Talk:5-HT2B receptor

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So, knockout-type gene studies in mice have shown that without this receptor, serious birth defects result in the heart. We've also got plenty of evidence now that chronic overstimulation of the receptor slowly causes a buildup by inducing non-cancerous cell division - basically, it makes it grow in an unhealthy manner, but its clearly needed for the growth in the first place. Near as I can tell, there has also not been significant experience with pure antagonists at a long-term level necessary to find out what happens with long-term total blockage of this receptor.

So, allow me to put forth a hypothesis for other researchers to consider when reading thru the available literature, as it continues to grow:

Given:

• the role of serotonin in the regulation of food intake (which is why some drugs worked as appetite suppressant in the first place)
• the fact that a slight amount of carbohydrate is overall healthier than fasting (hence the sugar drip) for a variety of organs
• the fact that carbohydrate intake is known to stimulate serotonin release
• the fact that total fasting results in the accumulation of a number of toxins in the bloodstream as a result of consumption of less than ideal stored fuels resulting in ketosis.

...could it be that these receptors exist primarily for the purpose of ensuring that cardiac cells reproduce at the optimal time when food to best do so is available? If this hypothesis were correct, direct stimulation of the receptors in organisms undergoing periods of fasting would likely have much worse cumulative effects than direct stimulation of the receptors during times when glucose was available to the cell even if the individual were restricting intake somewhat.

This would also explain nicely why problems became apparent during the "fen-phen" era: This was also the era when the low or zero-carb craze known as the Atkins diet was most popular. His company was founded in 1989, it went bankrupt in 2005, and during this time promotion of a carbohydrate-free malnutrition diet was at its highest. On the other hand, at the time Fenfluramine was initially approved (1973), the diet advice at the time given to people was to mainly to keep fat and cholesterol low (the risks of trans-fat were unknown at the time). Additionally Aspartame was not approved until the early 1980s meaning it was quite likely that dieters of the 1970s would still be exposed to sugars of some type in snacks, as the aftertaste of then-available sweeteners was unpleasant. Only after the development of aspartame did it become likely that a dieting person would totally eliminate simple sugars from their diet...

It may be possible that stimulation of these receptors is not a definite eventual death sentence, but rather, simply increases the risk of other already risky behaviors as a co-factor. If you see any articles supporting or refuting this possibility, I would greatly appreciate references to them.Zaphraud (talk) 04:37, 19 April 2009 (UTC)[reply]

Hello - I just wrote on the talk page of the psychotropic Agomelatine and I thought it would be worth mentioning here as well. I'll copy/paste what I wrote there because the idea is generally the same.

I know the serotonergic properties of Agomelatine are widely accepted as being limited to 5-HT2C receptor-site antagonism, although I found whilst looking through articles on pubmed a mentioning of the drug's antagonistic affinity for 5-HT2B which seems to be clinically significant. The link to the article follows - http://www.ncbi.nlm.nih.gov/pubmed/12750432 . Do all of you armchair psychopharmacologists think that this should be worth mentioning under the pharmacology section of the article or not? If so, then the drug should be listed as an antagonist on the 5-HT2B Wikipedia page as well. If not, why?

Should there be no response and/or no rejection of the addition of the drug as an antagonist at said site unmentioned, I'll amend the article appropriately after a period of time to allow for review. Basuraeuropea (talk) 21:25, 20 September 2014 (UTC)[reply]

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Given that 6-APB has been reported as having psychedelic effects it almost certainly is an agonist of the 5ht2a receptor. Therefore it cannot be said to be a selective agonist of the 5ht2b receptor. Unless I am missing something. — Preceding unsigned comment added by 92.7.162.43 (talk) 19:23, 10 December 2022 (UTC)[reply]