A nutrition and lifestyle team at The George Institute has indicated that even small reductions in cholesterol can substantially reduce heart attacks and strokes and this applies across a broad range of individuals, irrespective of age, sex or initial cholesterol level.
The leading cause of death among Australians is cardiovascular disease which accounts for more than 50,000 or one third of all deaths each year.
One of the main contributing factors to cardiovascular disease is raised blood cholesterol and one in every two Australian adults is thought to have a cholesterol reading above the recommended level.
Many people with high cholesterol remain unaware of the problem and the new research shows just how great an impact would be made if awareness was raised.
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According to researcher Dr. Rachel Huxley, the key change to reduce cholesterol levels is to lower the intake of saturated fats.
Dr. Huxley says almost everyone would benefit from lowering their blood cholesterol which means cutting down on full fat dairy products, convenience meals, takeaway foods, confectionary, cakes and biscuits.
The research has also revealed that as cholesterol levels are significantly influenced by diet, consuming the right types of food would deliver significant health benefits to the Australian population.
The current results provides the first mechanistic description of how diabetes takes away the ability of fast blood flow force to protect blood vessels, arguing that it does so by interfering with ERK5 and its signaling partners. Abe's team showed that molecules called advanced glycation end products (AGEs), produced in greater levels by patients with diabetes, interfere with ERK5 cardioprotection. Glycation reactions cause the release of oxidizing side products like hydrogen peroxide (H202) that drive free radical production, inflammation and cell damage in many diseases.
Researchers found that AGEs and H202 sabotage ERK5 by encouraging the attachment to it of a small ubiquitin-related modifier (SUMO), a protein tag used by cells to fine-tune their control over proteins. In normal function, a cell may extend a protein's lifespan, or send it from one part of the cell to another, by attaching a SUMO tag. In the current study, researchers found that AGEs and H202 induced ERK5-SUMOylation as part of disease.
In addition, the team found that ERK5-SUMOylation was increased in the aortas of diabetic mice. Along with Abe, Chang-Hoon Woo, Tetsuro Shishido and Carolyn McClain contributed to the work within the Aab Cardiovascular Research Center. Jae Hyang Lim and Jian-Dong Li within the Department of Microbiology & Immunology at the Medical Center contributed expertise, along with Jay Yang, professor of Anesthesiology at Columbia University.
This work is supported by grants from the America Heart Association and the National Institutes of Health. Our experiments found that taking away the SUMO tag from ERK protects blood vessels against diabetes, Abe said. We believe that the SUMOylation of ERK turns off good' genes that are important in countering atherosclerosis. In the next phase, we will be looking for drug candidates that can turn on ERK5 as diabetes attempts to shut it down.
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