Purpose of review Cardiovascular diseases
(CVDs) are the number one cause of death globally. The risk for the development of CVDs is significantly increased in obesity
, the product of white adipose tissue, appears to contribute to the development of CVDs in obesity
. Here, we discuss the premise that leptin
engages the sympathetic nervous system and contributes to elevated blood pressure (BP) developing in obesity
The long-term regulation of BP is dependent on the activity of the autonomic nervous system and specifically the sympathetic nervous system. Sympathetic nerve activity is significantly increased in obese rodents and humans. Leptin
increases sympathetic nerve activity in rodents and humans; however, leptin
only consistently increases BP chronically in rodents. The ability of leptin
to increase BP in rodents is via both hypothalamic and extrahypothalamic regions. In leptin
-deficient and leptin
receptor-deficient humans, leptin
appears to be the key reason for decreased systolic BP. However, in other research conducted in humans, chronic administration of leptin
does not elevate BP.
Further research into the role of leptin
in the development of CVDs, especially in humans, needs to be conducted.