Metabolic syndrome: what neurosurgeons should know

The term metabolic syndrome, first introduced in 1988, has evolved in concept since that time. While the strict definition is subject to ongoing debate, the syndrome generally involves glucose intolerance, obesity, dyslipidemia and high blood pressure, which increase the risk of developing cardiovascular disease. The complex pathophysiology underlying this syndrome similarly has yet to be agreed upon but can be attributed largely, although not entirely, to insulin resistance and dysfunctional glucose and fat metabolism. This multifactorial syndrome highlights the complex association between noninsulin-dependent diabetes mellitus, coronary artery disease, and hypertension. An overview of factors contributing to the pathogenesis of metabolic syndrome may help neurosurgeons gain an understanding of this increasingly encountered disorder. Insulin resistance and hyperinsulinemia are key pathophysiological components of metabolic syndrome. Glucose homeostasis requires that the feedback loop is maintained between insulinproducing pancreatic beta cells in response to a rise in serum glucose levels. In the setting of insulin resistance, the abnormally high levels of insulin produced in response to serum glucose elevations act not only to stimulate glucose uptake by muscles through a phosphatidylinositol 3-kinase pathway but also to induce mitogenic and proinflammatory effects via a MAP kinase pathway.