It became evident in the last years that an increased vascular risk is not
only associated with frank diabetes, but also already with states of insulin
resistance. This risk does not only affect the large vessels contributing to the
augmented cardiovascular risk often observed in insulin resistant patients, but also
various functions of the microvasculature. Here we present some evidence that
insulin resistant states are clearly associated with an increased formation of
reactive oxygen species (ROS) and linked to a state often called “oxidative stress”.
Various mechanisms (NADPH-oxidase, disturbed mitochondrial function,
uncoupling of nitric oxide synthase) may contribute to oxidative stress, but may
also aggravate insulin resistance. It is discussed whether both oxidative stress and
insulin resistance are causally linked and why oxidative stress leads to various
defects of microvascular function (changes in vasomotion, permeability, reduced
capillary bed, induction of apoptosis, changes in gene expression by activation of
transcription factors (NFkappB, AP-1, STAT).
