Obesity is a major risk for #hypertension or high blood pressure, which in turn increases the risk of cardiovascular diseases. Until now, there has been no precise explanation for the hypertension that follows weight gain. In a new study researchers describe how they found the hormone #leptin is the link between obesity and increased blood pressure. Leptin is a hormone that regulates the amount of fat that is stored in the body. It is released by fat cells and circulates in the bloodstream to reach the brain, where it controls signals that trigger storage of energy in fat reserves and also the release of energy from those reserves. As well as controlling energy expenditure, leptin also adjusts the sensation of hunger, which is why it is referred to as the satiety hormone. For their study, the team compared healthy mice and humans with counterparts who have problems producing or processing leptin. They found that an increase in leptin in diet-induced obese mice drove an increase in their blood pressure - but not if they were deficient in leptin, or could not process it because their brains lacked leptin receptors. The team found a similar effect in humans. Some people who lacked leptin or leptin receptors because of a genetic disorder, had low blood pressure, despite being obese. In another part of the study, the researchers showed that leptins effect on blood pressure is handled through circuits in a part of the brain known as the dorsomedial hypothalamus (DMH). Blocking either leptin or leptin receptors in this part of the brains of the diet-induced obese mice caused a rapid reduction in blood pressure - regardless of changes in weight - note the researchers. Lastly, the team carried out another experiment on diet-induced obese mice bred not to express the leptin receptor gene. When they switched the gene back on - the mices blood pressure went up. The authors conclude that these findings show that leptin couples changes in weight to changes in blood pressure in mammals.
Posted on: Sun, 07 Dec 2014 09:15:14 +0000
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