Key result
Systemic infusion of insulin results in a gradual increase in muscle sympathetic nerve activity, highlighting the sympathoexcitatory effects of hyperinsulinemia.
Hyperinsulinemia, even at low levels, can cause marked and long-lasting sympathoexcitation, contributing to blood pressure increases in obesity and metabolic syndrome.
Obesity and weight gain are frequently associ-ated with increases in blood pressure, driven inpart by sympathoexcitation (1). Obesity also islinked with insulin resistance and is associated with ongoing public health concerns, including the so-called metabolic syndrome (2). Even small increases in plasma insulin concentration (as low as one-fifth of that achieved after a mixed meal) (3) have marked and po-tentially long-lasting sympathoexcitatory effects (4). Such findings have important implications for the fluctuations in circulating catecholamines and blood pressure that occur in the postprandial state, as well as for conditions with sustained hyperinsulinemia. Yet the question remains, what are the mechanisms driving sympathoexcitation with hyperinsulinemia? In human studies, a systemic infusion of insulin has been shown to result in a gradual increase in muscle sympa-thetic nerve activity that remains elevated after plasma
No takes yet. Share an insight, caveat, or question.
Joyner et al. (2013) conducted an editorial in Obesity and insulin resistance. Insulin was evaluated. Systemic infusion of insulin results in a gradual increase in muscle sympathetic nerve activity, highlighting the sympathoexcitatory effects of hyperinsulinemia.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: