The relative contribution of nutrition-related chronic diseases to the total disease burden of the society and the health care costs has risen continuously over the last decades. Thus, there is an ...urgent necessity to better exploit the potential of dietary prevention of diseases. Carbohydrates play a major role in human nutrition – next to fat, carbohydrates are the second biggest group of energy-yielding nutrients. Obesity, type 2 diabetes mellitus, dyslipoproteinaemia, hypertension, metabolic syndrome, coronary heart disease and cancer are wide-spread diseases, in which carbohydrates could have a pathophysiologic relevance. Correspondingly, modification of carbohydrate intake could have a preventive potential. In the present evidence-based guideline of the German Nutrition Society, the potential role of carbohydrates in the primary prevention of the named diseases was judged systematically. The major findings were: a high carbohydrate intake at the expense of total fat and saturated fatty acids reduces the concentrations of total, LDL and HDL cholesterol. A high carbohydrate consumption at the expense of polyunsaturated fatty acids increases total and LDL cholesterol, but reduces HDL cholesterol. Regardless of the type of fat being replaced, a high carbohydrate intake promotes an increase in the triglyceride concentration. Furthermore, a high consumption of sugar-sweetened beverages increases the risk of obesity and type 2 diabetes mellitus, whereas a high dietary fibre intake, mainly from whole-grain products, reduces the risk of obesity, type 2 diabetes mellitus, dyslipoproteinaemia, cardiovascular disease and colorectal cancer at varying evidence levels. The practical consequences for current dietary recommendations are presented.
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The reference values for energy intake of the German, Austrian and Swiss nutrition societies for children, adolescents and adults are derived using the factorial method. For adults, a mean BMI of 22 ...kg/m² is taken as a basis given the current mean body size for adults residing in Germany (taken from the German Health Interview and Examination Survey for Adults, DEGS1). The determination of the energy expenditure for infants is based on data obtained using the doubly labelled water (DLW) method. The energy storage in growing tissue will be added for the purpose of deriving reference values for this age group. For pregnant women, given an increase in body weight of 12 kg during pregnancy, guiding values for additional energy intake in the second trimester of 250 kcal/day and in the third trimester of 500 kcal/day are indicated using DLW data sets and taking energy storage in growing tissue into account. In case of overweight prior to pregnancy as well as in the case of reduced physical activity during pregnancy, the additional requirement is lower. For women exclusively breastfeeding during the first 4–6 months, the guiding value for additional energy intake is quoted as 500 kcal/day.
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Background: In January 2017, the nutrition societies of Germany, Austria and Switzerland revised the reference values for sodium and chloride intake. Methods: For adults, the estimated value for ...sodium intake was derived on the basis of a balance study. The estimated values for children and adolescents were extrapolated from this estimated value considering differences in body mass. For infants aged 0 to under 4 months, an estimated value was set based on the sodium intake via breast milk. From this value the estimated value for infants aged 4 to under 12 months was also derived by extrapolation. The estimated value for lactating women takes into account the fact that the sodium loss via breast milk is compensated through homoeostatic mechanisms. Except for infants, the reference values for chloride intake were derived based on the estimated values for sodium intake. Results: For adults, pregnant and lactating women, the estimated values for sodium and chloride intake are set at 1,500 and 2,300 mg/day. Discussion and Conclusion: Reference values for sodium and chloride can be derived in terms of estimated values. Considering dietary recommendations for sodium and chloride, it must be taken into account that high intake of sodium chloride (salt) is associated with adverse health effects, for example, hypertension and cardiovascular diseases. Therefore, it is necessary to lower salt intake in the general population.
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Revised Reference Values for Potassium Intake Strohm, Daniela; Ellinger, Sabine; Leschik-Bonnet, Eva ...
Annals of nutrition & metabolism,
01/2017, Volume:
71, Issue:
1/2
Journal Article
Peer reviewed
Open access
Background: The nutrition societies of Germany, Austria and Switzerland have revised the reference values for potassium intake in January 2017. Methods: For adults, the estimated value was based on ...the 24-h urinary potassium excretion and on preventive considerations regarding hypertension and stroke. The estimated values for children and adolescents were extrapolated from the adult estimated value considering differences in body mass. For infants aged 0 to under 4 months, the estimated value was set based on the potassium intake via breast milk. From this reference value, the estimated value for infants aged 4 to under 12 months was also derived by extrapolation. The estimated value for lactating women takes into account the potassium loss via breast milk. Results: The estimated values for potassium intake are set at 400 mg/day for breastfed infants aged 0 to under 4 months, 600 mg/day for infants aged 4 to under 12 months, 1,100-4,000 mg/day for children and adolescents, 4,000 mg/day for adults and pregnant women and 4,400 mg/day for lactating women. Conclusions: The consumption of potassium-rich foods should be generally increased. Supplemental intake beyond the estimated values has no health benefit and is therefore not recommended.
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The nutrition societies of Germany, Austria and Switzerland are the joint editors of the ‘reference values for nutrient intake ’. They have revised the reference values for the intake of calcium and ...published them in June 2013. The reference values for the calcium intake for infants are derived from the calcium content of breast milk. For infants from 4 to <12 months of age, the calcium intake from solid foods is included in addition to the calcium intake from breast milk. Thus, the reference values for infants are estimated values; they are 220 mg/day for infants to <4 months and 330 mg/day for infants from 4 to <12 months of age. As a parameter for determining the calcium requirement in children and adolescents, calcium retention is taken into account. The average requirement is calculated by the factorial method. A balanced calcium metabolism is calculated based upon calcium balance studies and used as a parameter for the determination of the calcium requirement in adults. On the basis of the average requirement, recommended calcium intake levels for children, adolescents and adults are derived. Depending on age, the recommended calcium intake ranges between 600 mg/day for children aged 1 to <4 years and 1,200 mg/ day for adolescents aged 13 to <19 years; for adults, it is 1,000 mg/day.
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Die adipositasbedingte Insulinresistenz geht mit einer unterschwelligen Entzündungsreaktion einher. Als Antwort auf dieses Entzündungsgeschehen wird PGE2 unter anderem von Kupffer Zellen der Leber ...freigesetzt und kann seine Wirkung über vier PGE2-Rezeptorsubtypen (EP1-EP4) vermitteln. In vorangegangenen Arbeiten konnte gezeigt werden, dass PGE2 in Rattenhepatozyten über den EP3 R ERK1/2-abhängig die intrazelluläre Weiterleitung des Insulinsignals hemmt. Über die Modulation der Insulinrezeptorsignalkette durch andere EP-Rezeptoren war bisher nichts bekannt. Daher sollte in stabil transfizierten Zelllinien, die jeweils nur einen der vier EP-Rezeptorsubtypen exprimierten, der Einfluss von PGE2 auf die Insulinrezeptorsignalkette untersucht werden. Es wurden HepG2-Zellen, die keinen funktionalen EP-Rezeptor aufwiesen, sowie HepG2-Zellen, die stabil den EP1-R (HepG2-EP1), den EP3β-R (HepG2 EP3β) oder den EP4-R (HepG2 EP4) exprimierten, sowie die humane fötale Hepatozytenzelllinie, Fh hTert, die den EP2- und den EP4-R exprimierte, für die Untersuchungen verwendet. Die Zellen wurden für 330 min mit PGE2 (10 µM) vorinkubiert, um die pathophysiologische Situation nachzustellen und anschließend mit Insulin (10 nM) für 15 min stimuliert. Die insulinabhängige Akt- und ERK1/2-Phosphorylierung wurde im Western-Blot bestimmt.
In allen Hepatomzelllinien die EP-R exprimierten, nicht aber in der Zelllinie, die keinen EP R exprimierte, hemmte PGE2 die insulinstimulierte Akt-Phosphorylierung. In allen drei stabil transfizierten Zelllinien, nicht jedoch in den Fh-hTert-Zellen, steigerte PGE2 die basale und insulinstimulierte Phosphorylierung der Serin/Threoninkinase ERK1/2. In den HepG2 EP1- und den HepG2-EP3β-Zellen steigerte PGE2 mutmaßlich über die ERK1/2-Aktivierung die Serinphosphorylierung des IRS, welche die Weiterleitung des Insulinsignals blockiert. Die Hemmung der Aktivierung von ERK1/2 hob in EP3 R-exprimierenden Zellen die Abschwächung der Insulinsignalübertragung teilweise auf. In diesen Zellen scheint die ERK1/2-Aktivierung die größte Bedeutung für die Hemmung der insulinstimulierten Akt-Phosphorylierung zu haben. Da durch die Hemmstoffe die PGE2-abhängige Modulation nicht vollständig aufgehoben wurde, scheinen darüber hinaus aber noch andere Mechanismen zur Modulation beizutragen. In den Fh hTert-Zellen wurde die Insulinrezeptorsignalkette offensichtlich über einen ERK1/2-unabhängigen, bisher nicht identifizierten Weg unterbrochen.
Eine gesteigerte PGE2-Bildung im Rahmen der Adipositas ist nicht auf die peripheren Gewebe beschränkt. Auch im Hypothalamus können bei Adipositas Zeichen einer Entzündung nachgewiesen werden, die mit einer gesteigerten PGE2-Bildung einhergehen. Daher wurde das EP R-Profil von primären hypothalamischen Neuronen und neuronalen Modellzelllinien charakterisiert, um zu prüfen, ob PGE2 in hypothalamischen Neuronen die Insulinsignalkette in ähnlicher Weise unterbricht wie in Hepatozyten. In allen neuronalen Zellen hemmte die Vorinkubation mit PGE2 die insulinstimulierte Akt-Phosphorylierung nicht. In der neuronalen hypothalamischen Zelllinie N 41 wirkte PGE2 eher synergistisch mit Insulin. In durch Retinsäure ausdifferenzierten SH SY5Y-Zellen waren die Ergebnisse allerdings widersprüchlich. Dies könnte darauf zurückzuführen sein, dass die Expression der EP Rezeptoren im Verlauf der Kultur stark schwankte und somit die EP R-Ausstattung der Zellen zwischen den Zellversuchen variierte. Auch in den primären hypothalamischen Neuronen variierte die EP R-Expression abhängig vom Differenzierungszustand und PGE2 beeinflusste die insulinstimulierte Akt-Phosphorylierung nicht. Obwohl in allen neuronalen Zellen die Akt-Phosphorylierung durch Insulin gesteigert wurde, konnte in keiner der Zellen eine insulinabhängige Regulation der Expression von Insulinzielgenen (POMC und AgRP) nachgewiesen werden. Das liegt wahrscheinlich an dem niedrigen Differenzierungsgrad der untersuchten Zellen.
Im Rahmen der Adipositas kommt es zu einer Überaktivierung des Endocannabinoidsystems. Endocannabinoidrezeptoren sind mit den EP Rezeptoren verwandt. Daher wurde geprüft, ob Endocannabinoide die Insulinsignalweiterleitung in ähnlicher Weise beeinflussen können wie PGE2. Die Vorinkubation der N 41-Zellen für 330 min mit einem Endocannabinoidrezeptoragonisten steigerte die insulinstimulierte Akt-Phosphorylierung, was auf einen insulinsensitiven Effekt von Endocannabinoiden hindeutet. Dies steht im Widerspruch zu der in der Literatur beschriebenen endocannabinoidabhängigen Insulinresistenz, die aber auf indirekte, durch Endocannabinoide ausgelöste Veränderungen zurückzuführen sein könnte.
The obesity related insulin resistance is accompanied by a low grade inflammation. In response to inflammatory stimuli, PGE2 is released from Kupffer cells and signals through four G-Protein coupled PGE2-receptors (EP1-EP4). Previous work showed that PGE2 attenuated insulin signaling in rat hepatocytes through an EP3ß- and ERK1/2-dependent mechanism. Since EP-receptor expression on hepatocytes varies between species and physiological conditions, the effect of the individual EP receptor subtypes on insulin signaling was studied in hepatoma cell lines expressing individual EP receptor subtypes. HepG2 cells lacking functional EP-receptors, and derivatives stably expressing either EP1 receptor (HepG2-EP1), EP3ß receptor (HepG2-EP3ß) or EP4 receptor (HepG2-EP4) and Fh-hTert cells expressing EP2- and EP4-receptor were pre-incubated with PGE2 for 330 min to mimic the sub-acute inflammation. The cells were subsequently stimulated with insulin for 15 min. Akt and ERK1/2 activation was determined by Western Blotting with phospho-specific antibodies.
PGE2 inhibited insulin stimulated Akt phosphorylation in all cell lines expressing EP receptors, except in HepG2 cells which are lacking functional EP receptors. PGE2 increased insulin stimulated phosphorylation of the serine/threonine kinase ERK1/2 in all EP R expressing HepG2 cell lines except in Fh-hTert cells. In HepG2-EP1 and HepG2 EP3ß cells PGE2 increased the serine phosphorylation of the insulin receptor substrate, presumably through an ERK1/2 activation. This IRS-serine phosphorylation leads to attenuation of insulin signal transduction. Inhibiting ERK1/2 activation with a specific inhibitor attenuated the PGE2-dependent inhibition of insulin signal transmission in HepG2 EP3ß cells to some extent. ERK1/2 activation in these cells seems to be of major importance for the observed attenuation of insulin stimulated Akt phosphorylation. Application of inhibitors in the other cell lines stably expressing EP receptors provided evidence that other mechanisms contributed to the attenuation of insulin signaling. Insulin signal transduction in Fh-hTert cells by PGE2 was apparently blocked by an ERK1/2-independent mechanism.
Increased PGE2 production during obesity is not limited to the periphery. Signs of inflammation have been detected in the hypothalamus, which might be associated with an increased PGE2 production. Therefore, the EP receptor profile of primary neurons as well as neuronal cell models was characterised in order to investigate, whether PGE2 attenuates insulin signal transduction in neuronal cells similar to what was observed in hepatocytes. Pre-incubation with PGE2 did not attenuate insulin stimulated Akt phosphorylation in all neuronal cells. The EP receptor profile in SH SY5Y cells and in primary neurons varied depending on the differentiation status of the cells. Although Akt-kinase was phosphorylated in response to insulin stimulation in all neuronal cells studied, gene expression of insulin target genes (POMC, AgRP) was not modulated by insulin. This might be due to the low level of differentiation of the investigated cells.
In the course of obesity, an over-activation of the endocannabinoid system is detected. Since endocannabinoid receptors are related to EP receptors, it was investigated whether endocannabinoids can interfere with insulin signaling in a similar way as PGE2. Pre-incubation of the neuronal cell line N 41 for 330 min with an endocannabinoid receptor agonist, increased insulin stimulated Akt phosphorylation. This implies an insulin sensitising effect of endocannabinoids. This is contradictory to the endocannabinoid-dependent insulin resistance described in the literature and might be caused by indirect endocannabinoid-triggered mechanisms.
In Early Modern times, techniques of assembling, compiling and arranging pre-existing material were part of the established working methods in many arts. In the world of 18th-century opera, such ...practices ensured that operas could become a commercial success because the substitution or compilation of arias fitting the singer's abilities proved the best recipe for fulfilling the expectations of audiences. Known as »pasticcios« since the 18th-century, these operas have long been considered inferior patchwork. The volume collects essays that reconsider the pasticcio, contextualize it, define its preconditions, look at its material aspects and uncover its aesthetical principles.
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