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How many amino acids in orexins? Molecular weights of the peptide? —Preceding unsigned comment added by 12.158.118.18 ( talk) 18:23, 28 December 2007 (UTC)
ÁReferences, e.g. on the discovery of orexins, would be nice. JFW | T@lk 11:00, 14 July 2005 (UTC)
Well, great. Thanks for doing a {{ sofixit}} on me! JFW | T@lk 18:41, 14 July 2005 (UTC)
Sofixit is really nice when an anon complains on the talk page about his/her favourite theory or subject being underrepresented. To look more legitimate, it may be advisable to {{sofixit}}. JFW | T@lk 23:45, 14 July 2005 (UTC)
Article is a little heavy on the feeding/metabolism side which may be overplaying the role of orexin. Primarily seems to be important in regulating sleep/wake transition and maintaining high alertness, not so much involved in general arousal or ingestive activity.
Also would be good to ensure that either both names are used at all times or that one name is used consistently. Switching between orexin and hypocretin in the same paragraph is distracting. Until the literature settles on one name we should use both. Personally I strongly dislike hypocretin (hard to abbreviate, for one thing - OXA vs. HCRT-1 saves three keystrokes every time I type it) but think it is appropriate to include the name here. As article is titled "orexin" I placed this name first in all instances. - DrNixon 08:20, 1 February 2006 (UTC)
I don't think it's fair to say that the primary role of the orexins is either sleep/wake regulation or appetite regulation, or anything else at this point. Given the presence of long-form leptin receptors on orexin neurons, their coexpression with dynorphin in lateral hypothalamic neurons, and their connectivity with NPY neurons in the arcuate nucleus and lateral hypothalamus, I think it's fair to say that appetite regulation/ingestive behavior is not merely an incidental effect of the orexins. Many neuropeptides perform several functions. Is it fair to describe a single function as the primary function? I have studied other functions of the orexins besides sleep/wakefulness and appetite regulation, and I believe there is great potential for many other functions to be revealed.
As one who has administered orexin-A centrally to both rats and mice, I believe you are mistaken about arousal. We haven't published our data concerning arousal per se (it's not what we were studying), so all I have is my word, but mice are very much aroused beyond simple wakefulness upon central delivery of orexin-A. (Wang et al have reported increased spopntaneous activity in orexin-A-treated rats with free access to running wheels.) This might simply be a pharmacological effect, but it does point toward an endogenous role for orexins in arousal.
Also, in reference to the above comments on the discovery of the orexins, I think a reference to "clone 35" by Gautvik et al is in order. I'll get on it. Dcs002 ( talk) 10:13, 20 September 2009 (UTC)
This article was automatically assessed because at least one WikiProject had rated the article as start, and the rating on other projects was brought up to start class. BetacommandBot 16:30, 10 November 2007 (UTC)
Could someone do a text search in the article for "nympholepsy" and check if the usage is appropriate? or was it intended to be "narcolepsy"? According to a online dictionary, "nymplolepsy" means "an emotional frenzy" 137.92.97.114 ( talk) 03:10, 30 December 2007 (UTC)
Would it be useful to explain to the reader that peptides don't have much practical value as treatments because they can't cross the blood-brain barrier? Looie496 ( talk) 00:05, 7 October 2008 (UTC)
See Paul Kenny's article in the online Early Edition of the PNAS for the week of November 24, cited in Scientists find blocking a neuropeptide receptor decreases nicotine addiction LeadSongDog ( talk) 20:01, 25 November 2008 (UTC)
Can anyone clarify/confirm/deny the hypocretin effect on thyroid hormones suggested by www.naturalnews.com/025325.html unreliable fringe source? ? "... hypocretins are wired to many different aspects of nerve function. They provide input to the primary department in the hypothalamus gland that controls the production of TRH (thyroid releasing hormone), which has control of the pituitary (which makes TSH), and thus has overall control of thyroid hormone production. The message hypocretins deliver is as follows, "We are in a state of high stress alert wherein our brain must remain hyper-vigilant, however, to conserve fuel so we don't perish, turn down the production of thyroid hormone in the rest of the body (a self preservation strategy, especially during times of famine or infection).""
Some data at "Altered setting of the pituitary-thyroid ensemble in hypocretin-deficient narcoleptic men " but I'm not sure if it's too specific to a disease state. Rod57 ( talk) 11:23, 16 January 2009 (UTC)
I just added discovery of receptors, clarified authorship of Sakurai and colleagues, referenced clone 35 in the 3rd paragraph, and removed "dispute" from 4th paragraph.
Ever since the infancy of this article, the name Masashi Yanagisawa has been featured prominently, and I've wondered if he or someone in his lab had been editing this page to hail him as the sole discoverer of the orexins. The convention is usually that the first author of the paper is the first name credited with the contents of the paper. Many years ago I switched the reference from Masashi Yanagisawa (no "et al" or "and colleagues" at the time, just him) to Sakurai and colleagues, and I added the reference to de Lecea and colleagues, but within a few days my changes were erased and Yanagisawa was again hailed as the sole discoverer. And it's not just his name, it's Masashi Yanagisawa at the University of Texas Southwestern Medical Center at Dallas. No one else's affiliations are named in this article, and I'm not sure how appropriate it is. And until I inserted the reference to Gautvik and clone 35, Yanagisawa's name was always the one that appeared first, though that group's paper was actually the third to be published on these peptides.
I've always thought that Gautvik and colleagues and de Lecea and colleagues (same group really) should get the lion's share for the discovery of these peptides because a) they first identified clone 35, b) their work published in 1998 was a continuation of their earlier published work, which I think establishes them as the pioneering lab group, and c) well, their paper was published before Sakurai and colleagues, albeit only a month (which is really considered to be the same time). Sakurai and colleagues deserve a great deal of credit for the thoroughness of their description of the peptides, getting the exact sequence correct, describing one function (feeding) of these peptides, and most of all for discovering the receptors. (Maybe I'm also driven by what I perceive as the promotional nature this article has historically had in regards to Yanagisawa.)
The reason I removed the word "disputed" from the fourth paragraph is that I believe it connotes a sense of animosity that doesn't exist. Researchers simply publish under whichever name they prefer, being sure to mention the other name, and everyone seems to be waiting too see whether the field decides on one name or the other. That's the attitude I've seen at conferences anyway. Yes there are reasons given on both sides why the name should be one or the others, but these are more like competing proposals than a subject of real dispute. Dcs002 ( talk) 07:01, 24 September 2009 (UTC)
I have updated the nomenclature paragraph to recognize a nomenclature compromise. Having hypocretin refer to the gene and orexin refer to the peptide/proteins is reflected in GenBank database searches and the IUPHAR database or Guide to Pharmacology. That being said, individual authors and labs will probably continue to refer to orexin/hypocretin by whichever name suits them. 08:06, 7 September 2015 (UTC) 149.171.66.108 — Preceding unsigned comment added by 149.171.66.108 ( talk)
Removed reference to criticism of the use of the term 'orexin' because the feeding may be incidental to general arousal. That comment did not have a citation and a paper that might be relevant (Ida et al 1999) actually follows the orexin nomenclature. — Preceding unsigned comment added by 149.171.66.108 ( talk) 06:25, 3 October 2016 (UTC)
Why is there a link to CIMIT in this section? Is it here for a purpose other than garnering publicity for the organization? I think it should be removed. Dcs002 ( talk) 09:47, 9 October 2009 (UTC)
The orexin article says: "Hence obesity in narcoleptic patients may be due to orexin deficiency leading to brown-fat hypo activity and reduced energy expenditure." This is, however, impossible because adult humans do not have brown fat. — Preceding unsigned comment added by 141.20.48.39 ( talk) 10:01, 5 June 2012 (UTC)
Narcolepsy is mentioned several times before it is defined under “wakefulness.” I would suggest to either define it (or describe it) earlier in the article or just hyperlink it for people to read about it themselves. I also think the last paragraph under “wakefulness” can be categorized under a different heading. It does not directly relate to wakefulness, but is useful because it is talking about the problems that can occur if one does not have orexin-producing neurons. Under ‘food intake,’ why does orexin increase the craving for food? You could tie this in with the increased obesity rate for those with low levels of orexin. The ‘energy metabolism’ section could be expanded or even grouped with the ‘food intake’ section.
Overall, the article was very informative and had a lot of good content! Cbruha11 ( talk) 15:19, 28 March 2014 (UTC)
![]() | This article was the subject of an educational assignment in 2014 Q1. Further details were available on the "Education Program:Nebraska Wesleyan University/Psyc 180 Psychology of Sleep and Dreaming (2014)" page, which is now unavailable on the wiki. |
If higher levels of orexin correlate with improved mood and less depression, but also greater wakefulness, then how could orexin explain higher incidence of depression in narcoleptics? If anything it would suggest to me that narcoleptics should have lower incidences of depression, which the page doesn't read to suggest. Scuriusx86 ( talk) 23:55, 10 November 2015 (UTC)
It's been a while since I visited this page, but I just noticed this: "Studies suggest that orexin-A may be of greater biological importance than orexin-B." I know I've been away from orexin research for a long time now, but on its face this statement seems preposterous. First, the fact that orexin-B has been observed as less potent or less effective than orexin-A at anything only means we don't know if its main endogenous function is to do something we haven't thought to test. Orexin-A is clearly more effective at inducing feeding. Does that make it more biologically important? We don't know what we don't know here. We don't know all of the possible functions of these peptides. Second, when I was studying the orexins (which ended in 2006), orexin-A had simply been studied more than orexin-B. We knew more about it, so researchers had a lot more to build on, and therefore a lot more was published, building a clearer picture of its function in the brain. It was more effective at inducing the effects that we were looking for, but we have no idea what all of its effects are. We can't know that for any neuropeptide until we figure out exactly how the human brain works. Third, importance is a vague and dependent statement of a thing's value, and is nearly a meaningless thing to say on a scientific level. Scientists speak in specifics. Important for what? Appetite? Arousal? Memory? Important how? Activation? suppression? Survival under extreme conditions? The fact that orexin-B is preserved across so many species is compelling evidence of its evolutionary importance. We either need to source that claim or get rid of it. Dcs002 ( talk) 11:07, 24 May 2014 (UTC)
I agree. Orexin-A is certainly the go-to peptide for agonist-based studies and the OX1 receptor has got more selective antagonists for it, but that doesn't mean that OX-B or the OX2 receptor doesn't do anything. I have therefore removed that sentence. ( 149.171.66.108 ( talk) 06:29, 3 October 2016 (UTC))
We should probably add the epidemic (1,300 cases) of narcolepsy in Europe caused by the Pandemrix influenza vaccine, which triggered an autoimmune reaction to hypocretin receptor 2. An exposed region of the influenza nucleoprotein A shared residues with a fragment of the first extracellular domain of hypocretin receptor 2. People with HLA-DQB1*0602 haplotype developed protective immunity to influenza and an autoimmune reaction to hypocretin receptor 2, leading to death of the cells and incurable narcolepsy. There were 1,300 cases out of 30 million doses of Pandemrix, so it's a relatively rare reaction, on the order of the other known, rare risks of influenza vaccines.
Ahmed SS,Volkmuth W, Duca J, et al.
Antibodies to influenza nucleoprotein cross-react with human hypocretin receptor
http://stm.sciencemag.org/content/7/294/294ra105
Science Translational Medicine. 01 Jul 2015; 7(294):294ra105. DOI: 10.1126/scitranslmed.aab2354
Gretchen Vogel
Why a pandemic flu shot caused narcolepsy
http://news.sciencemag.org/health/2015/07/why-pandemic-flu-shot-caused-narcolepsy
Science. 1 July 2015 DOI: 10.1126/science.aac8792.
And Science calls it hypocretin. Is that the name now? -- Nbauman ( talk) 03:15, 6 July 2015 (UTC)
I'm not a specialist in this area, but it does appear that the clause, "but immunocytochemistry tactics revealed the various projections this area truly had to other parts of the brain. " from the second paragraph of the Discovery section needs some kind of verb.
..had to connect...???
I'm hoping that someone can add the right verb. — Preceding unsigned comment added by Joel1947 ( talk • contribs) 17:11, 29 July 2017 (UTC)
High plasma triglycerides (from a high fat diet) and low blood sugar ( hypoglycemia) increases orexin levels, which increases appetite through orexin-stimulated neuropeptide Y action. [1] A high fat diet more than a high calorie diet has been shown to increase obesity and orexin release. [2]
References
These are biomedical claims and therefore need secondary sources to support them. Here are a couple of possibilities:
Orexin and Obesity (page 34)
Section 13: OX and the Control of Glucose Homeostasis
Orexin signaling in feeding, energy homeostasis, obesity and diabetes
Boghog ( talk) 18:29, 3 February 2018 (UTC)
This article was the subject of a Wiki Education Foundation-supported course assignment, between 28 August 2023 and 15 December 2023. Further details are available
on the course page. Student editor(s):
Adn23 (
article contribs). Peer reviewers:
Achait2023.
— Assignment last updated by Achait2023 ( talk) 17:11, 5 December 2023 (UTC)
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How many amino acids in orexins? Molecular weights of the peptide? —Preceding unsigned comment added by 12.158.118.18 ( talk) 18:23, 28 December 2007 (UTC)
ÁReferences, e.g. on the discovery of orexins, would be nice. JFW | T@lk 11:00, 14 July 2005 (UTC)
Well, great. Thanks for doing a {{ sofixit}} on me! JFW | T@lk 18:41, 14 July 2005 (UTC)
Sofixit is really nice when an anon complains on the talk page about his/her favourite theory or subject being underrepresented. To look more legitimate, it may be advisable to {{sofixit}}. JFW | T@lk 23:45, 14 July 2005 (UTC)
Article is a little heavy on the feeding/metabolism side which may be overplaying the role of orexin. Primarily seems to be important in regulating sleep/wake transition and maintaining high alertness, not so much involved in general arousal or ingestive activity.
Also would be good to ensure that either both names are used at all times or that one name is used consistently. Switching between orexin and hypocretin in the same paragraph is distracting. Until the literature settles on one name we should use both. Personally I strongly dislike hypocretin (hard to abbreviate, for one thing - OXA vs. HCRT-1 saves three keystrokes every time I type it) but think it is appropriate to include the name here. As article is titled "orexin" I placed this name first in all instances. - DrNixon 08:20, 1 February 2006 (UTC)
I don't think it's fair to say that the primary role of the orexins is either sleep/wake regulation or appetite regulation, or anything else at this point. Given the presence of long-form leptin receptors on orexin neurons, their coexpression with dynorphin in lateral hypothalamic neurons, and their connectivity with NPY neurons in the arcuate nucleus and lateral hypothalamus, I think it's fair to say that appetite regulation/ingestive behavior is not merely an incidental effect of the orexins. Many neuropeptides perform several functions. Is it fair to describe a single function as the primary function? I have studied other functions of the orexins besides sleep/wakefulness and appetite regulation, and I believe there is great potential for many other functions to be revealed.
As one who has administered orexin-A centrally to both rats and mice, I believe you are mistaken about arousal. We haven't published our data concerning arousal per se (it's not what we were studying), so all I have is my word, but mice are very much aroused beyond simple wakefulness upon central delivery of orexin-A. (Wang et al have reported increased spopntaneous activity in orexin-A-treated rats with free access to running wheels.) This might simply be a pharmacological effect, but it does point toward an endogenous role for orexins in arousal.
Also, in reference to the above comments on the discovery of the orexins, I think a reference to "clone 35" by Gautvik et al is in order. I'll get on it. Dcs002 ( talk) 10:13, 20 September 2009 (UTC)
This article was automatically assessed because at least one WikiProject had rated the article as start, and the rating on other projects was brought up to start class. BetacommandBot 16:30, 10 November 2007 (UTC)
Could someone do a text search in the article for "nympholepsy" and check if the usage is appropriate? or was it intended to be "narcolepsy"? According to a online dictionary, "nymplolepsy" means "an emotional frenzy" 137.92.97.114 ( talk) 03:10, 30 December 2007 (UTC)
Would it be useful to explain to the reader that peptides don't have much practical value as treatments because they can't cross the blood-brain barrier? Looie496 ( talk) 00:05, 7 October 2008 (UTC)
See Paul Kenny's article in the online Early Edition of the PNAS for the week of November 24, cited in Scientists find blocking a neuropeptide receptor decreases nicotine addiction LeadSongDog ( talk) 20:01, 25 November 2008 (UTC)
Can anyone clarify/confirm/deny the hypocretin effect on thyroid hormones suggested by www.naturalnews.com/025325.html unreliable fringe source? ? "... hypocretins are wired to many different aspects of nerve function. They provide input to the primary department in the hypothalamus gland that controls the production of TRH (thyroid releasing hormone), which has control of the pituitary (which makes TSH), and thus has overall control of thyroid hormone production. The message hypocretins deliver is as follows, "We are in a state of high stress alert wherein our brain must remain hyper-vigilant, however, to conserve fuel so we don't perish, turn down the production of thyroid hormone in the rest of the body (a self preservation strategy, especially during times of famine or infection).""
Some data at "Altered setting of the pituitary-thyroid ensemble in hypocretin-deficient narcoleptic men " but I'm not sure if it's too specific to a disease state. Rod57 ( talk) 11:23, 16 January 2009 (UTC)
I just added discovery of receptors, clarified authorship of Sakurai and colleagues, referenced clone 35 in the 3rd paragraph, and removed "dispute" from 4th paragraph.
Ever since the infancy of this article, the name Masashi Yanagisawa has been featured prominently, and I've wondered if he or someone in his lab had been editing this page to hail him as the sole discoverer of the orexins. The convention is usually that the first author of the paper is the first name credited with the contents of the paper. Many years ago I switched the reference from Masashi Yanagisawa (no "et al" or "and colleagues" at the time, just him) to Sakurai and colleagues, and I added the reference to de Lecea and colleagues, but within a few days my changes were erased and Yanagisawa was again hailed as the sole discoverer. And it's not just his name, it's Masashi Yanagisawa at the University of Texas Southwestern Medical Center at Dallas. No one else's affiliations are named in this article, and I'm not sure how appropriate it is. And until I inserted the reference to Gautvik and clone 35, Yanagisawa's name was always the one that appeared first, though that group's paper was actually the third to be published on these peptides.
I've always thought that Gautvik and colleagues and de Lecea and colleagues (same group really) should get the lion's share for the discovery of these peptides because a) they first identified clone 35, b) their work published in 1998 was a continuation of their earlier published work, which I think establishes them as the pioneering lab group, and c) well, their paper was published before Sakurai and colleagues, albeit only a month (which is really considered to be the same time). Sakurai and colleagues deserve a great deal of credit for the thoroughness of their description of the peptides, getting the exact sequence correct, describing one function (feeding) of these peptides, and most of all for discovering the receptors. (Maybe I'm also driven by what I perceive as the promotional nature this article has historically had in regards to Yanagisawa.)
The reason I removed the word "disputed" from the fourth paragraph is that I believe it connotes a sense of animosity that doesn't exist. Researchers simply publish under whichever name they prefer, being sure to mention the other name, and everyone seems to be waiting too see whether the field decides on one name or the other. That's the attitude I've seen at conferences anyway. Yes there are reasons given on both sides why the name should be one or the others, but these are more like competing proposals than a subject of real dispute. Dcs002 ( talk) 07:01, 24 September 2009 (UTC)
I have updated the nomenclature paragraph to recognize a nomenclature compromise. Having hypocretin refer to the gene and orexin refer to the peptide/proteins is reflected in GenBank database searches and the IUPHAR database or Guide to Pharmacology. That being said, individual authors and labs will probably continue to refer to orexin/hypocretin by whichever name suits them. 08:06, 7 September 2015 (UTC) 149.171.66.108 — Preceding unsigned comment added by 149.171.66.108 ( talk)
Removed reference to criticism of the use of the term 'orexin' because the feeding may be incidental to general arousal. That comment did not have a citation and a paper that might be relevant (Ida et al 1999) actually follows the orexin nomenclature. — Preceding unsigned comment added by 149.171.66.108 ( talk) 06:25, 3 October 2016 (UTC)
Why is there a link to CIMIT in this section? Is it here for a purpose other than garnering publicity for the organization? I think it should be removed. Dcs002 ( talk) 09:47, 9 October 2009 (UTC)
The orexin article says: "Hence obesity in narcoleptic patients may be due to orexin deficiency leading to brown-fat hypo activity and reduced energy expenditure." This is, however, impossible because adult humans do not have brown fat. — Preceding unsigned comment added by 141.20.48.39 ( talk) 10:01, 5 June 2012 (UTC)
Narcolepsy is mentioned several times before it is defined under “wakefulness.” I would suggest to either define it (or describe it) earlier in the article or just hyperlink it for people to read about it themselves. I also think the last paragraph under “wakefulness” can be categorized under a different heading. It does not directly relate to wakefulness, but is useful because it is talking about the problems that can occur if one does not have orexin-producing neurons. Under ‘food intake,’ why does orexin increase the craving for food? You could tie this in with the increased obesity rate for those with low levels of orexin. The ‘energy metabolism’ section could be expanded or even grouped with the ‘food intake’ section.
Overall, the article was very informative and had a lot of good content! Cbruha11 ( talk) 15:19, 28 March 2014 (UTC)
![]() | This article was the subject of an educational assignment in 2014 Q1. Further details were available on the "Education Program:Nebraska Wesleyan University/Psyc 180 Psychology of Sleep and Dreaming (2014)" page, which is now unavailable on the wiki. |
If higher levels of orexin correlate with improved mood and less depression, but also greater wakefulness, then how could orexin explain higher incidence of depression in narcoleptics? If anything it would suggest to me that narcoleptics should have lower incidences of depression, which the page doesn't read to suggest. Scuriusx86 ( talk) 23:55, 10 November 2015 (UTC)
It's been a while since I visited this page, but I just noticed this: "Studies suggest that orexin-A may be of greater biological importance than orexin-B." I know I've been away from orexin research for a long time now, but on its face this statement seems preposterous. First, the fact that orexin-B has been observed as less potent or less effective than orexin-A at anything only means we don't know if its main endogenous function is to do something we haven't thought to test. Orexin-A is clearly more effective at inducing feeding. Does that make it more biologically important? We don't know what we don't know here. We don't know all of the possible functions of these peptides. Second, when I was studying the orexins (which ended in 2006), orexin-A had simply been studied more than orexin-B. We knew more about it, so researchers had a lot more to build on, and therefore a lot more was published, building a clearer picture of its function in the brain. It was more effective at inducing the effects that we were looking for, but we have no idea what all of its effects are. We can't know that for any neuropeptide until we figure out exactly how the human brain works. Third, importance is a vague and dependent statement of a thing's value, and is nearly a meaningless thing to say on a scientific level. Scientists speak in specifics. Important for what? Appetite? Arousal? Memory? Important how? Activation? suppression? Survival under extreme conditions? The fact that orexin-B is preserved across so many species is compelling evidence of its evolutionary importance. We either need to source that claim or get rid of it. Dcs002 ( talk) 11:07, 24 May 2014 (UTC)
I agree. Orexin-A is certainly the go-to peptide for agonist-based studies and the OX1 receptor has got more selective antagonists for it, but that doesn't mean that OX-B or the OX2 receptor doesn't do anything. I have therefore removed that sentence. ( 149.171.66.108 ( talk) 06:29, 3 October 2016 (UTC))
We should probably add the epidemic (1,300 cases) of narcolepsy in Europe caused by the Pandemrix influenza vaccine, which triggered an autoimmune reaction to hypocretin receptor 2. An exposed region of the influenza nucleoprotein A shared residues with a fragment of the first extracellular domain of hypocretin receptor 2. People with HLA-DQB1*0602 haplotype developed protective immunity to influenza and an autoimmune reaction to hypocretin receptor 2, leading to death of the cells and incurable narcolepsy. There were 1,300 cases out of 30 million doses of Pandemrix, so it's a relatively rare reaction, on the order of the other known, rare risks of influenza vaccines.
Ahmed SS,Volkmuth W, Duca J, et al.
Antibodies to influenza nucleoprotein cross-react with human hypocretin receptor
http://stm.sciencemag.org/content/7/294/294ra105
Science Translational Medicine. 01 Jul 2015; 7(294):294ra105. DOI: 10.1126/scitranslmed.aab2354
Gretchen Vogel
Why a pandemic flu shot caused narcolepsy
http://news.sciencemag.org/health/2015/07/why-pandemic-flu-shot-caused-narcolepsy
Science. 1 July 2015 DOI: 10.1126/science.aac8792.
And Science calls it hypocretin. Is that the name now? -- Nbauman ( talk) 03:15, 6 July 2015 (UTC)
I'm not a specialist in this area, but it does appear that the clause, "but immunocytochemistry tactics revealed the various projections this area truly had to other parts of the brain. " from the second paragraph of the Discovery section needs some kind of verb.
..had to connect...???
I'm hoping that someone can add the right verb. — Preceding unsigned comment added by Joel1947 ( talk • contribs) 17:11, 29 July 2017 (UTC)
High plasma triglycerides (from a high fat diet) and low blood sugar ( hypoglycemia) increases orexin levels, which increases appetite through orexin-stimulated neuropeptide Y action. [1] A high fat diet more than a high calorie diet has been shown to increase obesity and orexin release. [2]
References
These are biomedical claims and therefore need secondary sources to support them. Here are a couple of possibilities:
Orexin and Obesity (page 34)
Section 13: OX and the Control of Glucose Homeostasis
Orexin signaling in feeding, energy homeostasis, obesity and diabetes
Boghog ( talk) 18:29, 3 February 2018 (UTC)
This article was the subject of a Wiki Education Foundation-supported course assignment, between 28 August 2023 and 15 December 2023. Further details are available
on the course page. Student editor(s):
Adn23 (
article contribs). Peer reviewers:
Achait2023.
— Assignment last updated by Achait2023 ( talk) 17:11, 5 December 2023 (UTC)