Terma
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- May 8, 2017
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The way Glycine might hamper weight loss, besides affecting methyl consumption, water retention, receptors, TNF-alpha, and even Growth Hormone (if taken during fasting), is its activation of PPARgamma in healthy adipose tissue (linked in another thread) - but it seems to not do this in existing obesity, hence why it might not do that much, through this mechanism.
PPARgamma has effects reminiscent of Cortisol in adipocytes. It potentiates insulin and causes fat gain, while lowering inflammation.
In effect, PPARgamma is a major short-term PUFA antagonist, working through lipogenesis.
However if you administer either Cortisol or PPARgamma strong agonist during fasting, lipolysis actually increases. PPARgamma in fact increases lipolysis always but stimulates NEFA uptake and the net balance is fat gain (too many studies to link; see diabetes resources; e.g.: PPARgamma agonism increases rat adipose tissue lipolysis, expression of glyceride lipases, and the response of lipolysis to hormonal control. - PubMed - NCBI be careful when you read this, it's mainly a lipogenesis promoter)
In general on a RP-like diet, you have to limit Cortisol and PPARgamma activation, because constant carb and protein intake leads to insulin all day.
(There were some studies that showed that actually IGF-1 can lower 11b-HSD in tissues, which is a point in favor of milk, despite what I wrote earlier; so if you do well on milk, this can be part of the reason; although exogenous IGF-1 is suboptimal in other ways, and certainly no replacement for GH, so it's hard to say the net effect imo)
Conversely, IF lowers insulin, and Cortisol and PPARgamma become slightly fat burning, although I'm convinced it's mostly the Growth Hormone that gives its benefits, due to its repartitioning effects, and even increased Norepinephrine (since better circadian rhythm leads to amplified NAD production, which means higher SIRT1 and higher dopamine->norepinephrine in the morning, even without exercise; people emulate this already with caffeine, though).
This whole thing ties into inflammation and obesity, since endotoxin, inflammation, and macrophage action are thought to drive waist size and metabolic problems - both 11b-HSD for Cortisol and PPARgamma increase in adipose tissue in obesity to deal with the inflammation, through increasing lipogenesis.
So what I just described actually better fits other substances such as Abscissic Acid and some others mentioned and promoted on the forum, that work through PPARgamma. I think people even viewed PPARgamma in a positive light... this is deceptive. Glycine is only a problem circumstantially. Much like Vitamin A, which also affects weight loss.
[If you're reading this and confused by these statements and some of Cortisol's associations with insulin resistance, that's because it's species-specific and fat depot-specific and dose-dependent and dependent on food intake, the latter being the only one I described above - hopelessly confused; start here: Glucocorticoids Fail to Cause Insulin Resistance in Human Subcutaneous Adipose Tissue In Vivo | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic ]
PPARgamma has effects reminiscent of Cortisol in adipocytes. It potentiates insulin and causes fat gain, while lowering inflammation.
In effect, PPARgamma is a major short-term PUFA antagonist, working through lipogenesis.
However if you administer either Cortisol or PPARgamma strong agonist during fasting, lipolysis actually increases. PPARgamma in fact increases lipolysis always but stimulates NEFA uptake and the net balance is fat gain (too many studies to link; see diabetes resources; e.g.: PPARgamma agonism increases rat adipose tissue lipolysis, expression of glyceride lipases, and the response of lipolysis to hormonal control. - PubMed - NCBI be careful when you read this, it's mainly a lipogenesis promoter)
In general on a RP-like diet, you have to limit Cortisol and PPARgamma activation, because constant carb and protein intake leads to insulin all day.
(There were some studies that showed that actually IGF-1 can lower 11b-HSD in tissues, which is a point in favor of milk, despite what I wrote earlier; so if you do well on milk, this can be part of the reason; although exogenous IGF-1 is suboptimal in other ways, and certainly no replacement for GH, so it's hard to say the net effect imo)
Conversely, IF lowers insulin, and Cortisol and PPARgamma become slightly fat burning, although I'm convinced it's mostly the Growth Hormone that gives its benefits, due to its repartitioning effects, and even increased Norepinephrine (since better circadian rhythm leads to amplified NAD production, which means higher SIRT1 and higher dopamine->norepinephrine in the morning, even without exercise; people emulate this already with caffeine, though).
This whole thing ties into inflammation and obesity, since endotoxin, inflammation, and macrophage action are thought to drive waist size and metabolic problems - both 11b-HSD for Cortisol and PPARgamma increase in adipose tissue in obesity to deal with the inflammation, through increasing lipogenesis.
So what I just described actually better fits other substances such as Abscissic Acid and some others mentioned and promoted on the forum, that work through PPARgamma. I think people even viewed PPARgamma in a positive light... this is deceptive. Glycine is only a problem circumstantially. Much like Vitamin A, which also affects weight loss.
[If you're reading this and confused by these statements and some of Cortisol's associations with insulin resistance, that's because it's species-specific and fat depot-specific and dose-dependent and dependent on food intake, the latter being the only one I described above - hopelessly confused; start here: Glucocorticoids Fail to Cause Insulin Resistance in Human Subcutaneous Adipose Tissue In Vivo | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic ]
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