Serotonin Causes Obesity, Diabetes, Fibrosis,liver Damage ,increases Endotoxin And NO


Feb 26, 2018
Inspired by this thread Serotonin/endotoxin/PUFA As Primary Causes Of Depression And Diabetes; Can Be Easily Blocked
I was reading a few more recent studies on the detrimental effect of serotonin on ones health. It seems clear that by now it is known in medicine, that blocking it is highly therapeutic for many diseases.
Here we go:

Genetic deletion of mast cell serotonin synthesis prevents the development of obesity and insulin resistance. - PubMed - NCBI
In line with haiduts post ,when mice are lacking TPH , the enzyme that converts tryptophan to serotonin , it prevents obesity and insulin resistance .
And it also increases uncoupling (UCP1), which is highly therapeutic of it's own.

"These data suggest that therapies aimed at inhibiting mast cell Tph1 may represent a therapeutic approach for the treatment of obesity and type 2 diabetes."

Modulation of the Tryptophan Hydroxylase 1/Monoamine Oxidase-A/5-Hydroxytryptamine/5-Hydroxytryptamine Receptor 2A/2B/2C Axis Regulates Biliary Pro... - PubMed - NCBI
This is is another of the serotonin "modulation" studies which is the new word for antagonism. This a very recent study, so it really seems like it might be that we will read the term serotonin modulation more often than the term serotonin antagonism ,which they ironically do use in the actual study but not the in the headline.

"...treatment of these cell lines with 5HTR2A/2B/2C antagonists or TPH1 inhibitor decreased 5HT levels as well as expression of fibrosis and inflammation genes compared to controls."

The Role of Serotonin in Concanavalin A-Induced Liver Injury in Mice. - PubMed - NCBI

This is a great one as it shows serotonin as the fundamental initiator of disease/ stress hormones:It increases liver enzymes, induces cell death in liver cells ,increases NO and activates the TLR4 Receptor.
Ketanserine was actually therapeutic of that liver damage.

Serotonin is involved in the pathological processes of several liver diseases via the regulation of inflammatory response and oxidative stress. We aimed to investigate the role of serotonin in Concanavalin A- (Con A-) induced acute liver injury (ALI). ALI was induced in C57B/6 wild-type (WT) mice and tryptophan hydroxylase 1 (TPH1) knockout mice through tail vein injection of Con A (15 mg/kg body weight). Another group of TPH1 knockout ALI mice was supplied with 5-hydroxytryptophan (5-HTP) in advance to recover serotonin. The blood and liver tissues of mice were collected in all groups. Markedly increased serum levels of serotonin were identified after the injection of Con A. Increased serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and stronger hepatic tissue pathology were detected, suggesting that serotonin could mediate Con A-induced liver damage. Serotonin significantly facilitated the release of serum and intrahepatic inflammatory cytokines, including interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-17A (IL-17A), interferon-gamma (IFN-γ), and tumor necrosis-alpha (TNF-α), after the administration of Con A. In addition, serotonin significantly increased the intrahepatic levels of oxidative stress markers malonaldehyde (MDA), myeloperoxidase (MPO), and nitric oxide (NO) and decreased antioxidant stress indicator glutathione (GSH) in Con A-treated mice. Additionally, serotonin promoted hepatocyte apoptosis and autophagy based on B-cell lymphoma-2 (Bcl-2), Bcl-2-asociated X protein (Bax), and Beclin-1 levels and TUNEL staining. More importantly, serotonin activated nuclear factor kappa B (NF-κB) and upregulated the hepatic expressions of high mobility group protein B1 (HMGB1), toll-like receptor-4 (TLR4), and downstream molecules in Con A-mediated liver injury. Serotonin 2A receptor was upregulated in liver tissue after Con A injection, and serotonin 2A receptor antagonist Ketanserin protected against Con A-induced hepatitis. These results indicated that serotonin has the potential to aggravate Con A-induced ALI via the promotion of inflammatory response, oxidative stress injury, and hepatocyte apoptosis and the activation of hepatic HMGB1-TLR signaling pathway and serotonin 2A receptor.
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