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George Davey Smith - One of the best experts on this subject based on the ideXlab platform.
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substantial intergenerational increases in body mass index are not explained by the fetal Overnutrition hypothesis the cardiovascular risk in young finns study
The American Journal of Clinical Nutrition, 2007Co-Authors: Mika Kivimaki, Debbie A Lawlor, George Davey Smith, Marko Elovainio, Markus Jokela, Liisa Keltikangasjarvinen, Jorma Viikari, Olli T RaitakariAbstract:Background: According to the fetal Overnutrition hypothesis, intrauterine influences of maternal obesity increased lifelong obesity risk in the offspring. If the hypothesis is true, then the association between maternal body mass index (BMI; in kg/m 2 ) and offspring BMI should be stronger than the association between paternal BMI and offspring BMI, because only the mother directly influences the fetal environment. Objectives: We prospectively examined intergenerational change in BMI and tested the fetal Overnutrition hypothesis. Design:Dataonoffspringweightwereobtainedfrommothers.BMI was assessed from 2980 complete parent-offspring trios when the offspringwere3to18yofage.TheassessmentofoffspringBMIwas repeated 21 y later at age 24–39 y. Results: Adult BMI of the offspring was 1.21 units higher than the BMI of their parents at the same age, which indicates an increase in obesity levels across generations (P 0.0001). Maternal BMI was more strongly associated with offspring birth weight than was paternal BMI (P 0.0009). However, there were no such differences in parent-offspring associations for BMI at later developmental stages when offspring were aged 3-39 y (P 0.35). The results did not materially change in a sensitivity analysis for 1% to 15% nonpaternity. Conclusions: Because offspring share all genes with their parents, the observed substantially higher adult BMI for offspring than for parents is likely explained by environmental influences. No support was found for any specific influence from fetal environment on this intergenerational increase in adult obesity. The findings were consistentwiththefetalOvernutritionhypothesisonlyinrelationtobirth weight. Am J Clin Nutr 2007;86:1509–14.
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income inequality and the double burden of under and Overnutrition in india
Journal of Epidemiology and Community Health, 2007Co-Authors: S V Subramanian, Ichiro Kawachi, George Davey SmithAbstract:Objectives: Developing countries are increasingly characterised by the simultaneous occurrence of under- and Overnutrition. This study examined the association between contextual income inequality and the double burden of under- and Overnutrition in India. Design: A population-based multilevel study of 77 220 ever married women, aged 15–49 years, from 26 Indian states, derived from the 1998–99 Indian National Family Health Survey data. The World Health Organization recommended categories of body mass index constituted the outcome, and the exposure was contextual measure of state income inequality based on the Gini coefficient of per capita consumption expenditure. Covariates included a range of individual demographic, socioeconomic, behavioural and morbidity measures and state-level economic development. Results: In adjusted models, for each standard deviation increase in income inequality, the odds ratio for being underweight increased by 19% (p = 0.02) and the odds ratio for being obese increased by 21% (p Conclusions: Rapidly developing economies, besides experiencing paradoxical health patterns, are typically characterised by increased levels of income inequality. This study suggests that the twin burden of undernutrition and Overnutrition in India is more likely to occur in high-inequality states. Focusing on economic equity via redistribution policies may have a substantial impact in reducing the prevalence of both undernutrition and Overnutrition.
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Epidemiologic evidence for the fetal Overnutrition hypothesis: Findings from the Mater-University study of pregnancy and its outcomes
American Journal of Epidemiology, 2007Co-Authors: Debbie A Lawlor, Rosa Alati, George Davey Smith, Michael O'callaghan, Gail M Williams, Abdullah Al Mamun, Jacob M. NajmanAbstract:The fetal Overnutrition hypothesis proposes that greater maternal adiposity results in increased obesity throughout life in the offspring. The authors examined the associations between parental prepregnancy body mass index (BMI; weight (kg)/height (m)(2)), based on height and weight reported by the mother at her first antenatal clinic visit, and offspring BMI (height and weight measured at age 14 years) in 3,340 parent-offspring trios from a birth cohort based in Brisbane, Australia (mothers were recruited in 1981-1984). The maternal-offspring BMI association was stronger than the paternal-offspring BMI association. In the fully adjusted model, the increase in standardized offspring BMI at age 14 for a one-standard-deviation (SD) increase in maternal BMI was 0.362 SD (95% confidence interval: 0.323, 0.402), and the corresponding result for a one-SD increase in paternal BMI was 0.239 SD (95% confidence interval: 0.197, 0.282). There was statistical support for a difference in the magnitude of the association between maternal-offspring BMI and paternal-offspring BMI in all confounder-adjusted models tested (all p's < 0.0001). In sensitivity analyses taking account of different plausible levels of nonpaternity (up to 15%), the greater maternal effect remained. These findings provide some support for the fetal Overnutrition hypothesis.
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Patterns, distribution, and determinants of under- and Overnutrition: a population-based study of women in India
The American Journal of Clinical Nutrition, 2006Co-Authors: Sankaran Subramanian, George Davey SmithAbstract:Background: Little systematic evidence exists for the relation between socioeconomic position and nutritional status in countries experiencing the simultaneous presence of under- and Overnutrition. Objective: We investigated the socioeconomic distribution of nutritional status in India and whether state-level macroeconomic factors modify the relation between socioeconomic position and nutritional status. Design: Our analysis was based on a nationally representative sample of 77 220 women from India, with multiple categories of body mass index (BMI; in kg/m 2 ) as the outcome, namely,
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patterns distribution and determinants of under and Overnutrition a population based study of women in india
The American Journal of Clinical Nutrition, 2006Co-Authors: S V Subramanian, George Davey SmithAbstract:Background: Little systematic evidence exists for the relation between socioeconomic position and nutritional status in countries experiencing the simultaneous presence of under- and Overnutrition. Objective: We investigated the socioeconomic distribution of nutritional status in India and whether state-level macroeconomic factors modify the relation between socioeconomic position and nutritional status. Design: Our analysis was based on a nationally representative sample of 77 220 women from India, with multiple categories of body mass index (BMI; in kg/m 2 ) as the outcome, namely, <18.5 (underweight), 23-24.9 (pre-overweight), 25-29.9 (overweight), or ≥30 (obese), with 18.5-22.9 as the reference category. Results: In adjusted models, being underweight was inversely related to socioeconomic position, whereas socioeconomic position was positively related to being pre-overweight, overweight, and obese, and the socioeconomic gradient was most marked for obesity. State-level measures of affluence did not modify the positive association between socioeconomic position and categories of overweight. The risk of underweight was lower in affluent states, but this was seen mainly in women of high socioeconomic position. Conclusions: Undernutrition and Overnutrition are epidemics of the impoverished and the affluent, respectively, in India, and this association is consistent at the individual and ecologic levels. Policies should focus on the complex patterns of social distribution of both under- and Overnutrition in the Indian context.
Olli T Raitakari - One of the best experts on this subject based on the ideXlab platform.
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substantial intergenerational increases in body mass index are not explained by the fetal Overnutrition hypothesis the cardiovascular risk in young finns study
The American Journal of Clinical Nutrition, 2007Co-Authors: Mika Kivimaki, Debbie A Lawlor, George Davey Smith, Marko Elovainio, Markus Jokela, Liisa Keltikangasjarvinen, Jorma Viikari, Olli T RaitakariAbstract:Background: According to the fetal Overnutrition hypothesis, intrauterine influences of maternal obesity increased lifelong obesity risk in the offspring. If the hypothesis is true, then the association between maternal body mass index (BMI; in kg/m 2 ) and offspring BMI should be stronger than the association between paternal BMI and offspring BMI, because only the mother directly influences the fetal environment. Objectives: We prospectively examined intergenerational change in BMI and tested the fetal Overnutrition hypothesis. Design:Dataonoffspringweightwereobtainedfrommothers.BMI was assessed from 2980 complete parent-offspring trios when the offspringwere3to18yofage.TheassessmentofoffspringBMIwas repeated 21 y later at age 24–39 y. Results: Adult BMI of the offspring was 1.21 units higher than the BMI of their parents at the same age, which indicates an increase in obesity levels across generations (P 0.0001). Maternal BMI was more strongly associated with offspring birth weight than was paternal BMI (P 0.0009). However, there were no such differences in parent-offspring associations for BMI at later developmental stages when offspring were aged 3-39 y (P 0.35). The results did not materially change in a sensitivity analysis for 1% to 15% nonpaternity. Conclusions: Because offspring share all genes with their parents, the observed substantially higher adult BMI for offspring than for parents is likely explained by environmental influences. No support was found for any specific influence from fetal environment on this intergenerational increase in adult obesity. The findings were consistentwiththefetalOvernutritionhypothesisonlyinrelationtobirth weight. Am J Clin Nutr 2007;86:1509–14.
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Substantial intergenerational increases in body mass index are not explained by the fetal Overnutrition hypothesis: the Cardiovascular Risk in Young Finns Study.
Am J Clin Nutr, 2007Co-Authors: Olli T RaitakariAbstract:According to the fetal Overnutrition hypothesis, intrauterine influences of maternal obesity increased lifelong obesity risk in the offspring. If the hypothesis is true, then the association between maternal body mass index (BMI; in kg/m(2)) and offspring BMI should be stronger than the association between paternal BMI and offspring BMI, because only the mother directly influences the fetal environment.
Barry M Popkin - One of the best experts on this subject based on the ideXlab platform.
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the double burden of under and Overnutrition and nutrient adequacy among chinese preschool and school aged children in 2009 2011
European Journal of Clinical Nutrition, 2015Co-Authors: Carmen Piernas, Dantong Wang, Shufa Du, Bing Zhang, Zhihong Wang, Chang Su, Barry M PopkinAbstract:The double burden of under- and Overnutrition and nutrient adequacy among Chinese preschool and school-aged children in 2009–2011
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the burden of disease from undernutrition and Overnutrition in countries undergoing rapid nutrition transition a view from brazil
American Journal of Public Health, 2004Co-Authors: Carlos Augusto Monteiro, Wolney Lisboa Conde, Barry M PopkinAbstract:On the basis of 3 comparable population-based surveys conducted in Brazil, we identified clear changes in the relative magnitude of women’s undernutrition and Overnutrition. In 1975, there were almost 2 cases of underweight to 1 case of obesity, whereas in 1997, there were more than 2 cases of obesity to 1 case of underweight. In 1997, Brazilian low-income women were significantly more susceptible than high-income women to both underweight and obesity.
Manuel Tenasempere - One of the best experts on this subject based on the ideXlab platform.
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the hypothalamic inflammatory gliosis response to neonatal Overnutrition is sex and age dependent
Endocrinology, 2018Co-Authors: Pilar Argentearizon, Francisca Diaz, Vicente Barrios, Manuel Tenasempere, Luis M Garciasegura, Jesus Argente, Julie A ChowenAbstract:: Astrocytes participate in both physiological and pathophysiological responses to metabolic and nutrient signals. Although most studies have focused on the astrocytic response to weight gain due to high-fat/high-carbohydrate intake, surplus intake of a balanced diet also induces excess weight gain. We have accessed the effects of neonatal Overnutrition, which has both age- and sex-dependent effects on weight gain, on hypothalamic inflammation/gliosis. Although both male and female Wistar rats accumulate excessive fat mass as early as postnatal day (PND) 10 with neonatal Overnutrition, no increase in hypothalamic cytokine levels, markers of astrocytes or microglia, or inflammatory signaling pathways were observed. At PND 50, no effect of neonatal overnutriton was found in either sex, whereas at PND 150, males again weighed significantly more than their controls, and this was coincident with an increase in markers of inflammation and astrogliosis in the hypothalamus. Circulating triglycerides and free fatty acids were also elevated in these males, but not in females or in either sex at PND 10. Thus, the effects of fatty acids and estrogens on astrocytes in vitro were analyzed. Our results indicate that changes in circulating fatty acid levels may be involved in the induction of hypothalamic inflammation/gliosis in excess weight gain, even on a normal diet, and that estrogens could participate in the protection of females from these processes. In conclusion, the interaction of developmental influences, dietary composition, age, and sex determines the central inflammatory response and the associated long-term outcomes of excess weight gain.
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age and sex dependent effects of early Overnutrition on metabolic parameters and the role of neonatal androgens
Biology of Sex Differences, 2016Co-Authors: Pilar Argentearizon, Francisca Diaz, Vicente Barrios, Manuel Tenasempere, Esther Fuentemartin, Miguel A Sanchezgarrido, David Castrogonzalez, Jesus ArgenteAbstract:Background Males and females respond differently to diverse metabolic situations. Being raised in a small litter is reported to cause Overnutrition that increases weight gain and predisposes an individual to metabolic disturbances in adulthood; however, existing data are inconsistent. Indeed, significant weight gain and/or metabolic disturbances, such as hyperinsulinemia and hyperleptinemia, are sometimes not encountered. We hypothesized that these inconsistencies could be due to the animal’s sex and/or age at which metabolic parameters are measured.
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early postnatal Overnutrition increases adipose tissue accrual in response to a sucrose enriched diet
American Journal of Physiology-endocrinology and Metabolism, 2012Co-Authors: Esther Fuentemartin, Manuel Tenasempere, Jesus Argente, Cristina Garciacaceres, Miriam Granado, Miguel A Sanchezgarrido, Laura M Frago, Julie A ChowenAbstract:Both Overnutrition and an incorrect nutrient balance have contributed to the rise in obesity. Moreover, it is now clear that poor nutrition during early life augments the possibility of excess weight gain in later years. Our aim was to determine how neonatal Overnutrition affects later responses to a sucrose-enriched diet and whether this varies depending upon when the diet is introduced in postnatal life. Male Wistar rats raised in litters of four or 12 pups were given a 33% sucrose solution instead of water from weaning (day 21) or postnatal day (PND) 65. All rats received normal chow ad libitum until they were euthanized on PND 80. Body weight (BW) and food and liquid intake were monitored throughout the study. Fat mass, adipocyte morphology, serum biochemical and hormonal parameters, and hypothalamic neuropeptide mRNA levels were measured at study termination. Neonatal Overnutrition increased food intake, BW, and leptin levels, induced adipocyte hypertrophy, and decreased total ghrelin levels. The sucrose-enriched diet increased total energy intake, adipose accrual, and leptin, adiponectin, and acylated ghrelin levels but decreased BW. Most of these responses were accentuated in neonatally overnourished rats, which also had increased insulin and triglyceride levels. However, long-term sucrose intake induced adipocyte hypertrophy in rats from normal-sized litters but not in neonatally overfed rats. The results reported here indicate that neonatal Overnutrition increases the detrimental response to a diet rich in sucrose later in life. Moreover, the timing and duration of the exposure to a sucrose-enriched diet alter the adverse metabolic outcomes.
James R Sowers - One of the best experts on this subject based on the ideXlab platform.
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Overnutrition mtor signaling and cardiovascular diseases
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2014Co-Authors: Annayya R Aroor, Luis A Martinezlemus, James R SowersAbstract:The prevalence of obesity and associated medical disorders has increased dramatically in the United States and throughout much of the world in the past decade. Obesity, induced by excess intake of carbohydrates and fats, is a major cause of Type 2 diabetes, hypertension, and the cardiorenal metabolic syndrome. There is emerging evidence that excessive nutrient intake promotes signaling through the mammalian target of rapamycin (mTOR), which, in turn, may lead to alterations of cellular metabolic signaling leading to insulin resistance and obesity-related diseases, such as diabetes, cardiovascular and kidney disease, as well as cancer. While the pivotal role of mTOR signaling in regulating metabolic stress, autophagy, and adaptive immune responses has received increasing attention, there remain many gaps in our knowledge regarding this important nutrient sensor. For example, the precise cellular signaling mechanisms linking excessive nutrient intake and enhanced mTOR signaling with increased cardiovascular and kidney disease, as well as cancer, are not well understood. In this review, we focus on the effects that the interaction between excess intake of nutrients and enhanced mTOR signaling have on the promotion of obesity-associated diseases and potential therapeutic strategies involving targeting mTOR signaling.
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regulation of Overnutrition induced cardiac inflammatory mechanisms
CardioRenal Medicine, 2012Co-Authors: Vincent G Demarco, Adam Whaleyconnell, James R Sowers, Lakshmi PulakatAbstract:Background: Unlike conventional � -blockers, nebivolol, a third-generation � -adrenergic receptor blocker with vasodilator properties, promotes insulin sensitivity. Objective: The objective of this study was to determine whether nebivolol regulates Overnutrition-induced activation of cardiac nutrient sensor kinases and inflammatory signaling. Methods: Young Zucker obese (ZO) rats, a rodent model for Overnutrition, and age-matched Zucker lean rats were treated with nebivolol (10 mg/kg/day; 21 days) and cardiac function was monitored by echocardiography and pressure volume loop analysis. Activation status of nutrient sensor serine/threonine kinases mammalian target for rapamycin (mTOR), and p70 S6kinase (S6K1) and S6K1-substrate RPS6, inflammatory marker Janus kinase 2 (Jak2) and its substrate STAT1, and energy sensor AMP-dependent kinase (AMPK) were monitored by determining phosphorylation status of pSer 2448 of mTOR, pThr 389 of S6K1, pSer 235/236 of RPS6, pTyr 1007/1008 of Jak2, pTyr 701 of STAT1, and pThr 172 of AMPK, respectively. Results: Nebivolol reduced weight and improved cardiac function of ZO rats as shown by improvements in the myocardial performance index and a decrease in the diastolic parameter tau ( � ), the time constant of isovolumic relaxation. Nebivolol also attenuated excessive activation of the nutrient sensor kinases mTOR and S6K1 and their substrate
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role of trib3 in diabetic and Overnutrition induced atherosclerosis
Diabetes, 2012Co-Authors: James R SowersAbstract:Obesity caused by excess feeding (Overnutrition) has become a problem of epidemic proportions and is the underlying cause in metabolic disorders and chronic diseases such as diabetes and cardiovascular disease. Overnutrition is associated with systemic and tissue-related insulin resistance, an abnormality that promotes vascular disease as well as the development of diabetes (1,2). Thus, there is considerable interest in factors that link Overnutrition, insulin resistance, and hyperglycemia with vascular disease. There is emerging evidence that the expression of the Tribbles homolog 3 of Drosophila ( TRIB3 ) gene is increased in patients and animals with type 2 diabetes (3). The TRIB3 gene is located on the 20p13 region of the human chromosome. Its full-length translated mRNA is 1,074 base pairs, and its protein product is made up of 358 amino acids. Studies have shown that TRIB3 inhibits insulin metabolic signaling in liver (4–6), skeletal muscle (7), and vascular tissue (8). Further, these studies suggest that TRIB3 expression in skeletal muscle and liver tissue is increased with excessive nutrient intake as well as by hyperglycemia (3–7). Endoplasmic reticulum stress has also been shown to increase TRIB3 gene expression, and TRIB3 promotes cell death in response to endoplasmic reticulum stress (9) (Fig. 1). Several studies have shown that TRIB3 impairs insulin …
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adaptive mechanisms to compensate for Overnutrition induced cardiovascular abnormalities
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2011Co-Authors: Lakshmi Pulakat, Adam Whaleyconnell, Vincent G Demarco, Sivakumar Ardhanari, Anand Chockalingam, James R SowersAbstract:In conditions of Overnutrition, cardiac cells must cope with a multitude of extracellular signals generated by changes in nutrient load (glucose, amino acids, and lipids) and the hormonal milieu [increased insulin (INS), ANG II, and adverse cytokine/adipokine profile]. Herein, we review the diverse compensatory/adaptive mechanisms that counter the deleterious effects of excess nutrients and growth factors. We largely focus the discussion on evidence obtained from Zucker obese (ZO) and Zucker diabetic fatty (ZDF) rats, which are useful models to evaluate adaptive and maladaptive metabolic, structural, and functional cardiac remodeling. One adaptive mechanism present in the INS-resistant ZO, but absent in the diabetic ZDF heart, involves an interaction between the nutrient sensor kinase mammalian target of rapamycin complex 1 (mTORC1) and ANG II-type 2 receptor (AT2R). Recent evidence supports a cardioprotective role for the AT2R; for example, suppression of AT2R activation interferes with antihypertrophic/antifibrotic effects of AT1R blockade, and AT2R agonism improves cardiac structure and function. We propose a scenario, whereby mTORC1-signaling-mediated increase in AT2R expression in the INS-resistant ZO heart is a cardioprotective adaptation to Overnutrition. In contrast to the ZO rat, heart tissues of ZDF rats do not show activation of mTORC1. We posit that such a lack of activation of the mTOR↔AT2R integrative pathway in cardiac tissue under conditions of obesity-induced diabetes may be a metabolic switch associated with INS deficiency and clinical diabetes.
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Overnutrition and the cardiorenal syndrome use of a rodent model to examine mechanisms
CardioRenal Medicine, 2011Co-Authors: Adam Whaleyconnell, Lakshmi Pulakat, Vincent G Demarco, Melvin R Hayden, Javad Habibi, Erik J Henriksen, James R SowersAbstract:Obesity has reached epidemic proportions with far-reaching health care and economic implications. Overnutrition, characterized by excess intake of carbohydrates and fats, has been associated with end-organ damage in several tissues, including the heart and the kidney. Furthermore, Overnutrition is one of the most important modifiable and preventable causes of morbidity and mortality associated with cardiovascular and kidney diseases. Insulin resistance and compensatory hyperinsulinemia as well as associated mechanisms, including enhanced renin-angiotensin-aldosterone system activity, inflammation, and oxidative stress, have been implicated in obesity-related cardiorenal injury. In this review, the effect of Overnutrition on heart and kidney disease is assessed in a rodent model of Overnutrition and obesity, the Zucker obese rat.
