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The two major factors related to obesity and metabolic syndrome, sympathetic overactivity and insulin resistance, are closely
interrelated. Obesity is accompanied by an increase in sympathetic activity , particularly in the kidney, which could lead
to an increase in renin release and contribute to hypertension. Reactive hyperinsulinemia due to overeating, primary tissue
insulin resistance, hyperleptinemia and high free fatty acid levels all may promote enhanced sympathic outflow and metabolic
syndrome. Although acute administration of insulin in healthy subjects induces vasodilatation and is mediated by the release of
nitric oxide (NO), in insulin resistance the NO release is impaired, vasomotor tone increased due to enhanced calcium flux into
the vascular smooth muscle cells increasing the sympathetic nervous system activity. Anyhow the exact mechanisms through
which insulin resistance and hyperinsulinemia predispose to sympathtic overactivity are not well established. b-adrenergic
stimulation has also been shown to inhibit insulin signalling and decrease insulin induced glucose uptake in brown adipocytes.
As skletal muscle quantitatively account for the largest portion of whole body insulin resistance it not a surprise that factors
affecting muscular blood flow and nutrient delivery to the muscle are those of most importance in inducing insulin resistance.
Increased sympathetic drive induces small vessel rarefication or loss of capillary density causes vasoconstriction (via a-receptor)
and facilitate the shunting of glucose and insulin to less metabolically active skletal muscle beds. The metabolic properties of
antihypertensive agents give further credence to the hemodynamic model of insulin resistance. Vasoconstriction mediated by
b-blockers and vasodilatation by a-blockers parallel by their metabolic properties. Thus b-blockers that do vasoconstrict induce
insulin resistance, but those with a-blocking properties are not causing insulin resistance.
Biography
Risto Kaaja has completed his Ph.D at the age of 32 years from Helsinki University and postdoctoral studies from Helsinki University. He was an
obstetric physician for 23 years in the Women ́s Hospital of the Helsinki University Hospital and nowadays professor of Medicine in Turku University.
He has published more than 150 papers in reputed journals and the main topics of his publications have been related to manifestations of chronic
diseases in pregnancy. Of particular interest has been pre-eclampsia as a state of increased insulin resistance and sympathetic overactivity and of
increased risk for cardiovascular diseases later in life
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