Циљ истраживања је испитати утицај одабраних биљних естраката, фитоестрогена (генистеин, даидзеин), стероидних (естрадиол, прогестерон, тестостерон, дексаметазон) и пептидних хормона (соматостатин, калцитонин, грелин) на неуроендокрини систем и минералну хомеостазу пацова. Алтернатива хормонске супституционе терапије у виду биљних и других додатака исхрани интензивно се рекламирају за одржавање хормонске равнотеже, превенцију кардиоваскуларних проблема, атеросклерозе и остеопорозе у оба пола. Процена деловања ових супстанци на: (I) хипоталамо-хипофизно -адренални, -соматотропни, тироидни и гонадални систем; (II) неуроендокрине Ц-ћелије, кости, параштитасте жлезде и бубреге и (III) ћелијску механику, значајна је за евалуацију њихових жељених ефеката у односу на ризике при употреби у терапији канцера, кардиоваскуларних и других болести. Истраживања се спроводе на пацовима различите старости (млади, средње стари и стари пацови) и пола, а од посебног значаја су анимални модели андропаузе и менопаузе. Испитивања ћелијске механике обављају се у in vitro условима, на моделима еритроцита и ћелија канцера простате. Глукокортикоиди се у медицинској пракси користе у трудноћама са ризиком од превременог порођаја, како би се смањио неонатални морталитет и морбидитет. Међутим, овај третман убрзавајући матурационе процесе, доводи до трајних промена физиолошких система. Стога, краткорочни корисни ефекти пренаталне глукокортикоидне терапије су у исто време ти који повећавају дугорочне ризике метаболичких и ендокриних дисрегулација, укључујући одговор на стрес, раст и репродукцију. Ефекти пренаталног излагања глукокортикоидима испитује се на пацовима од феталног до адултног период живота.

Diabetes mellitus је комплексан метаболички поремећај који се манифестује у два основна облика, дијабетес тип 1 (ДТ1) и много чешћи облик, дијабетес тип 2 (ДТ2). Иако оба типа дијабетеса имају различите етиологије, оба карактерише хипергликемија због поремећене хомеостазе глукозе. Хипергликемија је последица недовољне концентрације инсулина у крви, што је случај у ДТ1, или неосетљивости циљних ћелија на деловање инсулина у ДТ2. У основи ДТ1 је аутоимуно обољење кога карактерише потпуни губитак β ћелија панкреаса које производе инсулин. Нестанак β ћелија у ДТ1 одвија се релативно брзо у поређењу са смањењем броја функционалних β ћелија у ДТ2 кога карактерише прогресиван губитак функционалности ћелија и потепено смањење њиховог броја. Разјашњење молекуларних механизама који регулишу функционалност ћелија и патолошке молекуларне процесе у дијабетесу, лежи у основи парадигме за терапију дијабетеса која предвиђа примену стратегија усмерених на побољшање функционалности и вијабилности β ћелија супресијом цитотоксичних сигналних путева и спречавањем активације процеса ћелијске смрти. Истраживања Одељења за молекуларну биологију фокусирана су на β ћелије, као и на хепатоците и кардиомиоците у контексту дијабетичних компликација. Експериментални системи које користимо су in vivo модел стрептозотоцином (СТЗ)-индукованог дијабетеса код лабораторијских пацова и in vitro модели базирани на различитим културама ћелијских линија.

Лабораторија проф. др Гордане Матић окупља групу младих научника који су посвећени изучавању неуроендокриних и нутриционистичких аспеката развоја метаболичког синдрома који постаје један од водећих здравствених проблема савременог доба. Наши научни напори су, пре свега, усмерени на разумевање молекуларних механизама деловања глукокортикоидних хормона у патогенези метаболичког синдрома, с обзиром да су ови хормони важни регулатори енергетске хомеостазе, метаболичке инфламације, као и сигналних путева инсулина и лептина. У наредне три године испитивања улоге стреса и исхране богате фруктозом у развоју метаболичког синдрома биће остварена у сарадњи са групом проф. др Luc Tapy-ја из Швајцарске уоквиру билатералног SCOPES пројекта под називом: Interactions between stress and dietary fructose in the development of the metabolic syndrome: role of glucocorticoids.

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83. Jelić M, Patenković A, Skorić M, Mišić D, Kurbalija Novičić Z, Bordács S, Várhidi F, Vasić I, Benke A, Frank G, Šiler B. Indigenous forests of European black poplar along the Danube River: genetic structure and reliable detection of introgression. Tree Genet Genomes. 2015;11(5):89.
84. Jevremović S, Lojić M, Jeknić Z, Trifunović-Momčilov M, Antonić D, Petrić M, Subotić A, Radojević L. In vitro propagation of Iris reichenbachii Heuff. and clonal fidelity of regenerated plants. Bot Serbica. 2015;39(2):129–36.
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91. Kalajdzic P, Kenig B, Andjelkovic M. Drosophila subobscura flies adapted to low lead concentration carry no fitness cost. Environ Pollut. 2015;204:90–8.
92. Kalauzi A, Nikolić L, Savić D, Radotić K. Cell death parameters as revealed by whole-cell patch-clamp and interval weighted spectra averaging: changes in membrane properties and current frequency of cultured mouse microglial cells induced by glutaraldehyde. J Membr Biol. 2015;248(1):117–23.
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