October often captures the American heart as a time of the year when the landscape takes on a warm autumn glow and children put on their favorite costumes, going door to door looking for candy. However, few realize that October is also recognized as Liver Awareness Month, which highlights many debilitating disorders, including fatty liver disease.
Fatty liver disease, also known as metabolic dysfunction-associated steatotic liver disease (MASLD), affects between 20% to 30% of the national adult population. Over the past 20 years, MASLD has nearly doubled in cases, becoming the most common liver disease in adolescents. When left untreated, MASLD can cause chronic liver injury, leading to scarring and ultimately, liver failure. Caleb Beimfohr, second-year PhD student, is dedicated to fighting fatty liver disease by examining the causes of obesity, which is considered the number one risk factor for the disease.
Beimfohr, who once planned to attend medical school, found his calling in lab research after taking a post-bachelor internship at Eli Lilly Research Labs for Diabetes, Obesity and Complications Therapeutic Area. From there, Beimfohr began his PhD journey at the IU School of Medicine's Department of Pharmacology and Toxicology, focusing on metabolism and weight loss research.
“Millions upon millions of people have obesity, and losing weight is incredibly difficult, especially when the odds are stacked against you with a Western diet,” Beimfohr said. “The end goal would be to create the perfect weight loss pill. Obviously, people need to be educated in what they are eating, but in situations where the system has failed, we could help them live longer, because excess weight is extremely detrimental to one’s health.”
Because obesity is often tied to fatty liver disease, Beimfohr recognized the need to protect the liver from excess fat accumulation and to develop a more effective way for the body to break down existing fat stores.
In the spring of 2025, Beimfohr began working with Brian DeBosch, MD, PhD, a professor of pediatrics at the IU School of Medicine and program leader of the Nutrition and Molecular Metabolism Research Program at the Herman B Wells Center for Pediatric Research. Beimfohr’s research supported DeBosch’s laboratory studies, which found that a form of sugar called trehalose induces liver fasting mechanisms by blocking sugar transporters and stimulating the production activation of fasting-induced genes. If this process went unbothered, the body would never be able to gain excess stores of fat. However, the body produces an enzyme (trehalase) that breaks down our dietary trehalose. Beimfohr hypothesized that if he could prevent the enzyme trehalase from breaking down the sugar trehalose, it might enable the body to enter into a controlled, fasting-like state.
In his latest study, presented at the 2025 Wells Center Retreat, Beimfohr used a compound similar to trehalose (6-Azide-Trehalose) to maximize liver fasting activation while resisting degradation by the enzyme trehalase. Before placing his lab mouse on a high carbohydrate diet for five days, Beimfohr administered 6-Azide-Trehalose for two days. The treatment successfully protected the mouse from both fat mass and liver mass gain.
“In just under five months as a part of my laboratory, Caleb has already done outstanding work toward understanding the role that glucose metabolism plays in the development of diabetes, obesity and fatty liver disease,” DeBosch said. “To augment his recent research impact, we are now doing mechanistic studies examining the degree to which urea cycle regulation by this novel compound mediates the overall therapeutic effect of 6-Azide-Trehalose on body weight, liver fat and pre-diabetes.”
When asked where he sees himself in 30 years, Beimfohr said that he sees himself having published many papers, leading his own lab and having one or two successful drugs attributed to his research.
