Obesity and hypertension come together

obedity and hypertentionObesity and hypertension are frequent companions. Hypertension is a “silent killer” because it often occurs with no symptoms and actually half of hypertensive patients just do not think about it and do not cure and often run up hopeless situation. But why do obesity and hypertension come together?

Leptin, hormone secreted by fat cells, increases significantly after weight gain and obesity. This hormone acts on the brain to increase blood pressure.

The link between obesity and cardiovascular disease is well known, so that being obese or overweight is a major risk factor for the development of hypertension and cardiovascular disease risk. But it has not been known clearly how obesity increases the risk of high blood pressure, making it difficult to develop evidence-based obesity, hypertension and heart disease therapies.

New study is to clarify the doubts about the link that unites them, beyond sharing the cardiovascular risk. What has discovered a team of researchers from Monash University (Australia), Warwick and Cambridge (UK), and several US universities, is that the hormone leptin, secreted by fat cells, was significantly elevated after weight gain and obesity, acting in the brain to increase blood pressure.

This research was published after experiments were conducted in animals and humans, including a unique cohort of patients lacking the hormone leptin or do not have leptin receptors. The results showed that both leptin block and leptin receptors removed from the brain act effectively in reducing obesity-induced hypertension.

About 80% of the common hypertension is caused by excess body fat and this study led by Professor Michael Cowley of Monash University describes how obesity raises blood pressure and opens new approaches to treating obesity-induced high blood pressure.

In genetically modified mice only subjects with normal leptin signaling showed an increase in blood pressure when they became obese. These data were confirmed in human studies. Patients with leptin deficiency and lacking the leptin receptor had lower systolic blood pressure.

Restored leptin receptors in the brain of obese mice elevated blood pressure and multiple methods of receptor blockade in the brain leptin reduced hypertension. Acute obstruction of the electrical activity of cells leptin receptor in the brain of hypertensive obese mice reduced blood pressure immediately, confirming the role of these neurons in the elevation of blood pressure in obesity.

This study shows that a hormone secreted by fat increases blood pressure and explains the mechanism of the relationship between obesity and hypertension. The data suggest that pharmacological approaches to alter the effect of leptin in the brain could potentially be a therapeutic target for the treatment of obesity-induced hypertension, and potentially could be exploited to reduce the effects of obesity induced cardiovascular disease.