Abstracts - Deutsche Zoologische Gesellschaft

84 Physiology SymposiumO PH.7 (Sa) - ENUCP1 is required for normal torpor behaviour and decreases reactive oxygen speciesproduction in brown adipose tissue mitochondriaRebecca Ölkrug, Martin Jastroch, Gerhard Heldmaier, Carola W. MeyerDepartment of Animal Physiology, Philipps-Universität MarburgIn small mammals and newborns, uncoupling protein 1 (UCP1) in brown adipose tissue (BAT)mitochondria produces heat by uncoupling respiratory chain from ATP synthesis (= non shiveringthermogenesis, NST). In mice, targeted inactivation of UCP1 (UCP1-KO) impairs maximal coldinduced heat production in vivo and leads to decreased survival in the cold. We sought to determineother phenotypic disadvantages associated with absence of UCP1 in BAT of mice. Here we demonstratethat a combination of cold exposure and food restriction induced torpor in wildtype mice(minimal body temperature (T b): 20-23°C) while KO mice only moderately lowered T b(29-34.5°C),or passively cooled off without defending T b. On the mitochondria level, presence of UCP1 in BATmitochondria was accompanied by barely detectable superoxide production levels (0.122 nmol /min*mg) which could be increased ~30 fold by inhibition of UCP1 with GDP. In contrast, KO mitochondriahad a 7.5-fold higher superoxide concentration which was GDP-insensitive.These resultsdemonstrate that UCP1 is not only required for cold induced heat production but also for entry intorpor. Furthermore, the UCP1-mediated reduction of superoxide production rates strongly suggeststhat the incorporation of mitochondrial uncoupling in NST allows maximising metabolic rates inBAT without the generation of deleterious oxidative stress.O PH.8 (Sa) - ENA Drosophila model to study the role of matrix metalloproteinases in asthmaKerstin IsermannZoophysiologie, Christian-Albrechts-Universität zu KielAsthma is a chronic disease of the airways with rapidly increasing prevalence. It is characterized bychronic inflammation of the respiratory tract accompanied by copious remodelling processes, whichcomprise all major parts of this organ. One of the most assured susceptibility genes for bronchialasthma is ADAM 33, coding for a metalloproteinase and desintegrin. Another family of metalloproteinasesthat has strongly been associated with the chronic forms of this disease are the matrixmetalloproteinases (mmp). Having the ability to degrade the extracellular matrix, these enzymesare believed to play a central role in airway remodelling. Although an association between diseasedevelopment and protease function is obvious, there has yet been no idea about their causal role inthis process. Predestined to study the fundamental molecular mechanisms of this process is the fruitfly Drosophila melanogaster, which has developed as a model organism for basic phenomena inbiomedical research. In the fly two mmps, mmp-1 and –2, are present. Resembling the situation observedin patients experiencing chronic inflammation of the airways, pathogen infected flies show asignificantly increased expression of the mmp-1 gene. Additionally, irregularities in the developmentof larval airways do not only occur in mmp-1 deficient but also in mmp-1 overexpressing mutants.These observations suggest a vital function for mmp-1 during tracheal development and point to itsprobable role in inflammation accompanied remodelling processes.