Research reveals connection between high blood pressure and diabetes

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Research is finally explaining the connection between patients suffering with high blood pressure (hypertension) and diabetes

Medical professionals have long questioned why so many patients who have been diagnosed with high blood pressure, also have diabetes. It appears that an international team led by the universities of Bristol, UK, and Auckland, New Zealand have finally shed some light on this.

This study has shown that a small protein cell glucagon-like peptide-1 (GLP-1) couples the body’s control of blood sugar and blood pressure.

Professor Julian Paton, a senior author, and Director of Manaaki Mãnawa – The Centre for Heart Research at the University of Auckland, said: “We’ve known for a long time that hypertension and diabetes are inextricably linked and have finally discovered the reason, which will now inform new treatment strategies.”

RNA sequencing helped to reveal connection

Having received contributions from collaborating scientists in Brazil, Germany, Lithuania, and Serbia, as well as the UK and New Zealand, the study is an amalgamation of knowledge from around the globe and shows the universal necessity to solve this long unknown mystery.

Using an unbiased, high-throughput genomics technique called RNA sequencing to read all the messages of the expressed genes in the carotid body in rats with and without high blood pressure, the university was Bristol researchers were able to find that the receptor that senses GLP-1 is located in the carotid body, but less so in hypertensive rats.

GLP-1 is released from the wall of the gut after eating and acts to stimulate insulin from the pancreas in order to control blood sugar levels. This was already common knowledge however it has now been revealed that GLP-1 also stimulates a small sensory organ called the carotid body located in the neck.

“Locating the link required genetic profiling and multiple steps of validation. We never expected to see GLP-1 come up on the radar, so this is very exciting and opens many new opportunities.” this is very exciting and opens many new opportunities,” said David Murphy, Professor of Experimental Medicine from Bristol Medical School: Translational Health Sciences (THS) and senior author.

“this is very exciting and opens many new opportunities.”

Even when receiving medication, a large number of people with hypertension and/or diabetes are at high risk of life-threatening cardiovascular disease and will remain at high risk. This is because most medications only treat symptoms and not causes of high blood pressure and high sugar.

“Blood pressure is notoriously difficult to control”

Professor Rod Jackson, epidemiologist from the University of Auckland, said: “We’ve known that blood pressure is notoriously difficult to control in patients with high blood sugar, so these findings are really important because by giving GLP-1 we might be able to reduce both sugar and pressure together, and these two factors are major contributors to cardiovascular risk.

“Drugs targeting the GLP-1 receptor are already approved for use in humans and widely used to treat diabetes. Besides helping to lower blood sugar these drugs also reduce blood pressure, however, the mechanism of this effect wasn’t well understood.”

According to Jackson and other study participants said: “This research has revealed that these existing drugs may actually work on the carotid bodies to enact their anti-hypertensive effect. Leading from this work, we are already planning translational studies in humans to bring this discover into practice so that patients most at risk can receive the best treatment available.”

The team anticipate that these breakthroughs will lead to future translational projects in human hypertensive and diabetic patients and GLP-1 is just the beginning in a long line of potential research.

Mr Audrys Pauža, a British Heart Foundation-funded PhD student, said: “The prevalence diabetes and hypertension is increasing throughout the world, and there is an urgent need to address this.”


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