Metformina - cudowny lek?

• Autorzy: Bauer A.
• Języki publikacji: PL

Słowa kluczowe

PL

metformina; cukrzyca; leczenie cukrzycy

EN

metformin; diabetes; diabetes treatment

• Wydawca: Politechnika Łódzka, Wydział Chemiczny
• Czasopismo: Eliksir
• Rocznik: 2017
• Tom: nr 1
• Strony: 6--10
• Opis fizyczny: Bibliogr. 30 poz., il. kolor., rys.

Twórcy

autor

Bauer A.

• Międzyresortowy Instytut Techniki Radiacyjnej, Wydział Chemiczny, Politechnika Łódzka

Bibliografia

• [1] Korzeniowska K., Jabłecka A., 2008, Cukrzyca (Część I), Farmacja Współczesna, 2, 231-235.
• [2] Grzybowska M., Bober J., Olszewska M., 2011, Metformina - mechanizmy działania i zastosowanie w terapii cukrzycy typu 2, Postępy Higieny Medycyny Doświadczalnej, 65, 277-285.
• [3] Hanisch U.K., Kettenmann H., 2007, Microglia: active sensor and versatile effectors cells in the normal and pathologic brain, Nature Neuroscience, 10, 1387-1394.
• [4] Pryor R., Cabreiro F., 2015, Repurposing metformin: an old drug with new tricks in its binding pockets, Biochemical Journal, 471, 307-322.
• [5] Hundal R.S., Krssak M. Dufour S., Laurent D., Lebon V., Chandramouli V., Inzucchi S.E., Schumann W.C., Petersen K.F., Landau B.R., Shulman G.I., 2000, Mechanism by which metformin reduces glucose production in type 2 diabetes, Diabetes, 49(12), 2063-2069.
• [6] Viollet B., Guigas B., Garcia N.S., Leclerc J., Foretz M., Andrelli F., 2012, Cellular and molecular mechanism of metformin: an overview, Clinical Science, 122, 253-270.
• [7] Hardie D.G., Carling D., Carlson M., 1998, The AMP-activated/ SNF1 protein kinase subfamily: metabolic sensors of the eukaryotic cell ? Annual Review of Biochemistry, 67, 821-855.
• [8] Kemp B.E., Mitchelhill K.I., Stapleton D., Michell B.J., Chen Z.P., 1999, Dealing with energy demand: the AMP-activated protein kinase, Trends in Biochemical Science, 24, 22-25.
• [9] Musi N., Hirshman M., Nygren J., Svanfeldt M., Bavenholm P., Rooyackers O., Zhou G., Williamson J.M., Ljunqvist O., Efendic S., Moller D.E., Thorell A., Goodyear L.J., 2002, Metformin increases AMP-activated protein kinase activity in skeletal muscle subjects with type 2 diabetes, Diabetes, 51(7), 2074-2081.
• [10] Luengo A., Sullivan L.B., Heiden M.G., 2014, Understanding the complex-I-ty of metformin action limiting mitochondria respiration to improve cancer therapy, BMC Biology, 12:82.
• [11] Evans J.M., Donnelly L.A., Emslie-Smith A., Alessi D.R., Morris A.D., 2005, Metformin and reduced risk of cancer in diabetic patients, British Medical Journal, 330, 1304-1305.
• [12] Bowker S.L., Majumdar S.R., Veugelers P., Johnson J.A., 2006, Increased cancer-related mortality for patients with type 2 diabetes who use sulfonylureas or insulin, Diabetes Care, 29, 2, 254-258.
• [13] http://www.naukowiec.org/wiedza/statystyka/iloraz-szans- -odds-ratio--szansa_456.html (data dostępu 27.02.2017).
• [14] http://ebm.org.pl/show.php?aid=15739 (data dostępu 27.02.2017).
• [15] Laplante M., Sabatini D.M., 2012, mTOR signaling in growth control and disease, Cell, 149, 274-293.
• [16] Cufi S., Vazquez-Martin A., Oliveras-Ferraros C., Martin- -Castillo B., Menendez J.J., Menendez A., 2010, Metformin against TGFβ-induced epithelial-to-mesenchymal transition (EMT): from cancer stem cells to aging-associated fibrosis, Cell Cycle, 9,22, 4461-4468.
• [17] Xiao H., Zhang J., Xu Z., Feng Y., Zhang M., Liu J., Chen R., Shen J., Lu Z., Fang X., Li J., Zhang Y., 2016, Metformin in a novel suppressor for trans forming growth factor (TGF)-β1, Scientific Reports, 6, 1-9.
• [18] UK Prospective Diabetes Study (UKPDS) Group, 1998, Effects of intensive blood glucose control with metformin on complication in overweight patients with type 2 diabetes (UKPDS 34), Lancet, 352, 854-865.
• [19] Roffi M., Brandle M., Robbins M.A., Mukherjee D., 2007, Current perspectives on coronary revascularization in the diabetic patient, Indian Heart Journal, 59, 124-136.
• [20] Beckman J.A., Creager M.A., Libby P,. 2002, Diabetes and atherosclerosis: epidemiology, pathophysiology, and management, Journal of the American Medical Association, 287, 2570-2581.
• [21] https://www.studyblue.com/notes/note/n/medical-term- -ch-10/deck/6056740 (data dostępu 25.02.2017).
• [22] Radomski M.W., Salas E., 1995, Nitric oxide — biological mediator, modular and factor of injury: its role in pathogenesis of atherosclerosis, Atherosclerosis, 118, S69-S80.
• [23] Nadar S., Blann A.D., Lip G.Y.H., 2004, Endothelial dysfunction: methods of assessment and application to hypertension, Current Pharmaceutical Design, 10, 3591-3605.
• [24] Obońska K., Grąbczewska Z., Fisz J., 2011, Ocena czynności śródbłonka naczyniowego - gdzie jesteśmy, dokąd zmierzamy? Folia Cardiologica Excerpta, 6, 667-671.
• [25] Marfella F., Acampora R., Verrazzo G., Ziccardi P., de Rosa N., Giunta R., Giugliano D., 1996, Metformin improves hemodynamic and rheological responses to L-arginine in NIDDM patients, Diabetes Care, 19(9), 934-939.
• [26] Algire C., Moiseeva O., Deschenes-Simard X., Amrein L., Petruccelli L., Birman E., Viollet B., Ferbeyre G., Pollak M.N., 2012, Metformin reduces endogenous reactive oxygen species and associated DNA damage, Cancer Prevention Research, 5(4), 536-543.
• [27] Murphy M.P., 2009, How mitochondria produce reactive oxygen species, Biochemical Journal, 417, 1-13.
• [28] Czajka A., 2006, Wolne rodniki tlenowe i mechanizmy obronne organizmu, Nowiny Lekarskie, 75, 6, 582-586.
• [29] Ewis S.A., Abdel-Rahman M.S., 1995, Effect of metformin on glutatione and magnesium in normal and streptozotocin-induced diabetic rats, Journal of Applied Toxicology, 15(5), 387-390.
• [30] Dai J., Liu M., Lin L., Deng K., Jing Y., Jia M., Wan J., Zhang L., 2014, Involvement of catalase in the protective benefits of metformin in mice with oxidative liver injury, Chemico-Biological Interactions216, 34-42.

Uwagi

Opracowanie rekordu w ramach umowy 509/P-DUN/2018 ze środków MNiSW przeznaczonych na działalność upowszechniającą naukę (2019).