@article{36062,
  author       = {{Schlegel-Matthies, Kirsten and Methfessel, Barbara}},
  journal      = {{Hauswirtschaft und Wissenschaft}},
  number       = {{1}},
  pages        = {{27--38}},
  title        = {{{ Alltagskultur: viel beschworen, wenig wissenschaftlich durchdrungen?!}}},
  volume       = {{52}},
  year         = {{2014}},
}

@article{54943,
  abstract     = {{Proteolytic activation is a unique feature of the epithelial sodium channel (ENaC). However, the underlying molecular mechanisms and the physiologically relevant proteases remain to be identified. The serine protease trypsin I can activate ENaC in vitro but is unlikely to be the physiologically relevant activating protease in ENaC-expressing tissues in vivo. Herein, we investigated whether human trypsin IV, a form of trypsin that is co-expressed in several extrapancreatic epithelial cells with ENaC, can activate human ENaC. In Xenopus laevis oocytes, we monitored proteolytic activation of ENaC currents and the appearance of $\gamma$ENaC cleavage products at the cell surface. We demonstrated that trypsin IV and trypsin I can stimulate ENaC heterologously expressed in oocytes. ENaC cleavage and activation by trypsin IV but not by trypsin I required a critical cleavage site (Lys-189) in the extracellular domain of the $\gamma$-subunit. In contrast, channel activation by trypsin I was prevented by mutating three putative cleavage sites (Lys-168, Lys-170, and Arg-172) in addition to mutating previously described prostasin (RKRK(178)), plasmin (Lys-189), and neutrophil elastase (Val-182 and Val-193) sites. Moreover, we found that trypsin IV is expressed in human renal epithelial cells and can increase ENaC-mediated sodium transport in cultured human airway epithelial cells. Thus, trypsin IV may regulate ENaC function in epithelial tissues. Our results show, for the first time, that trypsin IV can stimulate ENaC and that trypsin IV and trypsin I activate ENaC by cleavage at distinct sites. The presence of distinct cleavage sites may be important for ENaC regulation by tissue-specific proteases.}},
  author       = {{Haerteis, Silke and Krappitz, Annabel and Krappitz, Matteus and Murphy, Jane E. and Bertog, Marko and Krueger, Bettina and Nacken, Regina and Chung, Hyunjae and Hollenberg, Morley D. and Knecht, Wolfgang and Bunnett, Nigel W. and Korbmacher, Christoph}},
  journal      = {{Journal of Biological Chemistry}},
  number       = {{27}},
  pages        = {{19067–19078}},
  publisher    = {{Elsevier}},
  title        = {{{Proteolytic Activation of the Human Epithelial Sodium Channel by Trypsin IV and Trypsin I Involves Distinct Cleavage Sites}}},
  doi          = {{10.1074/jbc.m113.538470}},
  volume       = {{289}},
  year         = {{2014}},
}

@article{40219,
  author       = {{Wagenknecht, Inga and Meier-Gräwe, Uta}},
  issn         = {{1616-8836}},
  journal      = {{Zeitschrift für Paar-, Familien- und Sozialtherapie}},
  number       = {{2}},
  pages        = {{91--108}},
  publisher    = {{Psychosozial-Verlag}},
  title        = {{{Auf- und Ausbau Früher Hilfen in Zeiten knapper öffentlicher Kassen. Warum es sich lohnt, in Frühe Hilfen zu investieren}}},
  volume       = {{15}},
  year         = {{2014}},
}

@article{26910,
  abstract     = {{<jats:p>Non-alcoholic fatty liver disease (NAFLD) is closely associated with insulin resistance and obesity. Hence, carbohydrate quality could be of relevance to the risk of NAFLD, but prospective data are lacking. The aim of the present study was to investigate longitudinal associations between carbohydrate quality (including dietary glycaemic index (GI) and intakes of sugar, starch and fibre) and markers of liver function in an older Australian population. The analysis was based on 866 participants ( ≥ 49 years) of the Blue Mountains Eye Study with fasting blood specimens and dietary intake data at baseline and 5-year follow-up. Multi-level mixed regression analysis was used to relate dietary GI and sugar, starch and fibre intake to the liver enzymes alanine aminotransferase (ALT) and γ-glutamyltransferase (GGT), as well as fasting TAG and HDL-cholesterol (HDL-C). After adjustment for potential confounding factors, a lower fibre intake was cross-sectionally related to higher GGT (<jats:italic>P</jats:italic>= 0·02) and fasting TAG (<jats:italic>P</jats:italic>= 0·002) levels, with fruit fibre being the most relevant fibre source (<jats:italic>P</jats:italic>= 0·095 for GGT; <jats:italic>P</jats:italic>= 0·003 for TAG). A higher dietary GI was associated with lower HDL-C (<jats:italic>P</jats:italic>= 0·046). Changes in carbohydrate quality during 5 years were not related to changes in ALT, GGT, TAG or HDL-C (<jats:italic>P</jats:italic>≥ 0·08). In conclusion, the absence of longitudinal associations between carbohydrate quality and liver enzymes and serum lipids in this older population does not support a major role of carbohydrate nutrition in liver function among the elderly.</jats:p>}},
  author       = {{Goletzke, Janina and Buyken, Anette and Gopinath, Bamini and Rochtchina, Elena and Barclay, Alan W. and Cheng, Guo and Brand-Miller, Jennie C. and Mitchell, Paul}},
  issn         = {{0007-1145}},
  journal      = {{British Journal of Nutrition}},
  pages        = {{918--925}},
  title        = {{{Carbohydrate quality is not associated with liver enzyme activity and plasma TAG and HDL concentrations over 5 years in an older population}}},
  doi          = {{10.1017/s0007114512005867}},
  year         = {{2013}},
}

@article{26911,
  author       = {{Goletzke, J. and Herder, C. and Joslowski, G. and Bolzenius, K. and Remer, T. and Wudy, S. A. and Roden, M. and Rathmann, W. and Buyken, Anette}},
  issn         = {{0149-5992}},
  journal      = {{Diabetes Care}},
  pages        = {{1870--1876}},
  title        = {{{Habitually Higher Dietary Glycemic Index During Puberty Is Prospectively Related to Increased Risk Markers of Type 2 Diabetes in Younger Adulthood}}},
  doi          = {{10.2337/dc12-2063}},
  year         = {{2013}},
}

@article{26912,
  author       = {{Joslowski, Gesa and Remer, Thomas and Assmann, Karen E. and Krupp, Danika and Cheng, Guo and Garnett, Sarah P. and Kroke, Anja and Wudy, Stefan A. and Günther, Anke L. B. and Buyken, Anette}},
  issn         = {{1541-6100}},
  journal      = {{The Journal of Nutrition}},
  pages        = {{1147--1154}},
  title        = {{{Animal Protein Intakes during Early Life and Adolescence Differ in Their Relation to the Growth Hormone-Insulin-Like-Growth-Factor Axis in Young Adulthood}}},
  doi          = {{10.3945/jn.113.175877}},
  year         = {{2013}},
}

@article{27043,
  abstract     = {{<jats:p>Dietary fat intake in childhood may influence the risk for developing chronic diseases. The objective of the present study was to examine secular trends in the parameters of fat intake between 2000 and 2010 in a sample of German children and adolescents (<jats:italic>n</jats:italic> 808) participating in the Dortmund Nutritional and Anthropometric Longitudinally Designed (DONALD) Study. Dietary data from 4380 3 d weighed dietary records were analysed using repeated-measures regression to determine time trends in fat quantity, i.e. the intake of total fat, and in fat quality, i.e. the ratios of SFA, MUFA and PUFA. In young children (2–3 years) and in adolescents (13–18 years), total fat intake remained stable over time, but decreased by 0·08 % of total energy (%E) per year in 4–12-year-old children. In 2010, median fat intake was at the upper end of the recommendations. SFA intake decreased slightly in 2–3- and 4–12-year-old children by 0·09 and 0·05 %E per year, respectively. MUFA and PUFA intakes remained stable in all the age groups except in adolescents. Here, PUFA intake decreased initially, but increased between 2005 and 2010. In 2010, only between 3 and 18 % of the respective age groups had an intake of SFA or PUFA within the recommendations. In conclusion, fat quantity and quality did not change substantially between 2000 and 2010. Fat quality, in particular, needs to be improved, since a large percentage of our sample did not meet the recommended intakes for SFA and PUFA.</jats:p>}},
  author       = {{Libuda, Lars and Alexy, Ute and Kersting, Mathilde}},
  issn         = {{0007-1145}},
  journal      = {{British Journal of Nutrition}},
  pages        = {{141--150}},
  title        = {{{Time trends in dietary fat intake in a sample of German children and adolescents between 2000 and 2010: not quantity, but quality is the issue}}},
  doi          = {{10.1017/s0007114513002031}},
  year         = {{2013}},
}

@article{27061,
  author       = {{Libuda, Lars and Stimming, Madlen and Mesch, Christina and Warschburger, Petra and Kalhoff, Hermann and Koletzko, Berthold Viktor and Kersting, Mathilde}},
  issn         = {{1436-6207}},
  journal      = {{European Journal of Nutrition}},
  pages        = {{1335--1344}},
  title        = {{{Frequencies and demographic determinants of breastfeeding and DHA supplementation in a nationwide sample of mothers in Germany}}},
  doi          = {{10.1007/s00394-013-0633-4}},
  year         = {{2013}},
}

@article{27062,
  author       = {{Müller, Katrin and Libuda, Lars and Diethelm, Katharina and Huybrechts, Inge and Moreno, Luis A. and Manios, Yannis and Mistura, Lorenza and Dallongeville, Jean and Kafatos, Anthony and González-Gross, Marcela and Cuenca-García, Magdalena and Sjöström, Michael and Hallström, Lena and Widhalm, Kurt and Kersting, Mathilde}},
  issn         = {{0195-6663}},
  journal      = {{Appetite}},
  pages        = {{332--339}},
  title        = {{{Lunch at school, at home or elsewhere. Where do adolescents usually get it and what do they eat? Results of the HELENA Study}}},
  doi          = {{10.1016/j.appet.2013.09.002}},
  year         = {{2013}},
}

@article{27063,
  author       = {{Müller, K and Libuda, Lars and Gawehn, N and Drossard, C and Bolzenius, K and Kunz, C and Kersting, M}},
  issn         = {{0954-3007}},
  journal      = {{European Journal of Clinical Nutrition}},
  pages        = {{185--189}},
  title        = {{{Effects of lunch on children’s short-term cognitive functioning: a randomized crossover study}}},
  doi          = {{10.1038/ejcn.2012.209}},
  year         = {{2013}},
}

@article{27514,
  author       = {{Oepping, Anke and Schlegel-Matthies, Kirsten}},
  journal      = {{Schule NRW. Amtsblatt des Ministeriums für Schule und Weiterbildung}},
  pages        = {{10 -- 12}},
  title        = {{{Bildung für nachhaltige Entwicklung. Den Alltag gestalten – Teilhabe ermöglichen. Verbraucherbildung als Aufgabe von Schule}}},
  volume       = {{2}},
  year         = {{2013}},
}

@article{27515,
  author       = {{Schlegel-Matthies, Kirsten}},
  journal      = {{Haushalt in Bildung und Forschung (HiBiFo)}},
  number       = {{2}},
  pages        = {{61 -- 70}},
  title        = {{{Ethik, Konsumentenverantwortung und Verbraucherbildung im Spannungsfeld}}},
  volume       = {{2}},
  year         = {{2013}},
}

@article{27516,
  author       = {{Schlegel-Matthies, Kirsten}},
  journal      = {{Haushalt in Bildung und Forschung (HiBiFo)}},
  number       = {{2}},
  title        = {{{Fachliche Betreuung des Schwerpunktthemas: Ethik – Konsum – Verbraucherbildung. }}},
  volume       = {{2}},
  year         = {{2013}},
}

@book{27518,
  author       = {{Oepping, Anke and Schlegel-Matthies, Kirsten}},
  title        = {{{Ernährungs- und Verbraucherbildung im Unterricht }}},
  year         = {{2013}},
}

@article{27524,
  abstract     = {{<jats:p> Because of widespread irregular lunch consumption by both children and adults, information on the effects of lunch on short-term cognitive functioning is relevant to public health. In September 2012, a MEDLINE search was conducted for studies in which the effects of lunch on cognitive performance were examined. Eleven experimental studies published from 1981 to 1996 were found and evaluated; all involved adults. In three studies, the effects of lunch and lunch skipping were compared; the remaining studies involved a determination of the effects of lunch size and lunch composition. Results of studies in which lunch was compared with no lunch indicate that lunch leads to potential impairment of some aspects of cognitive functioning in the early afternoon. Lunch size may influence cognitive functioning, with impairment more likely to occur after a large lunch than a small lunch. Furthermore, in comparison with low-fat lunches, high-fat lunches seem to result in slower but more accurate responses to some cognitive tasks. However, these suggestions must be viewed with caution, as they are based on only a few studies and are not thoroughly supported by high-quality evidence. In addition, results obtained with adults are not applicable to children. Thus, the potential effects of lunch need further examination in children and adults. </jats:p>}},
  author       = {{Müller, Katrin and Libuda, Lars and Terschlüsen, Anna Maria and Kersting, Mathilde}},
  issn         = {{1486-3847}},
  journal      = {{Canadian Journal of Dietetic Practice and Research}},
  pages        = {{181--188}},
  title        = {{{A Review of the Effects of Lunch: On Adults’ Short-term Cognitive Functioning}}},
  doi          = {{10.3148/74.4.2013.181}},
  year         = {{2013}},
}

@article{27581,
  author       = {{Mesch, C. and Stimming, M.  and Wagner, A. and Libuda, Lars and Kersting, M.}},
  journal      = {{Ernährungsumschau International}},
  pages        = {{110--115}},
  title        = {{{Rekrutierung von Müttern mit Säuglingen in einer Interventionsstudie – erste Erkenntnisse aus der PINGU-Studie. }}},
  volume       = {{7}},
  year         = {{2013}},
}

@article{27732,
  author       = {{Assmann, K.E. and Joslowski, G. and Buyken, Anette and Cheng, G. and Remer, T. and Kroke, A. and Günther, A.L.B.}},
  issn         = {{1930-7381}},
  journal      = {{Obesity}},
  pages        = {{E782--E789}},
  title        = {{{Prospective association of protein intake during puberty with body composition in young adulthood}}},
  doi          = {{10.1002/oby.20516}},
  year         = {{2013}},
}

@article{27733,
  author       = {{Günther, Anke L. B. and Walz, Helena and Kroke, Anja and Wudy, Stefan A. and Riedel, Christina and von Kries, Rüdiger and Joslowski, Gesa and Remer, Thomas and Cheng, Guo and Buyken, Anette}},
  issn         = {{1932-6203}},
  journal      = {{PLoS ONE}},
  title        = {{{Breastfeeding and Its Prospective Association with Components of the GH-IGF-Axis, Insulin Resistance and Body Adiposity Measures in Young Adulthood – Insights from Linear and Quantile Regression Analysis}}},
  doi          = {{10.1371/journal.pone.0079436}},
  year         = {{2013}},
}

@article{36002,
  author       = {{Schlegel-Matthies, Kirsten and Methfessel, Barbara}},
  issn         = {{2193-8806}},
  journal      = {{Haushalt in Bidlung und Forschung}},
  number       = {{4}},
  pages        = {{49--60}},
  publisher    = {{Barbara Budrich}},
  title        = {{{Für eine veränderte Fachpraxis - Zur Kultur und Technik der Nahrungszubereitung und Mahlzeitengestaltung}}},
  volume       = {{2}},
  year         = {{2013}},
}

@article{54933,
  abstract     = {{In some patients with atypical cystic fibrosis (CF), only one allele of the CF transmembrane conductance regulator (CFTR) gene is affected. Mutations of the epithelial sodium channel (ENaC) may contribute to the pathophysiology of the disease in these patients. To functionally characterize a mutation in the $\beta$-subunit of ENaC ($\beta$V348M) recently identified in a patient with severe CF-like symptoms (Mutesa et al. 2009), we expressed wild-type (wt) $\alpha$$\beta$$\gamma$ENaC or mutant $\alpha$$\beta$V348M$\gamma$ENaC in Xenopus laevis oocytes. The $\beta$V348M mutation stimulated amiloride-sensitive whole-cell current ($\Delta$I(ami)) by $\sim$40% but had no effect on surface expression or single-channel conductance of ENaC. Instead the mutation increased channel open probability (P(o)). Proteolytic activation of mutant ENaC by chymotrypsin was reduced compared with that of wt ENaC ($\sim$3.0-fold vs. $\sim$4.2-fold), which is consistent with the increased baseline P(o) of mutant ENaC. Similarly, the ENaC activator S3969 stimulated mutant ENaC currents to a lesser degree (by $\sim$2.6-fold) than wt ENaC currents (by $\sim$3.5-fold). The gain-of-function effect of the $\beta$V348M mutation was confirmed by whole-cell current measurements in HEK293 cells transiently transfected with wt or mutant ENaC. Computational channel modeling in combination with functional expression of different $\beta$V348 mutants in oocytes suggests that the $\beta$V348M mutation increases channel P(o) by destabilizing the closed channel state. Our findings indicate that the gain-of-function effect of the $\beta$V348M mutation may contribute to CF pathophysiology by inappropriately increasing sodium and fluid absorption in the respiratory tract.}},
  author       = {{Rauh, Robert and Soell, Daniel and Haerteis, Silke and Diakov, Alexei and Nesterov, Viatcheslav and Krueger, Bettina and Sticht, Heinrich and Korbmacher, Christoph}},
  journal      = {{American Journal of Physiology-Lung Cellular and Molecular Physiology}},
  number       = {{1}},
  pages        = {{L43–L55}},
  publisher    = {{American Physiological Society}},
  title        = {{{A mutation in the $\beta$-subunit of ENaC identified in a patient with cystic fibrosis-like symptoms has a gain-of-function effect}}},
  doi          = {{10.1152/ajplung.00093.2012}},
  volume       = {{304}},
  year         = {{2013}},
}