A discovery into how fat cells work alongside the liver could have research implications for several diseases, including diabetes and cancer.
Scientists at UT Southwestern Medical Center report that fat cells help the liver to maintain blood sugar control, claiming they “have the liver’s back”.
These fat cells maintain tight regulation of a metabolite called uridine, which has many roles in the body, including storing glucose.
When the body is fasting, the fat cells take over from the liver in producing uridine. These findings were replicated in huma, mouse and rat studies.
The importance of uridine in the body and its relationship with fat cells could signal new research opportunities for understanding glucose regulation in diabetes, the researchers said.
Senior author Dr Phillip Scherer explained: “Like glucose, every cell in the body needs uridine to stay alive. Glucose is needed for energy, particularly in the brain’s neurons. Uridine is a basic building block for a lot of things inside the cell.
“We found that the liver serves as the primary producer of this metabolite only in the fed state. In the fasted state, the body’s fat cells take over the production of uridine.”
Levels of blood uridine were shown to increase during fasting and lower during feeding, with excess uridine released through bile.
“It turns out that having uridine in your gut helps you absorb glucose; therefore uridine helps in glucose regulatio,” said Scherer.
This fasting-induced rise in uridine was also linked to reduced body temperature due to disruption of the metabolism.
When the researchers tested the effects of a high-fat diet in dietary studies, body temperature was prevented from lowering, an effect also associated with obesity.
The study team later discovered that these findings were because of decreased uridine levels in response to fasting.
“Our studies reveal a direct link between temperature regulation and metabolism, indicating that a uridine-centred model of energy balance may pave the way for future studies on uridine balance and how this process is dysregulated in the diabetic state,” concluded Scherer.
The study has been published in the journal Science.

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