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Transcriptional upregulation of gastrin in response to peroxisome proliferator-activated receptor gamma agonist triggers cell survival pathways

100%

Ptak-Belowska A. , Pawlik M. W. , Krzysiek-Maczka G. , Brzozowski T. , Pawlik W. W.

tom 58

nr 4

Peroxisome proliferator-activated receptor (PPAR ) are members of the largest nuclear hormone receptor family of transcription factors (1). PPAR gamma (PPAR) plays an important role in adipogenesis, control of sensitivity to insulin, inflammation and atherosclerosis but recent studies also suggest that PPAR is involved in cell cycle withdrawal. PPAR can promote cell differentiation, exert an antiproliferative action and inhibit angiogenesis (2, 3). However, there are studies showing that activation of PPAR promotes the development of colon cancer (4). These data are in sharp contrast with studies that attribute anticancer effects to PPAR in gastrointestinal malignancies. Probably, the action of PPAR on cell cycle and proliferation depends on the cell type and presence of other stimuli that predispose cells to cancer development. Amidated and non-amidated gastrins may play an important role in the proliferation and carcinogenesis of GI cancers. It is known that gastrin peptides activate phosphorylation of Protein Kinase B (PKB/Akt) and anti-apoptotic signalling but there is little known about the link between gastrins and PPAR receptors in relation to apoptosis.

Potentiation of adipogenesis and insulinomimetic effects of a novel vanadium complex (N′-[(E)-(5-bromo-2oxophenyl)methylidene]-4methoxybenzohydrazide)oxido(1,10phenanthroline)vanadium(IV) in 3T3-L1 cells

84%

Kazek G. , Głuch-Lutwin M. , Mordyl B. , Menaszek E. , Szklarzewicz J. , Gryboś R. , Papież M.

2019

tom Vol. 4, no. 1

55--62

Recent research on the action of vanadium compounds shows its important effect on adipogenesis processes and adipocyte function. On the basis of previous screening tests in cellular models, the novel vanadium complex (N′-[(E)-(5-bromo-2-oxophenyl)methylidene]4-methoxybenzohydrazide)oxido(1,10-phenanthroline)vanadium(IV) was selected for this study. This complex exhibits potent inhibition of tyrosine phosphatases, and differences in the degree of inhibition were observed particularly for phosphatases. A significant increase in intracellular lipid accumulation and proliferative effect on 3T3-L1 preadipocytes confirmed the ability of this complex to enhance adipogenesis. The insulinomimetic activity of the tested complex was also demonstrated in fully differentiated 3T3-L1 adipocytes, in which glucose utilization was potentiated. The obtained results support the hypothesis that vanadium complexes show promising possibilities for use as new therapeutic strategies for the treatment of type 2 diabetes.