IRP Discoveries

Intermittent Fasting Boosts Endurance in Mouse Marathoners

runner tying his shoe

Food companies have long marketed carbohydrate-rich drinks and energy bars to athletes with the message that the energy those snacks provide is key to lifting heavier and running farther. A new mouse study by IRP researchers, however, suggests that skipping a meal (or several) might be far more effective for increasing athletic prowess1.

Unlike modern Americans used to three square meals a day, our ancient ancestors couldn’t exactly throw a TV dinner in the microwave whenever they felt a bit peckish. As a result, they probably found themselves hunting wooly mammoths and fending off saber-toothed tigers on an empty stomach.

“From an evolutionary perspective, animals in the wild – particularly predators – need to be able to function at a high level when they’re in a food-deprived state,” says IRP Senior Investigator Mark P. Mattson, Ph.D., the study’s senior author. “Individuals who were able to perform at a high level in a fasted state had a survival advantage.”

HIV Uses Host's Own Immune Molecules for Protection

an HIV-infected T cell

In one of Aesop’s classic fables, a clever wolf dons a sheep’s skin in order to move through the herd undetected. As it turns out, IRP researchers have discovered that in people with a specific set of immune system genes, the HIV virus uses a similar approach to hide from the body’s defenses.1

Nearly all cells in our bodies are coated with proteins called human leukocyte antigens (HLAs). These proteins allow the immune system to distinguish between healthy, native cells and those contaminated by unwelcome visitors like viruses or bacteria that must be destroyed. Each of the various HLA proteins is encoded by a different HLA gene and these genes vary considerably between individuals, causing different people to have different variants of each HLA protein.

“There are thousands of different forms of these HLA genes, and that variation allows us, as a species, to deal with virtually all infectious pathogens,” says IRP Senior Investigator Mary N. Carrington, Ph.D., the senior author of the new paper. “We’re really interested in the diversity of that part of the genome, since the risk of essentially every autoimmune disease, many cancers, and probably every infectious disease is associated with this set of genes.”

Gut Bugs May Convert High-Fat Fare into Cancer Risk

cartoon image of the gut microbiome showing microbes in the digestive tract

Researchers have a long history of fattening up mice to gain insight into the causes and consequences of weight gain in the human body. In one of the more recent studies of this kind, a team of IRP researchers found that that a high-fat diet consistently altered the collection of microbes residing in mice’s digestive tracts and that this diet-microbe combination might pre-dispose the mice – and, potentially, obese humans – to colon cancer by triggering certain changes in how genes behave.

Ebola Virus: Lessons from a Unique Survivor

Reblogged from The NIH Director's Blog.

Ebola virus (green) is shown on cell surface

There are new reports of an outbreak of Ebola virus disease in the Democratic Republic of Congo. This news comes just two years after international control efforts eventually contained an Ebola outbreak in West Africa, though before control was achieved, more than 11,000 people died—the largest known Ebola outbreak in human history. Many questions remain about why some people die from Ebola and others survive. Now, some answers are beginning to emerge thanks to a new detailed analysis of the immune responses of a unique Ebola survivor, a 34-year-old American health-care worker who was critically ill and cared for at the NIH Special Clinical Studies Unit in 2015.

Muscle Enzyme Explains Weight Gain in Middle Age

Reblogged from The NIH Director’s Blog.

using a weight scale

The struggle to maintain a healthy weight is a lifelong challenge for many of us. In fact, the average American packs on an extra 30 pounds from early adulthood to age 50. What’s responsible for this tendency toward middle-age spread? For most of us, too many calories and too little exercise definitely play a role. But now comes word that another reason may lie in a strong—and previously unknown—biochemical mechanism related to the normal aging process.

Little Fish in a Big Pond Reveal New Answers to Old Questions

Reblogged from The NICHD Connection.

Dr. Eric Horstick in the lab

Studying the neural control of behavior is a challenge. Researchers must consider an animal’s environment, past experiences, and motivations. Work in relatively simple organisms, for example the invertebrate C. elegans, has teased apart the neural circuitry of highly stereotyped behaviors, like foraging. But in mammals, very little is known, “and that’s surprising given just how important behaviors like this are,” said Dr. Eric Horstick, who studies the molecular mechanisms underlying animal behavior.

Cool Videos: Looking Inside Living Cells

Reblogged via the NIH Director's Blog.

ASCB Celldance 2016 — “Discovery Inside Living Cells in Multicellular Organisms” Roberto Weigert

Roberto Weigert is a cell biologist who specializes in intravital microscopy (IVM), an extremely high-resolution imaging tool that traces its origins to the 19th century. What’s unique about IVM is its phenomenal resolution can be used in living animals, allowing researchers to watch biological processes unfold in organs under real physiological conditions and in real time.

Find and Replace: DNA Editing Tool Shows Gene Therapy Promise

Reblogged from the NIH Director’s Blog.

This image represents an infection-fighting cell called a neutrophil. In this artist’s rendering, the DNA of a cell is being “edited” with a pen-like tool to help restore its ability to fight bacterial invaders.

For gene therapy research, the perennial challenge has been devising a reliable way to insert safely a working copy of a gene into relevant cells that can take over for a faulty one. But with the recent discovery of powerful gene editing tools, the landscape of opportunity is starting to change. Instead of threading the needle through the cell membrane with a bulky gene, researchers are starting to design ways to apply these tools in the nucleus—to edit out the disease-causing error in a gene and allow it to work correctly.

Simplifying HIV Treatment: A Surprising New Lead

Reblogged from the NIH Director's Blog.

CD4 cells in colon, SIV

The surprising results of an animal study are raising hopes for a far simpler treatment regimen for people infected with the AIDS-causing human immunodeficiency virus (HIV). Currently, HIV-infected individuals can live a near normal life span if, every day, they take a complex combination of drugs called antiretroviral therapy (ART). The bad news is if they stop ART, the small amounts of HIV that still lurk in their bodies can bounce back and infect key immune cells, called CD4 T cells, resulting in life-threatening suppression of their immune systems.