How obesity damages blood vessels: Severely overweight people secrete molecules from their fat tissue ‘which cause internal stress and narrowing of the arteries’
- Chinese scientists analysed more than 1,000 people with atherosclerosis
- Obese participants released ‘much higher levels’ of a protein called WNT5A
- WNT5A triggers ‘internal stress’, linked to mineral deposits in the blood vessels
Obesity damages the lining of blood vessels because fat tissue secretes a harmful protein, research suggests.
Chinese scientists analysed more than 1,000 people with atherosclerosis, which occurs when fatty deposits clog the arteries.
They found the obese participants released ‘much higher levels’ of a protein called WNT5A from their fat tissue.
WNT5A triggers ‘internal stress’ and was linked to the accumulation of mineral deposits in the blood vessels.
Over time, these deposits can stick to plaque, causing blood vessels to narrow further. This restricts oxygen to the vital organs, which can lead to heart attacks or stroke.
The scientist hope WNT5A may one day be targeted in treatments that prevent heart disease in obese people.
Obesity may damage the lining of the blood vessels, research suggests (stock)
The study was carried out by the Shanghai Jiao Tong University School of Medicine and led by Dr Pan Gao.
Around 39.8 per cent (93.3million) of adults in the US were obese between 2015 and 2016, according to the Center for Disease Control and Prevention.
And in the UK, 29 per cent of adults were classified as obese in 2017, NHS Digital data shows.
Heart disease is responsible for a quarter of all deaths in the US and UK, statistics show.
Vascular disease, when the blood vessels become inflamed and weak, is ‘the most common precursor to heart disease’, according to Circulation Foundation.
Obesity has been shown to change the secretion of molecules from fat tissue, the researchers wrote in the journal Science Translational Medicine.
These molecules influence the structure and function of blood vessels, they added.
The so-called Wnt signaling pathway, which allows cells to ‘communicate’, and ‘internal stress’ have both been linked to the onset of vascular disease.
However, the role obesity plays in these processes was unclear. To learn more, the researchers analysed 1,004 atherosclerosis patients.
Results suggested the obese participants had significantly higher levels of WNT5A in their plasma.
They also had ‘elevated expression’ of WNT5A’s receptors, Frizzled 2 and Frizzled 5, in the walls of their arteries.
In a separate experiment, the team found high WNT5A was linked to the build-up of hard, calcified plaque in 68 out of 70 patients with coronary artery disease.
WNT5A has previously been linked to ‘endothelial function’, with higher levels also being associated with diabetes, the researchers wrote.
They stress further investigation, including animal studies, is required before WNT5A can be targeted by a potential treatment.
WHAT IS ATHEROSCLEROSIS?
Atherosclerosis occurs when plaques made of fat, cholesterol, calcium and other substances accumulate in artery walls.
Over time, the blood vessels harden and narrow, which restricts the flow of blood around the body.
When these plaques rupture, they form a blood clot that can further block the flow of oxygen-rich blood.
Atherosclerosis is most serious when it reduces blood supply to the heart or brain, which can result in a heart attack or stroke, respectively.
The condition, and the diseases it can cause, is the single biggest cause of death in the developed world, with it being responsible for one in three fatalities.
Atherosclerosis often starts in childhood and worsens with age, however, most do not experience symptoms until middle age or older.
Risk factors include:
- High blood pressure
- Elevated cholesterol levels
- Poor nutrition
- Excessive alcohol consumption
All the above can damage the thin layer, the endothelium, that keeps the inside of our arteries smooth.
Once damaged, ‘bad’ cholesterol accumulates in the artery wall.
The body sends immune cells to clean up this cholesterol, which can then get stuck in the damaged site.
This causes plaque to build-up over time.
Source: Heart Research Institute