High cholesterol can cause bone loss
Sydney, Oct 16 (IANS) High cholesterol, which is a known factor for the decrease in heart health may harm more than our cardiovascular systems and lead to bone loss, say researchers including one of Indian-origin.
The new research conducted using animal models suggests that high levels of cholesterol can trigger mitochondrial oxidative stress on cartilage cells — connective tissue — causing them to die.
This may ultimately lead to the development of osteoarthritis — a type of arthritis that occurs when flexible tissue at the ends of bones wears down, said Indira Prasadam, a researcher at Queensland University of Technology in Brisbane, Australia.
For the study, Prasadam and her team used two different animal models to mimic human hypercholesterolemia.
The first was a mouse model that had an altered gene called Apolipoprotein E that made the animals hypercholesteremic.
The other was a rat model, and the animals were fed a high-cholesterol diet, causing diet-induced hypercholesterolemia.
Both models were fed a high-cholesterol diet or control normal diet, after which they underwent a surgery that mimics knee injuries in people and was designed to bring on osteoarthritis.
Both the mice and the rats that were subjected to surgery and fed with high-cholesterol diets showed more severe osteoarthritis development than seen in the normal diet group.
However, when both the mice and the rats were exposed to the cholesterol-lowering drug atorvastatin and mitochondrion-targeted antioxidants, the development of osteoarthritis was markedly decreased in relation to the untreated groups.
This study tested the potential therapeutic role of mitochondria targeting antioxidants in high-cholesterol-induced osteoarthritis, the researchers said.
“Our team has already begun working alongside dieticians to try to educate the public about healthy eating and how to keep cholesterol levels at a manageable level that won’t damage joints,” Prasadam said.
The research was published online in The FASEB Journal.