Tyler Shendruk | Fulcrum Staff
YOU EAT TOO much.
But so does everybody else. In North America and in many other places around the world, the majority of people take in more nutrients than is healthy. We all know that obesity and type-2 diabetes are nearly epidemic in Canada and the United States but our ample aliments lead to an abundance of ailments.
The researcher
In fact, according to the chairman of the Department of Biochemistry, Microbiology, and Immunology, Zemin Yao, non-alcoholic fatty liver disease is more prevalent than both obesity or diabetes. However, unlike obesity and diabetes, most affected people have few perceivable symptoms. The liver swells to a huge size, but this isn’t necessarily easy to see in a doctor’s office. It’s a nearly invisible disease, but that doesn’t mean it doesn’t impact millions of people’s health. Yao studies how the metabolism of lipids (tiny particles of fat), cholesterol, and the proteins associated with them are connected to non-alcoholic fatty liver disease.
The project
Your liver produces the proteins and chemicals used to breakdown and digest the food you eat. One important type of protein that it produces is called a lipoprotein. Since oily fat molecules don’t like to travel through the wet bloodstream to the cells that need these molecules, lipoproteins disguise the oily fat molecules and then carry the lipids through the bloodstream to their destination.
If lipoproteins aren’t formed, then fatty molecules from your food don’t leave the liver. This impairs the creation of fat tissue and can affect cholesterol levels, resulting in a need for statins, the most profitable drug in history. But the nutrients don’t just disappear; they stay in the liver. Over extended times, people with impaired lipoprotein production look skinny, but are in truth sick with fat in the liver, kidney, or heart.
The key
Yao knew that certain lab mice have a genetic disease that stops them from making fat-storage cells and he used this fact to track down the key to creating these lipoproteins. These mice were missing the gene for a protein called lipin. Lipin regulates the creation of lipoproteins that carry the fatty molecules through the blood by stopping and starting the transcription of metabolism genes. Yao found that lipin also transforms incoming fatty molecules into storage molecules that other proteins can carry. By doing both jobs in mice, lipin acts as the bridge between genetic control of metabolism and the biochemical transformation of fatty molecules.
Human beings have more than one form of lipin proteins, and so the situation is bound to be more complicated, but Yao sees lipin as the linchpin in understanding why fatty molecules might get stuck in the liver and cause fatty liver disease.
