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Cilj studije: Utvrditi izražaj gangliozida GM3 i njegovih glikosfingolipidnih preteča u bubregu i mišiću na štakorskim modelima šećerne bolesti tip 1 i tip 2. Metode: Model šećerne bolesti tip 1 (T1DM) induciran je intraperitonejskom injekcijom streptozotocina (STZ) u dozi od 55 mg/kg, a model šećerne bolesti tip 2 (T2DM) je induciran kombinacijom manje doze STZ-a (35 mg/kg) i masne hrane (udio masti 58%). Štakori su žrtvovani dva tjedna nakon induciranja šećerne bolesti, a zatim je analiziran izražaj gangliozida GM3 i njegovih sfingolipidnih preteča u tkivu bubrega i mišića metodama tankoslojne kromatografije visokog razlučivanja (HPTLC) i imunofluorescentnom mikroskopijom. PCR reakcijom u stvarnom vremenu određivan je izražaj gena za GM3 sintaze u tkivu bubrega skupine T1DM. Rezultati: U mišićima skupine T2DM statistički je značajno povećan sadržaj GM3 u u odnosu na kontrolnu skupinu. Sadržaj GM3 statistički je značajno povećan u tubulima bubrega štakora T1DM i T2DM u usporedbi s pripadajućim kontrolnim skupinama. Sadržaj GM3 je statistički povećan u glomerulima T1DM štakora. PCR metodom nađena je smanjena ekspresija gena za GM3 sintazu u bubrezima štakora T1DM. Zaključak: Povećani izražaj gangliozida GM3 u mišiću štakorskog modela šećerne bolesti tip 2 inducirane streptozotocinom i masnom prehranom potvrđuje dosadašnja istraživanja o posredovanju gangliozida GM3 u patogenezi šećerne bolesti tip 2. Povećani sadržaj GM3 u tubulima u oba modela šećerne bolesti može upućivati na ulogu gangliozida GM3 u patogenezi dijabetičke tubulopatije. Štakorski modeli šećerne bolesti tip 2 induciran streptozocinom i masnom hranom mogao bi se koristiti za istraživanja farmakoloških utjecaja na inzulinsku rezistenciju umjesto dosad korištenih modela., Aim of the study: was to determine the expression of the ganglioside GM3 and its sphingolipid precursors in kidneys and muscles in rat models of type 1 and 2 diabetes. Methods: the model of type 1 diabetes (T1DM) was induced with an intraperitoneal injection of streptozotocin (STZ) at a dose of 55 mg/kg, the model of type 2 diabetes (T2DM) was induced with a combination of a lower dose STZ (35 mg/kg) and a high-fat diet (58% fat). Rats were sacrificed two weeks after diabetes induction and then the expression of the ganglioside GM3 and its sphingolipid precursor in kidneys and muscles was analyzed by high performance thin layer chromatography (HPTLC) and immunofluorescence microscopy. The expression of the gene for GM3 synthase in kidney for the T1DM group was determined using real-time PCR. Results: In muscles of the T2DM group expression of GM3 was significantly increased compared to the control group. The expression of GM3 was significantly increased in tubules of T1DM and T2DM groups in comparison to their controls. The expression of GM3 was significantly increased in glomerules of T1DM rats. Using real time PCR method we found a decreased expression of GM3 synthase in kidneys of T1DM rats compared to controls. Conclusion: Increased expression of GM3 ganglioside in muscles of rat model for type 2 diabetes induced by streptozotocin and high-fat diet confirms recentlyobtained results showing that ganglioside GM3 plays one of key roles in pathogenesis of type 2 diabetes. Increased expression of GM3 in tubules of both diabetes models suggest that there is a significant role of ganglioside GM3 in pathogenesis of diabetic tubulopathy. The rat model for diabetes type 2 induced by streptozocine and a high-fat diet could be a new widely used model for researching pharmacological influences on insulin resistence instead of the models that are currently used.