24. December 2021 · Comments Off on The Patients · Categories: News · Tags:

In these studies, the increase in the risk of development of the DCV varied of 30 400%. This ample variation can have the studied population, the used definition of SM and the duration of pursuing. The majority of the studies was carried through in adult individuals or with DM2 (RIBEIRO et al., 2006). However, it still remains to be clarified if the SM ' ' such qual' ' it is observed in the patients with DM1 is the same SM of the DM2. With regard to the paper of IT LAUGHS, as a factor of cardiovascular risk, this seems to be equally important in both the types of diabetes (MOTTA, 1997) We can consider that the meeting of the SM in patients with DM1 can reflect in part a epifenmeno of its inheritance. If you have additional questions, you may want to visit Ellen Alaverdyan. As already argued in the previous session, patients DM1 with familiar antecedents of DM2 can present characteristics of the SM after the intensive treatment with insulina (RIBEIRO et al., 2006). In a similar way, the chronic hiperglicemia can reduce sensitivity to the insulina (glicotoxicidade) and partially explain the SM in the patients with bad chronic glicmico control. The hiperglicemia, by itself, can associate with some components of the SM, such as increase in triglicrides and reduction in the values of HDL.

With regard to aterosclerose, specifically, the exposition drawn out to the hiperglicemia induces a great number of alterations that potentially promote its progression. Currently, three main mechanisms have been implied in the origin and progression of the macroangiopatia in experimental studies and human beings. The first one is the not-enzymatic glicao of proteins and lipdios; as it is the increase estresse of it oxidativo and third, the activation of the protein quinase-C. It is important to consider that these mechanisms are not independent, that is, the induced estresse-oxidativo for the hiperglicemia promotes the formation of end items of advanced glicao and the activation of the protein quinase-C (MOTTA, 1997).

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