
People wary of cholesterol have reason to rejoice since a study has shown that there is another way to get rid of it.
Mark Brown of Wake Forest University School of Medicine said that "cholesterol really can't be broken down."
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To get rid of it, it must be excreted, and now Brown and his colleagues have new evidence for an alternate way to deliver cholesterol into the faeces.
The findings revise scientific dogma about cholesterol loss that goes back almost 40 years.
Textbooks say that white blood cells known as macrophages gobble up cholesterol from artery walls.
That cholesterol is then delivered to high-density lipoprotein [HDL, aka good cholesterol], which takes it back to the liver where it goes into bile.
"Bile is necessary under the model to deliver cholesterol to the intestine," said Brown.
In fact, studies in dogs unable to get cholesterol into bile showed that the animals actually experienced an increase in cholesterol loss.
And recent studies in mice showed a similar thing.
Researchers said that an alternative pathway has largely been ignored, and thus scientists have made very little progress in defining the molecular pathways and players involved.
Now, Brown and his colleagues offer new evidence that helps support and clarify this alternate path for cholesterol.
They report that mice made unable to secrete cholesterol into bile through genetic manipulation or surgery still lose cholesterol through the faeces at a normal rate.
Macrophages in those animals also continued to take up cholesterol from blood vessels.
The researchers believe that alternate path delivers cholesterol from the liver to the intestine directly through the bloodstream.
"The classic view of reverse cholesterol transport involved the delivery of peripheral cholesterol via HDL to the liver for secretion into bile. In parallel, we believe that the liver also plays a gatekeeper role for nonbiliary fecal sterol loss by repackaging peripheral cholesterol into nascent plasma lipoproteins that are destined for subsequent intestinal delivery," wrote the researchers.
For the purposes of cholesterol-lowering drug discovery, it may prove fruitful to consider those two pathways as "separate and complementary," said Brown.
The study is published in the July issue of Cell Metabolism.
Source: ANI
Textbooks say that white blood cells known as macrophages gobble up cholesterol from artery walls.
Advertisement
That cholesterol is then delivered to high-density lipoprotein [HDL, aka good cholesterol], which takes it back to the liver where it goes into bile.
"Bile is necessary under the model to deliver cholesterol to the intestine," said Brown.
In fact, studies in dogs unable to get cholesterol into bile showed that the animals actually experienced an increase in cholesterol loss.
And recent studies in mice showed a similar thing.
Researchers said that an alternative pathway has largely been ignored, and thus scientists have made very little progress in defining the molecular pathways and players involved.
Now, Brown and his colleagues offer new evidence that helps support and clarify this alternate path for cholesterol.
They report that mice made unable to secrete cholesterol into bile through genetic manipulation or surgery still lose cholesterol through the faeces at a normal rate.
Macrophages in those animals also continued to take up cholesterol from blood vessels.
The researchers believe that alternate path delivers cholesterol from the liver to the intestine directly through the bloodstream.
"The classic view of reverse cholesterol transport involved the delivery of peripheral cholesterol via HDL to the liver for secretion into bile. In parallel, we believe that the liver also plays a gatekeeper role for nonbiliary fecal sterol loss by repackaging peripheral cholesterol into nascent plasma lipoproteins that are destined for subsequent intestinal delivery," wrote the researchers.
For the purposes of cholesterol-lowering drug discovery, it may prove fruitful to consider those two pathways as "separate and complementary," said Brown.
The study is published in the July issue of Cell Metabolism.
Source: ANI
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