First of two part article I put together outlining that foods aren't nearly as noxious as people think, eating"clean" vs eating "dirty" is asinine, and why being fat/obese is far worse for health than any sort of diet-induced damage.

https://m.facebook.com/story.php?story_fbid=269530569920097&id=175556779317477

This post was edited by Balla on Jul 18 2014 09:30pm

Part 2 on adipocytes. Kept it basically nuance free.

https://m.facebook.com/story.php?story_fbid=269534363253051&id=175556779317477

Full text:
http://libgen.org/scimag/get.php?doi=10.2337%2Fdb14-0513

Interesting paper.
This shows adipose tissue plasticity, very exciting. This on top of the findings of irisin and meteorin-like, plus already known SNS and PGC-1 alpha, hopefully they can come up with some pharmacological intervention to modulate this system

"Improving type 2 diabetes through a distinct adrenergic signaling pathway involving mTORC2 that mediates glucose uptake in skeletal muscle"

http://diabetes.diabetesjournals.org/content/early/2014/07/02/db13-1860.short

"Acute Exercise Leads to Regulation of Telomere-Associated Genes and MicroRNA Expression in Immune Cells"

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0092088

Amazing. A molecular mechanism by which exercise boosts immune function. Chalk that up as yet another benefit.

Another paper on beige fat published this year:
http://www.readcube.com/articles/10.1038/ijo.2013.82

These findings + several molecular players are really starting to advance quickly. Let's see where it goes.

"The acute effects of four protein meals on insulin, glucose, appetite and energy intake in lean men."

http://www.ncbi.nlm.nih.gov/pubmed/20456814

Study shows a relation between the satiating effect of protein and the insulin response it evokes.. and differs between protein sources, showing that whey, which elicits a robust insulin response induces greater satiety. Makes sense as insulin is one of the bodies main long-term satiety signals (along with leptin).

What's interesting about insulin, however, is though it IS a satiety signal, there is some complex interplay going on.

This study: "ALTERED HYPOTHALAMIC FUNCTION IN DIET-INDUCED OBESITY"
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3383790/

Says, "Thus, insulin-induced hypoglycemia potently overrides virtually all of insulin’s central effects, an observation that for many years has confounded research in this field."

More information on the effects of hypoglycemia as as potent hunger stimulator can be found in this paper:
"Glucokinase as a Glucose Sensor in Hypothalamus - Regulation by Orexigenic and Anorexigenic Peptides"
http://cdn.intechopen.com/pdfs-wm/22056.pdf

This is more known of course, I just find it interesting about insulin: "Brain insulin controls adipose tissue lipolysis and lipogenesis"
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3061443/

Of course insulin decreases thermogenesis and attenuates lipolysis. Yet, it also causes satiety.

Yet, here's something strange about protein: http://ajcn.nutrition.org/content/29/9/984.abstract
Protein does of course induce a robust insulin response, esp certain ones. However, this also shows concomitant with protein induced insulin spike, you have an increase in FFAs, indicating lipolysis, even in the presence of mass insulin. CHOs don't have this binary effect.
I'm assuming much of this protein induced effect is due to a robust glucagon response along side the insulin - mitigating possible sublime hypoglycemia and allowing lipolysis. Interesting imo.

"Fatty acids from fish: the anti-inflammatory potential oflong-chain omega-3 fatty acids"

https://pdf.yt/d/dmpT_38qtuyV1112

Superb. Should help several people out there.

It's just important to make a quick note. Excess omega-3s can and will be deleterious to health, despite popular belief. It's because PUFAs are the most susceptible of all to lipid peroxidation.

"Δ9-THC-caused synaptic and memory impairments are mediated through COX-2 signaling."

http://ge.tt/4Voq73p1/v/0?c

"Cannabinoids attenuate norepinephrine-induced melatonin biosynthesis in the rat pineal gland by reducing arylalkylamine N-acetyltransferase activity without involvement of cannabinoid receptors."

http://libgen.org/scimag/index.php?s=Cannabinoids+attenuate+norepinephrine-induced+melatonin+biosynthesis+in+the+rat+pineal+gland+by+reducing+arylalkylamine+N-acetyltransferase+activity+without+involvement+of+cannabinoid+receptors.&siteid=&v=&i=&p=&redirect=1

"Mechano-growth factor peptide, the COOH terminus of unprocessed insulin-like growth factor 1, has no apparent effect on myoblasts or primary muscle stem cells"

http://ajpendo.physiology.org/content/306/2/E150.long

I'll probably get the full text to this soon. I still find it quite interesting though.. if this is true, why is it even expressed immediately post workout? Why does it go in cycles of this being upregulated while concomitantly IGF-1 is downregulated, then they switch? Doesn't make sense lol. It is known that the immediate response to exercise is a proliferation of satellite cells and an inhibition of differentiation/myonuclei induction (known due to increased in M-cadherin mRNA, increased beta-catenin mRNA, and increased myogenin mRNA during differentiation), so if the cycle of MGF and IGF aren't to blame.. what is? Yes, I'm aware there are also other factors, such as HGF, FGF, and PDFG that cause proliferation.. and other factors like Pax7, MyoD, and Myf5 cause differentiation. But, where does the cyclical aspect come from? What is causing one to upregulate while the other downregulates during muscle repair?

Actually, before I even got done with this post I found the full text:

http://libgen.org/scimag/index.php?s=10.1152ajpendo.00408.2013

e: regardless though, other studies have suggested otherwise, so until this is corroborated nothing is indeed definitive. Inherent variability is ever present


This post was edited by Balla on Jul 21 2014 10:28pm