Don't known if someone has already mentioned this recent news from this particular study here already or not, but definitely another point for Dr. Ray Peat.
"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."
"Tryptophan (Trp) is converted into serotonin (5-HT) within the brain by the enzyme tryptophan hydroxylase (TPH)2, where it both increases sympathetic nervous system signaling to brown adipose tissue (BAT) and suppresses appetite. In the gastrointestinal tract (GIT), Trp is converted to serotonin by the enzyme Tph1. Crane et al.6 find that reducing circulating serotonin by inhibition of Tph1 or deletion of the Tph1 gene increases the sensitivity of BAT cells to noradrenaline (NA) and β-adrenergic receptor (β-AR) signaling. This drives thermogenesis by fat and glucose oxidation via the actions of Ucp1. Sustained thermogenesis recruits additional fat and glucose from peripheral tissues for oxidation by BAT cells, which reduces fat storage in WAT as well as in undesirable locations such as skeletal muscle and the liver, thereby providing protection against obesity, skeletal muscle insulin resistance and NAFLD."
http://www.nature.com/nm/journal/v21/n2 ... .3797.html
"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."
"Tryptophan (Trp) is converted into serotonin (5-HT) within the brain by the enzyme tryptophan hydroxylase (TPH)2, where it both increases sympathetic nervous system signaling to brown adipose tissue (BAT) and suppresses appetite. In the gastrointestinal tract (GIT), Trp is converted to serotonin by the enzyme Tph1. Crane et al.6 find that reducing circulating serotonin by inhibition of Tph1 or deletion of the Tph1 gene increases the sensitivity of BAT cells to noradrenaline (NA) and β-adrenergic receptor (β-AR) signaling. This drives thermogenesis by fat and glucose oxidation via the actions of Ucp1. Sustained thermogenesis recruits additional fat and glucose from peripheral tissues for oxidation by BAT cells, which reduces fat storage in WAT as well as in undesirable locations such as skeletal muscle and the liver, thereby providing protection against obesity, skeletal muscle insulin resistance and NAFLD."
http://www.nature.com/nm/journal/v21/n2 ... .3797.html