The world wide prevalence of obesity and the metabolic syndrome is escalating. Contrary
to earlier experimental evidence, human obesity is characterised by sympathetic nervous
activation, with the outflows to both the kidney and skeletal muscle being activated.
While the mechanisms responsible for initiating the sympathetic activation remain
to be unequivocally elucidated, hyperinsulinemia, obstructive sleep apnoea, increased
circulating adipokines, stress and beta adrenergic receptor polymorphisms are implicated.
The pattern of sympathetic activation may be the pathophysiological mechanism underpinning
much obesity-related illnesses with the consequences including, amongst others, the
development of hypertension, insulin resistance, diastolic dysfunction and renal impairment.
While diet and exercise are the first line therapy for the treatment of obesity and
the metabolic syndrome, pharmacological interventions targeting the sympathetic nervous
system, either directly or indirectly are also likely to be of benefit. Importantly,
the benefit may not necessarily be weight related but may be associated with a reduction
in end organ damage.
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