Good news!
"Researchers led by scientists at Baylor College of Medicine (BCM) have unraveled just how an exercise-induced signaling metabolite, N-lactoyl-phenylalanine (Lac-Phe), travels a unique pathway to the brain and impacts the activity of one, and then two different neurons. It triggers a chain of events that ultimately suppresses appetite ..."
"... The researchers previously discovered that Lac-Phe is the most increased metabolite – a product of the body’s metabolism – in blood after intense exercise, not just in mice but also in humans and racehorses. The team’s previous work showed that giving Lac-Phe to obese mice reduced how much they ate and helped them lose weight without negative side effects. But until now, scientists didn’t fully understand how Lac-Phe works to suppress appetite. ...
The researchers studied two types of brain cells in mice. One type was AgRP neurons, which stimulate hunger and are in the arcuate nucleus of the hypothalamus. The other type was PVH neurons in the paraventricular nucleus of the hypothalamus. These neurons help suppress hunger.
AgRP and PVH neurons work together. Normally, AgRP neurons send signals that inhibit PVH neurons, making you feel hungry. But when AgRP neurons are turned off, PVH neurons become more active, reducing appetite.
He lab members and colleagues discovered that Lac-Phe directly inhibits AgRP neurons, which in turn activates PVH neurons. This chain of events resulted in mice eating less. The animals’ behavior remained normal, suggesting that Lac-Phe doesn’t cause unpleasant side effects. ..."
From the abstract:
"N-Lactoyl-phenylalanine (Lac-Phe) is a lactate-derived circulating metabolite that reduces feeding and obesity, but the molecular mechanisms that underlie the metabolic benefits of Lac-Phe remain unknown.
Here we show that Lac-Phe directly inhibits hypothalamic neurons that express Agouti-related protein (AgRP), resulting in an indirect activation of anorexigenic neurons in the paraventricular nucleus of the hypothalamus (PVH).
Both AgRP inhibition and PVH activation are required to mediate Lac-Phe-induced hypophagia.
Lac-Phe-mediated inhibition of AgRP neurons occurs through activation of the ATP-sensitive potassium (KATP) channel, whereas inhibition of the KATP channel blunts the effects of Lac-Phe to suppress feeding.
Together, these results reveal the molecular and neurobiological mechanisms by which Lac-Phe mediates metabolic improvements and suggest this exercise-induced metabolite might have therapeutic benefits in various human diseases."
New study sheds light on how exercise helps lose weight (original news release)
Lac-Phe induces hypophagia by inhibiting AgRP neurons in mice (no public access)
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