Hormonal Regulation Links Obesity to Blood Pressure

Leptin, a hormone that regulates the amount of fat stored in the body, also drives the increase in blood pressure (BP) that occurs with weight gain, according to a new study.

Researchers at Monash University (Melbourne, Australia) and the University of Cambridge (Cambridge, United Kingdom) conducted a study in mice and humans to see whether leptin (also known as the “satiety hormone”) couples changes in weight to changes in BP in mammalian species. The group found that obese people who were lacking the hormone due to a genetic disorder had low BP, despite being obese. This was also the case for people lacking the gene for the leptin receptor (LepR) in the brain, meaning that the brain was unable to respond to the hormone.

Modeling the human condition in rodents, the researcher showed that mice with normal leptin signaling developed an increase in BP when put on a high fat diet to enforce diet-induced obesity (DIO). These effects were not seen in mice that lacked leptin or with a defective or blocked LepR. The study found that leptin's effects on BP are mediated by neuronal circuits in the dorsomedial hypothalamus (DMH), as inhibiting the activity of LepR-expressing neurons in the DMH caused a rapid reduction of BP in DIO mice, independent of changes in weight; re-expression of the LepRs caused an increase in BP. The study was published on December 4, 2014, in the journal Cell.

“We now know that leptin regulates both our weight and our blood pressure through its action on the brain,” said study coauthor Prof. Sadaf Farooqi, PhD, of the Cambridge Wellcome Trust-Medical Research Council Institute of Metabolic Science. “Targeting this action could offer a useful way of helping people fight obesity and associated problems such as high blood pressure and heart disease.”

Leptin is a hormone made by fat cells which regulates the amount of fat stored in the body by adjusting both the sensation of hunger and energy expenditures. Hunger is inhibited when the amount of fat stored reaches a certain level, causing satiety; leptin is then secreted and circulates through the body, eventually activating leptin receptors in the arcuate nucleus of the DMH. Energy expenditure is then increased both by the signal to the brain, and directly via leptin receptors on peripheral targets. The effect of leptin is opposite to that of ghrelin (also known as the “hunger hormone”), which are on the same brain cells as leptin receptors, so these cells receive competing satiety and hunger signals.

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Monash University
University of Cambridge