"Capsaicin Induces “Brite” Phenotype in Differentiating 3T3-L1 Preadipocytes"

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4114566/

This is the beige (Brite) fat that is inducible in us.
Even more elucidation about it. Am getting ebullient tbh

However, for this study, capsaicin induces preadipocytes to differentiate into Beige fat aka express a brown fat phenotype (true brown fat comes from a different cellular lineage), as they expression the TRPV receptors capsaicin binds to, however, the fully differentiated adipocytes do not express that receptor, thus this won't be something too modulatory in our current state.

Pretty cool, the study also gives a list of some other agents that can induce browning of WAT: "Some pharmacological agents that can promote browning are sympathetic activators like BDNF and leptin, prostaglandins like PGE2 and PGI2, cardiac natriuretic peptides and neuropeptides, PPAR (both γ and α) modulators, some hormones like irisin and FGF-2."
I'll also add meteorin-like to that list: http://www.cell.com/cell/abstract/S0092-8674(14)00600-X -- as welll as t3 and PGC-1 alpha modulators

More on beige fat

"Eosinophils and Type 2 Cytokine Signaling in Macrophages Orchestrate Development of Functional Beige Fat"

http://www.cell.com/cell/abstract/S0092-8674(14)00601-1

It notes "Eosinophils and type 2 cytokines are required for biogenesis of beige fat"

e: full text; http://libgen.org/scimag/index.php?s=Eosinophils+and+Type+2+Cytokine+Signaling+in+Macrophages+Orchestrate+Development

This post was edited by Balla on Aug 7 2014 12:20am

New

"Fructose, high-fructose corn syrup, sucrose, and nonalcoholic fatty liver disease or indexes of liver health: a systematic review and meta-analysis"

http://ajcn.nutrition.org/content/early/2014/08/06/ajcn.114.086314.full.pdf#page=1&view=FitH

Suck it clean eaters:

"Conclusions: On the basis of indirect comparisons across study findings, the apparent association between indexes of liver health (ie, liver fat, hepatic de novo lipogenesis, alanine aminotransferase, AST, and g-glutamyl transpeptase) and fructose or sucrose intake appear to be confounded by excessive energy intake. Overall, the available evidence is not sufficiently robust to draw conclusions regarding effects of fructose, HFCS, or sucrose consumption on NAFLD"

Now I must prove to alan skittles can be your primary carbohydrate intake. Please link me to things to aid me on my quest

This post was edited by tommyd323 on Aug 8 2014 01:05am

Do it yourself pl0x

But could it? Was more my question

would be tough to do while maintaining insulin sensitivity.

Does this mean like avoiding diabetes? Lol

Yes



Well, when he poses it as using skittles for your PRIMARY intake.. I'd agree lol, that's extreme.
I'd say you can easily eat one full pack of poptarts, skittles, etc every single day and have zero deleterious health consequences

+ if you used a lot of skittles, such as tommy's post poses, if you ate them with fiber, protein, and fats, that'll mitigate most all of the celeritous digestion/absorption and thus the insulin spike too

"Histidine supplementation alleviates inflammation in the adipose tissue of high-fat diet-induced obese rats via the NF-κB- and PPARγ-involved pathways."

http://www.ncbi.nlm.nih.gov/pubmed/24833547