Einfluss einer hohen Natriumchlorid-Zufuhr und Kaliumbicarbonat-Ingestion auf Säure-Basen-Status und Proteinstoffwechsel
dc.contributor.advisor | Heer, Martina | |
dc.contributor.author | Bühlmeier, Judith | |
dc.date.accessioned | 2020-04-16T07:18:50Z | |
dc.date.available | 2020-04-16T07:18:50Z | |
dc.date.issued | 15.07.2011 | |
dc.identifier.uri | https://hdl.handle.net/20.500.11811/4738 | |
dc.description.abstract | Der charakteristische Muskelabbau der unteren Extremitäten in Immobilisation wird mit parallel beobachteten Proteinverlusten in Verbindung gebracht. Die selektive Atrophie wird auf eine Reduktion der mechanischen Belastung zurückgeführt, kann aber beispielsweise durch diätetische Einflussfaktoren verstärkt werden. So wird eine hohe Zufuhr von Natriumchlorid (NaCl) infolge azidogener Eigenschaften als unabhängiger Risikofaktor für Proteinverluste diskutiert. Ziel der Arbeit war es daher zum einen, die Auswirkungen einer hohen NaCl-Zufuhr auf den Säure-Basen-Status und Proteinstoffwechsel immobilisierter Versuchspersonen zu untersuchen. Da alkalische Mineralsalze bei metabolischer Azidose eine antikatabole Wirkung haben, sollte zum anderen der Einfluss einer oralen Gabe von Kaliumbicarbonat (KHCO3) auf NaCl-induzierte Veränderungen des Säure-Basen-Status und erwartete Proteinverluste untersucht werden. | en |
dc.description.abstract | Influences of high dietary sodium chloride and potassium bicarbonate supplements on acid base status and protein metabolism Immobilisation induces muscle loss, mainly occurring in the lower-limb muscles. This atrophy is associated with protein degradation. In addition to the direct effect of reduced mechanical loading, protein losses may be exacerbated by dietary impacts. Thus, a high NaCl intake is dicussed as a risk factor for protein losses due to observed acidic properties. The first aim of the present work was therefore to investigate influences of a high dietary NaCl intake on acid base status and protein metabolism in healthy immobilized humans. In contrast, administration of alkaline salts during metabolic acidosis has been shown to act anticatabolic. Hence, the second object was a monitoring of both systems when potassium bicarbonate (KHCO3) was supplemented during high NaCl intake. Acid base status and protein metabolism were examined in the frame of two stationary interventional studies (Salty Life 7 and 8), performed in the metabolic lab of the Institute of Aerospace Medicine, Cologne, Germany. Each study was divided into two campaigns that were completed by eight male volunteers in a randomized crossover design. During the interventional phase of the Salty Life 7 subjects were immobilized in 6º head-down-tilt bed rest (HDTBR) for 14 days and received either a high (7.0 mmol NaCl/kgBM/d) or a low (0.7 mmol NaCl/kgBM/d) NaCl intake. During the ten days of ambulatory intervention of the Salty Life 8 the subjects received a high NaCl-diet (7.3 mmol NaCl/kgBM/d) that was supplemented by oral administration of 3 x 30 mmol KHCO3/d in one campaign. The intervention phases of each study were preceded by a stationary adaptation phase. Nutrient intake was standardized and strictly controlled for the whole duration of both studies. To assess systemic acid base status we analysed blood gases, parameters of differential diagnosis (anion gap, serum chloride) as well as pH and net acid excretion in 24h urine. Changes of whole body protein content were measured by nitrogen balance, calculated from nitrogen intake and excretion in 24h urine. During the Salty Life 8 whole body protein kinetics were measured by Tracer Dilution Technique in the postabsorptive state. Serum concentration of IGF-1 and 24h urinary excretion of potentially bioactive glucocorticoids (GCs), cortisol and cortisone, were also analysed. During HDTBR high NaCl intake led to hyperchloremic, low-grade metabolic acidosis. Disuse-induced renal nitrogen losses were exacerbated by 180% and cortisol activity was concomitantly increased. KHCO3 during high NaCl intake counteracted postprandial NaCl-induced reduction of buffer substance, but failed to consistently compensate NaCl-induced low-grade metabolic acidosis. Excretion of potentially bioactive GCs was reduced. Though rates of phenylalanine hydroxylation, a sensitive marker of whole body net protein catabolism, slightly decreased, nitrogen balance was insensitive to those changes. To conclude: 1. High NaCl intake exacerbates disuse-induced protein losses. Concomitant changes in acid base status and increased GC activity seem to mediate this effect. 2. Administration of 3 x 30 mmol KHCO3/d appeared inadequate to compensate for NaCl-induced low grade metabolic acidosis. Even though temporary compensating led to reduced GC activity and net protein catabolism, NaCl-induced nitrogen losses were not prevented during ten days of high NaCl intake. | en |
dc.language.iso | deu | |
dc.rights | In Copyright | |
dc.rights.uri | http://rightsstatements.org/vocab/InC/1.0/ | |
dc.subject | Natriumchlorid | |
dc.subject | Säure-Basen Haushalt | |
dc.subject | Proteinstoffwechsel | |
dc.subject | Immobilisation | |
dc.subject | sodium chloride | |
dc.subject | acid base balance | |
dc.subject | protein metabolism | |
dc.subject.ddc | 630 Landwirtschaft, Veterinärmedizin | |
dc.title | Einfluss einer hohen Natriumchlorid-Zufuhr und Kaliumbicarbonat-Ingestion auf Säure-Basen-Status und Proteinstoffwechsel | |
dc.type | Dissertation oder Habilitation | |
dc.publisher.name | Universitäts- und Landesbibliothek Bonn | |
dc.publisher.location | Bonn | |
dc.rights.accessRights | openAccess | |
dc.identifier.urn | https://nbn-resolving.org/urn:nbn:de:hbz:5N-25828 | |
ulbbn.pubtype | Erstveröffentlichung | |
ulbbnediss.affiliation.name | Rheinische Friedrich-Wilhelms-Universität Bonn | |
ulbbnediss.affiliation.location | Bonn | |
ulbbnediss.thesis.level | Dissertation | |
ulbbnediss.dissID | 2582 | |
ulbbnediss.date.accepted | 11.03.2011 | |
ulbbnediss.fakultaet | Landwirtschaftliche Fakultät | |
dc.contributor.coReferee | Remer, Thomas |
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