"In the presence of adequate nicotinic acid maximum growth was obtained when DL-tryptophan constituted 0.2%, or more, of the diet."
QUANTITATIVE DL-TRYPTOPHAN REQUIREMENT OF THE WEANLING PIG
D. C. SHELTON, W. M. BEESON & E. T. MERTZ
Purdue University
https://t.co/GNZgeuf0st
@SunnyT44321328 @jakeglmn Why the common “alternatives” don’t work — and often cause harm
1. “Just eat more meat” does not fix the problem
Dietary tryptophan from protein is protein-bound, not free.
Under metabolic stress (dieting, inflammation, obesity), tryptophan is preferentially diverted into...
"Since disturbed Trp affects biosynthesis of serotonin and might be associated w/ susceptibility for mood disturbances and carb craving, strategies to supplement Trp while dieting could be highly useful in treating uncontrolled weight gain or preventing neuropsychiatric symptoms"
@SunnyT44321328 @jakeglmn Effects of a caloric restriction weight loss diet on tryptophan metabolism and inflammatory biomarkers in overweight adults | European Journal of Nutrition
https://t.co/oXJXNg5OcJ
“The nicotinic acid GPR109A receptor regulated the structure of the gut microbiota & that the microbial populations were different between WT and Gpr109a- mice. Bacteroidetes & Firmicutes
These findings indicate that GPR109A regulates the gut microbiota”
https://t.co/5j9AvbIpYD
@0interestrates@cremieuxrecueil “Antibiotics” were “shown” during PELLAGRA from niacin/tryptophan-deficient diet, NOT “infectious” disease, to “improve” growth by frying intestine freeing tryp to compensate for niacin’s lack — as “evidence” from thereon that rebranded Nazi war agents kill fabricated “pathogens”
"In the presence of adequate nicotinic acid maximum growth was obtained when DL-tryptophan constituted 0.2%, or more, of the diet."
QUANTITATIVE DL-TRYPTOPHAN REQUIREMENT OF THE WEANLING PIG
D. C. SHELTON, W. M. BEESON & E. T. MERTZ
Purdue University
https://t.co/GNZgeuf0st
RHEO
"Despite tremendous efforts, effective pharmacological agents for the treatment of obesity are still limited. Here, we showed that in contrast to lactate receptor GPR81, niacin receptor GPR109A-deficient mice had progressive weight gain and hepatic fat accumulation. Using..
high-fat diet-induced mouse model of obesity, we demonstrated that niacin treatment apparently protected against obesity without affecting food intake in wild-type mice but not in GPR109A-deficient mice. Further investigation showed that niacin treatment led to a remarkable..
inhibition of hepatic de novo lipogenesis. Additionally, we demonstrated that niacin treatment triggered brown adipose tissue and/or white adipose tissue thermogenic activity via activation of GPR109A. Moreover, we observed that mice exposed to niacin exhibited a dramatic..
decrease in intestinal absorption of sterols and fatty acids. Taken together our findings demonstrate that acting on GPR109A, niacin shows the potential to maintain energy homeostasis through multipathways, representing a potential approach to the treatment of obesity, diabetes..
RHEO
"Despite tremendous efforts, effective pharmacological agents for the treatment of obesity are still limited. Here, we showed that in contrast to lactate receptor GPR81, niacin receptor GPR109A-deficient mice had progressive weight gain and hepatic fat accumulation. Using..
decrease in intestinal absorption of sterols and fatty acids. Taken together our findings demonstrate that acting on GPR109A, niacin shows the potential to maintain energy homeostasis through multipathways, representing a potential approach to the treatment of obesity, diabetes..