Hormonal
Obesity induces 'selective leptin resistance' where the appetite-suppressing effects of leptin are blunted, but the blood pressure-raising effects (via SNS activation) remain intact.
Your body produces high levels of leptin, but your brain ignores its 'stop eating' command. However, it still listens to leptin's command to raise blood pressure. This mismatch makes losing weight and controlling blood pressure harder. Treatments that mimic or bypass leptin signaling (like GLP-1 agonists) may help by addressing these pathways.
However, obesity may induce selective leptin resistance, whereby the RSNA responses to leptin are maintained while the appetite suppressant effects of leptin are attenuated
Why this rating
Supported by rodent studies and human observations of MC4R deficiency.
Source
Obesity-induced Hypertension: Role of Sympathetic Nervous System, Leptin, and Melanocortins
John E. Hall et al. · Journal of Biological Chemistry · 2010
DOI 10.1074/jbc.r110.113175
More from this paper
- Excess weight gain causes hypertension primarily through activation of the sympathetic nervous system (SNS), mediated by leptin and melanocortin receptors, leading to increased renal sodium reabsorption and impaired pressure natriuresis.Good
- Activation of the central melanocortin 4 receptor (MC4R) is necessary for obesity to increase sympathetic nervous system activity and arterial pressure.Good
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