New research from the Division of Nutritional Sciences helps explain how fat tissue develops in mammals and could one day contribute to biomedical treatments for obesity and related diseases.

Daniel Berry, assistant professor in the division, studies the cellular and molecular mechanisms that govern the lineage of adipose cells, or how fat tissue develops from a fertilized embryo and how that path can change in response to diet and environmental conditions. 

Mammals have two types of fat tissue: white adipose tissue (WAT), which stores energy, and brown adipose tissue, which generates heat. To meet energy needs, the body generates new white adipocytes — or fat cells — from stem cell-like precursor cells. These precursor cells are defined when a mammal is still an embryo, but it is still unknown how they go on to produce new fat cells when that mammal is an adult. 

Berry’s previous research revealed that the adult cells can take one of two paths: form new adipocytes or maintain existing tissue. Now the most recent research from his lab, published in iScience, identifies an important step in defining that path. 

A protein called platelet-derived growth factor receptor beta (Pdgfrβ) acts as a molecular regulator and is critical for white adipose tissue homeostasis and maintenance. The absence of Pdgfrβ results in dysfunctional white adipose tissue growth and inflammation. 

“If we remove this controller, fat cell precursors become macrophages instead of adipocytes, promoting Type 2 diabetes and inflammation,” Berry says. “Thus, Pdgfrβ maintains a fat cell precursor state that is crucial for preserving healthy fat tissue.”

While healthy fat tissue helps the body with important functions like regulating hormones, controlling temperature and absorbing certain nutrients, dysfunctional fat tissue is associated with conditions like Type 2 diabetes, hypertension and cardiovascular disease. Berry says that understanding the mechanisms behind the formation of fat cells and the expansion of white adipose tissue may lead to more effective strategies for treating obesity and metabolic diseases.

“How new fat cells form is a very important question,” Berry said. “We need to identify how the body forms healthy fat tissue and how we can protect fat from becoming dysfunctional in response to unhealthy diets.” 

The paper’s lead author is Abigail Benvie, a graduate student in the field of molecular nutrition, with co-authors Derek Lee ’21, M.S. ’23; Yuwei Jiang, an assistant professor in physiology and biophysics at the University of Illinois at Chicago; and Berry. The research was funded by a grant from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). 

Future studies in Berry’s lab aim to define the embryonic fat cell lineage and how we can use pharmacological approaches to control fat cell number and function.