Tsunayoshi Sawada
Iron
- Joined
- Dec 23, 2019
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https://www.nature.com/articles/s41366-018-0047-8
Conclusions
Human obesity is characterized by an increased capacity to produce and release 5-HT from the proximal small intestine, which is strongly linked to higher body mass, and glycemic control. Gut-derived 5-HT is likely to be an important driver of pathogenesis in human obesity and dysglycemia.
Obesity is a major risk factor for chronic disease. A new study in mice reveals that lowering levels of the signaling molecule serotonin outside of the brain reduces obesity and its complications by increasing brown adipose tissue (BAT) energy expenditure.
However more than 90% of our bodies serotonin is actually made in the gut, which cannot enter the brain to affect mood.
"We know from a raft of recent high profile publications that gut-derived serotonin causes diabetes and obesity, but we didn't know if this was relevant to such disorders in humans.
University of Adelaide Senior Research Fellow, Associate Professor Richard Young, says these findings also indicate that obese humans secrete excess serotonin from the upper gut at rest, as well as during a meal.
derived serotonin is the link through which the gut microbiome affects host glucose metabolism. The key evidence supporting this conclusion is that the combination of depleted EC cell 5-HT and gut antibiotic-associated microbiota perturbation did not show any additive effect compared to the individual
“We found that the microbiome worsens our metabolism by signalling to cells in the gut that produce serotonin. They drive up serotonin levels, which we previously showed to be increased in obese humans, and this rise in blood serotonin causes significant metabolic problems.”
the study found that increased serotonin levels resulting from high temperature likely contributed to increased impulsivity and a higher risk of crimes. “
https://www.cell.com/current-biology/fulltext/S0960-9822(19)31382-X?_returnURL=https://linkinghub.elsevier.com/retrieve/pii/S096098221931382X?showall=true
serotonin as a chemical that triggers the body’s startle response
https://www.sciencedirect.com/science/article/abs/pii/S0165032718330751
“…The relative peripheral levels of PUFA species are associated with neuropsychiatric illnesses, with elevated AA in proportion to DHA and EPA in MDD (Lin et al., 2010) and suicide risk
pufa and 5-ht works together and potentie each other
https://ichgcp.net/clinical-trials-registry/NCT03018340<== sletcive serotonin antagonits potent anti depresant
Compared with placebo, pimavanserin reduced weighted HAMD-17 total scores in both stages (least-square means difference = –1.7; P = .04). Patients who received pimavanserin in the first stage separated from the placebo group on the HAMD-17 by the end of the first week (difference = –1.7; P = .04) and had significantly improved on the HAMD-17 by week 5 (difference = –4; P < .001).”
https://www.nature.com/articles/s41380-018-0074-9
. Roughly 20% of patients with mitochondrial disease also have bipolar disorder
Enhanced serotonergic activity may then further impair mitochondria in a vicious cycle
Conclusions
Human obesity is characterized by an increased capacity to produce and release 5-HT from the proximal small intestine, which is strongly linked to higher body mass, and glycemic control. Gut-derived 5-HT is likely to be an important driver of pathogenesis in human obesity and dysglycemia.
Obesity is a major risk factor for chronic disease. A new study in mice reveals that lowering levels of the signaling molecule serotonin outside of the brain reduces obesity and its complications by increasing brown adipose tissue (BAT) energy expenditure.
However more than 90% of our bodies serotonin is actually made in the gut, which cannot enter the brain to affect mood.
"We know from a raft of recent high profile publications that gut-derived serotonin causes diabetes and obesity, but we didn't know if this was relevant to such disorders in humans.
University of Adelaide Senior Research Fellow, Associate Professor Richard Young, says these findings also indicate that obese humans secrete excess serotonin from the upper gut at rest, as well as during a meal.
derived serotonin is the link through which the gut microbiome affects host glucose metabolism. The key evidence supporting this conclusion is that the combination of depleted EC cell 5-HT and gut antibiotic-associated microbiota perturbation did not show any additive effect compared to the individual
“We found that the microbiome worsens our metabolism by signalling to cells in the gut that produce serotonin. They drive up serotonin levels, which we previously showed to be increased in obese humans, and this rise in blood serotonin causes significant metabolic problems.”
the study found that increased serotonin levels resulting from high temperature likely contributed to increased impulsivity and a higher risk of crimes. “
https://www.cell.com/current-biology/fulltext/S0960-9822(19)31382-X?_returnURL=https://linkinghub.elsevier.com/retrieve/pii/S096098221931382X?showall=true
serotonin as a chemical that triggers the body’s startle response
https://www.sciencedirect.com/science/article/abs/pii/S0165032718330751
“…The relative peripheral levels of PUFA species are associated with neuropsychiatric illnesses, with elevated AA in proportion to DHA and EPA in MDD (Lin et al., 2010) and suicide risk
pufa and 5-ht works together and potentie each other
https://ichgcp.net/clinical-trials-registry/NCT03018340<== sletcive serotonin antagonits potent anti depresant
Compared with placebo, pimavanserin reduced weighted HAMD-17 total scores in both stages (least-square means difference = –1.7; P = .04). Patients who received pimavanserin in the first stage separated from the placebo group on the HAMD-17 by the end of the first week (difference = –1.7; P = .04) and had significantly improved on the HAMD-17 by week 5 (difference = –4; P < .001).”
https://www.nature.com/articles/s41380-018-0074-9
. Roughly 20% of patients with mitochondrial disease also have bipolar disorder
Enhanced serotonergic activity may then further impair mitochondria in a vicious cycle
