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Factors in the Blood During Dieting May Have Anti-Diabetes Properties

Taking Vitamin D May Benefit People with MS

Two Alzheimer’s risk genes linked to brain atrophy, promise future blood markers




Released: 01/09/16


Factors in the Blood During Dieting May Have Anti-Diabetes Properties

Factors in the blood from calorie-restricted rats can modify energy-producing mitochondria within the insulin-producing cells that regulate blood sugar levels, new research shows. This has a positive impact on glucose-stimulated insulin secretion and protects cells from fatty acid and glucose toxicity.

The findings suggest that insulin-producing cells’ mitochondria may be altered by signals independent of the body’s fuel levels and may represent a useful therapeutic target in type 2 diabetes. Additionally, identifying these blood factors may open even more targetable interventions against the disease.

“Our findings support the concept that the impact of diet on insulin secreting cells is mediated by signals traveling through the blood rather than the nutrients and metabolites themselves. These signals may be generated elsewhere in other organs such as fat tissue, liver, brain or even the immune cells,” said Dr. Orian Shirihai, co-author of The FEBS Journal study. “Our findings also suggest that at least in part the beneficial effect of reducing caloric intake is mediated by the appearance of a protective signal rather than the elimination of a harmful one. This study describes an experimental system through which such signals can be identified and characterized with the hope that in the future it can potentially be mimicked using a small compound.”

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The above post is reprinted from materials provided by Wiley. Note: Materials may be edited for content and length.

Links: Materials:  http://www.wiley.com/WileyCDA/PressRelease/pressReleaseId-122762.html

 

Wiley  http://www.wiley.com/WileyCDA/Brand/id-35.html

Released: 01/04/16


Taking Vitamin D May Benefit People with MS

Taking a high dose of vitamin D3 is safe for people with multiple sclerosis (MS) and may correct the body’s hyperactive immune response, according to a study published in the December 30, 2015, online issue of Neurology®, the medical journal of the American Academy of Neurology.

Low levels of vitamin D in the blood are tied to an increased risk of developing MS. People who have MS and low levels of vitamin D are more likely to have greater disability and more disease activity.

For the study, 40 people with relapsing-remitting MS received either 10,400 IU or 800 IU of vitamin D3 supplements per day for six months. The current recommended daily allowance of vitamin D3 is 600 IU. Blood tests at the start of the study and again at three and six months measured the amount of vitamin D in the blood and the response in the immune system’s T cells, which play a key role in MS.

Side effects from the vitamin supplements were minor and were not different between the people taking the high dose and the people taking the low dose. One person in each group had a relapse of disease activity.

The people taking the high dose had a reduction in the percentage of T cells related to MS activity. When the increase in vitamin D in the blood was greater than 18 nanograms per milliliter (ng/ml), every 5 ng/ml increase in vitamin D led to a 1 percent decrease in the percentage of interleukin 17 T cells in the blood. The people taking the low dose did not have any changes in their T cells.

While researchers are still determining the optimal level of vitamin D in the blood for people with MS, the people in the study taking the high dose of vitamin D reached a level that has been proposed as a target for people with MS. Vitamin D levels above 30 ng/ml are considered sufficient for the general population, but researchers noted that for people with MS, it may be that levels above 50 ng/ml are necessary to reduce disease activity. The group taking the low dose did not reach this target.

“These results are exciting, as vitamin D has the potential to be an inexpensive, safe and convenient treatment for people with MS,” said study author Peter A. Calabresi, MD, of Johns Hopkins University School of Medicine in Baltimore, MD, and a Fellow of the American Academy of Neurology. “More research is needed to confirm these findings with larger groups of people and to help us understand the mechanisms for these effects, but the results are promising.”

The study was supported by the Kenneth and Claudia Silverman Family Foundation, Montel Williams Foundation and National Multiple Sclerosis Society. To learn more about multiple sclerosis, please visit www.aan.com/patients.

 

Neurology®http://www.neurology.org/content/early/2015/12/30/WNL.0000000000002316.short?rss=1

American Academy of Neurology:   https://www.aan.com/

www.aan.com/patients.:  www.aan.com/patients.

Released: 01/04/16


Two Alzheimer’s risk genes linked to brain atrophy, promise future blood markers

Two genetic variants previously linked to Alzheimer's disease have been more specifically tied to brain atrophy that is characteristic of the disease.

A newly reported study, led by Liana Apostolova, M.D., Barbara and Peer Baekgaard Professor of Alzheimer's Disease Research at the Indiana University School of Medicine, also found that the proteins produced by the genes and circulating in the blood were associated with the brain atrophy and could be used in Alzheimer's-related tests in the future.

The study is believed to be the first to directly link common variants of the genes -- ABCA7 and MA4A6A -- to atrophy in cortical and hippocampal regions of the brain, which are associated with memory and other key functions. It's also believed to be the first to link the atrophy to protein levels in the blood produced by the genes.

"We also found that the levels of the protein products of these genes, circulating in the peripheral blood, were associated with the cortical and hippocampal atrophy. This finding suggests that those results of gene expression could become useful biomarker blood tests for Alzheimer's disease," Dr. Apostolova said.

The study was published in the advance online edition of the journal Neurobiology of Aging.

Alzheimer's disease is a progressive illness that is the leading cause of dementia and the sixth leading cause of death in the United States, according to the Alzheimer's Association. There is no cure for the disease and currently available treatments can slow, but cannot stop, the deterioration.

Although scientists have been linking a growing number of gene variants to the risk of developing Alzheimer's disease, most of the associations have not identified the specific mechanisms that would increase the risk of developing the disease.

For the new study, the researchers identified the top nine genetic variants that have been associated with Alzheimer's disease risk, not including the APOe4 gene that has long been linked to increased risk for several characteristics of Alzheimer's disease.

Using magnetic resonance imaging tools to measure brain size and genetic analysis, the researchers looked for associations between the genetic variants and atrophy in the cortical and hippocampal regions of the brain, which are established physical biomarkers of Alzheimer's disease. The studies were conducted in 50 participants with no cognitive difficulties and 90 who had been diagnosed with mild cognitive impairment, a condition that is associated with increased risk of developing Alzheimer's disease. All of the participants were 50 years or older.

Just two of the genetic variants -- known as ABCA7 and MA4A6A -- appeared to be associated with the changes in brain structure.

Funding from the following sources supported the research: National Institutes of Health grants R01 AG040770, K02 AG048240, P50 AG16570 and P30 AG010133; and the Easton Consortium for Alzheimer’s Drug Discovery and Biomarker Development.

 

In addition to Dr. Apostolova, researchers contributing to the study were Leslie M. Ramirez of the Drexel University College of Medicine, Giovanni Coppola, Naira Goukasian, Sona Hurtz, Eric Klein, Shai Porat, Renee Sears, and Benjamin Wang of UCLA, Kristy S. Hwang of the Oakland University William Beaumont School of Medicine, Jennifer A. Eastman of the Northwestern University Feinberg School of Medicine and Nouchee Vang of the University of Minnesota.

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