"Glucagon is essential for adaptive thermogenesis in brown adipose tissue"

http://press.endocrine.org/doi/pdf/10.1210/en.2014-1175

Lawd. Yet another player elucidated in browning of adipose tissue. This one was knonw, but now they find it players a larger role than previously thought. It works, most likely, through FGF21, which I also posted about on the previous page with mTOR signaling.

hf with nearly 0% brown adipose left in anyone over the age of 5 lawl

They've shown, in humans, white AT can be induced into beige AT, which acts and morphologically looks just like brown adipose tissue. This is the "browning" as brown adipose and white adipose tissues come from diff cellular lineages. But yeah.. it's on a link in the past 4 pages or so. Essentially, this implies adipose tissue is "plastic" similar to neurons, highly subject to change, and can be shifted just through living in an area that's very cold vs living in an area that's very hot.

"Differentially regulated protein kinase A (PKA) activity in adipose tissue and liver is associated with resistance to diet-induced obesity and glucose intolerance in mice that lack PKA regulatory subunit type-IIα"

http://press.endocrine.org/doi/abs/10.1210/en.2014-1122

Another epigenetic gem, possibly. Selective inhibition of this subunit could be a great tool for obesity and related deragements afterward

P.S. sorry for flood of studies brothers, just thought they were highly interesting and were related to health

This post was edited by Balla on Aug 2 2014 10:06pm

"Exogenous Leptin Administered Intramuscularly Induces Sex Hormone Disorder and Ca Loss via Downregulation of GnRH and PI3K Expression."

http://www.researchgate.net/publication/264165123_Exogenous_Leptin_Administered_Intramuscularly_Induces_Sex_Hormone_Disorder_and_Ca_Loss_via_Downregulation_of_Gnrh_and_PI3K_Expression

This would cause significant testosterone declines.

"Brown fat and vascular heat dissipation"

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110100/

More recent input into brown fat.
Apparently brown fat causes reduced peripheral vasoconstriction, mediating heat loss, which then triggers further adaptive thermogenesis via t3 and others.
Perhaps brown fat could also protect from hypertension and thus CV disease then, not just obesity and insulin resistance.

Full text: https://www.sendspace.com/file/1rw3xc
They're essentially saying glucose deprivation falls under metabolic stress-mediated hypertrophy, whichs falls within the paradigm of lactic acid and other metabolites that challenge cellular integrity. They're saying muscular contraction at a high intensity causes arterial and venous compression (during the actual lift), that occludes the muscle from receiving nutrient rich blood flow, even in such a transient manner.

I see where they're going with this and it's actually quite enthralling. They're looking for the specific mediators of anabolic pathway signaling due to exercise.. such as the hypothesized phospolipase D expression cleaving membrane lipids to phosphatidic acid, activating mTOR. Thus, they show here that the brief glucose deprivation stimatules the mTOR pathway as well. However;

they gathered cells in a glucose-free medium at 30, 60, 120, or 180 min. I don't see anywhere near 30 mins of glucose deprivation occuring during training. During the actual contraction process, a lift MAY take 1 min, and that's on the far end. That will occur many times over during a workout, and assuming a high volume, hypertrophy-oriented routine, maybe 12 mins of glucose occlusion (assuming 45 secs/set * 16 sets). Now, 12 mins, intermittently spread out every 1-2 mins is not at all the same as 12 mins or especially 30 mins straight.
Irrespective of the times they used, and applicability to real life, I would surmise that the brief periods of glucose deprivation/nutrient rich blood flow occlusion may absolutely contribute to anabolic signaling under the paradigm of metabolic stress. Even though brief, the brief period is during the time glucose is gravely needed aka active contraction, so the effect should be augmented. This study shows that the brief deprived periods cause significant mTOR pathway during the recovery/reavailability of glucose.

They also show glucose deprivation alone robustly induces AMPK. This gives another signaling mechanism that contributes to its activation, apart from general ATP & glycogen depletion, ROS induction, and Ca2+ signaling. Further, they showed the AMPK expression didn't induce MAFbx (a ubiquitin ligase, causes muscle atrophy by degrading them via the proteasome), corroborating studies finding AMPK-alpha 2 is induced via exercise, which doesn't inhibit anabolic pathways and contribute greatly to catabolism.

Last, aiming to elucidate mechanisms by which it contributes to mTOR upregulation, they found NOS is activated, upregulating NO production, contributing greatly to the mTOR activation. It also seems the AMPK that's strongly upregulated by the glucose depri mediates the NOS induction, aiming to increase glucose uptake.

"Effect of Salt Intake and Potassium Supplementation on Serum Renalase Levels in Chinese Adults: A Randomized Trial"

http://journals.lww.com/md-journal/Fulltext/2014/07030/Effect_of_Salt_Intake_and_Potassium.4.aspx

This study has incredible clinical health implications. Renalase is an enzyme that breaks down catecholamines. They show it has a significant correlation with salt intake.. whereby high salt diets cause robust decline of the enzyme, causing a more sustained level of plasma NE and EPI, possibly contributing greatly to the higher blood pressure seen in those with very high salt intakes, and thus the increase in indicidence of CV disease. However, there wasn't a significant correlation between renalase activity and BP, making the whole study quite dubious. More work needs to be done.

"Nicotine enhances modulation of food-cue reactivity by leptin and ghrelin in the ventromedial prefrontal cortex"

http://onlinelibrary.wiley.com/doi/10.1111/adb.12167/abstract

"Acute effects of three high-fat meals with different fat saturations on energy expenditure, substrate oxidation and satiety."

http://www.ncbi.nlm.nih.gov/pubmed/19010571

Hmm.. so maybe there is even more to the idea of all calories aren't created equally? That's obviously true when you compare entropic differences between each major macronutrient. However, this gives more veracity to the fact some foods in the same macro group will induce a greater thermogenic response, or slightly less thermogenic response, etc.. it doesn't seem to be too significant for anything though.

From the study (no full text atm): "Fat oxidation rates increased nonsignificantly after the two meals rich in unsaturated fatty acids and decreased nonsignificantly after the high-saturated fatty acid meal. Postprandial respiratory quotient, protein and carbohydrate oxidation, and satiety measures were similar among meals."

However, it does also say, "Five-h postprandial thermogenesis was higher by 28% after the high-polyunsaturated meal (p=0.039) and by 23% higher after the high-monounsaturated meal (p=0.035) compared with the high-saturated meal."
Those % increases seem large.. however, let's put fat TEF at 5% (it's around that), and assume 500 cals of it consumed = 25 kcals thermogenically disperses. 25*0.28=7 kcals. So 32kcals burned vs 25kcals burned.