@article{StadionSchuermann2020, author = {Stadion, Mandy and Sch{\"u}rmann, Annette}, title = {Intermittent fasting}, series = {Psychotherapeut}, volume = {66}, journal = {Psychotherapeut}, number = {1}, publisher = {Springer}, address = {New York}, issn = {0935-6185}, doi = {10.1007/s00278-020-00471-5}, pages = {23 -- 27}, year = {2020}, abstract = {A long-term positive energy balance leads to overweight and obesity. Adiposity is the main risk factor for cardiovascular diseases, type 2 diabetes and cancer and is often accompanied by depression. The increasing prevalence creates a major problem for the healthcare system. The conservative management of obesity strives for weight loss by reducing the daily caloric intake and increasing physical activity as well as an improvement in the quality of life supported by psychological interventions. For reducing body weight, intermittent fasting represents an alternative to continuous calorie restriction as it can be easily integrated into daily life. In this form of diet calorie intake is limited in time, i.e. on 2 days in the week or 6-10 h per day. Animal and human studies provide evidence that intermittent fasting over a longer time period is a suitable method to decrease body fat and to improve many metabolic parameters. Fasting alters metabolism and activates specific cellular pathways. These have not only cardioprotective effects but also neuroprotective and antidepressive effects. In this article the currently discussed mechanisms induced by intermittent fasting are highlighted and the essential observations from randomized controlled human trials are presented.}, language = {de} } @article{LehmannFlorisWoiteketal.2017, author = {Lehmann, Andreas and Floris, Jo{\"e}l and Woitek, Ulrich and Ruehli, Frank J. and Staub, Kaspar}, title = {Temporal trends, regional variation and socio-economic differences in height, BMI and body proportions among German conscripts, 1956-2010}, series = {Public Health Nutrition}, volume = {20}, journal = {Public Health Nutrition}, number = {3}, publisher = {Cambridge Univ. Press}, address = {Cambridge}, issn = {1368-9800}, doi = {10.1017/S1368980016002408}, pages = {391 -- 403}, year = {2017}, abstract = {Objective: We analyse temporal trends and regional variation among the most recent available anthropometric data from German conscription in the years 2008-2010 and their historical contextualization since 1956. Design/setting/subjects: The overall sample included German conscripts (N 13 857 313) from 1956 to 2010. Results: German conscripts changed from growing in height to growing in breadth. Over the analysed 54 years, average height of 19-year-old conscripts increased by 6.5 cm from 173.5 cm in 1956 (birth year 1937) to 180.0 cm in 2010 (birth year 1991). This increase plateaued since the 1990s (1970s birth years). The increase in average weight, however, did not lessen during the last two decades but increased in two steps: at the end of the 1980s and after 1999. The weight and BMI distributions became increasingly right-skewed, the prevalence of overweight and obesity increased from 11.6 \% and 2.1 \% in 1984 to 19.9 \% and 8.5 \% in 2010, respectively. The north-south gradient in height (north = taller) persisted during our observations. Height and weight of conscripts from East Germany matched the German average between the early 1990s and 2009. Between the 1980s and the early 1990s, the average chest circumference increased, the average difference between chest circumference when inhaling and exhaling decreased, as did leg length relative to trunk length. Conclusions: Measuring anthropometric data for military conscripts yielded year-by-year monitoring of the health status of young men at a proscribed age. Such findings contribute to a more precise identification of groups at risk and thus help with further studies and to target interventions.}, language = {en} } @misc{KozielHermanussenGomulaetal.2017, author = {Koziel, Slawomir and Hermanussen, Michael and Gomula, Alexandra and Swanson, James and Kaczmarek, Maria and El-Shabrawi, Mortada and Elhusseini, Mona and Satake, Takashi and Martinovic Klaric, Irena and Scheffler, Christiane and Morkuniene, Ruta and Godina, Elena and Sasa, Missoni and Tutkuviene, Janina and Siniarska, Anna and Nieczuja-Dwojacka, Joanna and Nunez, Javier and Groth, Detlef and Barbieri, Davide}, title = {Adolescence - a Transition to Adulthood Proceedings of the 24th Aschauer Soiree, held at Jurata, Poland, November 5th 2016}, series = {Pediatric Endocrinology Reviews}, volume = {14}, journal = {Pediatric Endocrinology Reviews}, number = {3}, publisher = {Medical Media}, address = {Netanya}, issn = {1565-4753}, pages = {326 -- 334}, year = {2017}, abstract = {Eighteen scientists met at Jurata, Poland, to discuss various aspects of the transition from adolescence to adulthood. This transition is a delicate period facing complex interactions between the adolescents and the social group they belong to. Social identity, group identification and identity signalling, but also stress affecting basal salivary cortisol rhythms, hypertension, inappropriate nutrition causing latent and manifest obesity, moreover, in developing and under-developed countries, parasitosis causing anaemia thereby impairing growth and development, are issues to be dealt with during this period of the human development. In addition, some new aspects of the association between weight, height and head circumference in the newborns were discussed, as well as intrauterine head growth and head circumference as health risk indicators.}, language = {en} } @article{HauffeRathSchelletal.2021, author = {Hauffe, Robert and Rath, Michaela and Schell, Mareike and Ritter, Katrin and Kappert, Kai and Deubel, Stefanie and Ott, Christiane and J{\"a}hnert, Markus and Jonas, Wenke and Sch{\"u}rmann, Annette and Kleinridders, Andr{\´e}}, title = {HSP60 reduction protects against diet-induced obesity by modulating energy metabolism in adipose tissue}, series = {Molecular Metabolism}, volume = {53}, journal = {Molecular Metabolism}, publisher = {Elsevier}, address = {Amsterdam, Niederlande}, issn = {2212-8778}, doi = {10.1016/j.molmet.2021.101276}, pages = {1 -- 14}, year = {2021}, abstract = {Objective Insulin regulates mitochondrial function, thereby propagating an efficient metabolism. Conversely, diabetes and insulin resistance are linked to mitochondrial dysfunction with a decreased expression of the mitochondrial chaperone HSP60. The aim of this investigation was to determine the effect of a reduced HSP60 expression on the development of obesity and insulin resistance. Methods Control and heterozygous whole-body HSP60 knockout (Hsp60+/-) mice were fed a high-fat diet (HFD, 60\% calories from fat) for 16 weeks and subjected to extensive metabolic phenotyping. To understand the effect of HSP60 on white adipose tissue, microarray analysis of gonadal WAT was performed, ex vivo experiments were performed, and a lentiviral knockdown of HSP60 in 3T3-L1 cells was conducted to gain detailed insights into the effect of reduced HSP60 levels on adipocyte homeostasis. Results Male Hsp60+/- mice exhibited lower body weight with lower fat mass. These mice exhibited improved insulin sensitivity compared to control, as assessed by Matsuda Index and HOMA-IR. Accordingly, insulin levels were significantly reduced in Hsp60+/- mice in a glucose tolerance test. However, Hsp60+/- mice exhibited an altered adipose tissue metabolism with elevated insulin-independent glucose uptake, adipocyte hyperplasia in the presence of mitochondrial dysfunction, altered autophagy, and local insulin resistance. Conclusions We discovered that the reduction of HSP60 in mice predominantly affects adipose tissue homeostasis, leading to beneficial alterations in body weight, body composition, and adipocyte morphology, albeit exhibiting local insulin resistance.}, language = {en} } @misc{HauffeRathSchelletal.2022, author = {Hauffe, Robert and Rath, Michaela and Schell, Mareike and Ritter, Katrin and Kappert, Kai and Deubel, Stefanie and Ott, Christiane and J{\"a}hnert, Markus and Jonas, Wenke and Sch{\"u}rmann, Annette and Kleinridders, Andr{\´e}}, title = {HSP60 reduction protects against diet-induced obesity by modulating energy metabolism in adipose tissue}, series = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe}, journal = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe}, publisher = {Universit{\"a}tsverlag Potsdam}, address = {Potsdam}, issn = {1866-8372}, doi = {10.25932/publishup-54800}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-548002}, pages = {1 -- 14}, year = {2022}, abstract = {Objective Insulin regulates mitochondrial function, thereby propagating an efficient metabolism. Conversely, diabetes and insulin resistance are linked to mitochondrial dysfunction with a decreased expression of the mitochondrial chaperone HSP60. The aim of this investigation was to determine the effect of a reduced HSP60 expression on the development of obesity and insulin resistance. Methods Control and heterozygous whole-body HSP60 knockout (Hsp60+/-) mice were fed a high-fat diet (HFD, 60\% calories from fat) for 16 weeks and subjected to extensive metabolic phenotyping. To understand the effect of HSP60 on white adipose tissue, microarray analysis of gonadal WAT was performed, ex vivo experiments were performed, and a lentiviral knockdown of HSP60 in 3T3-L1 cells was conducted to gain detailed insights into the effect of reduced HSP60 levels on adipocyte homeostasis. Results Male Hsp60+/- mice exhibited lower body weight with lower fat mass. These mice exhibited improved insulin sensitivity compared to control, as assessed by Matsuda Index and HOMA-IR. Accordingly, insulin levels were significantly reduced in Hsp60+/- mice in a glucose tolerance test. However, Hsp60+/- mice exhibited an altered adipose tissue metabolism with elevated insulin-independent glucose uptake, adipocyte hyperplasia in the presence of mitochondrial dysfunction, altered autophagy, and local insulin resistance. Conclusions We discovered that the reduction of HSP60 in mice predominantly affects adipose tissue homeostasis, leading to beneficial alterations in body weight, body composition, and adipocyte morphology, albeit exhibiting local insulin resistance.}, language = {en} } @article{WarschburgerGmeinerMorawietzetal.2017, author = {Warschburger, Petra and Gmeiner, Michaela Silvia and Morawietz, Marisa and Rinck, Mike}, title = {Battle of plates}, series = {Public health nutrition : PHN / The Nutrition Society}, volume = {21}, journal = {Public health nutrition : PHN / The Nutrition Society}, number = {2}, publisher = {Cambridge Univ. Press}, address = {Cambridge}, issn = {1368-9800}, doi = {10.1017/S1368980017002701}, pages = {426 -- 434}, year = {2017}, abstract = {Objective: Approach-avoidance training (AAT) is a promising approach in obesity treatment. The present study examines whether an AAT is feasible and able to influence approach tendencies in children and adolescents, comparing implicit and explicit training approaches. Design/Setting/Subjects: Fifty-nine overweight children and adolescents (aged 8-16 years; twenty-six boys) participated in an AAT for food cues, learning to reject snack items and approach vegetable items. Reaction times in the AAT and an implicit association rest (IAT) were assessed pre- and post-intervention. Results: A significant increase in the AAT compatibility scores with a large effect (eta(2) = 0.18) was found. No differences between the implicit and explicit training approaches and no change in the IAT scores were observed. Conclusions: Automatic tendencies in children can be trained, too. The implementation of AAT in the treatment of obesity might support the modification of an unhealthy nutrition behaviour pattern. Further data from randomized controlled clinical trials are needed.}, language = {en} } @article{LaegerCastanoMartinezWernoetal.2018, author = {Laeger, Thomas and Castano-Martinez, Teresa and Werno, Martin W. and Japtok, Lukasz and Baumeier, Christian and Jonas, Wenke and Kleuser, Burkhard and Sch{\"u}rmann, Annette}, title = {Dietary carbohydrates impair the protective effect of protein restriction against diabetes in NZO mice used as a model of type 2 diabetes}, series = {Diabetologia : journal of the European Association for the Study of Diabetes (EASD)}, volume = {61}, journal = {Diabetologia : journal of the European Association for the Study of Diabetes (EASD)}, number = {6}, publisher = {Springer}, address = {New York}, issn = {0012-186X}, doi = {10.1007/s00125-018-4595-1}, pages = {1459 -- 1469}, year = {2018}, abstract = {Aims/hypothesis Low-protein diets are well known to improve glucose tolerance and increase energy expenditure. Increases in circulating fibroblast growth factor 21 (FGF21) have been implicated as a potential underlying mechanism. Methods We aimed to test whether low-protein diets in the context of a high-carbohydrate or high-fat regimen would also protect against type 2 diabetes in New Zealand Obese (NZO) mice used as a model of polygenetic obesity and type 2 diabetes. Mice were placed on high-fat diets that provided protein at control (16 kJ\%; CON) or low (4 kJ\%; low-protein/high-carbohydrate [LP/HC] or low-protein/high-fat [LP/HF]) levels. Results Protein restriction prevented the onset of hyperglycaemia and beta cell loss despite increased food intake and fat mass. The effect was seen only under conditions of a lower carbohydrate/fat ratio (LP/HF). When the carbohydrate/fat ratio was high (LP/HC), mice developed type 2 diabetes despite the robustly elevated hepatic FGF21 secretion and increased energy expenditure. Conclusion/interpretation Prevention of type 2 diabetes through protein restriction, without lowering food intake and body fat mass, is compromised by high dietary carbohydrates. Increased FGF21 levels and elevated energy expenditure do not protect against hyperglycaemia and type 2 diabetes per se.}, language = {en} } @misc{Schulze2018, author = {Schulze, Matthias Bernd}, title = {Metabolic health in normal-weight and obese individuals}, series = {Diabetologia : journal of the European Association for the Study of Diabetes (EASD)}, volume = {62}, journal = {Diabetologia : journal of the European Association for the Study of Diabetes (EASD)}, number = {4}, publisher = {Springer}, address = {New York}, issn = {0012-186X}, doi = {10.1007/s00125-018-4787-8}, pages = {558 -- 566}, year = {2018}, abstract = {Cardiovascular complications are commonly associated with obesity. However, a subgroup of obese individuals may not be at an increased risk for cardiovascular complications; these individuals are said to have metabolically healthy obesity (MHO). In contrast, metabolically unhealthy individuals are at high risk of cardiovascular disease (CVD), irrespective of BMI; thus, this group can include individuals within the normal weight category (BMI 18.5-24.9kg/m(2)). This review provides a summary of prospective studies on MHO and metabolically unhealthy normal-weight (MUHNW) phenotypes. Notably, there is ongoing dispute surrounding the concept of MHO, including the lack of a uniform definition and the potentially transient nature of metabolic health status. This review highlights the relevance of alternative measures of body fatness, specifically measures of fat distribution, for determining MHO and MUHNW. It also highlights alternative approaches of risk stratification, which account for the continuum of risk in relation to CVD, which is observable for most risk factors. Moreover, studies evaluating the transition from metabolically healthy to unhealthy phenotypes and potential determinants for such conversions are discussed. Finally, the review proposes several strategies for the use of epidemiological research to further inform the current debate on metabolic health and its determination across different stages of body fatness.}, language = {en} } @phdthesis{Hauffe2021, author = {Hauffe, Robert}, title = {Investigating metabolic consequences of an HSP60 reduction during diet-induced obesity}, doi = {10.25932/publishup-50929}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-509294}, school = {Universit{\"a}t Potsdam}, pages = {xxi, 116}, year = {2021}, abstract = {The mitochondrial chaperone complex HSP60/HSP10 facilitates mitochondrial protein homeostasis by folding more than 300 mitochondrial matrix proteins. It has been shown previously that HSP60 is downregulated in brains of type 2 diabetic (T2D) mice and patients, causing mitochondrial dysfunction and insulin resistance. As HSP60 is also decreased in peripheral tissues in T2D animals, this thesis investigated the effect of overall reduced HSP60 in the development of obesity and associated co-morbidities. To this end, both female and male C57Bl/6N control (i.e. without further alterations in their genome, Ctrl) and heterozygous whole-body Hsp60 knock-out (Hsp60+/-) mice, which exhibit a 50 \% reduction of HSP60 in all tissues, were fed a normal chow diet (NCD) or a highfat diet (HFD, 60 \% calories from fat) for 16 weeks and were subjected to extensive metabolic phenotyping including indirect calorimetry, NMR spectroscopy, insulin, glucose and pyruvate tolerance tests, vena cava insulin injections, as well as histological and molecular analysis. Interestingly, NCD feeding did not result in any striking phenotype, only a mild increase in energy expenditure in Hsp60+/- mice. Exposing mice to a HFD however revealed an increased body weight due to higher muscle mass in female Hsp60+/- mice, with a simultaneous decrease in energy expenditure. Additionally, these mice displayed decreased fasting glycemia. Opposingly, male Hsp60+/- compared to control mice showed lower body weight gain due to decreased fat mass and an increased energy expenditure, strikingly independent of lean mass. Further, only male Hsp60+/- mice display improved HOMA-IR and Matsuda insulin sensitivity indices. Despite the opposite phenotype in regards to body weight development, Hsp60+/- mice of both sexes show a significantly higher cell number, as well as a reduction in adipocyte size in the subcutaneous and gonadal white adipose tissue (sc/gWAT). Curiously, this adipocyte hyperplasia - usually associated with positive aspects of WAT function - is disconnected from metabolic improvements, as the gWAT of male Hsp60+/- mice shows mitochondrial dysfunction, oxidative stress, and insulin resistance. Transcriptomic analysis of gWAT shows an up regulation of genes involved in macroautophagy. Confirmatory, expression of microtubuleassociated protein 1A/1B light chain 3B (LC3), as a protein marker of autophagy, and direct measurement of lysosomal activity is increased in the gWAT of male Hsp60+/- mice. In summary, this thesis revealed a novel gene-nutrient interaction. The reduction of the crucial chaperone HSP60 did not have large effects in mice fed a NCD, but impacted metabolism during DIO in a sex-specific manner, where, despite opposing body weight and body composition phenotypes, both female and male Hsp60+/- mice show signs of protection from high fat diet-induced systemic insulin resistance.}, language = {en} } @phdthesis{Seebeck2020, author = {Seebeck, Nicole}, title = {Regulation of the organokines FGF21 and chemerin by diet}, doi = {10.25932/publishup-47114}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-471140}, school = {Universit{\"a}t Potsdam}, pages = {i, 132}, year = {2020}, abstract = {The hepatokine FGF21 and the adipokine chemerin have been implicated as metabolic regulators and mediators of inter-tissue crosstalk. While FGF21 is associated with beneficial metabolic effects and is currently being tested as an emerging therapeutic for obesity and diabetes, chemerin is linked to inflammation-mediated insulin resistance. However, dietary regulation of both organokines and their role in tissue interaction needs further investigation. The LEMBAS nutritional intervention study investigated the effects of two diets differing in their protein content in obese human subjects with non-alcoholic fatty liver disease (NAFLD). The study participants consumed hypocaloric diets containing either low (LP: 10 EN\%, n = 10) or high (HP: 30 EN\%, n = 9) dietary protein 3 weeks prior to bariatric surgery. Before and after the intervention the participants were anthropometrically assessed, blood samples were drawn, and hepatic fat content was determined by MRS. During bariatric surgery, paired subcutaneous and visceral adipose tissue biopsies as well as liver biopsies were collected. The aim of this thesis was to investigate circulating levels and tissue-specific regulation of (1) FGF21 and (2) chemerin in the LEMBAS cohort. The results were compared to data obtained in 92 metabolically healthy subjects with normal glucose tolerance and normal liver fat content. (1) Serum FGF21 concentrations were elevated in the obese subjects, and strongly associated with intrahepatic lipids (IHL). In accordance, FGF21 serum concentrations increased with severity of NAFLD as determined histologically in the liver biopsies. Though both diets were successful in reducing IHL, the effect was more pronounced in the HP group. FGF21 serum concentrations and mRNA expression were bi-directionally regulated by dietary protein, independent from metabolic improvements. In accordance, in the healthy study subjects, serum FGF21 concentrations dropped by more than 60\% in response to the HP diet. A short-term HP intervention confirmed the acute downregulation of FGF21 within 24 hours. Lastly, experiments in HepG2 cell cultures and primary murine hepatocytes identified nitrogen metabolites (NH4Cl and glutamine) to dose-dependently suppress FGF21 expression. (2) Circulating chemerin concentrations were considerably elevated in the obese versus lean study participants and differently associated with markers of obesity and NAFLD in the two cohorts. The adipokine decreased in response to the hypocaloric interventions while an unhealthy high-fat diet induced a rise in chemerin serum levels. In the lean subjects, mRNA expression of RARRES2, encoding chemerin, was strongly and positively correlated with expression of several cytokines, including MCP1, TNFα, and IL6, as well as markers of macrophage infiltration in the subcutaneous fat depot. However, RARRES2 was not associated with any cytokine assessed in the obese subjects and the data indicated an involvement of chemerin not only in the onset but also resolution of inflammation. Analyses of the tissue biopsies and experiments in human primary adipocytes point towards a role of chemerin in adipogenesis while discrepancies between the in vivo and in vitro data were detected. Taken together, the results of this thesis demonstrate that circulating FGF21 and chemerin levels are considerably elevated in obesity and responsive to dietary interventions. FGF21 was acutely and bi-directionally regulated by dietary protein in a hepatocyte-autonomous manner. Given that both, a lack in essential amino acids and excessive nitrogen intake, exert metabolic stress, FGF21 may serve as an endocrine signal for dietary protein balance. Lastly, the data revealed that chemerin is derailed in obesity and associated with obesity-related inflammation. However, future studies on chemerin should consider functional and regulatory differences between secreted and tissue-specific isoforms.}, language = {en} } @article{WarschburgerKroellerHaertingetal.2016, author = {Warschburger, Petra and Kr{\"o}ller, Katja and Haerting, Johannes and Unverzagt, Susanne and van Egmond-Fr{\"o}hlich, Andreas}, title = {Empowering Parents of Obese Children (EPOC): A randomized controlled trial on additional long-term weight effects of parent training}, series = {Appetite : multidisciplinary research on eating and drinking}, volume = {103}, journal = {Appetite : multidisciplinary research on eating and drinking}, publisher = {Elsevier}, address = {London}, issn = {0195-6663}, doi = {10.1016/j.appet.2016.04.007}, pages = {148 -- 156}, year = {2016}, abstract = {Although inpatient lifestyle treatment for obese children and adolescents can be highly effective in the short term, long-term results are unconvincing. One possible explanation might be that the treatment takes place far from parents' homes, limiting the possibility to incorporate the parents, who play a major role in establishing and maintaining a healthy lifestyle in childhood and adolescence. The main goal was to develop a brief behaviorally oriented parent training program that enhances 'obesity-specific' parenting skills in order to prevent relapse. We hypothesized that the inclusion of additional parent training would lead to an improved long-term weight course of obese children. Parents of obese children (n = 686; 7-13 years old) either participated in complementary cognitive-behavioral group sessions (n = 336) or received written information only (n = 350) during the inpatient stay. Children of both groups attended multidisciplinary inpatient rehabilitation. BMI-SDS as a primary outcome was evaluated at baseline, post-intervention and at 6- and 12-month follow-up. Intention-to-treat (ITT) as well as per-protocol analyses (PPA) were performed. A significant within-group decrease of 0.24 (95\% CI 0.18 to 0.30) BMI-SDS points from the beginning of the inpatient stay through the first year was found, but no group difference at the one-year follow-up (mean difference 0.02; 95\% CI -0.04 to 0.07). We also observed an increase in quality of life scores, intake of healthy food and exercise for both groups, without differences between groups (ITT and PPA). Thus, while the inpatient treatment proved highly effective, additional parent training did not lead to better results in long-term weight maintenance or to better psychosocial well-being compared to written psycho-educational material. Further research should focus on subgroups to answer the question of differential treatment effects.}, language = {en} } @article{WarschburgerKroeller2016, author = {Warschburger, Petra and Kr{\"o}ller, Katja}, title = {Loss to follow-up in a randomized controlled trial study for pediatric weight management (EPOC)}, series = {BMC PEDIATRICS}, volume = {16}, journal = {BMC PEDIATRICS}, publisher = {BioMed Central}, address = {London}, issn = {1471-2431}, doi = {10.1186/s12887-016-0727-2}, pages = {9}, year = {2016}, abstract = {Background: Attrition is a serious problem in intervention studies. The current study analyzed the attrition rate during follow-up in a randomized controlled pediatric weight management program (EPOC study) within a tertiary care setting. Methods: Five hundred twenty-three parents and their 7-13-year-old children with obesity participated in the randomized controlled intervention trial. Follow-up data were assessed 6 and 12 months after the end of treatment. Attrition was defined as providing no objective weight data. Demographic and psychological baseline characteristics were used to predict attrition at 6- and 12-month follow-up using multivariate logistic regression analyses. Conclusions: The minor differences between the completers and the non-completers suggest that our retention strategies were successful. Further research should focus on prevention of attrition in families with a lower educational background.}, language = {en} } @article{CaliendoGehrsitz2016, author = {Caliendo, Marco and Gehrsitz, Markus}, title = {Obesity and the labor market: A fresh look at the weight penalty}, series = {Inorganics : open access journal}, volume = {23}, journal = {Inorganics : open access journal}, publisher = {Elsevier}, address = {Amsterdam}, issn = {1570-677X}, doi = {10.1016/j.ehb.2016.09.004}, pages = {209 -- 225}, year = {2016}, language = {en} } @article{HoffmannWarschburger2015, author = {Hoffmann, Svenja and Warschburger, Petra}, title = {Body image in obese children and adolescents. Body dissatisfaction and body size perception in relation to quality of life and weight loss}, series = {Psychotherapeut}, volume = {60}, journal = {Psychotherapeut}, number = {6}, publisher = {Springer}, address = {New York}, issn = {0935-6185}, doi = {10.1007/s00278-015-0060-5}, pages = {498 -- 504}, year = {2015}, abstract = {Body dissatisfaction and an unrealistic perception of own body size are particularly common in obese children and adolescents; however, little is known about the association with weight-related quality of life and the impact on successful long-term weight loss. At the beginning of an inpatient child obesity rehabilitation program, 408 children and adolescents aged 9-12 years completed a questionnaire on body image (body silhouettes) and a body weight-specific questionnaire for overweight and obese children and adolescents (GW-LQ-KJ) on quality of life. Height and weight were measured by a physician at the beginning and 1 year after inpatient hospitalization. Of the participants 91.9 \% reported body dissatisfaction and 75.7 \% underestimated their own body size. There were no gender-specific differences in body dissatisfaction but boys perceived their body size more realistically than girls. Participants with body dissatisfaction and realistic body size perception showed a reduced weight-related quality of life. Those participants who realistically perceived their body size also lost less weight in the long term. The subjective underestimation of body size proved to be important for reduced weight-related quality of life and more pronounced long-term weight loss; therefore, body image should be taken into account in multimodal treatment programs.}, language = {de} } @article{Warschburger2015, author = {Warschburger, Petra}, title = {SRT-Joy - computer-assisted self-regulation training for obese children and adolescents: study protocol for a randomized controlled trial}, series = {Trials}, volume = {16}, journal = {Trials}, publisher = {BioMed Central}, address = {London}, issn = {1745-6215}, doi = {10.1186/s13063-015-1078-2}, pages = {10}, year = {2015}, abstract = {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.}, language = {en} } @article{MummSchefflerHermanussen2014, author = {Mumm, Rebekka and Scheffler, Christiane and Hermanussen, Michael}, title = {Developing differential height, weight and body mass index references for girls that reflect the impact of the menarche}, series = {Acta paediatrica : nurturing the child}, volume = {103}, journal = {Acta paediatrica : nurturing the child}, number = {7}, publisher = {Wiley-Blackwell}, address = {Hoboken}, issn = {0803-5253}, doi = {10.1111/apa.12625}, pages = {e312 -- e316}, year = {2014}, abstract = {Aim Growth is both a matter of amplitude and tempo. We aimed to develop references for body height, body weight and body mass index (BMI) with respect to tempo of maturity. Methods Data obtained from the German KiGGS study (2003-2006) on body height, body weight and presence or absence of the menarche were re-analysed in 3776 girls, aged 10-17years. We developed smoothed centiles for BMI-, body-height- and body-weight-for-age using the LMS method for premenarcheal and postmenarcheal girls. Results Body height, body weight and BMI differed significantly between premenarcheal and postmenarcheal girls. On average, postmenarcheal girls aged 11-17years were 5.3cm taller and 9.7kg heavier, and their BMI was 2.9kg/m2 higher than in premenarcheal girls of the same calendar age. Conclusion Adolescent BMI rises with calendar age and biological age. New reference charts for adolescent girls aged 10-18years were generated to be inserted into the currently used references to avoid misclassifying underweight and overweight pubertal girls.}, language = {en} } @article{WarschburgerKuhne2014, author = {Warschburger, Petra and Kuhne, Daniela}, title = {Psychosocial determinants of quality of life in parents of obese children seeking inpatient treatment}, series = {Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation}, volume = {23}, journal = {Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation}, number = {7}, publisher = {Springer}, address = {Dordrecht}, issn = {0962-9343}, doi = {10.1007/s11136-014-0659-y}, pages = {1985 -- 1995}, year = {2014}, abstract = {To examine and identify predictors of parental health-related quality of life (HRQoL) in a sample of obese and very obese children participating in an inpatient program for treating obesity.}, language = {en} } @article{WarschburgerKroeller2012, author = {Warschburger, Petra and Kr{\"o}ller, Katja}, title = {"Childhood overweight and obesity maternal perceptions of the time for engaging in child weight management"}, series = {BMC public health}, volume = {12}, journal = {BMC public health}, number = {12}, publisher = {BioMed Central}, address = {London}, issn = {1471-2458}, doi = {10.1186/1471-2458-12-295}, pages = {8}, year = {2012}, abstract = {Background: There is an increasing awareness of the impact of parental risk perception on the weight course of the child and the parent's readiness to engage in preventive efforts, but only less is known about factors related to the parental perception of the right time for the implementation of preventive activities. The aim of this study was to examine parental perceptions of the appropriate time to engage in child weight management strategies, and the factors associated with different weight points at which mothers recognize the need for preventive actions. Methods: 352 mothers with children aged 2-10 years took part in the study. We assessed mothers' perceptions of the actual and preferred weight status of their child, their ability to identify overweight and knowledge of its associated health risks, as well as perceptions of the right time for action to prevent overweight in their child. A regression analysis was conducted to examine whether demographic and weight related factors as well as the maternal general risk perception were associated with recognizing the need to implement prevention strategies. Results: Although most of the parents considered a BMI in the 75th to 90th percentile a valid reason to engage in the prevention of overweight, 19\% of the mothers were not willing to engage in prevention until their child reached the 97th percentile. Whereas the child's sex and the identification of an elevated BMI were significant predictors for parents' recognition of the 75th percentile as right point to engage in prevention efforts, an inability to recognize physical health risks associated with overweight silhouettes emerged as a significant factor predicting which parents would delay prevention efforts until a child's BMI reached the 97th percentile. Conclusion: Parental misperceptions of overweight and associated health risks constitute unfavorable conditions for preventive actions. Feedback on the health risks associated with overweight could help increase maternal readiness for change.}, language = {en} } @article{CaliendoLee2013, author = {Caliendo, Marco and Lee, Wang-Sheng}, title = {Fat chance! - Obesity and the transition from unemployment to employment}, series = {Economics and human biology}, volume = {11}, journal = {Economics and human biology}, number = {2}, publisher = {Elsevier}, address = {Amsterdam}, issn = {1570-677X}, doi = {10.1016/j.ehb.2012.02.002}, pages = {121 -- 133}, year = {2013}, abstract = {This paper focuses on estimating the magnitude of any potential weight discrimination by examining whether obese job applicants in Germany get treated or behave differently from non-obese applicants. Based on two waves of rich survey data from the IZA Evaluation dataset, which includes measures that control for education, demographic characteristics, labor market history, psychological factors and health, we estimate differences in job search behavior and labor market outcomes between obese/overweight and normal weight individuals. Unlike other observational studies which are generally based on obese and non-obese individuals who might already be at different points in the job ladder (e.g., household surveys), in our data, individuals are newly unemployed and all start from the same point. The only subgroup we find in our data experiencing any possible form of negative labor market outcomes is obese women. Despite making more job applications and engaging more in job training programs, we find some indications that they experienced worse (or at best similar) employment outcomes than normal weight women. Obese women who found a job also had significantly lower wages than normal weight women.}, language = {en} } @misc{WarschburgerKroeller2016, author = {Warschburger, Petra and Kr{\"o}ller, Katja}, title = {Loss to follow-up in a randomized controlled trial study for pediatric weight management (EPOC)}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-100359}, pages = {9}, year = {2016}, abstract = {Background Attrition is a serious problem in intervention studies. The current study analyzed the attrition rate during follow-up in a randomized controlled pediatric weight management program (EPOC study) within a tertiary care setting. Methods Five hundred twenty-three parents and their 7-13-year-old children with obesity participated in the randomized controlled intervention trial. Follow-up data were assessed 6 and 12 months after the end of treatment. Attrition was defined as providing no objective weight data. Demographic and psychological baseline characteristics were used to predict attrition at 6- and 12-month follow-up using multivariate logistic regression analyses. Results Objective weight data were available for 49.6 (67.0) \% of the children 6 (12) months after the end of treatment. Completers and non-completers at the 6- and 12-month follow-up differed in the amount of weight loss during their inpatient stay, their initial BMI-SDS, educational level of the parents, and child's quality of life and well-being. Additionally, completers supported their child more than non-completers, and at the 12-month follow-up, families with a more structured eating environment were less likely to drop out. On a multivariate level, only educational background and structure of the eating environment remained significant. Conclusions The minor differences between the completers and the non-completers suggest that our retention strategies were successful. Further research should focus on prevention of attrition in families with a lower educational background.}, language = {en} } @article{WarschburgerKroeller2016, author = {Warschburger, Petra and Kr{\"o}ller, Katja}, title = {Loss to follow-up in a randomized controlled trial study for pediatric weight management (EPOC)}, series = {BMC pediatrics}, volume = {16}, journal = {BMC pediatrics}, publisher = {BioMed Central}, address = {London}, issn = {1471-2431}, doi = {10.1186/s12887-016-0727-2}, pages = {9}, year = {2016}, abstract = {Background Attrition is a serious problem in intervention studies. The current study analyzed the attrition rate during follow-up in a randomized controlled pediatric weight management program (EPOC study) within a tertiary care setting. Methods Five hundred twenty-three parents and their 7-13-year-old children with obesity participated in the randomized controlled intervention trial. Follow-up data were assessed 6 and 12 months after the end of treatment. Attrition was defined as providing no objective weight data. Demographic and psychological baseline characteristics were used to predict attrition at 6- and 12-month follow-up using multivariate logistic regression analyses. Results Objective weight data were available for 49.6 (67.0) \% of the children 6 (12) months after the end of treatment. Completers and non-completers at the 6- and 12-month follow-up differed in the amount of weight loss during their inpatient stay, their initial BMI-SDS, educational level of the parents, and child's quality of life and well-being. Additionally, completers supported their child more than non-completers, and at the 12-month follow-up, families with a more structured eating environment were less likely to drop out. On a multivariate level, only educational background and structure of the eating environment remained significant. Conclusions The minor differences between the completers and the non-completers suggest that our retention strategies were successful. Further research should focus on prevention of attrition in families with a lower educational background.}, language = {en} } @phdthesis{Leicht2008, author = {Leicht, Katja}, title = {Positionelle Klonierung von Tbc1d1 als Kandidatengen f{\"u}r Adipositas}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus-34610}, school = {Universit{\"a}t Potsdam}, year = {2008}, abstract = {Nob1 (New Zealand obese 1) bezeichnet einen Adipositas-QTL auf Chr. 5 der Maus (LODBMI >3,3), der in einem R{\"u}ckkreuzungsexperiment der Mausst{\"a}mme NZO (adip{\"o}s) und SJL (schlank) identifiziert wurde. Um Kandidatengene f{\"u}r Adipositas zu finden, wurden mehr als 300 Nob1-Transkripte mit Hilfe von Genexpressionsanalysen auf Unterschiede in stoffwechselrelevanten Geweben zwischen beiden Mausst{\"a}mmen untersucht. Sieben Gene zeigten eine differentielle Expression: 2310045A20Rik, Tbc1d1, Ppp1cb, Mll5, Insig1, Abhd1 und Alox5ap. Die codierenden Bereiche dieser Gene wurden anschließend auf Sequenzunterschiede zwischen NZO und SJL untersucht. Nur im Gen Tbc1d1, das im Peak-Bereich des Nob1 lokalisiert ist, wurde eine SJL-spezifische Deletion von sieben Basen detektiert, die zu einer Leserasterverschiebung und einem vorzeitigen Abbruch des Proteins in der funktionellen Rab-GAP-Dom{\"a}ne f{\"u}hrt (Loss-of-Function-Mutation). Interessanterweise wurde eine Variante von TBC1D1 (R125W) in Kopplungsanalysen mit Adipositas beim Menschen assoziiert (Stone et al., 2006). TBC1D1 zeigt eine hohe Homologie zu TBC1D4 (AS160), das im Insulinsignalweg eine wichtige Rolle spielt. In 17 weiteren Genen im Peak-Bereich des Nob1 wurde keine weitere SJL-spezifischen Mutation detektiert. Bei NZO-Tieren erfolgte die Tbc1d1-mRNA-Expression vorwiegend in glycolytischen Fasern des Skelettmuskels. Zudem wurden zwei gewebsspezifisch exprimierte Tbc1d1-Isoformen identifiziert, die sich durch alternatives Splicen der Exone 12 und 13 unterscheiden. Die im Rahmen dieser Arbeit gefundenen Ergebnisse machen Tbc1d1 zu einem plausiblen Kandidatengen f{\"u}r den Nob1-QTL. Welche Funktion Tbc1d1 im Glucose- und Fettstoffwechsel des Skelettmuskels hat, muss in weiteren Analysen untersucht werden.}, language = {de} } @phdthesis{Andres2008, author = {Andres, Janin}, title = {Untersuchungen {\"u}ber Regulationsmechanismen der 11beta-Hydroxysteroid Dehydrogenase Typ 1}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus-33033}, school = {Universit{\"a}t Potsdam}, year = {2008}, abstract = {Die 11beta-HSD1 reguliert intrazellul{\"a}r die Cortisolkonzentration durch Regeneration von Cortison z.B. aus dem Blutkreislauf, zu Cortisol. Daher stellt diese ein wichtiges Element in der Glucocorticoid-vermittelten Genregulation dar. Die 11beta-HSD1 wird ubiquit{\"a}r exprimiert, auf hohem Niveau besonders in Leber, Fettgewebe und glatten Muskelzellen. Insbesondere die Bedeutung der 11beta-HSD1 in Leber und Fettgewebe konnte mehrfach nachgewiesen werden. In der Leber f{\"u}hrte eine erh{\"o}hte Aktivit{\"a}t aufgrund einer {\"U}berexpression in M{\"a}usen zu einer verst{\"a}rkten Gluconeogeneserate. Des Weiteren konnte gezeigt werden, dass eine erh{\"o}hte Expression und erh{\"o}hte Enzymaktivit{\"a}t der 11beta-HSD1 im subkutanen und viszeralen Fettgewebe assoziiert ist mit Fettleibigkeit, Insulinresistenz und Dyslipid{\"a}mie. {\"U}ber die Regulation ist jedoch noch wenig bekannt. Zur Untersuchung der Promotoraktivit{\"a}t wurde der Promotorbereich von -3034 bis +188, vor und nach dem Translations- und Transkriptionsstart, der 11beta-HSD1 kloniert. 8 Promotorfragmente wurden mittels Dual-Luciferase-Assay in humanen HepG2-Zellen sowie undifferenzierten und differenzierten murinen 3T3-L1-Zellen untersucht. Anschließend wurde mittels nicht-radioaktiven EMSA die Bindung des TATA-Binding Proteins (TBP) sowie von CCAAT/Enhancer-Binding-Proteinen (C/EBP) an ausgew{\"a}hlte Promotorregionen analysiert. Nach der Charakterisierung des Promotors wurden spezifische endogene und exogene Regulatoren untersucht. Fetts{\"a}uren modifizieren die Entstehung von Adipositas und Insulinresistenz. Ihre Wirkung wird u.a. PPARgamma-abh{\"a}ngig vermittelt und kann durch das Inkretin (Glucose-dependent insulinotropic Peptide) GIP modifiziert werden. So wurden die Effekte von unterschiedlichen Fetts{\"a}uren, vom PPARgamma Agonisten Rosiglitazon sowie dem Inkretin GIP auf die Expression und Enzymaktivit{\"a}t der 11beta-HSD1 untersucht. Dies wurde in-vitro-, tierexperimentell und in humanen in-vivo-Studien realisiert. Zuletzt wurden 2 Single Nucleotide Polymorphismen (SNP) im Promotorbereich der 11beta-HSD1 in der Zellkultur im Hinblick auf potentielle Funktionalit{\"a}t analysiert sowie die Assoziation mit Diabetes mellitus Typ 2 und K{\"o}rpergewicht in der MeSyBePo-Kohorte bei rund 1.800 Personen untersucht. Die Luciferase-Assays zeigten basal eine zell-spezifische Regulation der 11beta-HSD1, wobei in allen 3 untersuchten Zelltypen die Bindung eines Repressors nachgewiesen werden konnte. Zudem konnte eine m{\"o}gliche Bindung des TBPs sowie von C/EBP-Proteinen an verschiedene Positionen gezeigt werden. Die Transaktivierungsassays mit den C/EBP-Proteinen -alpha, -beta und -delta zeigten eben-falls eine zellspezifische Regulation des 11beta-HSD1-Promotors. Die Aktivit{\"a}t und Expression der 11beta-HSD1 wurde durch die hier untersuchten endogenen und exogenen Faktoren spezifisch modifiziert, was sowohl in-vitro als auch in-vivo in unterschiedlichen Modellsystemen dargestellt werden konnte. Die Charakterisierung der MeSyBePo-Kohorte ergab keine direkten Assoziationen zwischen Polymorphismus und klinischem Ph{\"a}notyp, jedoch Tendenzen f{\"u}r eine erh{\"o}htes K{\"o}rper-gewicht und Typ 2 Diabetes mellitus in Abh{\"a}ngigkeit des Genotyps. Der Promotor der 11beta-HSD1 konnte aufgrund der Daten aus den Luciferaseassays sowie den Daten aus den EMSA-Analysen n{\"a}her charakterisiert werden. Dieser zeigt eine variable und zell-spezifische Regulation. Ein wichtiger Regulator stellen insbesondere in den HepG2-Zellen die C/EBP-Proteine -alpha, -beta und -delta dar. Aus den in-vivo-Studien ergab sich eine Regulation der 11beta-HSD1 durch endogene, exogene und pharmakologische Substanzen, die durch die Zellkulturversuche best{\"a}tigt und n{\"a}her charakterisiert werden konnten.}, language = {de} }