The discovery of leptin and its multiple biologic actions, including sympathetic nervous system (SNS) activation, has provided a possible link between obesity and hypertension. Short-term leptin administration directly into the brain stimulates sympathetic activity, and long-term leptin infusion, at rates that mimic plasma concentrations found in obesity, increases arterial pressure via adrenergic activation in nonobese rodents. Short-term studies suggest that the sympathetic effects of leptin may depend on interactions with other neurochemical pathways in the hypothalamus, such as melanocortin receptors. However, it is still unclear whether there is resistance to the long-term SNS and blood pressure effects of leptin in obesity. Results from clinical trials using long-term leptin administration in humans in an attempt to reduce body weight should help to answer some of these questions.
|Original language||English (US)|
|Number of pages||5|
|Journal||Current Opinion in Endocrinology and Diabetes|
|State||Published - Jun 23 1999|
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism