Impact Stories

What was your journey toward your current area of study?  

With a background in nutritional science, my research focuses on the intersection of gut health and dietary behavior. Despite evidence-based knowledge of metabolic health, navigating the modern food environment remains a significant behavioral challenge. Understanding that cravings for foods like pizza and burgers activate the brain’s dopamine reward pathway and taste so good, it is not easy to say no to them. We understand that this is human nature. 

These areas of interest led me to working with two mentors: Dr. Patrick Tso, a distinguished expert in lipid metabolism at UC, and Dr. Steven Woods, a distinguished professor in the field of psychiatry and the neuroscience of obesity, also at UC. This work propelled me to start studying the gut and the brain circuits.  

When I began working with Dr. Tso, who was my former postdoc mentor, he asked me a simple question: How does the body make two apolipoprotein B proteins — B-48 in the small intestine and B-100 in the liver? That is when I started my journey with apolipoproteins.  

What is your primary research focus? 

In my lab, we are focused on the apolipoprotein mechanisms that are at work during lipid metabolism. If we do not have a balanced diet, we know lipids or glucose induce obesity and metabolic disorders like type 2 diabetes, cardiovascular disease and inflammatory bowel disease emerge.  

I am studying the apolipoprotein A4 (APOA4) protein, alongside a neuropeptide called cholecystokinin, or CCK. Both are well-recognized gut-derived peptides involved in satiety (suppressing food intake) – and secreted by the gut in response to dietary fat intake. Since I began my postdoc work at UC, this research has been supported by the American Heart Association and the National Institutes of Health, and I have been able to continue it in my own lab at Ohio University.  

You were part of a research team that published a study in Obesity examining how APOA4 could play a part in combatting weight gain. Why were those findings significant? 

We found that APOA4 has short-term effects on satiation, which confirms findings in the literature. But we also found that introducing APOA4 into mice eating a high-fat diet resulted in no additional body weight gain — and increased whole-body energy expenditure without making any changes to their diet or activity levels. This was an important finding. After we published our findings, another research group in Denmark confirmed our data.  

Many physicians and patients will be familiar with GLP-1 agonist medications. How does APOA4 differ from GLP-1? 

This is a question we are still exploring. Both APOA4 and GLP-1 are naturally secreted by the gut, though in distinct parts of it, and they have similar physiological functions. GLP-1 can inhibit food intake, stimulate insulin secretion and increase insulin sensitivity. APOA4 has a similar function, but as a short-term food intake suppressor. If you consider the therapeutic potential, introducing exogenous APOA4 results in whole-body energy expenditure without altering food intake and physical activity, which contrasts with the diet and exercise regimens that must be used with GLP-1 agonists to combat nutrient deficiency-related side effects. We are studying this and creating data to better explain the difference between them.  

How has funding from the Osteopathic Heritage Foundation helped further your research? 

I very much appreciate the Foundation for providing me with this support. It has helped me focus on several areas of additional inquiry into APOA4, including further research into how APOA4 might be used to treat fatty livers, regulate insulin action and potentially reduce inflammatory bowel disease. The support from the Foundation has enabled my lab to obtain preliminary data in several of these areas and pursue additional funding. 

In addition, the Foundation’s support has enabled me to engage student scientists in my work, and this is especially important to me. I am currently working with an osteopathic medical student in my lab and am able to provide a stipend for their research assistance. I am also exploring accepting additional students to assist in the lab, one of whom is preparing her application for the Heritage College. In this way, the Foundation is helping me support the development of future researchers. I love research and I always encourage my students to consider becoming researchers, too, and to help solve complex issues to better help people who need obesity care.  

You collaborate with a broad team of researchers, many of whom are also affiliated with osteopathic institutions. How has the osteopathic philosophy influenced your research? 

I greatly appreciate the osteopathic philosophy and its holistic approach to patient care because we understand the body’s entire system is interdependent – every part interacts with others. Because of my affiliation with the Heritage College and the Diabetes Institute, I can collaborate with colleagues and together, we can learn more about one another’s research and explore new areas of discovery. For instance, these collaborations allow us to look at the effects of APOA4 on various tissue, like liver tissue, adipose tissue, skeletal muscles, as well as processes like energy homeostasis. The osteopathic philosophy helps us understand these systems are all interdependent and I am fortunate to extend this philosophy into my research. 

Where is your research heading next? 

Receptors are important for future drug development. In 2021, low density lipoprotein receptor-related protein 1 (LRP1) was identified as a novel APOA4 receptor that mediates glucose uptake in adipose tissue.  Our first area of focus is the liver, to see how APOA4 interacts with its receptors. We already have preliminary data showing that APOA4 can increase the LRP1 receptor in the liver and we want to understand how APOA4 works with LRP1 to regulate lipid metabolism and potentially reduce fat in the liver.  

The second area we are concentrating on is how APOA4 interacts with the LRP1 receptor to regulate insulin action. Obese people have hyperinsulinemia, or high insulin levels. This is why they become insulin resistant. The liver and kidney are key organs for clearing insulin from circulation, and based on our project, we already know that APOA4 supplementation could reduce glucose-induced circulating insulin levels in obese mice. So, is that possible because the APOA4 also increases insulin clearance? This is what we are investigating.  

I also want to work more closely with my colleagues and explore the possibility that APOA4 could reduce inflammatory bowel diseases. We already have preliminary data showing that APOA4 can reduce aging-mediated obesity. We are preparing the manuscript and hope to publish these findings soon.