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Archive - Jul 4, 2019

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Tiny Molecular Change Reverses Prediabetes in Obese Mice; Remarkable Results Point to Potential Diabetes Drug Target and Highlight Possible Role for Ceramides in Sensing Nutrition

A small chemical change -- shifting the position of two hydrogen atoms -- makes the difference between mice that are healthy and mice with insulin resistance and fatty liver, major risk factors for diabetes and heart disease. Making the change prevented the onset of these symptoms in mice fed a high-fat diet and reversed prediabetes in obese mice. The scientists changed the trajectory of metabolic disease by deactivating an enzyme called dihydroceramide desaturase 1 (DES1). Doing so stopped the enzyme from removing the final hydrogens from a fatty lipid called ceramide, having an effect of lowering the total amount of ceramides in the body. The finding highlights a role for ceramides in metabolic health and pinpoints DES1 as a "druggable" target that could be used to develop new therapies for metabolic disorders such as prediabetes, diabetes, and heart disease -- that affect the health of hundreds of millions of Americans. Scientists at University of Utah Health and Merck Research Laboratories led the research, published online in Science on July 4, 2019. The article is titled “Targeting a Ceramide Double Bond Improves Insulin Resistance and Hepatic Steatosis.” "We have identified a potential therapeutic strategy that is remarkably effective, and underscores how complex biological systems can be deeply affected by a subtle change in chemistry," says Scott Summers (at right in photo), PhD, Chair of Nutrition and Integrative Physiology at U of Utah Health, who was co-senior author on the study with David Kelley, MD, formerly of Merck Research Laboratories. "Our work shows that ceramides have an influential role in metabolic health," says Dr. Summers. "We're thinking of ceramides as the next cholesterol." This isn't the first time that Dr.

Scientists Apply Bacterial Homing Capability to Enable Stem Cells to Home to Heart Tissue; Approach Offers “Enormous Potential” for Millions Suffering from Heart Disease Around the Globe

In a world first, scientists have found a new way to direct stem cells to heart tissue. The findings, led by researchers at the University of Bristol in the UK and published recently in Chemical Science, could radically improve the treatment for cardiovascular disease, which causes more than a quarter of all deaths in the UK. The open-access article is titled “Designer Artificial Membrane Binding Proteins to Direct Stem Cells to the Myocardium.” To date, trials using stem cells, which are taken and grown from the patient or donor and injected into the patient's heart to regenerate damaged tissue, have produced promising results. However, while these next-generation cell therapies are on the horizon, significant challenges associated with the distribution of the stem cells have remained. High blood flow in the heart combined with various “tissue sinks” that circulating cells come into contact with, means the majority of the stem cells end up in the lungs and spleen. Now, researchers from Bristol's School of Cellular and Molecular Medicine have found a way to overcome this by modifying stem cells with a special protein so the stem cells “home” to heart tissue. Dr. Adam Perriman, the study's lead author, Associate Professor in Biomaterials, UKRI Future Leaders Fellow and founder of the cell therapy technology company CytoSeek (https://www.cytoseek.uk/), explained: "With regenerative cell therapies, where you are trying to treat someone after a heart attack, the cells rarely go to where you want them to go. Our aim is to use this technology to re-engineer the membrane of cells, so that when they're injected, they'll home to specific tissues of our choice.”