NEW HAVEN, Conn.—High levels of free radicals have been found to increase satiety and help reduce diet-induced obesity, according to a new study published in the journal Nature Medicine.
Researchers at Yale School of Medicine conducted a study of brain circuits that control hunger and satiety in mice. After the mice ate, the team saw that the neurons responsible for stopping overeating had high levels of free radicals. The process is driven by the hormone leptin and glucose, which signal the brain to modulate food intake. When mice ate, leptin and glucose levels and free radical levels increased. However, in mice with diet-induced obesity, the same neurons displayed impaired firing and activity (leptin resistance); in these mice, levels of free radicals were buffered by peroxisomes, preventing the activation of these neurons and thus the ability to feel sated after eating.
They concluded elevating free radical levels in the hypothalamus directly or indirectly suppresses appetite in obese mice by activating satiety-promoting melanocortin neurons. Free radicals, however, are also thought to drive the aging process.
"It's a catch-22," the researchers said. “On one hand, you must have these critical signaling molecules to stop eating. On the other hand, if exposed to them chronically, free radicals damage cells and promote aging."
According to the researchers, the crucial role of free radicals in promoting satiety as well as degenerative processes associated with aging may explain why it has been difficult to develop successful therapeutic strategies for obesity without major side effects.
