Fri, Mar-20-15, 16:41
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Senior Member
Posts: 15,075
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Plan: mostly milkfat
Stats: 190/152.4/154
BF:
Progress: 104%
Location: Ontario
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Quote:
Vitamin D prevents diabetes and clogged arteries in mice
Washington University diabetes researcher Carlos Bernal-Mizrachi, MD, shown with a mouse that lacks the ability to process vitamin D in key immune cells. Without adequate vitamin D in those cells, the animals developed diabetes and atherosclerosis.
Credit: Robert Boston
In recent years, a deficiency of vitamin D has been linked to type 2 diabetes and heart disease, two illnesses that commonly occur together and are the most common cause of illness and death in Western countries. Both disorders are rooted in chronic inflammation, which leads to insulin resistance and the buildup of artery-clogging plaque.
Now, new research in mice at Washington University School of Medicine in St. Louis suggests vitamin D plays a major role in preventing the inflammation that leads to type 2 diabetes and atherosclerosis. Further, the way key immune cells behave without adequate vitamin D may provide scientists with new therapeutic targets for patients with those disorders.
The study appears March 19 in the journal Cell Reports.
Studying mice that lacked the ability to process vitamin D in immune cells involved in inflammation, the researchers found that the animals made excess glucose, became resistant to insulin action and accumulated plaques in their blood vessels.
“The finding that vitamin D helps regulate glucose metabolism may explain previous epidemiological studies identifying an increased risk of diabetes in patients with vitamin D deficiency,” said senior investigator Carlos Bernal-Mizrachi, MD, associate professor of medicine and of cell biology and physiology. “In our study, inactivation of the vitamin D receptor induced diabetes and atherosclerosis, so normalizing vitamin D levels may have the opposite effect.”
In addition, he said inadequate vitamin D turned immune cells into transporters of fat. That may help researchers better understand how diabetes and atherosclerosis are linked and provide new possibilities for therapy.
For years, researchers have been studying vitamin D’s possible roles in inflammation and inflammatory diseases, such as type 2 diabetes and atherosclerosis. By engineering mice without the vitamin D receptor on important immune cells called monocytes and macrophages, the researchers were able to learn how those conditions are linked, according to Bernal-Mizrachi.
Monocytes are white blood cells made in the bone marrow that circulate in the bloodstream. After a few days, they typically move into the body’s tissues where they mature into cells called macrophages.
“Inactivating the vitamin D receptor on monocytes and macrophages promotes inflammation of the liver and in artery walls,” he said. “It also increases the ability of monocytes in the blood to adhere and migrate into blood vessel walls, where they deposit cholesterol and secrete inflammatory substances that lead to diabetes and heart disease.”
He said the findings suggest that getting enough vitamin D may reduce those properties in immune cells, decreasing inflammation and reducing the onset of a combination of heart disease and diabetes, which is often referred to as cardiometabolic disease. In addition, the researchers found that without vitamin D, monocytes carried fat to the walls of blood vessels, which is something that hadn’t been observed previously.
“We knew that when monocytes matured and became macrophages, they would eat cholesterol deposited inside the blood vessel wall,” said co-first author Amy E. Riek, MD, assistant professor of medicine. “But in these experiments, we found that when they don’t have vitamin D, the monocytes, while they’re still in circulation, also eat up cholesterol and carry it in the bloodstream.”
That’s an important discovery, Riek explained, because it’s much easier to find treatments that target something in the blood than it is to target the same cells after they move into the wall of a blood vessel.
“So that provides us, potentially, with a new target for therapy,” she said.
It also changes the way that scientists think about how lipids are carried into the blood vessel wall to cause plaques. Scientists already knew that LDL, the so-called bad cholesterol, carried fat deposits to the vessel wall. Now this study suggests that when monocytes don’t have enough vitamin D, they can do it, too.
“The monocytes were laden with fat in the absence of vitamin D receptor,” Bernal-Mizrachi said. “And they carried that fat into the artery, so that’s a new understanding of another way fat may get into blood-vessel walls in patients who are vitamin D deficient.”
Interestingly, the problem was reversible in the mice. When the animals that had developed type 2 diabetes and atherosclerosis received bone marrow transplants from mice with healthy vitamin D receptors on their monocytes and macrophages, their inflammation levels decreased, and the animals had lower blood glucose and became more sensitive to insulin.
Currently, Bernal-Mizrachi and Riek are conducting clinical studies in people who have type 2 diabetes, treating them with vitamin D to see whether it can prevent some of the complications of diabetes and inflammation in humans, too.
“As part of that study, we’re actually isolating monocytes from the blood of patients before and after vitamin D therapy,” Riek said. “So we can look at the inflammatory properties of those cells to see whether vitamin D is causing any changes.”
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http://www.sciencedaily.com/release...50319123634.htm
In the related stories on the same page, from 2012;
Quote:
Vitamin D may prevent clogged arteries in diabetics
People with diabetes often develop clogged arteries that cause heart disease. New research has found that when vitamin D levels are adequate in people with diabetes, blood vessels are less likely to clog. But in patients with insufficient vitamin D, immune cells bind to blood vessels near the heart, then trap cholesterol to block those blood vessels.
People with diabetes often develop clogged arteries that cause heart disease, and new research at Washington University School of Medicine in St. Louis suggests that low vitamin D levels are to blame.
In a study published Nov. 9 in the Journal of Biological Chemistry, the researchers report that blood vessels are less like to clog in people with diabetes who get adequate vitamin D. But in patients with insufficient vitamin D, immune cells bind to blood vessels near the heart, then trap cholesterol to block those blood vessels.
"About 26 million Americans now have type 2 diabetes," says principal investigator Carlos Bernal-Mizrachi, MD. "And as obesity rates rise, we expect even more people will develop diabetes. Those patients are more likely to experience heart problems due to an increase in vascular inflammation, so we have been investigating why this occurs."
In earlier research, Bernal-Mizrachi, an assistant professor of medicine and of cell biology and physiology, and his colleagues found that vitamin D appears to play a key role in heart disease. This new study takes their work a step further, suggesting that when vitamin D levels are low, a particular class of white blood cell is more likely to adhere to cells in the walls of blood vessels.
Vitamin D conspires with immune cells called macrophages either to keep arteries clear or to clog them. The macrophages begin their existence as white blood cells called monocytes that circulate in the bloodstream. But when monocytes encounter inflammation, they are transformed into macrophages, which no longer circulate.
In the new study, researchers looked at vitamin D levels in 43 people with type 2 diabetes and in 25 others who were similar in age, sex and body weight but didn't have diabetes.
They found that in diabetes patients with low vitamin D -- less than 30 nanograms per milliliter of blood -- the macrophage cells were more likely to adhere to the walls of blood vessels, which triggers cells to get loaded with cholesterol, eventually causing the vessels to stiffen and block blood flow.
"We took everything into account," says first author Amy E. Riek, MD, instructor in medicine. "We looked at blood pressure, cholesterol, diabetes control, body weight and race. But only vitamin D levels correlated to whether these cells stuck to the blood vessel wall."
Riek and Bernal-Mizrachi say what's not yet clear is whether giving vitamin D to people with diabetes will reverse their risk of developing clogged arteries, a condition called atherosclerosis. They now are treating mice with vitamin D to see whether it can prevent monocytes from adhering to the walls of blood vessels near the heart, and they also are conducting two clinical trials in patients.
In one of those studies, the researchers are giving vitamin D to people with diabetes and hypertension to see whether the treatment may lower blood pressure. In the second study, African Americans with type 2 diabetes are getting vitamin D along with their other daily medications, and the research team is evaluating whether vitamin D supplements can slow or reverse the progression of heart disease.
Sometime in the next several months, the scientists hope to determine whether vitamin D treatment can reverse some of the risk factors associated with cardiovascular disease.
"In the future, we hope to generate medications, potentially even vitamin D itself, that help prevent the deposit of cholesterol in the blood vessels," Bernal-Mizrachi explains. "Previous studies have linked vitamin D deficiency in these patients to increases in cardiovascular disease and in mortality. Other work has suggested that vitamin D may improve insulin release from the pancreas and insulin sensitivity. Our ultimate goal is to intervene in people with diabetes and to see whether vitamin D might decrease inflammation, reduce blood pressure and lessen the likelihood that they will develop atherosclerosis or other vascular complications."
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I think this is an important point in the connection between atherosclerosis and blood cholesterol levels... the stuff doesn't just accidentally end up in the artery wall, there are mechanisms that actively pursue that end. Maybe at some point cholesterol could be rate-limiting, that's not the same as it being the cause of atherosclerosis. |
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I actually keep forgetting to take it lately. I mean to take 5000 IU a day, though.
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