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Selective serotonin reuptake inhibitors (SSRIs) are currently widely used antidepressants, which produce antidepressant effects by selectively inhibiting the reuptake of 5-HT
.
Previous studies have shown that the central nervous system serotonin signal has the effect of inhibiting eating, and there is a weight loss in patients with depression a few months before SSRIs treatment
.
However, more and more clinical studies have shown that long-term use of SSRIs (greater than 1 year) is associated with weight gain
.
This contradictory result is considered to be the third major side effect of SSRIs
.
On October 21, 2021, the Patricia Ducy research team of Columbia University revealed that the side effects of long-term use of SSRIs to cause weight gain depend on serotonin signaling, and further discovered that Mc4r agonists can improve this side effect
.
Mouse weight gain after oral fluoxetine.
Researchers found that normal mice daily oral fluoxetine for 6 weeks and 12 weeks promoted diet, increased body weight, and white adipose tissue content also increased, but it did not affect the energy consumption and exercise of the mice.
Ability
.
In fact, on the 5th day after oral fluoxetine, the mice's food intake began to increase significantly during the nocturnal activities, and the weight also increased
.
Transparent brain technology reveals neuronal activity in the whole brain.
Further transparent brain technology realizes c-FOS activation labeling.
It was found that the dorsal raphe nucleus (DRN), arcuate nucleus (ARC) and the paraventricular nucleus of the hypothalamus after acute oral fluoxetine (PVN) and other key brain areas that regulate food intake decrease in activity
.
In more detail, the activity of pro-amelanocortin (POMC, which drives satiety) neurons in the ARC brain area decreases, and the α-melanocyte-stimulating hormone (α-MSH) neurons that drive satiety in the PVN brain area Activity is also reduced
.
After the activity of the neurons that promote satiety in the brain decreases, the mice continue to eat
.
Immunofluorescence experiments show that fluoxetine can quickly inhibit serotonergic neurons in the DRN brain area
.
Short-term oral fluoxetine in mice after knocking out Tph2 (the gene encoding the serotonin rate-limiting enzyme) or knocking out the serotonin transporter SERT did not cause pro-amelanocortin neurons in the ARC brain area and PVN brain area α -MSH neuron activity is reduced, and body weight will not increase
.
Previous studies have shown that pro-amelanocortin neurons in the ARC brain area inhibit food intake through the serotonin receptor Htr2c, and neurons in the DRN brain area express the autoreceptor of the inhibitory serotonin receptor Htr1a
.
Researchers use pharmacological means to inhibit Htr1a or activate Htr2c to block the weight gain caused by fluoxetine
.
These results indicate that the effect of short-term fluoxetine in promoting diet depends on serotonin signaling
.
In addition, long-term oral fluoxetine (6 weeks) significantly reduced the level of α-MSH in the PVN brain area, but activation of Htr2c did not prevent the weight gain caused by fluoxetine
.
α-MSH suppresses hunger through the melanocortin 4 receptor (Mc4r) expressed on PVN neurons
.
They exogenously administered lipocalin-2 (Lipocalin-2, which directly generates anorexia hormone signal through Mc4r in the hypothalamus), but it can prevent the weight gain caused by chronic fluoxetine
.
In general, this article found that fluoxetine causes weight gain through two different mechanisms: short-term fluoxetine administration causes Htr1a to autologously inhibit DRN serotonergic neurons, and reduces the activity of POMC neurons in the ARC brain area, and promotes food intake
.
Long-term use of fluoxetine reduces the expression of Htr2c in the ARC brain area, reduces the level of α-MSH, and promotes feeding behavior
.
[References] https://doi.
org/10.
1172/JCI151976 The pictures in the article are from the references
Selective serotonin reuptake inhibitors (SSRIs) are currently widely used antidepressants, which produce antidepressant effects by selectively inhibiting the reuptake of 5-HT
.
Previous studies have shown that the central nervous system serotonin signal has the effect of inhibiting eating, and there is a weight loss in patients with depression a few months before SSRIs treatment
.
However, more and more clinical studies have shown that long-term use of SSRIs (greater than 1 year) is associated with weight gain
.
This contradictory result is considered to be the third major side effect of SSRIs
.
On October 21, 2021, the Patricia Ducy research team of Columbia University revealed that the side effects of long-term use of SSRIs to cause weight gain depend on serotonin signaling, and further discovered that Mc4r agonists can improve this side effect
.
Mouse weight gain after oral fluoxetine.
Researchers found that normal mice daily oral fluoxetine for 6 weeks and 12 weeks promoted diet, increased body weight, and white adipose tissue content also increased, but it did not affect the energy consumption and exercise of the mice.
Ability
.
In fact, on the 5th day after oral fluoxetine, the mice's food intake began to increase significantly during the nocturnal activities, and the weight also increased
.
Transparent brain technology reveals neuronal activity in the whole brain.
Further transparent brain technology realizes c-FOS activation labeling.
It was found that the dorsal raphe nucleus (DRN), arcuate nucleus (ARC) and the paraventricular nucleus of the hypothalamus after acute oral fluoxetine (PVN) and other key brain areas that regulate food intake decrease in activity
.
In more detail, the activity of pro-amelanocortin (POMC, which drives satiety) neurons in the ARC brain area decreases, and the α-melanocyte-stimulating hormone (α-MSH) neurons that drive satiety in the PVN brain area Activity is also reduced
.
After the activity of the neurons that promote satiety in the brain decreases, the mice continue to eat
.
Immunofluorescence experiments show that fluoxetine can quickly inhibit serotonergic neurons in the DRN brain area
.
Short-term oral fluoxetine in mice after knocking out Tph2 (the gene encoding the serotonin rate-limiting enzyme) or knocking out the serotonin transporter SERT did not cause pro-amelanocortin neurons in the ARC brain area and PVN brain area α -MSH neuron activity is reduced, and body weight will not increase
.
Previous studies have shown that pro-amelanocortin neurons in the ARC brain area inhibit food intake through the serotonin receptor Htr2c, and neurons in the DRN brain area express the autoreceptor of the inhibitory serotonin receptor Htr1a
.
Researchers use pharmacological means to inhibit Htr1a or activate Htr2c to block the weight gain caused by fluoxetine
.
These results indicate that the effect of short-term fluoxetine in promoting diet depends on serotonin signaling
.
In addition, long-term oral fluoxetine (6 weeks) significantly reduced the level of α-MSH in the PVN brain area, but activation of Htr2c did not prevent the weight gain caused by fluoxetine
.
α-MSH suppresses hunger through the melanocortin 4 receptor (Mc4r) expressed on PVN neurons
.
They exogenously administered lipocalin-2 (Lipocalin-2, which directly generates anorexia hormone signal through Mc4r in the hypothalamus), but it can prevent the weight gain caused by chronic fluoxetine
.
In general, this article found that fluoxetine causes weight gain through two different mechanisms: short-term fluoxetine administration causes Htr1a to autologously inhibit DRN serotonergic neurons, and reduces the activity of POMC neurons in the ARC brain area, and promotes food intake
.
Long-term use of fluoxetine reduces the expression of Htr2c in the ARC brain area, reduces the level of α-MSH, and promotes feeding behavior
.
[References] https://doi.
org/10.
1172/JCI151976 The pictures in the article are from the references
