This week we profile a recent publication in Cell Metabolism from
Dr. Evan Rosen’s (pictured) lab at the Beth Israel Deaconess Medical Center.
Can you provide a brief overview of your lab’s current research focus?
We are focused on understanding how adipose tissue functions normally, and how adipose dysfunction leads to metabolic diseases like obesity and Type 2 diabetes. We use state-of-the-art genetic and genomic technologies to identify and characterize the molecules that enable adipocytes to develop normally and to respond to nutritional, inflammatory, and thermal stress.
What is the significance of the findings in this publication?
The lymphatic system has long been assumed to play a passive role in physiology, draining fluid and immune cells away from tissues and returning them to the circulation. Contrary to this notion, there are longstanding data that suggest a much more active role of the lymphatic system in adipose tissue. Thus, defects in lymphatic development lead to obesity, and conversely, obesity causes lymphatic dysfunction. To date, no one has demonstrated how local lymphatic vessels communicate with adipocytes within the fat pad. We show in this paper that cells of the lymphatic system secrete a hormone called neurotensin (NTS), which inhibits thermogenesis in brown fat. Cold exposure increases brown fat heat production in part by shutting off NTS production and release from lymphatics.
What are the next steps for this research?
We believe that this story represents the tip of the iceberg in adipocyte-lymphatic cross-talk. We are now working to identify additional factors that are produced by lymphatics that affect fat function, and vice versa.
Funding Sources:
We are supported by the NIH.
