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Former good article Insulin was one of the Natural sciences good articles, but it has been removed from the list. There are suggestions below for improving the article to meet the good article criteria. Once these issues have been addressed, the article can be renominated. Editors may also seek a reassessment of the decision if they believe there was a mistake.
Article milestones
Date Process Result
December 20, 2005 Good article nominee Listed
January 20, 2009 Good article reassessment Delisted
On this day... Facts from this article were featured on Wikipedia's Main Page in the "On this day..." column on July 27, 2004, January 11, 2005, July 27, 2005, January 11, 2006, July 27, 2006, January 11, 2007, January 11, 2008, January 11, 2009, January 11, 2010, July 27, 2011, July 27, 2012, and July 27, 2015.
Current status: Delisted good article

QUALITY CONTROL: Article has become too long and unfocused[edit]

It occurs to me a great deal of the information in this article is related to insulin therapy as a treatment for diabetes (not to mention the lengthy section on it's use as a performance enhancer), whereas there isn't all that much information on the many actions of insulin throughout the body (effects on different tissues, enzymes, possible role in atherogenenesis and Alzheimer's etc). I'd suggest the article would benefit by being split up into two - one that focuses on the hormone and it's actions, and the other that discusses therapeutic and non-therapeutic uses. Thoughts? Andybellenie (talk) 23:49, 5 November 2008 (UTC)

I agree. The article is currently 76 KB long. According to Article_length#A_rule_of_thumb, the article "probably should be divided". The entire section entitled "5 As a medication" could easily be split out into a new article entitled Insulin therapy and replaced with a short paragraph in this article with a link to the new article. Boghog2 (talk) 05:32, 6 November 2008 (UTC)
I agree that the article is long, and even that it is unfocused, """but""", the underlying subject matter is immense and multi-variate. An article which reflects the reality, as WP articles are enjoined to do, will necessarily be long and unfocused. The length recommendations are rules of thumb, not inflexible edicts.
Philosophically, there are both splitters amongst the WP editorial community and lumpers. I am neither, being more concerned with the experience of the Average reader. It's been my experience in my own writing, on and off WP, and in observing discussion here, that our AR (for whom we are writing) is, like most everyone save specialists 9eg, physicians and scholars) ill-equiped by training or inclination to be able to assemble a coherent picture of a subjects rea from scattered and interlinked coverage of subparts here and there. For articles of first resort, which this really is insulin being so central and basic to so many aspects of human and other physiology and biochemistry, we here should endeavor to avoid forcing such organization on our AR. It will be a disservice, and a decrease in WP quality.
I oppose the proposed split and suggest instead better writing to cover the necessary subparts of a largish topic. Always needed, that brilliant writing, after all; whether in split out articles or lumped ones. ww (talk) 14:58, 6 November 2008 (UTC)
I understand your point, but I still feel that insulin therapy is a large and complex enough subject in itself to justify it's own article. For better or worse, people often use WP to look up medical information and so a focused topic on the subject is desirable Andybellenie (talk) 23:01, 6 November 2008 (UTC)
The topic of insulin therapy (which would fall under the umbrella of WP:MED + WP:PHARM) is important and broad enough such that it deserves its own article. The insulin article could then concentrate on the function and properties of endogenously produced insulin protein and would be covered under WP:MCB. On a somewhat related issue, I noticed that there is a separate insulin gene article (also within the scope of WP:MCB). I think separating the information about the gene and the protein into two articles is unnatural since the two topics are so closely related (and much more closely related compared to the topics of insulin protein vs. insulin therapy). Hence I think the protein and gene articles should be merged and at the same time, the "5 As a medication" section should be split out into a new article to prevent the insulin article from becoming too long. Boghog2 (talk) 22:27, 10 November 2008 (UTC)
Agree wholeheartedly, insulin therapy is the subject of entire textbooks and worthy of a separate article. I disagree with ww because being a substantial topic is no reason to have an unwieldy article; the entire planet Earth has an article no longer than this one. Certainly insulin therapy should be mentioned here, but it shouldn't consume half the article and 30ish kB. Insulin therapy once existed but was crappy and deleted here. - Draeco (talk) 05:27, 19 November 2008 (UTC)
Agree as well. Insulin therapy deserves its own articles under the same logic that hematopoietic stem cell transplantation has its own article from bone marrow, and arsenic poisoning has its own article from arsenic. The subject is already discussed in great length, so it would have no problem existing as a seperate article without the fear of being too short, or in any way too specific. On a slightly different point, I suggest a mention of Hans Christian Hagedorn in this new article, as he was one of the founding fathers of modern insulin treatment, and because the laboratory he founded still exists today as the company Novo Nordisk, which still markets insulin worldwide. He even had the NPH (Neutral Protamine Hagedorn) Insulin named after him. I would gladly add this to the article myself should it be split - I am in possession of a somewhat rare biography of Hagedorn. Bobber0001 (talk) 21:30, 19 November 2008 (UTC)

Article split[edit]

As discussed above and in the spirit of WP:BOLD, I went ahead and split out the material that was previously in the "as a medication" section of this article into a newly created insulin therapy article. In addition, I merged the insulin gene article into this article. Obviously there is a lot editing that should be done to both this and the insulin therapy article. Cheers. Boghog2 (talk) 00:11, 10 December 2008 (UTC)

Charles Best, Clark Noble, and the coin toss.[edit]

I understand the comment about the coin toss being unfortunate for Clark Noble may come close to the neutral point of view policy, but it doesn't make sense to keep removing the statement. The reference at the end of the sentance is a reference to an article about how Clark Noble's career took a different path as a result of losing the coin toss to Charles Best. Removing the part about the coin toss being unfortunate for Noble makes the reference at the end of the sentance meaningless.

One of the references notes that the account of the coin toss was fabricated by a Canadian newspaper reporter and denied by Noble and Best. The entire story is suspect. In addition, the article is about insulin, not someone's unfortunate career misturn. This aspect of the article should be kept to a minimum because of it. --MartinezMD (talk) 05:54, 21 February 2009 (UTC)
Here's the reference: "Stevenson stated in a footnote that "Drs. Best and Noble agree that the coin-tossing story is fiction, invented here by a newspaper reporter," that "Noble was not in the best of health at the time", and that "he left at once for a holiday."26 Charles Best maintained that the story of the coin toss was made up by a reporter for the Toronto Star"

First, the article is indeed about insulin, but the subheading is about the history of its discovery, and the people involved in it. Noble may have narrowly missed the chance to work with Banting in the summer of 1921, but he was later charged by Macleod to do work on insulin purification in 1922, and made significant contributions to the early characterization of insulin. E. Clark Noble deserves mention in the section about the discovery of insulin. The working relationship between Banting, Best, Collip and Noble is relevant to this part of the article. The only reasonable alternative would be to create a second article about the discovery of insulin, and leave this one to deal with the properties of the protein itself. I don’t know if anyone’s interested in doing that.

Second, the source of Lloyd Stevenson’s footnote about the coin toss story is obscure, and a personal communication from Charles Best’s son in 2002, claiming that the coin toss story from 1921 was a fabrication doesn’t necessarily make the entire story suspect. Especially when both Frederick Banting and Clark Noble himself claimed it was true. I’m pretty sure there isn’t a single story in the annals of human history that doesn’t have at least one detractor, but the official story, attributed to both Banting and Noble has been that the coin toss determined which student would work with Banting.

The claim that the coin toss didn’t take place was attributed to Best in later years. However, Best’s motives in claiming there was no coin toss have been questioned in a very compelling way by Banting biographer Michael Bliss, who presented convincing evidence that Best probably recanted a number of events surrounding the discovery of insulin to play up his own role in its discovery, and downplay the role of Macleod. For example he claims that he chose to work with Banting because he believed in his idea (at a time when Macleod didn’t), and that Macleod hadn’t select him as one of two students to work with Banting. Rather, he chose to work with Banting on his own volition because he believed in Banting’s idea. Thus, arbitrary selection by Macleod, and a coin toss to determine who would work with Banting would make his association with the discovery of insulin seem too much like luck rather than foresight and intent. So he denied that it took place. The link to Bliss’ argument is here:

The coin toss story is not so much suspect as it is controversial, with two of the principals claiming it happened and the third claiming it didn’t, with at least one important biographer questioning the motives behind the latter claim. Since the story is both interesting and relevant to the history of the discovery of insulin I wanted to include it, but didn’t want to get into the controversy. So, I just included the more common version of the story, without touching on the controversy. I’d rather not remove it from the article, but if you insist on making an issue of it, I can expand it to include both sides of the controversy.

  • I didn't revert the edits or remove your additions to the section any further because I agree the history is important. However, *this* article is about insulin, not primarily the history of it's discovery or the principals. The history of its discovery is growing and will approach a cumbersome size if not already there. I put forth the premise that in this article these issues should be more superficially covered, and a more in-depth article should be created about the discovery of insulin as was done with "Insulin Therapy". --MartinezMD (talk) 06:41, 22 February 2009 (UTC)

On second thought I'm going to ask Michael Bliss, the foremost living expert on this history, if he'd be interested in writing an article on the discovery. There's certainly enough material to warrant it. Thank you.

The discovery section while very relevant and well written is starting to overwhelm the rest of the article due to its length. I would therefore support splitting out this material into a new article. Cheers. Boghog2 (talk) 12:51, 22 February 2009 (UTC)

fully deuterated insulin[edit]

new drug invention public domain Deuterium is less than a quarter a gram deuterated insulin is likely to have last much longer from the isotope effect

Deuterium is less than a quarter a gram deuterated insulin is likely to have last much longer from the isotope effect fully deuterating 20 milligrams of insulin which would be a bunch as its a medically active peptide would cost less than half a ¢

modern insulins are produced via genetically engineered cultured material solitary microorganisms have been bred to survive an all deuterium culture fluid Thus breeding a current insulin producing organism to survive a deuterium environment is likely

wikipedia says words rather like The rate of a reaction involving a C-H group is typically 6 to 10 times faster than the corresponding C-D group

the deuterated version lasts longer

as a multiunit peptide there is also the opportunity to deuterate just part of the structure

anyway I think it would make it have different pharmacodynamics which could be worth the deuterium at less than part of a ¢ —Preceding unsigned comment added by (talk) 23:22, 12 October 2009 (UTC)

Hexamer, Monomers[edit]

Insulin is synthesised and stored in the pancreas as a hexamer, while the active form is the monomer. The articles does not mention this at all. Should it? (talk) 22:36, 14 May 2009 (UTC)

I'm adding it. (talk) 09:55, 19 May 2009 (UTC)

Synthesis, physiological effects, and degradation[edit]


Insulin is produced in the pancreas and released when any of the several stimuli is detected. The stimuli include ingested protein and glucose in the blood produced from digested food. Carbohydrate produces glucose, although not all types of carbohydrate produce glucose and thereby increase blood glucose levels. In target cells, they initiate a signal transduction, which has the effect of increasing glucose uptake and storage. Finally, insulin is degraded, terminating the response.

"Carbohydrate produces glucose, although not all types of carbohydrate produce glucose..."---(What the heck?!!). This sounds confused and contradictory. It can surely be reworded in a better way. Perhaps it is sombunall (some but not all) carbs which produce glucose? (I dunno; that's why I'm asking) Shanoman (talk) 01:06, 6 August 2009 (UTC)

   Physiological effects

The following section has been copied from page 108 of book the book “Thrive with Diabetes” from Laurence Chalem. Increased glycogen synthesis – insulin forces storage of glucose in liver (and muscle) cells in the form of glycogen; lowered levels of insulin cause liver cells to convert glycogen to glucose and excrete it into the blood. This is the clinical action of insulin, which is directly useful in reducing high blood glucose levels as in diabetes.[citation needed]

I suggest change it for: Induce glycogen synthesis - Insulin decrease glucose concentration on blood by inducing intake of glucose by the cell. It is possible because Insulin causes the insertion of GLUT4 receptor in the cell membranes of muscle and fat tissues which allows the glucose to enter the cell.[1] Also, when glucose levels are too high, insulin induce the formation of glycogen in liver and muscle cells to storage the excess of glucose, until it is needed.[2]Carmenmilagros (talk) 01:32, 25 May 2017 (UTC)

bidirectional transport glut2 vs glut4 confusion[edit]

The second sentence of this article states:

"Insulin causes cells in the liver, muscle, and fat tissue to take up glucose from the blood, storing it as glycogen in the liver and muscle, and stopping use of fat as an energy source."

The problem I see with this is that the sentence implies that liver cells have glut4 transporters--they don't--they have glut2 (passive) transporters. Insulin only directly "causes" cells with glut4 transporters to take up glucose. However, insulin does increase the consumption of glucose in liver cells, changing the concentration gradient across the cell membrane and driving glucose into the cell. It could be said that insulin causes glucose to be taken up by the liver, but it is only an indirect effect. Sure insulin is necessary, but without increased metabolism, there would be no increase in glucose transport.

I don't know if it is really all that necessary, but when I was reading it I got confused. I was thinking the only change that should be made would be something like "Insulin causes cells in the liver, muscle, and fat tissue to both directly and indirectly take up glucose..." I won't make any changes until I get some feedback.

My source is: Susan P. Porterfield. Endocrine Pancreas. C 2001. 2nd ed. Mosby, Inc.

Bjf624 (talk) 14:00, 2 September 2009 (UTC)

I take it that your problem with current wording is the lumping together of different transporters. Your proposed fix also lumps them together, but in a different way. It may be useful to Our Reader to make this distinction. If so we will have to add some wording to clarify the distinction. I suggest you be bold and have it.
I myself think it would be useful. ww (talk) 09:54, 3 September 2009 (UTC)

Requesting edit concerning Nikolae Paulescu.[edit]

Nikolae Paulescu was denied the Nobel Prize not because his findings were subpar, but because of his Antisemitic views and beliefs. I'm requesting permission to put that fact in the article, because where it says that Paulescu did not receive the Nobel Prize and that "Professor Ian Murray was particularly active in working to correct the historical wrong against Paulescu" and why Paulescu should have received it, it never stated why Paulescu didn't get the Nobel Prize. I think it would fill up a small hole in this article if I edit that part of the article.

--I am Gogandantess! The Greatest Swordsman of All the Demons! User:Gogandantess (talk) 18:03, 29 October 2009 (UTC)

I don't think that kind of detail is appropriate to add to this article whose main focus should remain on the insulin protein and not the discoverers. I do think however it would be appropriate to add that kind of information to the Nicolae Paulescu article. Cheers. Boghog (talk) 18:21, 29 October 2009 (UTC)
Concur with Bgohog. Further, it's my understanding that the Nobel Committees do not make public the list of people being considered, the reasons for rejecting any candidate. No information is made available for something like 50 years (at least 'recently'). So I'd be curious about the data source(s) for this claim. And, there are several Nobel Prize winners I know of who were quite anti-Semitic, one at least from this era. So why the Committee would object in Paulescu's case but not in others? Puzzling.
Finally, you don't need nayone's permission to edit the article. I trust what you wee after here was other editors' perspectives, not permission. :) ww (talk) 19:20, 29 October 2009 (UTC)
Yeah, thats what I meant. Just checked out the Nikolae page and its already in there. Yeah, I guess it wouldn't belong, but I just think it would confirm that it wasn't the fact that he wasn't worthy. User:Gogandantess (talk) 18:03, 29 October 2009 (UTC)

Insulin pump[edit]

how much insulin dose a insulin pump hold? Dose anyone have any idea?

Thank you Cindy Champlin Ridgeland, SC —Preceding unsigned comment added by (talk) 20:10, 3 February 2010 (UTC)

Check under Insulin pump --MartinezMD (talk) 22:26, 3 February 2010 (UTC)

Section does not make sense.[edit]

This appears to be just sort of a jumble of words :S

"Signal transduction pathway

When insulin receptor receipt ligand in its dimeric from, activated by tyrosine domain phosphorylation, it binds IRS-1 through its SH2 domains, afterward multiple tyrosine residues of IRS-1 itself are then phosphorylated, which binds to PI3K which cleaves PIP2 in PIP3, it generates a binding site of PKB (AKT), and also for PDK1 which being associated with PKB, can activated PKB by phosphorylation. p-PKB downstream of insulin have two important forward, once can phosphorylate serine 21 in GSK-3a and serine 9 in GSK-3b, which inhibited phosphorylation of glycogen synthase(GS), that’s phospho-dependent mechanism of GS. [21]Other can phosphorylates TBC1D4, which inhibits the GTPase-activating domain associated with TBC1D4, which leaves proteins into downward and stimulates GLUT4 translocate into plasma membrane to uptake glucose, which can be convert to glucose-6-phosphate it’s allosteric activation of GS.[22]"

Could someone who knows about this please improve it? —Preceding unsigned comment added by (talk) 14:15, 26 January 2011 (UTC)

Yes, I agree that that section was very opaque. I have rewritten it and merged it with the closely related Insulin#Signal_transduction section. The pathway is very complex, but I hope the section now make a little more sense. Cheers. Boghog (talk) 21:48, 26 January 2011 (UTC)
 Yes, This section is very confusing. I suggest the following:

The effects of insulin are caused by the binding of it to a glycoprotein receptor in the cell membrane. This receptor has two α-subunits and two β subunits. The β subunits has tyrosine kinase enzyme activity which is triggered by the insulin binding. This activity provokes the autophosphorylation of the β subunit itself and the phosphorylation of other proteins inside the cell like IRS-1 and IRS-2. This phosphorylation cause the non- covalent binding of other proteins (PI3-kinase, Grb2 and SHP2) to them which initiate a cascade of events that activates some nuclear proteins like Ras and MAP kinase. This activation will eventually activate nuclear transcription factors for the regulation of glucose transport and for the synthesis of glycogen and proteins.[3]Carmenmilagros (talk) 01:34, 25 May 2017 (UTC)

Terrible mistake in Ian Murray quote[edit]

How is it possible to misquote ? In refference 27 of the article, 1st page, line number 10, clearly states: "Insufficient recognition has been given to Paulesco, the...[]"

INsufficient, not sufficient, as quoted in the wiki page !!

Bogdan Nacuta 25.02.2011 —Preceding unsigned comment added by (talk) 13:02, 25 February 2011 (UTC)

It's amazing how this sole word "insufficient" is the base of the Romanian far right to assume the fascist Nicolae Paulescu should have received a Nobel Prize. (talk) 10:04, 7 February 2014 (UTC)

Paulescu's work should be nullified ???[edit]

"Also, the French Minister of Health, stated that all his scientific merit must be nullified because of his "brutal inhumanity" of expressing anti-jewish views. " - can anyone confirm this, did the French minister of Health actually make this statement? If he did, it's revolting and should have received a harsh and severe response from the Romanian government. — Preceding unsigned comment added by (talk) 18:23, 24 August 2011 (UTC)

How is insulin an enzyme?[edit]

To be an enzyme, a protein must catalyze a chemical reaction. Receptor binding is not a chemical reaction. What chemical reaction does insulin catalyze? — Preceding unsigned comment added by Hjimker (talkcontribs) 21:28, 8 May 2012 (UTC)

Corrected. Thank you. — Preceding unsigned comment added by (talk) 17:52, 16 May 2012 (UTC)

Insulin causes liver cells to take up glucose?[edit]

The introduction to this article states that "Insulin causes cells in the liver, muscle, and fat tissue to take up glucose from the blood". I thought I learned that in liver cells insulin stimulates the conversion of glucose into glycogen, but that liver cells aren't insulin-dependent for glucose uptake because they don't use a Glut4 transporter. Could a specialist please confirm ? —Preceding unsigned comment added by Callacatacat (talkcontribs) 12:47, 30 September 2010 (UTC)

Thats right. There are some cells that are not dependent on insulin for glucose uptake. These are liver, brain, erythrocytes, intestinal epithelial cells, cornea, kidney. — Preceding unsigned comment added by (talk) 06:13, 24 May 2012 (UTC)

Proposed new edit regarding method of introduction of insulin[edit]

An editor has been trying to add content like the following to the article:

The pharmacokinetic nature of insulin depends upon the way of administration. Here there are two types of administration one is with using Catheter and another one is using with micro needles. Catheter is a very large needle and is more painful when administered intradermally. However administration is more difficult as it is administered in such a way that right below the skin. And this method creates very fear in patients. In case of micro needle method we use a thin needle and is less painful when administered.It has fast pharmacokinetic nature and post pandrailglycemic response. Patients feel less fear and also brings glucose levels to normal glucose levels. These are the advantages of micro needle technique when compared to Catheter method. The only disadvantage of micro needle method is when piercing a small bulb is formed though it will be recovered in one day. It can be used in children as it has rapid insulin absorption.

sourced to:

<ref name="pmid21355717">{{cite journal | author = Gupta J, Felner EI, Prausnitz MR | title = Rapid pharmacokinetics of intradermal insulin administered using microneedles in type 1 diabetes subjects | journal = Diabetes Technol. Ther. | volume = 13 | issue = 4 | pages = 451–6 | year = 2011 | month = April | pmid = 21355717 | pmc = 3131988 | doi = 10.1089/dia.2010.0204 }}</ref>

There's a couple of problems: 1) The sourcing fails WP:MEDRS--it's a primary study on 5 people written by the guy selling the patent license on the products used in the study, 2) It's not written very clearly, 3) It appears to be written in a style that is promoting the product used. Could you please provide a WP:MEDRS-compliant source and help us get the content expressed more clearly? Thank you. Zad68 13:30, 12 October 2012 (UTC)

I've reverted the difficult-to-follow and misplaced edits pending further discussion here. Looking at the content, I really don't see much that adds to the article. I agree that medical claims require secondary sources (like high-quality review articles). We welcome a new contributor but some coaching may be required - cannot do that without some interaction. -- Scray (talk) 11:13, 13 October 2012 (UTC)
Agreed, these edits are definitely misplaced. Some time ago (see discussion), this article was split into two, the first covering the insulin gene/protein and the normal function of endogenously produced insulin, and a second (insulin therapy), covering the use of insulin to treat diabetes. The recently added material belongs in the insulin therapy article, not this one. Furthermore any health related information that is added to insulin therapy must be supported by reliable secondary sources. Boghog (talk) 12:19, 13 October 2012 (UTC)
I agree with the reversion of the "difficult-to-follow and misplaced edits". If you had not reverted I would have reverted for similar and additional reasons. Darrell_Greenwood (talk) 17:36, 13 October 2012 (UTC)

Is there an error in the figure?[edit]

In the synthesis section, the figure showed the preproinsulin inside the lumen of the RER, and the signal peptide is cleaved after the protein folded (which was what the text implied before I modified it). From my understanding, the signal peptide is removed in the process of translocation into the lumen or very soon afterwards, otherwise the proinsulin may not fold properly, for example as suggested by this paper. Can someone check again and modify the figure? I can probably do it some time later if no one will, but I need to be sure that this is the current consensus opinion of the sequence of events. Hzh (talk) 15:03, 2 December 2012 (UTC)

confusion in Physiological effects[edit]

the article says:

"Increased lipid synthesis – insulin forces fat cells to take in blood lipids, which are converted to triglycerides; lack of insulin causes the reverse."

this is not a description of synthesis of lipids. it is uptake or synthesis then? and then the next bullet:

"Increased esterification of fatty acids – forces adipose tissue to make fats (i.e., triglycerides) from fatty acid esters; lack of insulin causes the reverse."

this seems to be what is described in the previous bullet. i suspect the first explanation being incorrect. can someone clarify? does insulin increases lipid synthesis? or only triglyceride synthesis from lipids? (talk) 10:07, 6 July 2013 (UTC)

The article currently has these two confusing statements:

Increased lipid synthesis – insulin forces fat cells to take in blood glucose, which is converted into triglycerides; increase of insulin causes the reverse.[57] Increased esterification of fatty acids – forces adipose tissue to make neutral fats (i.e., triglycerides) from fatty acids; increase of insulin causes the reverse

If "increase of insulin causes the reverse." is correct, then an explanation is needed. Does it mean insulin stops the synthesis of triglycerides from sources other than glucose and stops the esterification of fatty acids to produce triglycerides? — Preceding unsigned comment added by (talk) 00:37, 3 November 2016 (UTC)

Glucose Transporter[edit]

Glucose is not transported into beta cells by GLUT2. GLUT2 is found only in rodent cells. GLUT1 & GLUT3 are present in human cells for uptake of glucose to trigger metabolic pathways. — Preceding unsigned comment added by (talk) 01:17, 31 March 2014 (UTC)

Incorrect unit conversion[edit]

Conversion of U to moles using the factor of 6.945 is incorrect. Unfortunately, this incorrect factor has been propagated to numerous sources on the internet and even the AMA cites it. The correct unit conversion is a factor of 6. Please see [4] [5] for more complete discussions.

metabolism of carbs and "fats"?[edit]

"It regulates the metabolism of carbohydrates and fats by promoting the absorption of glucose from the blood to skeletal muscles and fat tissue and by causing fat to be stored rather than used for energy." 

Insulin regulates the metabolism of fat? And carbohydrates? OK, i'm no scientist. But i thought insulin regulated the distribution of glucose. Could someone please take a look at this and verify or correct. ThankeeLonginus876 (talk) 14:47, 2 July 2015 (UTC)

Numerical error in Insulin article.[edit]

In the fourth paragraph of the article, it is stated that insulin is a protein of 110 amino acid residues, with a molecular mass of 5808 Da. It is preproinsulin that has a polypeptide length of 110 residues, and a molecular mass closer to 12,500 Da. After proteolytic processing prior to secretion, the active hormone insulin is composed of 51 residues in two chains crosslinked by cystine residues. The isotope-average molecular mass of the 51-residue insulin monomer is very close to 5808. (talk) 15:42, 28 January 2016 (UTC)

CAN WE TALK INSULINE AS A ALCOHOL — Preceding unsigned comment added by (talk) 08:07, 31 July 2016 (UTC)

Errors in discussion on Type 1 and 2 diabetes[edit]

Was briefly reading through the article when I located what I believe to be erroneous statements:

When the pancreatic beta cells are destroyed by an autoimmune process, insulin can no longer be synthesized or be secreted into the blood. This results in type 2 diabetes mellitus...

In type 1 diabetes mellitus the destruction of beta cells is less pronounced than in type 2 diabetes, and probably not due to an autoimmune process.

These statements are mixed up for Type 1 and 2 diabetes as far as I understand. There may be even more errors, a full review of the Insulin article by subject matter expert is highly recommended.

FinalStage (talk) 16:25, 29 August 2016 (UTC)

Intranasal insulin should get its own header/section I believe[edit]

I believe a new header should be added titled "Intranasal Insulin" as Intranasal Insulin has differing effects as traditional routes of administration for insulin.

It is important for people to know how Intranasal Insulin differs from subcutaneous injections. For example Intranasal Insulin has been researched to not cause hypoglycemia (source: and does not affect systemic glucose control (source: --CuriousGeorge16 (talk) 02:46, 23 January 2017 (UTC)

Question: Since this article has been critiqued as too long and unfocused does anyone agree that Intranasal Insulin should be briefly discussed here and linked to a new wikipedia article titled "Intranasal Insulin"? link to credible research studies on Intranasal Insulin here — Preceding unsigned comment added by CuriousGeorge16 (talkcontribs) 02:51, 23 January 2017 (UTC)

Expand on Inhaled Insulin?[edit]

There was only one mention of inhaled Insulin on this page. Do you guys think it would be beneficial to add that inhaled insulin has been linked to cancer or has at least been shown to be dangerous? (source here

Also I think we should distinguish between Inhaled Insulin and Intranasal Insulin as they seem similar to the layman but have vastly different effects and safety profiles. --CuriousGeorge16 (talk) 02:56, 23 January 2017 (UTC)

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  1. ^
  2. ^
  3. ^
  4. ^ Heinemann, L (June 2010). "Insulin assay standardization: leading to measures of insulin sensitivity and secretion for practical clinical care: response to Staten et al.". Diabetes care. 33 (6): e83; author reply e84. PMID 20508228. 
  5. ^ Takayama, M; Yamauchi, K; Aizawa, T (March 2014). "Quantification of insulin.". Diabetic medicine : a journal of the British Diabetic Association. 31 (3): 375–6. PMID 24147803.