Rising rural body-mass index is the main driver of the global obesity epidemic in adults

Body-mass index (BMI) has increased steadily in most countries in parallel with a rise in the proportion of the population who live in cities 1,2 . This has led to a widely reported view that urbanization is one of the most important drivers of the global rise in obesity 3�6 . Here we use 2,009 population-based studies, with measurements of height and weight in more than 112 million adults, to report national, regional and global trends in mean BMI segregated by place of residence (a rural or urban area) from 1985 to 2017. We show that, contrary to the dominant paradigm, more than 55 of the global rise in mean BMI from 1985 to 2017�and more than 80 in some low- and middle-income regions�was due to increases in BMI in rural areas. This large contribution stems from the fact that, with the exception of women in sub-Saharan Africa, BMI is increasing at the same rate or faster in rural areas than in cities in low- and middle-income regions. These trends have in turn resulted in a closing�and in some countries reversal�of the gap in BMI between urban and rural areas in low- and middle-income countries, especially for women. In high-income and industrialized countries, we noted a persistently higher rural BMI, especially for women. There is an urgent need for an integrated approach to rural nutrition that enhances financial and physical access to healthy foods, to avoid replacing the rural undernutrition disadvantage in poor countries with a more general malnutrition disadvantage that entails excessive consumption of low-quality calories. © 2019, The Author(s)

Aggregatory behaviour of platelets incubated with subcellular fractions of normal and chagasic human syncytiotrophoblast Comportamento agregatório das plaquetas incubadas com frações subcelulares de sinciciotrofoblasto humano normal e chagásico

The surface of human syncytiotrophoblast does not induce maternal blood platelet aggregation even though it is not an endothelium. It can be surmised that as occurs in endothelial injury the subcellular components of the syncytiotrophoblast may have pro-or antiaggregatory activity. During congenital Chagas' disease which is associated to trophoblast lesions, platelets may play a role in the development of T. cruzi-induced placentitis. In the present work the aggregatory behaviour of normal human blood platelets was recorded after their challenging with subcellular fractions of syncytiotrophoblast isolated from normal and chagasic women. Nuclear, Mitochondrial, Microsomal and Supernatant fractions isolated from normal and chagasic syncytiotrophoblast failed to induce per se any aggregatory reaction on platelets. When samples of platelet-rich plasma (PRP) were preincubated with normal and chagasic nuclear fractions and then stimulated with collagen at threshold level (CT-PRP) an inhibition of the aggregatory response was observed. Treatment of CT-PRP with normal and chagasic mitochondrial fractions induced inhibition of platelet aggregation whereas only chagasic fraction reduced latency time. Microsornal fraction from normal placentas showed no significant effects on platelet aggregation. It is concluded that subcellular fractions of normal human syncytiotrophoblast do not exhibit any effect on platelet aggregation, whereas those subcellular fractions enriched in intracellular membrane components isolated from chagasic placentas inhibit platelet aggregation.<br>A superficie do sinciciotrofoblasto humano não induz agregação das plaquetas maternas apesar de não ser um endotélio. Lesões endoteliais propiciam o aparecimento de agregados plaquetários, o que nos leva a questionar se os componentes subcelulares do sinciciotrofoblasto também poderiam propiciar eventos semelhantes. Na doença de Chagas congênita, que está associada a lesões a nivel de trofoblasto, as plaquetas poderiam desempenhar algum papel no desenvolvimento da placentitis induzida pelo T. cruzi. Neste trabalho estudou-se o comportamento agregatório das plaquetas humanas normais expostas a frações subcelulares do sinciciotrofoblasto isolado de placentas de mulheres normais e chagásticas. As frações Nuclear, Mitocondrial, Microsomal e Sobrenadante isoladas do sincicitrofoblasto normal ou chagásico não induziram per se reação agregatória de plaquetas. Quando amostras de plasma rico em plaquetas (PRP) foram pré-incubadas com fração nuclear de placentas normais ou chagásicas e pós-estimuladas com doses limiares de colágeno (DLC-PRP) observou-se uma inibiçâo da resposta agregatória. O tratamento de DLC-PRP com fração Mitocondrial de trofoblasto normal e chagásico também induziu inibição da agregação plaquetária porém somente a fração chagásica diminuiu o tempo de latência. A fração Microsomal das placentas normais não provocou diferenças significativas na agregação plaquetária. Conclui-se que as frações subcelulares do sinciciotrofoblasto humano normal não tem ação significativa na agregação plaquetária, enquanto que a incubação com frações subcelulares de placentas chagásicas, enriquecidas em componentes membranosos intracelulares, induziu a inibiçâo da agregação plaquetária