Quote (Balla @ Feb 12 2014 12:56am)

http://www.eurekalert.org/pub%5Freleases/2014-02/uob-nrs021014.php

Pretty cool, but I have some thoughts.
As far as possible mechanisms, lactate produced in astrocytes is transported to neurons via the lactate transporter (MCT1), which triggers depolarization and excitation of neurons.
It's involved on glucose sensing in the hypothalamus, regulating energy and hunger. Usage of glucose leads to the lactate I talked about in the first thought, and the transportation. These shifts modulate neuropeptide expression (shifts sensed largely by Glucokinase), example - hypoglycemia/depleted reserves can induce hypothalamic AMPK expression, leading to NPY and AgRP (and vice versa) expression increased and thus hunger.
As for this study, it makes sense. Lactate production would indicate glycogen depletion and glucose usage. Norepinephrine/epi induce glycogenolysis and such to increase glucose concentrations.
It also fits in w/ my first statement. Norepi/epi (sympathetic nervous system mediators) innervate ghrelin, the main gut hunger hormone, which also acts at the ARC of the hypothalamus to shift to hunger pathways, as described above.
At least, that's how I think about it, iirc

Quote (Balla @ Feb 17 2014 12:13am)

http://mobile.journals.lww.com/nsca-jscr/%5Flayouts/oaks.journals.mobile/articleviewer.aspx?year=9000&issue=00000&article=97467

Protein expression differences from overtraining

Most striking is the significant up regulation of MAFbx.
It's a potent catabolic protein, it utilizes the proteasome system.. Aka it tags something (our muscle protein fibers in this case) with ubiquitin, which is then degraded by the proteasome intracellularly.

The other responses are expected. Myod and myogenin are also degraded via the proteasome too! So, I do wonder if those particularly are only down regulated from increased degradation from MAFbx.
The authors apparently, don't seem to have done PCR to actually measure my question, only western blot. I feel it's important in any experiment measuring protein levels and such, to do both such tests, to see it from a transcription view, as well as translated one

Quote (Bubbler @ Feb 21 2014 12:41am)

If you simply care about up regulation of a specific protein there is no need to do pcr, bc while there may be changes in transcription, the bottom line will still be defined by the protein count aka what gets translated, which is probably why they didn't do pcr as it would take much time and effort to develop a protocol to quantify it for no reason

Quote (Balla @ Feb 20 2014 11:56pm)

Well you're right that the question I'm asking isn't all too important.. In this sense actually they were only wondering about the protein levels themselves and that is what's important, so I know what you mean. I'm just curious to know where the down regulation occurs lol. And PCR isn't much effort.. Maybe 7 hours?

Quote (Bubbler @ Feb 21 2014 01:10am)

The actually pcr technique wouldn't take that long but this isn't some cookie cutter experiment you do in your molecular bio or what have you class where every step has been done before, meaning defining an adequate protocol will take a lot of time

However, you are right that it would be good to gain insight into if Myod and myogenin are being downregulated at a transcriptional level so you can rule it out and confirm/deny that ubiquitination via MAFbx is the primary method of downregulation

Quote (Afficionado @ Feb 22 2014 04:08pm)

Some articles on meal frequency and relevancy of eating breakfast. Nothing new, everyone knows this stuff, just wanted to make it readily available.



http://www.ncbi.nlm....pubmed/14513075



Breakfast skipping reduced overall weight in overweight students, with out other variables controlled.

This one is fairly weak as the total intake isn't controlled..



http://www.ncbi.nlm..../pubmed/9155494



This one essentially says that some studies do show an inverse relationship between meal frequency and adiposity, but these studies don't control  calorie intake...which is ridiculous...



...and concludes that no studies have ever shown that on controlled calorie diets multiple meals have any advantage over one meal, and in fact, they have yielded the same results. Thus defeating meal timing.



http://www.ncbi.nlm....pubmed/19943985



This is only the abstract. It essentially says, more favorable gut peptide profiles do not exist in higher meal frequencies. Weight loss is NOT enhanced by higher meal frequency alone, and better appetite control or diet adherence has not been shown in higher meal frequencies.



Ghrelin levels also remained unaltered by increasing meal frequency.

Quote (Balla @ Feb 22 2014 10:49pm)

Eh I don't really agree with the last bit. I don't think any gut hormonal shift is necessarily beneficial, but overtime on a specific meal frequency, your body will adapt and shift rhythmic secretion of hormones, such as ghrelin. Like with IF, ghrelin becomes a bit lower during the early parts of the day vs normally eating then, but later in the day, you'll get large spikes of ghrelin reaching a zenith. This isn't "bad" or "good" but it does happen, and is probably intuitive if you think about it