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Does leptin cause an increase in blood pressure in animals and humans?
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Simonds, Stephanie E., Pryor, Jack T. and Cowley, Michael A. (2016) Does leptin cause an increase in blood pressure in animals and humans? Current Opinion in Nephrology and Hypertension, 26 (1). pp. 20-25. doi:10.1097/MNH.0000000000000287 ISSN 1062-4821.
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Official URL: http://dx.doi.org/10.1097/MNH.0000000000000287
Abstract
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. Leptin, 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.
Recent findings
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.
| Item Type: | Journal Article | ||||
|---|---|---|---|---|---|
| Divisions: | Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School | ||||
| Journal or Publication Title: | Current Opinion in Nephrology and Hypertension | ||||
| Publisher: | Wolters Kluwer Health | ||||
| ISSN: | 1062-4821 | ||||
| Official Date: | 1 January 2016 | ||||
| Dates: |
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| Volume: | 26 | ||||
| Number: | 1 | ||||
| Page Range: | pp. 20-25 | ||||
| DOI: | 10.1097/MNH.0000000000000287 | ||||
| Status: | Peer Reviewed | ||||
| Publication Status: | Published | ||||
| Access rights to Published version: | Restricted or Subscription Access |
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