20 February 2012
Obesity and high blood pressure are two of the world’s biggest health problems. In a novel study that examines both conditions in parallel, neuroscientists at Bristol University are examining how mechanisms in the brain and body adjust to nutritional intake. Their research aims to identify the signalling pathways that disrupt energy levels and trigger weight gain and hypertension.
Despite an overwhelming volume of scientific research into obesity, little is known about how nutrients such as glucose and fatty acids alter neuronal function. RCUK Research Fellow Dr Nina Balthasar is keen to understand the significance of neuronal activity in the brain corresponding to our physiological state, and the relationships between the various neuronal, nutrient and hormonal mechanisms that underpin the body’s ability to regulate energy homeostasis – and in the case of obesity, why they become dysfunctional.
“How does the brain sense, integrate and adjust to metabolic states, how does it know we have just eaten and how does the brain get the metabolic information from the rest of the body and then signal to other physiological processes that the body needs to adjust in response?” Dr Balthasar hopes to find the answers that might illuminate scientific and clinical understanding of the body’s regulatory systems.
“Current therapeutics for reducing body weight frequently fail because not enough is understood about the neuronal and cell signalling pathways involved, so the potential to cause side effects is high,” explains Dr Balthasar. “Obesity is closely linked to hypertension and most drugs that reduce appetite unfortunately also increase blood pressure. By looking at the mechanisms behind obesity-induced hypertension, our research could ultimately help with the development of drugs that are not so counterproductive.”
Dr Balthasar’s lab focuses on the hypothalamus, one of the key regions of the brain which regulates hunger. The group is interested in how hormones and nutrients are released from peripheral tissues, how these then elicit a signal in the hypothalamus, and what responses then occur in the central nervous system.
Studies with animal models have revealed how neuronal mechanisms adjust to glucose levels from food intake and crucially, how this impacts on gene function – the role of these genes in maintaining homeostasis and regulating appetite could lead to further insights about the physiological causes of not only obesity, but also type 1 diabetes, where failure of neurons to sense glucose levels appropriately has devastating consequences.
Dr Balthasar explains: “When trying to work out how a disease process occurs, it is necessary to explore the pathways that go wrong. Recent research has begun to unravel some of the neuronal pathways regulating body weight, but the exact mechanisms by which signals from the rest of the body are sensed and translated into a coordinated response are still unclear. The neuronal focus taken at Bristol is fairly unique – by combining a range of in vitro studies with imaging techniques, genetic manipulation and phenotypic analyses at the systems level, we hope to add much needed detail to our understanding of how metabolic balance is maintained, and the exact central pathways that lead to obesity-induced hypertension.”
Please contact Aliya Mughal for further information.
Obesity is closely linked to hypertension and most drugs that reduce appetite unfortunately also increase blood pressure.