Patients with CHF have persistent activation of their sympathetic nervous system (SNS) (Reaven etal., 1996; Scherrer and Sartori, 1997), and excessive activation of the SNS might lead to insulin resistance. In normal individuals, adrenaline infusion leads to acute insulin resistance (Scherrer and Sartori, 1997).
Insulin increases skeletal muscle uptake of glucose. In healthy subjects, acute SNS activation decreases glucose uptake by skeletal muscles. Unloading of cardiopulmonary receptors, a manoeuvre that leads to selective reflex sympathetic activation in skeletal muscle, reduces insulin-induced stimulation of muscle glucose uptake by up to 25% (Scherrer and Sartori, 1997).
Stimulation of ^-receptors in humans increases lipolysis, resulting in raised plasma free fatty acid (FFA) levels (Schiffelers etal., 2001). In normal subjects infusion of norepinephrine results in increased plasma levels of FFAs (Marangou etal., 1988). In patients with CHF, norepinephrine concentrations have been correlated with FFA concentrations (Paolisso etal., 1991). The FFAs impair insulin-mediated glucose disposal in human skeletal muscle (Roden, 2004) and can stimulate hepatic gluconeogenesis (Lam etal., 2003), further potentiating hyperglycaemia.
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