Talk:Insulin resistance

Treatment of Subject Missing the Forest for All the Trees!
In the entire treatment here, I can't find any reference to systemic inflammation or inflammatory signaling, which a lot of work suggests underpins IR - obesity causes upregulation of inflammatory signaling, as does lack of exercise, Western diet pattern, sleep deprivation, and Vit D deficiency - all factors in IR, metabolic syndrome and type II diabetes. How does this treatment include so many details, and miss the big picture so completely? dfwatt, HMS. —Preceding unsigned comment added by 209.6.180.11 (talk) 16:08, 24 April 2011 (UTC)

I
I added another meta-analysis to the page to the prevention and management section. This covers exercise effects on insulin resistance on adolescents. -Kirost200--Kirost2000 (talk) 04:05, 8 December 2021 (UTC)

I added back the reference to the presentation of Dr. Andrew P. Selwyn on CME on Diabetes that has been deleted during (I suppose) a spamming done a few days ago. This source has been used for the Pathophysiology section. -Eridanis

Why is there an IP number on top of this article? 205.174.22.25 03:36, 6 February 2007 (UTC)

There is a lot of vague, speculative, or unsourced information in this article. Just speaking as an avid fan of Wikipedia and a non-expert regarding the subject of insulin, it isn't very useful -- in fact I think anyone who doesn't look at it with a critical eye could be misled re: topics like what causes insulin resistance by some of the speculation and unsourced, original research in this article. If the science hasn't established these things, the article should just say so. —Preceding unsigned comment added by 124.168.112.203 (talk) 12:21, 26 December 2010 (UTC)

Agreed: the article is a mess, and needs not simply attention from an expert, but outright cleanup. Unreferenced assertions should be deleted. They make the article unnecessarily long, are frequently factually inaccurate, and just rob the whole article of its credibility.--Rhombus (talk) 12:26, 28 January 2011 (UTC)

The above comments are all quite old, but there are still some issues with this article. I have never before seen a link to a random blogpost put directly into the main text of a wikipedia article, and as far as I can see the article still not only contains a lot of unsourced claims but also probably some factual inaccuracies - the "If this compensatory increase does not occur, blood glucose concentrations increase and type 2 diabetes occurs" passage in the first paragraph is, as far as I know, simply not true - T2's do increase their production of insulin when insulin resistance increases, the increased production of insulin just is not enough to meet the body's needs in the long run. I'm not really an expert in this matter, but I do know enough about the subject to tell that this article still has some issues. In my experience, when there are inaccuracies in the first paragraph of an article it gets much harder to trust the rest of the material even if it's ok (which some of it probably isn't, given the unsourced claims that are still around). Knowledgelover121 (talk) 10:04, 13 September 2011 (UTC)


 * I agree. I'm curious as to how correct information is inserted into the Wikipedia text. In the side section there is a statement "Insulin is a hormone that facilitates the transport of glucose from blood into cells, thereby reducing blood glucose (blood sugar)." Since the topic is insulin resistance perhaps a sentence following the first could be: "In the presence of insulin resistance the blood sugar rises since transport from the blood into the cells is thwarted".
 * T2DMcoach (talk) 00:38, 5 July 2023 (UTC)

Spam
An anon keeps on inserting an animal study linking bisphenol A with insulin resistance. We have to be very very selective with animal studies. Only if they display a major trend in research, a very useful animal model, or somesuch, are they worthy of inclusion. I agree with this link should stay out until its relevance in humans becomes known. JFW | T@lk  23:35, 18 December 2005 (UTC)

This article is a little heavy for the lay person like myself. Could someone maybe make it a bit more readable for the non medically trained? Pipedreambomb 23:37, 3 March 2006 (UTC)

Intelligibility
Someone should really re-write that opening sentence in English, no? I think I understand what it's saying, but I'm not confident enough to re-explain it.

...in fact, that goes for much of this article. At the minimum, medical jargon which is likely to be unfamiliar to the educated lay reader should be linked. --Oolong 21:12, 5 June 2006 (UTC)


 * I have rewritten the introduction in what I believe is simpler terms and more detail, making wikilinks to all of the medical terms. I hope that this satisfies you. It looks better to me. --Ben Best 14:39, 6 June 2006 (UTC)

identical to "metabolic syndrome" ?
Since I'm being flamed for edits, I'll just leave the reference, so an approved editor can deal with it:

http://www.ajcn.org/cgi/content/abstract/83/6/1237

The article is heavy. It should also note that there are many causes of insulin resistance including atrophy and cells already being plump with glycogen, autoimmunity is just one, and that both cells and people can be so referred to, since some cells in an individual can be insulin resistant while others aren't.

The essential point is that insulin is a hormone - just the messenger. It requests cells that "excess" glucose be stored as glycogen. If the message isn't acted on, for whatever reason (including not getting to the cell as in autoimmunity), that's "insulin resistance" or at most what parents refer to as "selective hearing." (to be much too flip)

Again, I'm being flamed for contributions, so I will leave this editing task to someone in the inner circle, or much closer to it.

Monounsaturated Fat-Olive Oil leads to Insulin Resistance? Polyunsaturated Fats All Good?
The one study that I've seen that promotes this hypothesis concerning olive oil is the one this article refers to. There are many more studies that cite olive oil (and other monounsaturated fats)as neutral to good. Additionally, the blanket statement that polyunsaturates (which include omega-6 and omega-3 oils) lessen/mitigate insulin resistance sidesteps the extreme difference in effects of the two on hormone production and inflammation. In essence, the information on fats and insulin resistance appears both biased toward a limited amount of evidence for one hypothesis about monounsaturates(to the exclusion of the greater body of evidence), and a gross generalization that could lead people to believe that all polyunsaturated fats are equal (omega-3's are known to lessen inflammation, while most omega-6's are known for inflammatory properties). I've read that a quarter of the adult population has developed, or is at risk for developing some form of insulin resistance. That's a lot of people who could be coming here for guidance after the doctor has told them they are pre-diabetic, and they deserve better.

-Believe it or not, there are interesting individuals out there (Perricone fans?) who think that fish-based omega-3s reduce inflammation while plant-based omega-3s increase it. I wish I knew where they were getting this.--Dseilhan 21:38, 20 March 2007 (UTC)

Connecting the Dots
The National Insulin Resistance Council (NIRC) appreciates both the technical complexity and the mystery of how insulin resistance starts and works. While scientific research goes on, NIRC believes that there are enough dots to be connected into a pretty clear picture. And the picture leads us to believe that there are specific things that can be done to improve it by a wide margin.

Consider this logic: No one doubts the links between insulin resistance (IR), diabetes and IR and CVD. Nor are the links between IR and PCOS and metabolic syndrome in question. Intervention with IR patients even when they have become symptomatic prolongs healthy life, and defers disease. The villian in IR is hyperinsulinemia, having too much insulin too much of the time. Insulin is suspect in liver signaling related to glycogen creation. Insulin is caustic and erodes the inner linings of vascular tissue and the outer sheathing of certain nerve tissue. These effects occur whether a patient is symptomatic or not. IR appears to be genetically programmed, evidenced by the epidemiological data relating family diabetes and CVD histories. IR certainly is aggravated by excess weight, and may be triggered by it. If IR is the staging for consequential illness, and its effects occur unseen until symptoms like high blood pressure, elevated blood sugar or menstrual disruption show up, then why don't we seek to identify its presence early, before it does so much of its slow, relentless damage? More logic, this part social: There are 21+ million active diabetics in the US today and over 400 thousand fatal heart attacks not attributable to cholesterol. Related sick care costs all taxpayers nearly 30% of Medicare expenses, all linked to IR. PCOS, caused by IR, is a significant cause of fertility issues, but the proportion is not known for lack of tracking. In addition to the costs of active non-infectious disease care, who would guess at the cost of all the avoidable cases of PCOS, hypertension, gestational diabetes, diabetes, and CVD? The children and young adults of today with undetected IR are tomorrow's diabetics and CVD victims, yet they don't have to be. Why aren't we scrambling to find ways to prevent non-infectious disease as hard as we scramble to deal with it?

NIRC proposes specific actions: 1. Immediate efforts to find the easist, least costly, least intrusive, and most effective means to screen children and young adults for IR should be started and the best ones rolled out. 2. The CDC should track and report the incidence of IR. Today, it does not even include IR in its index of conditions. 3. The CDC should track and report the incidence of PCOS and especially the fertility complications from it. 4. The CDC should track and report the incidence of metabolic syndrome.

Decades before the tobacco industry conceded that smoking caused cancer, warnings were put on their products. Shouldn't people who have IR know it, so they can take action to blunt its effects before their lives have been shortened by it?

The National Insulin Resistance Council's purpose is to educate health care professionals and the public about IR, its effects and to propogate workable interventions.

151.200.237.196 00:59, 17 May 2007 (UTC)fs@insulinresistancecouncil.org

NIRC, source your edits
First, Wikipedia is not the place for starting social change, or making social commentary. Wikipedia is a place for facts, and NIRC's comments above in "Connecting the Dots" are inappropriate. Secondly, NIRC makes a verifiable claim, to wit: "Nevertheless, metformin, the 8th most often prescribed drug in the US, is often prescribed for pre-diabetes and insulin resistance, despite FDA instructions". I am deleting this phrase, but anyone may feel free to re-add it should they be able to properly cite a reference for it. Finally, the use of "NIRC ED" to distinguish edits made by NIRC is inappropriate. The proper place to note the source of a fact is in a footnote to that effect, and anything that is not a fact, if it deserves to be in the article (e.g. connecting text), does not deserve to be especially distinguished from the rest of the article.

--Popefelix 18:54, 8 October 2007 (UTC)

I do have a problem with Wikipedia is a place for facts when it comes to nutrition and/or drug statements. These "facts" change so often. What was yesterday a fact is changed. Something else then becomes a "fact". It would be nice to have the changes that come about earlier rather then later. WSNRFN (talk) 21:14, 2 September 2008 (UTC)WSNRFN

I tend to agree with WSNRFN. This article, in addition to being generally turgid and difficult to read, is woefully unbalanced in its presentation of current thinking on insulin resistance. I recognize that Wikipedia is not the place to debate differing theories on the possible causes of insulin resistance, but the article reads as though the causes are well known, which they most definitely are not. This article is fundamentally misleading in this regard. (\\FB\\) — Preceding unsigned comment added by 24.136.172.22 (talk) 16:07, 4 November 2015 (UTC)

History: Who the XXXX was Wilhelm Falta?
I added the reference about Wilhelm Falta who wrote about insulin resistance in 1931, 5 years before Harry Himsworth. Although much less known than Himsworth's paper (maybe because it is in German language and in a hard-to-find journal issue), Falta's paper has been quoted at least a dozen times in reviews on insulin resistance. However, I have not been able to find the paper itself, not even the abstract. My guess is that there is not an available abstract and of course neither a DOI of the paper. Probably the only way to find the paper would be to look for a physical copy in some well-stocked medical library.

About Wilhelm Falta himself there seems to be no information available on the Web, besides the fact that he wrote the paper. A review by E. Gale in "Diabetes" states that he worked in Vienna, but doesn't say in which institution, nor describes his work.

The journal itself is quoted in all reviews as Klin Wochenschr, but it could possibly be the Wiener klinische Wochenschrift, as the Klinische Wochenschrift was edited in Berlin (it was the result of the union of the Berliner klinische Wochenschrift and the Therapeutische Halbmonatshefte in 1921).

Maybe somebody can find Falta's paper and/or add a little more background on Wilhelm Falta. I really would like to give a look at what this guy did. About the authors who quoted his paper in reviews, my guess is that most of them never saw it and are just passing the reference around. Tipically, Himsworth's experiments are described, but Falta is only mentioned.

85.155.148.159 (talk) 19:41, 30 June 2008 (UTC)

You've put Falta in the article, which is right? If you get a named user account and convince me you can read the German I might be convinced to take a trip down to the bowels of the library. I guess the paper could be put up on WikiSource as it's out of copyright now? Ianmc (talk) 20:45, 30 June 2008 (UTC)

Ja, bitte! By all means, please do it, put it on Wikisource or send me a scanned copy!. My account name is drjmartinez, in case it does not show up. My email should be also available, or send it to martinezAT madridDOTcom. Danke vielmals!! Drjmartinez (talk) 15:35, 1 July 2008 (UTC)

Open Directory Project Links
The DMOZ search template, and by implication all DMOZ search links, is being considered for deletion because it violates WP:ELNO #9. Anyone interested in discussing the fate of Open Directory Project (DMOZ) search links is invited to join the discussion at Templates for deletion. Qazin (talk) 05:19, 8 November 2008 (UTC)

Cushing's syndrome
Sorry for my english first! I'm quite surprised about the absence of Cushing's syndrome argument on insulin-resistance topic,why? —Preceding unsigned comment added by 91.80.226.194 (talk) 16:54, 14 April 2009 (UTC)

Why do not talk better about the relationship between cortisol excess and insulinresistance and therefore diabetes?

Weight gain
I am certain that I am an insulin resistance person, and what I have to contribute is based on my experience and therefore anecdotal, so that is why I am keeping it confined to the discussion section. I will voluntarily delete this section if I have misunderstood the talk guidelines and my contribution is not appropriate.

If anyone were to ask me what I think caused me to become IR, I would tell them that I noticed having the symptoms associated with IR following a period during which I consumed too much processed white-flour- and refined-sugar-containing foods and did not get enough exercise. Based on what I have read here and elsewhere online, I suspect my family history of diabetes and overweightness made me more likely to become IR as a result of poor lifestyle choices. I endeavor to avoid Type 2 Diabetes through getting enough exercise and appropriate dietary choices.

Weight gain is listed in the article as one of the constellation of symptoms of IR. My own experience would suggest that the condition of being IR makes this weight-gain permanent and irreversible for all practical purposes. I realize this statement may be controversial because of the moral judgements that often exist around personal body-weight. Nonetheless, I think this possible aspect of IR would be a worthwhile avenue of further research on this condition. Witchydude (talk) 15:27, 24 April 2009 (UTC)witchydude


 * Yes we can discuss these sorts of things here. Without refs we however cannot add it to the article page.  Weight loss is difficult for everyone as discussed on the obesity page.  Surgery is often the only effective measure for many people with a BMI > 40 and lead to long term weight loss.  Extreme exercise is also effective ( for example military recruits ).  Getting ride of motorized transportation and only traveling by bicycle or walking is effective for the general population but few people are willing to do this.  Losing weight improves IR. Doc James  (talk · contribs · email) 15:04, 22 April 2010 (UTC)


 * Haven't found any references to the following thinking, so it's probably original research (so also not allowed to be added to article) Has anyone else considered the importance of maintaining glucose homoeostasis WITHIN individual cells wrt to insulin resistance? If cells have high levels of glucose AND glycogen, would it be in the best interest of those individual cells to to follow the "request" given by the insulin? If not, and they "know"/can enact such knowledge, would it not manifest as insulin resistance? Such cells could be accused of seeing high blood glucose as Somebody Else's Problem.


 * Sometimes symptoms/side effects get listed because of a reasoning "it should cause/has been like that/is like that". Insulin is often assumed to cause weight gain/make weight loss difficult, and insulin resistance tends to result in very high levels of insulin being produced/needed. Certainly with injected insulin in type 2 that can be verified as being a debatable assumption-check out the NICE guidelines on management of type 2 diabetics -http://guidance.nice.org.uk/CG66/Guidance/pdf/English My partner DXed with mild type 2 a few years ago went through all the "normal" type 2 meds being ill (more so with the "stronger" meds). Her Hba continued rising fair sharply until eventually basal insulin was tried (without other meds, at very low levels to see if she'd tolerate it) - Results to nearly normal Hba, felt much better, and even weight loss. NB fairly sure she wasn't tested for IR, so it may/may not be such(her BMI is VERY high, so I can partially understand why it wasn't tested)
 * 82.47.212.82 (talk) 01:19, 4 November 2010 (UTC)

Confusion
New comment - not sure how to get the header (wiki-newbie) I've edited the first few paragraphs of this article. There is some confusion within this article about whether it relates to insulin resistance as a concept, or the insulin resistance syndrome (or metabolic syndrome). In both cases, insulin resistance is associated with reduced insulin action, but only in the second case is it associated with dyslipidaemia, hypertension, etc. The causes of insulin resistance as a concept are many and varied, whereas the cause of the insulin resistance (metabolic) syndrome is obesity. My edits focus on the insulin resistance syndrome.

The other area of confusion was between insulin resistance and reduced insulin secretion. Any amount of insulin resistance will not cause high blood glucose concentrations as long as pancreatic beta cells cmpnsate by secreting proportionately more insulin. It is only if this compensation fails that impaired fasting glucose or impaired glucose tolerance occur.

I'm a researcher in insulin resistance, but my study is all in dogs. Not sure if that makes me an expert for this purpose or not - dogs are one of the better models of obesity-induced insulin resistance.

I hope this helps.

Kurt Verkest (talk) 12:06, 22 April 2010 (UTC)K —Preceding unsigned comment added by Kurt Verkest (talk • contribs) 10:23, 22 April 2010 (UTC)


 * Welcome to Wikipedia. We have a page on metabolic syndrome.  This page I would say is more about the concept of insulin resistance on its own. Doc James  (talk · contribs · email) 15:08, 22 April 2010 (UTC)

hormone production in fat cells?!
Signs and Symptoms #6's needs review: "Weight gain, fat storage, difficulty losing weight. For most people, too much weight is due to high amounts of fat storage. The fat in IR is generally stored in and around abdominal organs in both males and females. It is currently suspected that hormone production in that fat are a precipitating cause of insulin resistance"

The article thus indicates that adipose tissue gains volume, and thus turns into a hormone producer. (Minimally needs source, and probably needs full article link) What hormone specifically is being produced that causes insulin resistance? There is a reference (#14 to a paper on growth hormone replacement therapy, but fat cells do not cause someone to undergo growth hormone replacement therapy). How does this tissue gain this ability to produce the hormone?

Suggest deleting the 2nd-4th sentences, leaving just: Weight gain, fat storage, difficulty losing weight.

Long thought of merely as depot storage for triglyceride, adipose tissue is now known to be an important endocrine tissue. Major active products are leptin, which is critical in the regulation of weight, adiponectin, IL-6, to name but a few. Ianmc (talk) 21:41, 30 April 2010 (UTC)

Cool -- never heard that before :) However,  - on the leptin page there is no mention of it causing insulin resistance (perhaps off-topic);  - the last sentence of the cited area does not specify leptin;  - and the phrase "the fat in IR is generally stored" doesn't seem to make sense -- Insulin Resistance itself doesn't store fat. Instead, it may cause additional fat storage. (perhaps, "The fat caused by IR is generally stored..." - Perhaps the 'hormone production in that fat' should be linked to [Adipose_derived_hormones], and the 2 articles referenced on that page should be cited here. —Preceding unsigned comment added by 216.145.56.15 (talk) 19:49, 6 May 2010 (UTC)

Tobacco
From what I can gauge studies on whether or not tobacco increases insulin resistance have produced mixed results. you should either provide a source for the claim, remove the claim, or at least mention the ambiguity that surrounds the issue.

W66w66 (talk) 21:30, 28 May 2010 (UTC)


 * Yes I agree we should. Let me know if you need help finding / accessing sources. Doc James  (talk · contribs · email) 21:46, 28 May 2010 (UTC)

Insulin Sensitivity
At the moment the google for insulin sensitivty gets redirected to resistance. Can i suggest it would be just as easy putting an entry for insulin sensivity, because to the layman who doesn't understand what it is (and most people doing a google enquire about this for the first time won't know anything about it) a direct entry for insulin sensitivity would be beneficial.

The entry can read something as basic as;

If body tissue is insulin sensntive, it easily and readily accepts nutrients from the body. If body tissue is insulin resistant, it does not accept nutrients as easily

user quartzuk —Preceding unsigned comment added by Quartzuk (talk • contribs) 11:29, 20 June 2010 (UTC)

Original research in symptoms list
I flagged the symptom list as original research and removed the statement, "Symptoms list was quoted in part from various websites that are trying to educate the public about the illness, but were edited for accuracy." from the references. This section needs specific references for items in the list and sources that support supposed inaccuracy and correction. —Chris Capoccia T⁄C 15:21, 4 October 2010 (UTC)

coffee
It says coffee decreases insulin resistance on the Gout page, under Cause/Lifestyle and its referenced. 203.161.68.25 (talk) 11:11, 18 November 2010 (UTC)

Claim that foods high in fat cause excess adipose tissue.
Under the causes of insulin resistance is the following:

"Long term intake of highly fatty foods leads to the formation of fatty tissue that chronically release free fatty acids in the blood stream. This has been found in many studies to contribute to diminished insulin sensitivity. [11]"

which references the following article: ^ Schinner, S.; Scherbaum, W. A.; Bornstein, S. R.; Barthel, A. (2005). "Molecular mechanisms of insulin resistance". Diabetic Medicine 22 (6): 674. doi:10.1111/j.1464-5491.2005.01566.x..

However, the only relevant section in the paper's abstract is this statement:

"Furthermore, we have now increasing evidence that the adipose tissue not only produces free fatty acids that contribute to insulin resistance, but also acts as a relevant endocrine organ producing mediators (adipokines) that can modulate insulin signalling."

The statement assumes that excess adipose tissue in humans is caused primarily by high fat foods. The reference makes no mention of this claim.

Please substantiate this claim or modify the original text.

207.7.59.69 (talk) 23:21, 29 March 2011 (UTC)


 * I agree. This sentence is, at the very least, misleading. I added a 'citation needed' tag; i'm not sure if this is appropriate or not as i have never edited a page before (62.40.51.113 (talk) 10:54, 16 April 2011 (UTC))

A saturated fat worsened insulin sensitivity; a mono-saturated fat improved it. Mono-SFAs  may help uptake and utilization of glucose in normal and insulin-resistant muscle.
Dimopoulos N, Watson M, Sakamoto K, Hundal HS.

Differential effects of palmitate and palmitoleate on insulin action and glucose utilization in rat L6 skeletal muscle cells.

Biochem J. 2006 Nov 1;399(3):473-81.

Abstract

An increase in circulating levels of specific NEFAs (non-esterified fatty acids) has been implicated in the pathogenesis of insulin resistance and impaired glucose disposal in skeletal muscle. In particular, elevation of SFAs (saturated fatty acids), such as palmitate, has been correlated with reduced insulin sensitivity, whereas an increase in certain MUFAs and PUFAs (mono- and poly-unsaturated fatty acids respectively) has been suggested to improve glycaemic control, although the underlying mechanisms remain unclear. In the present study, we compare the effects of palmitoleate (a MUFA) and palmitate (a SFA) on insulin action and glucose utilization in rat L6 skeletal muscle cells. Basal glucose uptake was enhanced approx. 2-fold following treatment of cells with palmitoleate. The MUFA-induced increase in glucose transport led to an associated rise in glucose oxidation and glycogen synthesis, which could not be attributed to activation of signalling proteins normally modulated by stimuli such as insulin, nutrients or cell stress. Moreover, although the MUFA-induced increase in glucose uptake was slow in onset, it was not dependent upon protein synthesis, but did, nevertheless, involve an increase in the plasma membrane abundance of GLUT1 and GLUT4. In contrast, palmitate caused a substantial reduction in insulin signalling and insulin-stimulated glucose transport, but was unable to antagonize the increase in transport elicited by palmitoleate. Our findings indicate that SFAs and MUFAs exert distinct effects upon insulin signalling and glucose uptake in L6 muscle cells and suggest that a diet enriched with MUFAs may facilitate uptake and utilization of glucose in normal and insulin-resistant skeletal muscle.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1615906/?tool=pubmed

Free PMC Article

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1615906/?tool=pubmed

http://www.biochemj.org/bj/399/0473/bj3990473.htm

Source

Division of Molecular Physiology, Centre for Interdisciplinary Research, Faculty of Life Sciences, University of Dundee, Dundee DD1 5EH, UK. — Preceding unsigned comment added by Ocdnctx (talk • contribs) 02:11, 26 May 2011 (UTC)

How to write about science and medicine: Start with things a non-specialist can follow.
This article starts with a highly technical discussion of glucose levels and triglycerides and such, only getting on to symptoms (or anything a non-specialist is going to get much of a handle on) about two pages in. This is not the way to do it, seriously - if a topic has potential interest or implications for the general lay public - which this obviously does - please try to spell them out within the first paragraph or two, preferably before you start using too many words with four syllables or more. I don't have time to do a good job of this myself, but this would be a much more useful article if someone (preferably someone with some background in this stuff) were to write up a lay summary to open the entry with... --Oolong (talk) 10:05, 11 May 2012 (UTC)

Agreed. The intro needs to be clearly separated as it's delves too quickly into detail. Although very informative and precise are the contributions, nevertheless, an encylopedia has a responsibility to guide the layman. Preroll (talk)

Other drugs that cause insulin resistance?
The article currently only discusses protease inhibitors used to treat HIV/AIDS as being one cause of insulin resistance. My significant other suffered from IR due to the medication she was on for epilepsy and depression. According to her the prescribing doctor informed her of the possibility of IR. She subsequently gained about 20kg within about a year (from ~64kg to 84kg). Unfortunately my partner is uncertain about whether the IR is due to only one particular drug or is caused by interaction between two or more of the handful of pills she took daily. At her most recent checkup a month ago her doctor changed almost all of her daily medication to eliminate the IR side effect (as well as the "over-stabilisation" of her emotions) - she has since lost about 5kg in spite of drastically reduced exercise due to knee surgery she had in the same week. From this story it is obvious that HIV/AIDS drugs are not the only pharmaceutical culprits. If someone knows something (and has MEDRS sources) about drugs other than protease inhibitors that cause IR please add the information to the article. Roger (Dodger67) (talk) 13:16, 11 December 2014 (UTC)

Pathogenesis
From JCI: 10.1172/JCI77812 JFW &#124; T@lk  09:14, 5 January 2016 (UTC)

External links modified
Hello fellow Wikipedians,

I have just modified 3 external links on Insulin resistance. Please take a moment to review my edit. If you have any questions, or need the bot to ignore the links, or the page altogether, please visit this simple FaQ for additional information. I made the following changes:
 * Added archive https://web.archive.org/web/20121004215938/http://www.uoguelph.ca/hhns/grad/courses/HHNS6700F10WeeklyReadings/UngerandScherer.pdf to http://www.uoguelph.ca/hhns/grad/courses/HHNS6700F10WeeklyReadings/UngerandScherer.pdf
 * Added archive https://web.archive.org/web/20120113012814/http://www.ysonut.es/pdf/Ysodoc/D060302.pdf to http://www.ysonut.es/pdf/Ysodoc/D060302.pdf
 * Added archive https://web.archive.org/web/20071121193025/http://www.dlife.com/diabetes-news/2007/11/ucsd_researchers_discover_infl.html to http://www.dlife.com/diabetes-news/2007/11/ucsd_researchers_discover_infl.html

When you have finished reviewing my changes, you may follow the instructions on the template below to fix any issues with the URLs.

Cheers.— InternetArchiveBot  (Report bug) 16:38, 29 December 2017 (UTC)

Add one citation about vitamin D deficiency and insulin resistance - and conflict of interest
Hello, I suggest adding a reference to the paragraph:

"Lifestyle and factors". "Vitamin D deficiency has also been associated with insulin resistance.[6][new reference]"

new reference: doi: 10.1055/a-0895-5166 title: Insulin Resistance in Adults with Type 1 Diabetes is Associated with Lower Vitamin D Serum Concentration

Conflict of interest statement: I am co-author of the cited article. I did not get any personal fee for suggesting the citation. — Preceding unsigned comment added by Mikolajek94 (talk • contribs) 18:59, 5 February 2020 (UTC)

Fasting Insulin levels
Hi @Shaileshkumar1966 According to the citation you added, the two most commonly reported conversion factors between conventional and SI units for human insulin are 1 μIU/mL = 6.945 pmol/L (incorrect) and 1 μIU/mL = 6.00 pmol/L (correct) so a fasting level of 174 pmol/L corresponds to 29μIU/mL so I have adjusted the figure and transposed the cite. Regards CV9933 (talk) 13:26, 9 January 2023 (UTC)