaussian process regression model to estimate prevalence with 95% uncertainty intervals (UIs).FindingsWorldwide, the proportion of adults with a body-mass index (BMI) of 25 kg/m(2) or greater increased between 1980 and 2013 from 28·8% (95% UI 28·4-29·3) to 36·9% (36·3-37·4) in men, and from 29·8% (29·3-30·2) to 38·0% (37·5-38·5) in women. Prevalence has increased substantially in children and adolescents in developed countries; 23·8% (22·9-24·7) of boys and 22·6% (21·7-23·6) of girls were overweight or obese in 2013. The prevalence of overweight and obesity has also increased in children and adolescents in developing countries, from 8·1% (7·7-8·6) to 12·9% (12·3-13·5) in 2013 for boys and from 8·4% (8·1-8·8) to 13·4% (13·0-13·9) in girls. In adults, estimated prevalence of obesity exceeded 50% in men in Tonga and in women in Kuwait, Kiribati, Federated States of Micronesia, Libya, Qatar, Tonga, and Samoa. Since 2006, the increase in adult obesity in developed countries has slowed down.InterpretationBecause of the established health risks and substantial increases in prevalence, obesity has become a major global health challenge. Not only is obesity increasing, but no national success stories have been reported in the past 33 years. Urgent global action and leadership is needed to help countries to more effectively intervene.FundingBill & Melinda Gates Foundation.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2005.09.037 Byline: Judith J. Eckert (a)(b), Amanda McCallum (a), Andrew Mears (a), Martin G. Rumsby (c), Iain T. Cameron (b), Tom P. Fleming (a) Keywords: Protein kinase C; Mouse embryo; Trophectoderm; Tight junction; ZO-1; Cell contact pattern; Inner cell mass; ZO-2 Abstract: In mouse early development, cell contact patterns regulate the spatial organization and segregation of inner cell mass (ICM) and trophectoderm epithelium (TE) during blastocyst morphogenesis. Progressive membrane assembly of tight junctional (TJ) proteins in the differentiating TE during cleavage is upregulated by cell contact asymmetry (outside position) and suppressed within the ICM by cell contact symmetry (inside position). This is reversible, and immunosurgical isolation of the ICM induces upregulation of TJ assembly in a sequence that broadly mimics that occurring during blastocyst formation. The mechanism relating cell contact pattern and TJ assembly was investigated in the ICM model with respect to PKC-mediated signaling and gap junctional communication. Our results indicate that complete cell contact asymmetry is required for TJ biogenesis and acts upstream of PKC-mediated signaling. Specific inhibition of two PKC isoforms, PKC[delta] and I[paragraph], revealed that both PKC activities are required for membrane assembly of ZO-2 TJ protein, while only PKCI[paragraph] activity is involved in regulating ZO-1[alpha]+ membrane assembly, suggesting different mechanisms for individual TJ proteins. Gap junctional communication had no apparent influence on either TJ formation or PKC signaling but was itself affected by changes of cell contact patterns. Our data suggest that the dynamics of cell contact patterns coordinate the spatial organization of TJ formation via specific PKC signaling pathways during blastocyst biogenesis. Author Affiliation: (a) University of Southampton, School of Biological Sciences, Bassett Crescent East, Southampton, SO16 7PX, UK (b) University of Southampton, Developmental Origins of Health and Disease Division, School of Medicine, Coxford Road, Southampton, SO16 5YA, UK (c) University of York, Department of Biology, York, YO1 5DD, UK Article History: Received 19 May 2005; Revised 1 September 2005; Accepted 22 September 2005

During early mammalian development, blastocyst morphogenesis is achieved by epithelial differentiation of trophectoderm (TE) and its segregation from the inner cell mass (ICM). Two major interrelated features of TE differentiation required for blastocoel formation include intercellular junction biogenesis and a directed ion transport system, mediated by [Na.sup.+]/[K.sup.+] ATPase. We have examined the relative contribution of intercellular signalling mediated by protein kinase C (PKC) and gap junctional communication in TE differentiation and blastocyst cavitation. The distribution pattern of four ([delta], [theta], [iota]/[lambda], [zeta]) PKC isoforms and PKC[micro]/PKD1 showed partial colocalisation with the tight junction marker ZO-1[alpha]+ in TE and all four PKCs ([delta], [theta], [iota]/[lambda], [zeta]) showed distinct TE/ICM staining patterns (predominantly at the cell membrane within the TE and cytoplasmic within the ICM), indicating their potential contribution to TE differentiation and blastocyst morphogenesis. Specific inhibition of PKC[delta] and [zeta] activity significantly delayed blastocyst formation. Although modulation of these PKC isoforms failed to influence the already established programme of epithelial junctional differentiation within the TE, [Na.sup.+]/[K.sup.+] ATPase [alpha]1 submit was internalised from membrane to cytoplasm. Inhibition of gap junctional communication, in contrast, had no influence on any of these processes. Our results demonstrate for the first time that distinct PKC isotypes contribute to the regulation of cavitation in preimplantation embryos via target proteins including [Na.sup.+]/[K.sup.+] ATPase. Keywords: Protein kinase C; Mouse embryo; Blastocyst; Trophectoderm; Inner cell mass; Tight junction; ZO-1; [Na.sup.+]/[K.sup.+] ATPase; Cavitation