The Fat Flip

Mystery behind fat storage mechanism revealed

Today we’re talking about two types of fat cells:  brown fat and white fat.  White fat cells store energy and contribute to weight gain, while brown fat expends energy and promotes weight loss.   Understanding what triggers white fat to go brown and back again could provide great insights into how to treat obesity, a major risk factor for heart disease, diabetes and cancer.   Experimental research published in Cell Metabolism investigated how the process of energy expenditure and storage works in both obese and normal weight mice. 

Researchers focused on the brain, specifically a hypothalamic protein and insulin receptor called TCPTP, observing the effects of limiting or reducing TCPTP during meals.  At its most basic level, after meals, concentrations of both insulin and glucose increase in the blood, signaling the browning of fat increasing energy expenditure, while when insulin concentration in the blood is low, white fat is signaled for energy storage.  Lead researcher, Professor Tony Tiganis, explains that in the context of obesity, the switch stays on all the time and doesn’t turn off after feeding repressing the conversion of white fat to brown, leading to energy conservation. 

As a result of this study, there is a better understanding of the key role TCPTP plays in this process.  Investigators were able to see that removing TCPTP in obese subjects turned on browning of fat after feeding to promote weight loss.  They even saw that when TCPTP was completely withheld, obesity was avoided, even with overfeeding.  There is excitement around these results because for the first time the mechanism behind the switch from brown fat to white fat and brown again has been revealed.      

While we continue to understand how this “switch” works in humans, there’s no quick fix to shed pounds.  The best recommendation to achieve a healthy weight is to stay active and eat a balanced diet rich in fruit and vegetables, which may reduce your risk for obesity and chronic disease.    

Published October 1, 2017