Overweight and obesity are associated with many health problems—type 2 diabetes, heart disease, hypertension, cancer, and more. But why? The short answer is that fat tissue (specifically white adipose tissue) is not just a storage depot for excess energy; it also functions as an endocrine organ, secreting factors into the bloodstream. As adipose tissue expands, secretion of these factors—many of which promote inflammation—increases and largely drives the negative health consequences of obesity.
This explanation, however, oversimplifies the situation. In addition to white adipose tissue, which is generally harmful to health, there is brown fat, which is beneficial and counteracts many of the adverse effects of white fat. Brown fat is abundant in infants but rare in adults, where it helps burn calories to generate heat, boosting metabolism—especially in cold conditions. It also improves blood sugar and lipid control, potentially lowering the risk of metabolic disease.
In this study, researchers at Rockefeller University genetically depleted brown fat in mice and found that the animals subsequently developed hypertension. What is the molecular mechanism underlying this effect? Could drugs be developed to activate or expand brown fat? Do any existing blood pressure medications act through this pathway? What genetic programs control the balance between white and brown fat, and can this balance be shifted pharmacologically? Could such an approach help address the obesity epidemic?
