9.Internatıonal Moleculer Bıology and Bıotechnology Congress (9.Molbiotech-2020), Kars, Türkiye, 6 - 10 Aralık 2020, cilt.1, ss.60
Necrosis is induced from cell death types by the activation of Ripk1 (Receptor interacting protein kinases),
which are formed as a result of cellular stress. This study was planned to investigate the effect of quinoa
application on the Ripk1 gene one of the necrotic markers, in rats with experimental insulin resistance by
applying glucocorticoid. For this purpose, 42 male Wistar-Albino rats weighing 200-250 g were used. Six
experimental groups, each consisting of 7 rats; control (C), quinoa given (Q), insulin resistance induceddexamethasone
(D), insulin resistance created and quinoa given (DQ), insulin resistance created and metformin
given (DM), quinoa given and insulin resistance created (QD) groups were formed. D, DQ, DM, QD group rats
were administered dexamethasone (1mg / kg / day) for 7 days to cause insulin resistance. Group D was sacrificed
at the end of 7 days. Then, quinoa feed was given to DQ and metformin was given 40 mg / kg / day to DM, for 6
days. For QD, quinoa feed for 6 days and then insulin resistance (7 days) was created with dexamethasone. The
control group received physiological serum for 7 days, and the quinoa group received quinoa for 6 days. At the
end of the experiment, the animals were sacrificed and their livers were taken. RNA was obtained from liver
tissues and converted into cDNA. Then, Ripk1 gene expression levels of the groups were determined by RTqPCR
method. Accordingly, one of the necrotic genes, Ripk1 was found to be 10-fold upregulated in the insulin
resistance (D) group, 7-fold in the quinoa treatment (DQ) group, 6-fold in the quinoa protection (QD) group, 3-
fold in the treatment control (DM) group. Expression in the quinoa (Q) group was found to be lower than the
control. As a result, it was determined that the necrotic damage in the liver caused by increased glucose in
experimental insulin resistance decreased with the application of quinoa.