Recent research has already started to uncover how your nervous system regulates your body weight and cardiovascular function, and how to manage certain pathways that control how this information is processed, up until now it has remained unclear which exact mechanisms allow your brain to sense and translate these signals into co-ordinated metabolic and cardiovascular responses.
Yet the team from the University of Bristol team, with funding from the British Heart Foundation (BHF), has now found a target that is not only critical to your brain’s regulation of body weight, but also in the development of obesity-associated conditions. The mechanism behind a key molecule, known as melanocortin-4-receptor (MC4R), can cause severe obesity with type 2 diabetes when it becomes mutated or lost in both human and animal models, say the researchers.
The mechanism that the team identified works, via MC4R, to regulate of the activity of your autonomic nervous system, which maintains appropriate blood pressure and insulin levels. This nervous system regulates your internal organs and processes and is split into the parasympathetic and sympathetic nervous system, which commonly exert opposing influences on the structures they supply with nerves.
The team showed that activating MC4R could inhibit the parasympathetic neurons in the brain stem area of the central nervous system (CNS), and, at the same time, activate the sympathetic neurons in the spinal cord. Therefore, the MC4R carefully balances positive and negative forces on the autonomic nervous system, and maintains your equilibrium of appropriate blood pressure and insulin levels.
According to Dr Nina Balthasar, one of the study’s lead authors and a researcher in the University’s School of Physiology and Pharmacology, ‘Obesity is a major risk factor for cardiovascular disease with recent statistics showing that obese adults are three to four times more likely to develop high blood pressure.’
She added, ‘In order to curb the escalating incidence of obesity and obesity-related diseases, a primary prevention goal must be to understand the physiological processes underlying our vulnerability to weight gain – knowledge that is central to the development of novel, effective therapies. Our data illustrate the complexity of the CNS pathways governing the body’s metabolic balance and highlight the challenges ahead for the development of safe therapies.’