The sympathetic nervous system SNS and insulin resistance

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).

Skeletal muscle

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).

Adipose tissue

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.

Norepinephrine and epinephrine also inhibit pancreatic insulin secretion in humans and stimulate hepatic gluconeogenesis and glycogenolysis, further worsening hyperglycaemia (Nonogaki, 2000).

Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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