The question the researchers sought to resolve was, does post-meal fat storage predict where the increase in adiposity will occur in the future?
According to the researchers, that is answer NO ( damnit! )
If you store alot of post-meal fat in your belly, theres no garauntee it will be there next week, or even tomorrow. This flies in the face of the calories argument, because it suggests that regardless of what you eat, each of your fat cells have thier own agenda as to how big or small they prefer to be.
Indeed, This next study builds on that theory. The paper is a review describing the infrastructure of adipose tissue. It talks about how long term over-feeding upregulates genes involved with angiogenesis, extracellular matrix deposition, i.e. when your fat cells see they are being forced to store larger amounts of fat for extended periods, they modify themselves to increase vasculature. Think of it like a tree growing. As the tree grows, it also increases its underground root network in size.
There are important implications for people looking to reduce fat mass discussed aswell. Short-term reductions in fat mass do not appear to reduce adipose tissue vasculature, but, it was reported that long-term reductions in fat mass did modulate genes involved with extracellular matrix deposition and cell death at >=33weeks. ( 1 ).
This suggests that a fat reduced state must be maintained for an extended period such to as allow for significant changes in adipose tissue vasculature to occur that favour maintanence of the new reduced size. This makes sense because short-term reductions in fat mass usually only involves reductions in the lipid droplet size in the adipocyte, this probably makes the adipocyte freak out and throw trantrums like a baby ( probably by refusing to make leptin ) and thus create an environment that favors fat storage.
Shrinking the fat cell's lipid droplet is not enough, one must also reduce its vasculature, and perhaps even kill it off completely ( apoptosis ).
Infact, going a step above leptin, the paper has a short mention at how drugs that reduce angiogenesis are able to reduce fat mass in leptin deficient mice that is "on par" with leptin administration itself!
The paper speculates that angiogenic-derived signals in adipose tissue may modify hunger and satiety, this is because reductions in fat mass produced from angiogenesis inhibiting drugs reduce food intake despite reductions in leptin and hypothalamic neuropeptides that modify bodyweight. Could adipose tissue vasculature be downstream of leptin signalling? As in, hypothalamic leptin signalling inhibits adipose tissue vasculature, while lack of hypothalamic leptin signalling promotes adipose tissue vasculature?
Don't forget we have atleast one study showing how leptin injections in the brain cause fat cell death by apoptosis. Sounds a bit convenient to me...... And lets not forget our old friend insulin, AKA insulin injection sites in type 1 diabetics cause localised fat tissue hypertrophy. I can only wonder if angiogenesis is downstream of insulin signalling in fat cells aswell.
It is clear that over a more prolonged period the supportive structures (vascular and extracellular membrane) needed to maintain adipose tissue expansion begin to predominate. This is accompanied by down-regulation of apparent nutrient-sensing pathways that are the permissive to this tissue expansion.