judge-mental
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http://www.mindandmuscle.net/forum/index.php?showtopic=22247
lets start by quoting the ALRI "Tactics" writeup
QUOTE
One reason we accumulate fat is due to insulin. Insulin is likely one of the most anabolic to muscle substances on the planet, but it has an evil side in that it is anabolic to fat cells too. The reason is partitioning meaning that insulin can store calories in fat or muscle.
As we gain fat, muscle cells tend to become less sensitive to insulin (Insulin Insensitivity) and fat cells tend to become ever so accommodating. So the result is that fat get the lion’s share of calories coming in. When you diet or cut calorie intake the muscle start to shrink and the fat cells have the upper hand in the fight for calories which is why most lose more muscle than fat when dieting.
The goal is to stimulate muscle cell insulin sensitivity and decrease fat cell feeding frenzies… Repartitioning!
Peroxisome proliferator-activated receptor (PPAR)-gamma activators are widely used in the treatment of type 2 diabetes because they improve the sensitivity of insulin receptors. Punica granatum flower (PGF) has been used as an anti-diabetic medicine in Unani medicinal literature. In several studies the reported active compound in this friendly herb that causes this cool event is gallic acid. You are already aware of the research that shows gallic acid inhibits fat cell feeding on glucose, but the right extraction has been shown in mammal studies to induce muscle cell insulin sensitivity. When fat is starved and muscle is fed…well, you do the math.
I'm totally so not sold on this. PPAR gamma should antagonised in dieting IMO. they almost got me(nice ingrideints except that one) until that point. their logic is totally flowed.
here I go:
off the bat - it is SO widely known PPAR GAMMA (from now on will just say PPAR-G) stimulates adipogenesis and weight gain. so it helps IR obviously by adding cells. but not so good usualy for fat loss, unless you had lyposuction. PPAR gamma is bad news, its the body's way to handle excess food, may be good for bolimic diabetes, but for dieters (who are bolimic when on deiting probably but I'd live that for now)for instance alcohol manifests its adipogenci effects directly through PPAR-G2.
further more PPAR-G markedly induce adipocyte glycerol kinase (GyK) gene expression. This is surprising, as standard textbooks indicate that adipocytes lack GyK and thereby avoid futile cycles of triglyceride breakdown and resynthesis from glycerol and FFAs. By inducing GyK, TZDs markedly stimulate glycerol incorporation into triglyceride and reduce FFA secretion from adipocytes. so it helps IR by lowering FFA but it sucks for fat moblization. this specifically may involve some futile cycle calorie burning (as all fed signals do) but not sure its worth it.
oh yeah and ppar gamma makes your stem cells and sattelite cells into adipocytes. COOL!
so why are PPAR-gamma needed to be specifically activated in type II syndromXish folks?
basically VAT has a toatlly different cyokine production profile and particularly its low in PPAR gamma. so IR people need more femoral, "healthy", normally responding fat to signal adipognesis
and spook adds:
so - ALRI will give us those nice female hips we are dreaming of, ah?QUOTE
... thats why the PPAR-gamma agonists are given to overweight diabetics. It really depends on body fat distrobution. femoral obesity is generally plauged with more than ample cell number. Central or peripheral though often show signs on needing more. Of course if they would juse lose weight there endocrine profile would improve as well, but thats easier said than done.
all readily verified on pubemd. I about to be very dissapointed if there isn't a last second twist to the plot because they have seriously dropped the ball.
