News in nootropic drugs.. Noopept increases GLP-1 secretion. Noopept is one of the most widely used nootropics out there, and was found to increase BDNF and NGF neuronal activity actually. It has potential and positive benefits (such as via increasing choline uptake, an AMPAkine effect, subtly potentiating LTP, and the upregulates BDNF and NGF), however the increased BDNF signaling will downregulate the TrkB receptor, attenuating full on memory and cognitive function overtime, so there's a fine line.
Now, for this study, after that bit of background on noopept.
"Noopept Normalizes Parameters of the Incretin System in Rats with Experimental Diabetes."
http://www.ncbi.nlm.nih.gov/pubmed/25065315To summarize these findings, and add a lot of information about GLP-1, especially as a neuronal agent, and add some ostensible implications, I'll put some thoughts about it.
Noopept protects from diabetes by increasing release of glucagon like peptide-1. It's an incretin, which essentially means it causes a robust insulin secretion. This is part of normal physiology, and is the reason that ingesting glucose orally stimulates a far more pronounced insulin spike than injecting it and by-passing that system. GLP-1 and GIP (as well as other incretins) are targets for diabetes, as they are an impetus for an increased insulin response, which tends to decline in the diabetic patient (this wouldn't necessarily work for a self-induced type 2 diabetic, however, who will, at first, have massive levels of insulin to counteract the resistance). Moreover, GLP-1 has been found to be highly protective on the beta-cells of the pancreas (which secretes insulin), and actually helps restore function in those areas, which is why they are big targets for those type of metabolic derangements. Specifically, it can cause proliferation of beta cells and inhibit their apoptosis.
GLP-1 is also a potent satiety signal and modulator of food intake. It inhibits gastic emptying, enhancing satiety (fullness). Furthermore, it will act on vagal afferents, which then signal to the brain stem then hypothalamus to cause satiety directly at the central centers there. Moreover, GLP-1 also binds to the D2 dopamine receptors in the amygdala, aiming to attenuate the "reward" from the food, further modulating intake.
Now that we've noted GLP-1 can have central effects, it's important to note that GLP-1 is also even produced by neurons. GLP-1 seems to actually protect from neuronal apoptosis via inhibiting Bim. IIRC, there was a study that noted neurite outgrowth mediated by GLP-1, similar to NGF-induced outgrowth (but doesn't affect proliferation). Keep in mind, I believe it was in vitro, in rat medullary cells or something related. In vivo medulla (in the brainstem) action of GLP-1 does happen (those cells contain GLP receptors) also indicates the possibility of SNS action. This study notes how GLP-1 actually also causes secretion of NGF (nerve growth factor) in the insular cortex. The insular cortex has been impliciated in profound things such as consciousness and emotion (involved in neural circuits, for instance with the thalamus and amygdala).
Now, a few interesting things about GLP-1 are also:
http://www.ncbi.nlm.nih.gov/pubmed/12749025?dopt=Abstract[1] - protects hippocampal neurons against glutatmate mediated apoptosis and mitigated levels of amyloid-beta peptide (in vivo) and APP (in vitro).
http://www.ncbi.nlm.nih.gov/pubmed/12925848?dopt=Abstract[2] - Study notes that overexpression of the GLP-1 receptor augments learning & memory (would this also hold true for simply increases in GLP-1 itself I wonder? It has a very short half-life I believe).
Thus, this study notes that noopept actually augments secretion of GLP-1 from the gut.. which implies oral administration is key if you want this GLP-1 effect. I suppose that MOST people take it sublingually, which wouldn't allow this effect to even take place. Perhaps there's good reason to up the dose of noopept by 10-30mg or so and take it orally instead? Simply surmise at this point, esp in terms of actual physiological significance, which I doubt there's much (but who knows at this point).