Journal
TOXICOLOGY MECHANISMS AND METHODS
Volume 23, Issue 5, Pages 297-302Publisher
TAYLOR & FRANCIS LTD
DOI: 10.3109/15376516.2012.759305
Keywords
Diabetes; glucose; mitochondria; NADH; NADPH; oxidative stress
Categories
Funding
- Fundacao para a Ciencia e a Tecnologia [SFRH/BD/38467/2007]
- Fundacao para a Ciencia e Tecnologia, Portugal, under the frame of Programa Operacional Tematico Factores de Competitividade (COMPTE) do Quadro Comunitario de Apoio III [PTDC/QUI/72826/2006, PTCD/QUI-BIC/103514/2008]
- Fundo Comunitario Europeu (FEDER)
- Fundação para a Ciência e a Tecnologia [SFRH/BD/38467/2007, PTDC/QUI/72826/2006] Funding Source: FCT
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The reductive power provided by nicotinamide adenine dinucleotides is invaluable for several cellular processes. It drives metabolic reactions, enzymatic activity, regulates genetic expression and allows for the maintenance of a normal cell redox status. Therefore, the balance between the oxidized (NAD(+)) and the reduced (NADH) forms is critical for the cell's proper function and ultimately, for its survival. Being intimately associated with the cells' metabolism, it is expected that alterations to the NAD(+)/NADH ratio are to be found in situations of metabolic diseases, as is the case of diabetes. NAD(+) is a necessary cofactor for several enzymes' activity, many of which are related to metabolism. Therefore, a decrease in the NAD(+)/NADH ratio causes these enzymes to decrease in activity (reductive stress), resulting in an altered metabolic situation that might be the first insult toward several pathologies, such as diabetes. Here, we review the importance of nicotinamide adenine dinucleotides in the liver cell and its fluctuations in a state of type 2 diabetes mellitus.
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