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Starting in 2009, the German state of Saxony distributed sports club membership vouchers among all 33,000 third graders in the state. The policy’s objective was to encourage them to develop a long-term habit of exercising. In 2018, we carried out a large register-based survey among several cohorts in Saxony and two neighboring states. Our difference-in-differences estimations show that, even after a decade, awareness of the voucher program was significantly higher in the treatment group. We also find that youth received and redeemed the vouchers. However, we do not find significant short- or long-term effects on sports club membership, physical activity, overweightness, or motor skills.
Gut bacteria exert beneficial and harmful effects in metabolic diseases as deduced from the comparison of germfree and conventional mice and from fecal transplantation studies. Compositional microbial changes in diseased subjects have been linked to adiposity, type 2 diabetes and dyslipidemia. Promotion of an increased expression of intestinal nutrient transporters or a modified lipid and bile acid metabolism by the intestinal microbiota could result in an increased nutrient absorption by the host. The degradation of dietary fiber and the subsequent fermentation of monosaccharides to short-chain fatty acids (SCFA) is one of the most controversially discussed mechanisms of how gut bacteria impact host physiology. Fibers reduce the energy density of the diet, and the resulting SCFA promote intestinal gluconeogenesis, incretin formation and subsequently satiety. However, SCFA also deliver energy to the host and support liponeogenesis. Thus far, there is little knowledge on bacterial species that promote or prevent metabolic disease. Clostridium ramosum and Enterococcus cloacae were demonstrated to promote obesity in gnotobiotic mouse models, whereas bifidobacteria and Akkermansia muciniphila were associated with favorable phenotypes in conventional mice, especially when oligofructose was fed. How diet modulates the gut microbiota towards a beneficial or harmful composition needs further research. Gnotobiotic animals are a valuable tool to elucidate mechanisms underlying diet-host-microbe interactions.
Adipositas gilt seit einigen Jahren als eine der häufigsten chronischen Erkrankungen des Kindes- und Jugendalters. Welche Faktoren zu einer erfolgreichen Behandlung der Adipositas im Kindes- und Jugendalter führen, sind jedoch noch immer nicht ausreichend geklärt. Ein wichtiger – bisher jedoch weitgehend unbeachteter – Faktor, welcher möglicherweise wegweisend für den Therapieverlauf sein kann, ist das subjektive Krankheitskonzept der betroffenen Kinder. Das bedeutsamste theoretische Modell, welches den Einfluss der individuellen Krankheitsvorstellungen auf den Regulationsprozess eines Menschen im Umgang mit Erkrankungen beschreibt, ist das Common Sense Model of Illness Representation (CSM) von Howard Leventhal. Ziel der vorliegenden Arbeit war es die subjektiven Krankheitskonzepte adipöser Kinder zu erfassen und ihren Einfluss auf den Regulationsprozess zu analysieren. In einer ersten Untersuchung wurde mittels Daten von 168 adipösen Kindern im Alter von 8 bis 12 Jahren zunächst ein Fragebogen zur Erfassung der subjektiven Krankheitskonzepte entwickelt. Die Ergebnisse weisen darauf hin, dass der Fragebogen als reliabel und valide eingeschätzt werden kann. Mit Hilfe dieses Fragebogens konnte nachgewiesen werden, dass adipöse Kinder Konstrukte über ihre Erkrankung haben, welche in eigenständigen Dimensionen gespeichert werden. Die gefundenen initialen Krankheitskonzepte adipöser Kinder ergeben ein homogenes erwartungskonformes Bild. In einer zweiten Untersuchung wurden anschließend die subjektiven Krankheitskonzepte adipöser Kinder, die Bewältigungsstrategien sowie gesundheits- und krankheitsrelevante Kriteriumsvariablen untersucht. Die Befragungen erfolgten vor Beginn einer stationären Reha (T1), am Ende der Reha (T2) sowie sechs Monate nach Reha-Ende (T3). Von 107 Kindern liegen Daten zu allen drei Messzeitpunkten vor. Es konnte ein Zusammenhang zwischen Krankheitskonzepten, Bewältigungsstrategien und spezifischen Kriteriumsvariablen bei adipösen Kindern nachgewiesen werden. Die Analyse der Wirkzusammenhänge konnte zeigen, dass die kindlichen Krankheitskonzepte – neben den indirekten Einflüssen über die Bewältigungsstrategien – die Kriteriumsvariablen vor allem auch direkt beeinflussen können. Der Einfluss der initialen Krankheitskonzepte adipöser Kinder konnte hierbei sowohl im querschnittlichen als auch im längsschnittlichen Design bestätigt werden. Zudem konnten vielfältige Einflüsse der Veränderung der subjektiven Krankheitskonzepte während der Therapie gefunden werden. Die Veränderungen der Krankheitskonzepte wirken sowohl mittelfristig auf die individuellen Bewältigungsstrategien am Ende der Reha als auch längerfristig auf die adipositasspezifischen Kriteriumsvariablen Gewicht, Ernährung, Bewegung und Lebensqualität. Die Befunde stärken die Relevanz und das Potential der zielgerichteten Modifikation adaptiver bzw. maladaptiver Krankheitskonzepte innerhalb der stationären Therapie der kindlichen Adipositas. Zudem konnte bestätigt werden, dass subjektive Krankheitskonzepte und ihre Veränderung innerhalb der Therapie einen relevanten Beitrag zur Vorhersage des kindlichen Therapieerfolgs über einen längerfristigen Zeitraum leisten können.
Background: Obesity is not only a highly prevalent disease but also poses a considerable burden on children and their families. Evidence is increasing that a lack of self-regulation skills may play a role in the etiology and maintenance of obesity. Our goal with this currently ongoing trial is to examine whether training that focuses on the enhancement of self-regulation skills may increase the sustainability of a complex lifestyle intervention.
Methods/Design: In a multicenter, prospective, parallel group, randomized controlled superiority trial, 226 obese children and adolescents aged 8 to 16 years will be allocated either to a newly developed computer-training program to improve their self-regulation abilities or to a placebo control group. Randomization occurs centrally and blockwise at a 1:1 allocation ratio for each center. This study is performed in pediatric inpatient rehabilitation facilities specialized in the treatment of obesity. Observer-blind assessments of outcome variables take place at four times: at the beginning of the rehabilitation (pre), at the end of the training in the rehabilitation (post), and 6 and 12 months post-rehabilitation intervention. The primary outcome is the course of BMI-SDS over 1 year after the end of the inpatient rehabilitation. Secondary endpoints are the self-regulation skills. In addition, health-related quality of life, and snack intake will be analyzed.
Discussion: The computer-based training programs might be a feasible and attractive tool to increase the sustainability of the weight loss reached during inpatient rehabilitation.
Background: Obesity is a risk factor for diseases including type 2 diabetes mellitus (T2DM) and cardiovascular disorders. Diabetes itself contributes to cardiac damage. Thus, studying cardiovascular events and establishing therapeutic intervention in the period of type T2DM onset and manifestation are of highest importance. Mitochondrial dysfunction is one of the pathophysiological mechanisms leading to impaired cardiac function. Methods: An adequate animal model for studying pathophysiology of T2DM is the New Zealand Obese (NZO) mouse. These mice were maintained on a high-fat diet (HFD) without carbohydrates for 13 weeks followed by 4 week HFD with carbohydrates. NZO mice developed severe obesity and only male mice developed manifest T2DM. We determined cardiac phenotypes and mitochondrial function as well as cardiomyocyte signaling in this model. Results: The development of an obese phenotype and T2DM in male mice was accompanied by an impaired systolic function as judged by echocardiography and MyH6/7 expression. Moreover, the mitochondrial function only in male NZO hearts was significantly reduced and ERK1/2 and AMPK protein levels were altered. Conclusions: This is the first report demonstrating that the cardiac phenotype in male diabetic NZO mice is associated with impaired cardiac energy function and signaling events.
Past research indicates an association in adults and young people of emotional and contextual factors with a higher risk for the development of eating disorders or obesity. Few studies focus on problematic eating patterns in childhood, especially in association with parental feeding strategies. 482 mothers completed a questionnaire about eating behaviors and the weight status of their 1- to 10-year-old child as well as their own feeding strategies. A classification of the child's eating behavior (food responsiveness, emotional eating, external eating, eating time and meal structure) using hierarchical cluster analysis revealed a conspicuous eating pattern (10 %) showing above-average values in all eating behaviors. Controlling for weight and demographic variables mothers of children with conspicuous eating patterns were characterized by restrictive strategies and were less likely to encourage or facilitate their child to control his or her eating. Similar problematic eating patterns were also identified in early childhood. The association of maternal feeding strategies - beyond weight control issues - with conspicuous eating patterns in children might indicate a possibility of early prevention through parent training.
Prevention and anthropology
(2014)
Screening is an important issue in medicine and is used to early identify unrecognised diseases in persons who are apparently in good health. Screening strongly relies on the concept of "normal values". Normal values are defined as values that are frequently observed in a population and usually range within certain statistical limits. Screening for obesity should start early as the prevalence of obesity consolidates already at early school age. Though widely practiced, measuring BMI is not the ultimate solution for detecting obesity. Children with high BMI may be "robust" in skeletal dimensions. Assessing skeletal robustness and in particularly assessing developmental tempo in adolescents are also important issues in health screening.
Yet, in spite of the necessity of screening investigations, appropriate reference values are often missing. Meanwhile, new concepts of growth diagrams have been developed. Stage line diagrams are useful for tracking developmental processes over time. Functional data analyses have efficiently been used for analysing longitudinal growth in height and assessing the tempo of maturation. Convenient low-cost statistics have also been developed for generating synthetic national references.
As a tumor suppressor and the most frequently mutated gene in cancer, p53 is among the best-described molecules in medical research. As cancer is in most cases an age-related disease, it seems paradoxical that p53 is so strongly conserved from early multicellular organisms to humans. A function not directly related to tumor suppression, such as the regulation of metabolism in nontransformed cells, could explain this selective pressure. While this role of p53 in cellular metabolism is gradually emerging, it is imperative to dissect the tissue-and cell-specific actions of p53 and its downstream signaling pathways. In this review, we focus on studies reporting p53's impact on adipocyte development, function, and maintenance, as well as the causes and consequences of altered p53 levels in white and brown adipose tissue (AT) with respect to systemic energy homeostasis. While whole body p53 knockout mice gain less weight and fat mass under a high-fat diet owing to increased energy expenditure, modifying p53 expression specifically in adipocytes yields more refined insights: (1) p53 is a negative regulator of in vitro adipogenesis; (2) p53 levels in white AT are increased in diet-induced and genetic obesity mouse models and in obese humans; (3) functionally, elevated p53 in white AT increases senescence and chronic inflammation, aggravating systemic insulin resistance; (4) p53 is not required for normal development of brown AT; and (5) when p53 is activated in brown AT in mice fed a high-fat diet, it increases brown AT temperature and brown AT marker gene expression, thereby contributing to reduced fat mass accumulation. In addition, p53 is increasingly being recognized as crucial player in nutrient sensing pathways. Hence, despite existence of contradictory findings and a varying density of evidence, several functions of p53 in adipocytes and ATs have been emerging, positioning p53 as an essential regulatory hub in ATs. Future studies need to make use of more sophisticated in vivo model systems and should identify an AT-specific set of p53 target genes and downstream pathways upon different (nutrient) challenges to identify novel therapeutic targets to curb metabolic diseases
As a tumor suppressor and the most frequently mutated gene in cancer, p53 is among the best-described molecules in medical research. As cancer is in most cases an age-related disease, it seems paradoxical that p53 is so strongly conserved from early multicellular organisms to humans. A function not directly related to tumor suppression, such as the regulation of metabolism in nontransformed cells, could explain this selective pressure. While this role of p53 in cellular metabolism is gradually emerging, it is imperative to dissect the tissue-and cell-specific actions of p53 and its downstream signaling pathways. In this review, we focus on studies reporting p53's impact on adipocyte development, function, and maintenance, as well as the causes and consequences of altered p53 levels in white and brown adipose tissue (AT) with respect to systemic energy homeostasis. While whole body p53 knockout mice gain less weight and fat mass under a high-fat diet owing to increased energy expenditure, modifying p53 expression specifically in adipocytes yields more refined insights: (1) p53 is a negative regulator of in vitro adipogenesis; (2) p53 levels in white AT are increased in diet-induced and genetic obesity mouse models and in obese humans; (3) functionally, elevated p53 in white AT increases senescence and chronic inflammation, aggravating systemic insulin resistance; (4) p53 is not required for normal development of brown AT; and (5) when p53 is activated in brown AT in mice fed a high-fat diet, it increases brown AT temperature and brown AT marker gene expression, thereby contributing to reduced fat mass accumulation. In addition, p53 is increasingly being recognized as crucial player in nutrient sensing pathways. Hence, despite existence of contradictory findings and a varying density of evidence, several functions of p53 in adipocytes and ATs have been emerging, positioning p53 as an essential regulatory hub in ATs. Future studies need to make use of more sophisticated in vivo model systems and should identify an AT-specific set of p53 target genes and downstream pathways upon different (nutrient) challenges to identify novel therapeutic targets to curb metabolic diseases.
The intake of high-fat diets (HFDs) containing large amounts of saturated long-chain fatty acids leads to obesity, oxidative stress, inflammation, and insulin resistance. The trace element selenium, as a crucial part of antioxidative selenoproteins, can protect against the development of diet-induced insulin resistance in white adipose tissue (WAT) by increasing glutathione peroxidase 3 (GPx3) and insulin receptor (IR) expression. Whether selenite (Se) can attenuate insulin resistance in established lipotoxic and obese conditions is unclear. We confirm that GPX3 mRNA expression in adipose tissue correlates with BMI in humans. Cultivating 3T3-L1 pre-adipocytes in palmitate-containing medium followed by Se treatment attenuates insulin resistance with enhanced GPx3 and IR expression and adipocyte differentiation. However, feeding obese mice a selenium-enriched high-fat diet (SRHFD) only resulted in a modest increase in overall selenoprotein gene expression in WAT in mice with unaltered body weight development, glucose tolerance, and insulin resistance. While Se supplementation improved adipocyte morphology, it did not alter WAT insulin sensitivity. However, mice fed a SRHFD exhibited increased insulin content in the pancreas. Overall, while selenite protects against palmitate-induced insulin resistance in vitro, obesity impedes the effect of selenite on insulin action and adipose tissue metabolism in vivo.