The research comes as British politicians and health experts debate proposals for a UK ‘sugar tax’ in which a 20% duty on sugary drinks would be imposed to discourage the public – especially children – away from unhealthy food and drink options.
The study also highlights the potential health risks of regularly consuming large amounts of rich, sugary foods. With healthy eating among the most common New Year’s resolutions, the findings add more incentive to reduce food intake all year round.
Dr Richard Rainbow led researchers from the University of Leicester in the first study to show direct evidence of blood vessel contraction due to glucose. The team manged to demonstrate this effect even at glucose levels observed after a large meal.
The researchers believe the result provides a foundation for finding a therapeutic target to improve outcomes following a heart attack or stroke. The research team previously demonstrated in 2010 that high glucose from any cause, not just diabetes, was an indicator of a ‘worse outcome’ following a heart attack.
Further research in 2014 by the team showed that glucose has potentially damaging effects on the normal function of the heart, such as arrhythmia and abolishing the built-in protective mechanisms that the heart can activate on stress.
This study adds to current understanding of the potentially damaging effects of glucose. High glucose at the time of heart attack could make the block in a coronary artery more severe by causing the blood vessel to contract, leading to a higher risk of complications.
Currently, clinicians are being advised by the American Heart Association (AHA), the UK's National Institute for Health and Care Excellence (NICE) and the European Society for Cardiology that blood glucose is a key factor when looking at cardiovascular disease.
“Blood glucose at the time of heart attack is indicative of a poor outcome for patients. What isn’t clear, as yet, is whether the glucose is the cause and this is an ongoing area of research,” Rainbow told us.
“We demonstrate that the glucose is causing some degree of blood vessel contraction which may worsen arterial narrowing. But we cannot, at this time, state whether glucose could trigger a heart attack."
Using electrophysiology and myography techniques to examine the impact of glucose on arterial cells that make up the tissue of blood vessels, the team experimented on rat mesenteric, porcine coronary and human internal mammary arteries.
They identified a known signalling protein family, protein kinase C, as a key part of the enhanced contractile response of blood vessels.
Protein kinase C: Frustrating researchers since 1982
Protein kinase C has been a frustrating target for drug discovery ever since it was first identified in 1982. Initial therapeutic efforts focused on cancer, with additional indications - including diabetic complications and heart failure, targeted later as researchers developed a better understanding of these proteins in health and disease. Unfortunately, efforts have yet to result in the approval of a single new drug that specifically targets protein kinase C.
Additional studies about this mechanism and its role in blood vessel contraction are varied and amongst the most researched. High blood glucose concentration is known to increase cellular levels of the protein kinase C activator, DAG in a variety of tissues, including arterial smooth muscle.
“This team have shown that, in multiple species, it is possible to use protein kinase C as a target to block blood vessel constriction caused by high levels of glucose in the blood,” said Professor Jeremy Pearson, Associate Medical Director at the British Heart Foundation.
“This opens up the possibility for improved treatment for patients where recovery from heart attack is complicated by raised glucose levels.”
Source: British Journal of Pharmacology
First published online 9 December 2015, doi: 10.1111/bph.13399.
“Distinct and complementary roles for α and β isoenzymes of protein kinase C in mediating vasoconstrictor responses to acutely elevated glucose.”
Authors: Jackson R, Brennan S, Fielding P, Sims MW, Challiss RA, Adlam D, Squire IB, Rainbow RD.