Dr. Barrow, a recent hire in the College of Human Ecology at Cornell, received an exploratory R21 grant ($566,000 over three years) from the National Institutes of Health in 2019. Her research focuses on human metabolism, metabolic disease, and obesity.

Dr. Barrow received her undergraduate and graduate degrees from the University of Florida and was a postdoctoral fellow at the Dana-Farber Cancer Institute/Harvard Medical School. She joined the faculty at Cornell in 2018.

Adipose tissue (commonly called fat) is made up of two types of cells: white adipose and brown/beige adipose. White adipose cells store energy in a fat droplet, and release that energy in response to insulin. Brown adipose cells are a lot less common throughout the body - they contain a large number of mitochondria and are able to produce heat and prevent hypothermia. Hibernating mammals and newborn babies have a lot of brown adipose, but for a long time it was thought that almost all of it goes away by the time you’re an adult.

In most cells, mitochondria produce energy in the form of ATP, by creating an imbalance (gradient) of protons across a membrane. This gradient is energetically unfavorable, which means that the protons need to flow back across the membrane to even things out. By controlling the flow of protons back in, the mitochondria can harness that energy to make ATP.

But there is a protein called UCP1 that is only found in brown adipose cells, which creates lots of new openings in the mitochondrial membrane, allowing a much larger, less controlled flow of protons back across the membrane. This produces a lot of energy, but because it isn’t channeled into making ATP, it gets released as heat.

In her R21, Dr. Barrow proposes to study a protein called Nipsnap1, which she thinks helps control UCP1’s function. Her exploratory grant provides fundin for her to focus on trying to understand what Nipsnap1 does and how.