Moving Toward Answers in ME/CFS

Woman in bed

Thinkstock/Katarzyna Bialasiewicz

Imagine going to work or school every day, working out at the gym, spending time with family and friends—basically, living your life in a full and vigorous way. Then one day, you wake up, feeling sick. A bad cold maybe, or perhaps the flu. A few days pass, and you think it should be over—but it’s not, you still feel achy and exhausted. Now imagine that you never get better— plagued by unrelenting fatigue not relieved by sleep. Any exertion just makes you worse. You are forced to leave your job or school and are unable to participate in any of your favorite activities; some days you can’t even get out of bed. The worst part is that your doctors don’t know what is wrong and nothing seems to help.

Unfortunately, this is not fiction, but reality for at least a million Americans—who suffer from a condition that carries the unwieldy name of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), a perplexing disease that biomedical research desperately needs to unravel [1]. Very little is currently known about what causes ME/CFS or its biological basis [2]. Among the many possibilities that need to be explored are problems in cellular metabolism and changes in the immune system.

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Creative Minds: The Worm Tissue-ome Teaches Developmental Biology for Us All

C. elegans

Caption: An adult Caenorhabditis elegans, 5 days
Credit: Coleen Murphy, Princeton University, Princeton, NJ

In the nearly 40 years since Nobel Prize-winning scientist Sydney Brenner proposed using a tiny, transparent soil worm called Caenorhabditis elegans as a model organism for biomedical research, C. elegans has become one of the most-studied organisms on the planet. Researchers have determined that C. elegans has exactly 959 cells, 302 of which are neurons. They have sequenced and annotated its genome, developed an impressive array of tools to study its DNA, and characterized the development of many of its tissues.

But what researchers still don’t know is exactly how all of these parts work together to coordinate this little worm’s response to changes in nutrition, environment, health status, and even the aging process. To learn more, 2015 NIH Director’s Pioneer Award winner Coleen Murphy of Princeton University, Princeton, NJ, has set out to analyze which genes are active, or transcribed, in each of the major tissues of adult C. elegans, building the framework for what’s been dubbed the C. elegans “tissue-ome.”

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Feed a Virus, Starve a Bacterium?

Woman eating hot soup in bed

Thinkstock/Stockbyte

Yes, the season of colds and flu is coming. You’ve probably heard the old saying “feed a cold and starve a fever.” But is that sound advice? According to new evidence from mouse studies, there really may be a scientific basis for “feeding” diseases like colds and flu that are caused by viruses, as well as for “starving” certain fever-inducing conditions caused by bacteria.

In the latest work, an NIH-funded research team found that providing nutrition to mice infected with the influenza virus significantly improved their survival. In contrast, the exact opposite proved true in mice infected with Listeria, a fever-inducing bacterium. When researchers forced Listeria-infected mice to consume even a small amount of food, they all died.

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Progress Toward Stem Cell Treatment for Diabetes

patient-derived pancreatic beta cells

Caption: Insulin-containing pancreatic beta cells (green) derived from human stem cells. The red cells are producing another metabolic hormone, glucagon, that regulates blood glucose levels. Blue indicates cell nuclei.
Credit: The Salk Institute for Biological Studies, La Jolla, CA

In people with type 1 diabetes, the immune system kills off insulin-producing beta cells of the pancreas needed to control the amount of glucose in their bloodstream. As a result, they must monitor their blood glucose often and take replacement doses of insulin to keep it under control. Transplantation of donated pancreatic islets—tissue that contains beta cells—holds some promise as a therapy or even a cure for type 1 diabetes. However, such donor islets are in notoriously short supply [1]. Recent advances in stem cell research have raised hopes of one day generating an essentially unlimited supply of replacement beta cells perfectly matched to the patient to avoid transplant rejection.

A couple of years ago, researchers took a major step toward this goal by coaxing induced pluripotent stem cells (iPSCs), which are made from mature human cells, to differentiate into cells that closely resembled beta cells. But a few things were troublesome. The process was long and difficult, and the iPSC-derived cells were not quite as good at sensing glucose and secreting insulin as cells in a healthy person. They also looked and, in some ways, acted like beta cells, but were unable to mature fully in the lab. Now, an NIH-funded team has succeeded in finding an additional switch that enables iPSC-derived beta cells to mature and produce insulin in a dish—a significant step toward moving this work closer to the clinical applications that many diabetics have wanted.

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Obesity Research: Study Shows Significant Benefits of Modest Weight Loss

5% weight lossFor the one in three American adults who are obese, recommendations to lose substantial amounts of weight through a combination of diet and exercise can seem daunting and, at times, hopeless. But a new study should come as encouraging news for all those struggling to lose the extra pounds: even a modest goal of 5 percent weight loss delivers considerable health benefits.

In the NIH-funded study, people with obesity who lost just 5 percent of their body weight—about 12 pounds on average—showed improvements in several risk factors for type 2 diabetes and heart disease. They also showed metabolic improvements in many parts of the body, including the liver, pancreas, muscle, and fat tissue. While people who lost additional weight enjoyed further improvements in their health, the findings reported in the journal Cell Metabolism show that sometimes it really does pay to start small [1].

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