Talk:Leptin

Leptin and Alzheimer's
According to BBC News, Alzheimer's risk is linked to Leptin http://news.bbc.co.uk/1/hi/health/8414989.stm --Gohan2091 02:56, 16 December 2009 (GMT)

Leptin as an immune mediator
Would be happy to put my 2 cents. Leptin is a potent stimulator of the immune system. Leptin receptors on monocytes cause the release intracellularly of STAT3 which cause the monocytes to release IL-6, IL-12 and TNF alpha. The IL-6 goes to the liver and increases production of CRP. All of these cytokines are elevated in obesity because of increased leptin levels. As monocytes only live 1 week they don't become leptin resistant. Fat on the other hand does and as a result adiponectin levels drop. Adiponectin is an inhibitor of TNF alpha and so this goes even higher.

for more can see www.hungerhormones.com

Todd Burstain, MD Associate Professor of Medicine University of Iowa College of Medicine. e-mail address removed —Preceding unsigned comment added by 129.255.246.56 (talk) 16:51, 7 September 2007 (UTC)

I think we need a new paragraph. Does anyone want to contribute? Horia 20:19, 24 April 2007 (UTC)

Yeah I agree but I don't know enough about the topic to be able to contribute personally. --Meridius 10:41, 20 May 2007 (UTC)

Confusing dates
This article starts with Leptin being discovered in 1994 and then a couple of sentences later, "leptin was cloned ... in 1950 ..." Perhaps I missed something or does this need to be clarified? Dennybara 08:59, 15 December 2005 (UTC)
 * You missed something. The mutation that produced ob/ob mice occurred in 1950, but the precise nature of the genetic defect was not known until the 1990s. You don't clone a gene or a protein, but the gene was sequenced and reproduced in the early 1990s. alteripse 01:45, 25 January 2006 (UTC)


 * I think you missed something. It clearly says that - Leptin was cloned by studying mutant obese mice that arose at random within a mouse colony at the Jackson Laboratory in 1950. - Cloning was invented in the '90s, wasn't it? - Boris 02:02, 25 January 2006 (UTC)
 * I said: The mutated mice date back to 1950; their specific mutation was not understood until the 1990s. No one knew about leptin or its connection to the mice until after 1990. If you dont think the article is clear, then change it. alteripse 03:40, 25 January 2006 (UTC)

Does an increased leptin level lead to an increase or a decrease in appetite?

It leads to a decrease in appetite. It inhibits the orexigenic peptides, AgRP and NPY, in the arcuate nucleus.

Leptin's link to obesity/hunger?
The reason leptin levels are high in obese people is they are leptin resistant just like insulin levels are high in type 2 DM. So while the leptin levels are high, the output from the leptin receptor in the arcuate nucleus is low. This leads to higher AGRP, NPY and lower alpha MSH release even in the setting of high leptin and low ghrelin. The result is a lower metabolic rate than would be predicted and more hunger even though the blood levels of these two hormones would predict the opposite. Todd Burstain, MD Associate Professor of Medicine, University of Iowa. todd-burstain@uiowa.edu —Preceding unsigned comment added by 129.255.246.56 (talk) 18:36, 21 September 2007 (UTC)

I was reading this article... www.mercola.com/2000/mar/5/exercise_lowers_fat_hormone.htm and it seems strange that we'd be different from rats. I think that this study is biasing the results a bit. Let's think about it... exercise in humans decreases leptin. Leptin causes weight loss in rats. Fat people have higher levels of leptin. Does this mean that leptin causes weight gain in humans? Certainly not! I think leptin, rather than influencing fat storage levels, may be linked to hunger. Rats, being a slave to instinct, stop eating when they get leptin. In humans, when exercising (especially at higher intensities) hunger vanishes, we puke our food up and empty our bowels. Yes, exercise necessitates, but not actually when exercising. so what I think leptin does is it deactivates hunger. Why do overweight people have higher levels of leptin? They're probably not as hungry, it could be a defence against weight loss. Of course, the person is still hungry, because he is addicted to the pleasure response in the food, so the leptin isn't enough to stop him from eating, and as he eats more and more, more and more leptin is produced to try and counteract the hunger! What do you think? Tyciol 20:25, 9 February 2006 (UTC)


 * Overall I think that you have a good grasp on what leptin does, but I think that you may be a bit confused on some small points. Leptin does not influence fat storage levels; rather, leptin is secreted by fat stores. You are right in that leptin deactivates hunger. It does so by inactivating NPY & AgRP (hunger) neurons, and activating POMC (satiety) neurons. Obese people have high levels of leptin because they have a lot of fat. Why doesn’t this high level of leptin stop them from eating? Well, the answer is complicated. Human hunger is regulated by physiology, like in rats, but we have the added caveat of having out hunger regulated by our psychology. Additionally, the more obese a person is the less able leptin is to cross the blood brain barrier. These are just a couple of the known reasons why obese people have really high levels of leptin. Overall, pretty good analysis. (Sorry for bad formating, this is my first post) Leptin Resistant 03:00, 11 February 2007 (UTC)


 * No. It is a very common mistake, but leptin doesn't regulate hunger, it regulates the amount of adipose issue. A mutation in leptin means that fat grows uncontrollably, sucking up all the nutrients that someone eats. Mice, rats or people with leptin mutations are hungry because they are actually starving - all their other organs are entering starvation mode because the fat is taking in all the available energy. So the increase in appetite is entirely secondary. For example, if you take a mouse with leptin deficiency, then restrict its calorie intact to that of a normal mouse it cannot overeat at all. Do you end up with a normal lean mouse? No, you end up with an obese runted mouse, with a small brain, small kidneys, small bones, etc. In fact, you can restrict the food of these mice so severely that they will starve to death - and at the point of starvation they will still be obese. In other words - leptin suppresses fat growth, in the absence of leptin the fat grows uncontrollable so that people need to eat constantly to prevent all of their other organs would starve to death.

It is not obesity that directly causes leptin resistance, but high levels of circulating serum triglycerides. Serum triglycerides are often a symptom of obesity, but people taking TZDs (PPAR-gamma agonists), which promote fat storage while lowering serum triglycerides, actually help insulin and leptin signaling. The high levels of serum triglycerides impair leptin from crossing the blood-brain-barrier, by inhibiting a saturable transporter. Read this article: Diabetes 53:1253-1260, 2004. Triglycerides Induce Leptin Resistance at the Blood-Brain Barrier William A. Banks1, Alan B. Coon1, Sandra M. Robinson1, Asif Moinuddin1, Jessica M. Shultz1, Ryota Nakaoke1,2, and John E. Morley1

A comment about the above. High triglycerides (and low HDL) are not the cause of leptin resistance but a symptom of it. Leptin normally stimulates the release of adiponectin. But with leptin resistance adiponectin levels fall. Adiponectin is responsible for the activation of an enzyme called lipoprotein lipase which is responsible for the conversion of triglycerides into VLDL and for the conversion of IDL into HDL. As a result triglycerides are elevated and HDL is decreased, a pattern called Type IV hyperlipidemia. Todd Burstain, MD Associate Professor of Medicine, University of Iowa. todd-burstain@uiowa.edu   —Preceding unsigned comment added by 129.255.246.56 (talk) 18:40, 21 September 2007 (UTC)

The way I see it, high levels of serum triglycerides usually signal starvation (via triglyceride breakdown). Thus, it would not be optimal to have leptin signaling in the brain during starvation (since it would lead to increased energy expenditure, increased metabolism and satiety). Obesity, ironically, leads to the same signal! Of course, during the evolution of our metabolic systems, obesity was not all that relevant. It just happens to be that those with higher lipid profiles will have high serum triglycerides, as a natural consequence.

To resolve the three different situations you posed: a) leptin decreases after exercising because you want to find food now, since you just expended a lot of energy, b) exogenous leptin administration in rats leads to the activation of signaling pathways involved in energy expenditure and satiety (overall, promoting weight loss) and c) obese individuals have larger adipose stores and leptin is released in proportion to adipose weight; they continue to eat because though leptin circulates in high concentration, leptin resistance (from higher levels of serum triglycerides) leads to the brain not receiving this signal to stop eating and to expend energy.

-Daniel Vowinkel

Astonishly, the wikipedia article, for all its detail, does not say what leptin "does".Sfahey 23:40, 13 February 2006 (UTC)
 * Well, it is annoying, yeah. It's not wrong to be lacking assertiveness about a function, since it might be hard for certain compounds. Look at all that junk DNA humans have, for example, who knows what potential functions those might have. I bet there's a lot of stuff we don't know about. Even so, when scientists begin to agree on a solid theory of a compound's function (which I think applies to Leptin) then it should be mentioned. Should we add it? I just want to resolve what it actually does, for both animals and humans, before posting it in. Tyciol 17:14, 14 February 2006 (UTC)

Adipocytes are cells present in adipose tissue, the cells secrete leptin , which signals to the brain that we have had enough to eat! scottydog

Among the many many places that Leptin binds, a major target is the Ventral Medial nucleus of the Hypothalamus, also known as the "satiety center." When Leptin binds there, it causes signals to be produced that make you feel full, or satiated. Having sufficient fat stores causes enough Leptin to be produced that your brain knowns you don't need to eat very much more. I will submit the change although I am not a registered user. -- A medical student

Can anyone tell me what foods or herbs stimulate the production of Leptins in the body? Bernard


 * Hey Bernard, Any kind of food stimulates production of leptin. You take in food, the food is digested, and the nutrients from the digested food go to fat cells. Once the fat cells have taken in the nutrients, they release leptin. So eating releases leptin. But of course this is probably not what you wanted to hear. The best way to loose weight is still exercise and diet.Leptin Resistant 03:11, 11 February 2007 (UTC)

Ob Lep
I added in that Ob stood for obese, relating to the obese mice, and Lep for Leptin, the name given to the hormone discovered, right alongside the abbreviation to make it simpler to understand. This page is looking great!

Gene expression
The RNA expression map shows that (apart from the placenta) leptin (or at least its mRNA) is also produced in heart muscle cells, cerebral peduncles and the adrenal cortex in at least the same concentration as in adipose tissue. What is function of leptin in these tissues/from these tissues? There is no mention of that in the article. For systemic levels it's probably not that important because there is much more adipose tissue than those other tissues in the body. Icek (talk) 23:28, 11 December 2007 (UTC)

Jargon
Overall this is a very good article. Towards improving it further, I'd like to see the lead rewritten to be in more of a "plain English" style. The detailed information should be moved into an appropriate section further down in the article. Some chemical compounds are little-known enough that the only article we can really have on them is a very technical one, but in the case of Leptin, there's enough mainstream coverage that the majority of the article should be readable by mainstream readers. --Elonka 01:45, 20 March 2008 (UTC)

The problem with "mainstream coverage" is that nearly all of it is anecdote, pushing a private agenda, or just plain garbage. I don't really know how to present a factual, objective article on a metabolic hormone or regulatory molecule without using "jargon." Perhaps a paragraph at the beginning of the article explaining in non-technical terms that leptin is a biomolecule, found in mammals, and that it appears to be involved in storage and metabolism of sugars in the body, and leave the nontechnical inforation at that. Maybe even throw in references to insulin, glucose, glycans, and even mellatonin.

The way I see it, it's very difficult to have a nontechnical discussion that doesn't rapidly regress into rampant factionalism, with each party pushing their own agenda, and objectivity taking a rapid departure out the window. --NReitzel (talk) 15:58, 29 October 2008 (UTC)

The original post is absolutely correct. Wikipedia standards dictate that Wikipedia is written specifically FOR the "mainsteam." This is not a detriment. This is its benefit. I appreciate that this article is written by highly educated individuals who are keen on precision. That's great. But the lead needs to be written in plain English -- most especially the first sentence. When a reader comes across this article, and are hit in the very first sentence that defines leptin as "a 16-kDa adipokine" it dissuades them from even trying to read any further. It is important that Wikipedia articles avoid an air of academic elitism, where only the privileged few deserve the benefit of learning about a complex subject. Believe me, there are plenty of subjects that can be written in a way that would confound and confuse scientists too. Furthermore, a good writer and communicator has the ability to synthesize complex information in a way that it can be understood by the mainstream. Richard Feynman jumps to mind, as does Carl Sagan. Quantum Mechanics is far more complex than a hormone.

This problem is an ongoing one with scientific articles, where the writers get lost in the weeds, seemingly excited to compete with each other as to who can produce the deepest minutiae that is technically correct -- but loses the audience in the process. Wikipedia is not a textbook, nor a graduate course in biochemistry. It's an encyclopedia meant for mass consumption. I'm not suggesting to simplify the entire article, but the introduction needs to be simplified. Madscribbler (talk) 17:26, 16 December 2013 (UTC)

Liptin Producer
The Question was: "Can anyone tell me what foods or herbs stimulate the production of Leptins in the body? Bernard"

And the Answer: "Hey Bernard, Any kind of food stimulates production of leptin. You take in food, the food is digested, and the nutrients from the digested food go to fat cells. Once the fat cells have taken in the nutrients, they release leptin. So eating releases leptin. But of course this is probably not what you wanted to hear. The best way to loose weight is still exercise and diet".

So if I eat, Liptin gets produced, and therefore I should stop feeling hungry. Yes?

If I now stop eating there is a shortage of Liptin which should give me hungry feeling. Surely there must be something to take as a supliment with your meal (reduced) to "kickstart" Liptin production, having the effect of reduced intake coupled with high Liptin levels supressing appetite. —Preceding unsigned comment added by 196.207.47.60 (talk) 11:53, 26 August 2008 (UTC)

Yes there is a supplement now available to lower leptin and increase your sensitivity. Double Blind Studies and patented. I use it and my wife and it works. Thomasinwinnipeg (talk) 15:55, 21 October 2008 (UTC)

reverted edits April 2009
http://en.wikipedia.org/w/index.php?title=Leptin&oldid=283562122 http://en.wikipedia.org/w/index.php?title=Leptin&oldid=283562496 I do not believe that these edits are 'unproductive' as tagged by User:Madhero88. Celefin (talk) 14:22, 13 April 2009 (UTC)
 * The link I removed was to the website leptinresearch.org that seems to exist to promote a supplement in some dubious way connected to leptin
 * I inserted a link to the wikipedia page on the ob/ob mouse - this is the mutant mouse that led to the discovery of leptin
 * I am so sorry for those reverts, that was my mistake Maen. K. A. (talk) 14:29, 13 April 2009 (UTC)

Regulator of cardiovascular function?
I'm not clear enough on what this means to try to incorporate it into the article without some more reading first, but here's something interesting: "These findings have prompted the speculation that leptin in the physiological range may serve as a physiological regulator of cardio-vascular function ... ." --Dan Wylie-Sears 2 (talk) 12:50, 3 September 2009 (UTC)

Pulsatile secretion, ghrelin
And here are a couple more tidbits to be worked in somewhere: "Leptin inhibits both the secretion of gastric ghrelin and the stimulation of feeding by ghrelin. ... Leptin is secreted in a pulsatile manner with a frequency of discharge similar to that of ghrelin (5,6) (Fig. 3). However, in marked contrast to the acceleration in ghrelin secretion, energy deprivation diminishes leptin pulse amplitude, thereby diminishing overall leptin output."  --Dan Wylie-Sears 2 (talk) 13:22, 3 September 2009 (UTC)

Effects on the brain
As mentioned in the article, leptin is a protein and is therefore unlikely to cross the blood-brain barrier.

There is evidence that some of leptin's effects are mediated by the Vagus nerve: http://ajpregu.physiology.org/cgi/content/abstract/288/4/R879

MBVECO (talk) 21:19, 18 February 2010 (UTC)MBVECO

Discovery section
This section has gotten way out of control and needs to be significantly condensed. Much of the controversy about who discovered what would be reduced if WP:SECONDARY sources were used. Furthermore this section contains a lot of WP:PEACOCK phrases (e.g., "major scientific advance") and excessive detail about specific publications that needs to be removed. Boghog (talk) 20:20, 8 August 2013 (UTC)

EVIDENCE FOUND FOR RELATION BETWEEN LEPTIN AND CHRONIC FATIGUE SYNDROME
The study lead by Dr. Ian Lipkin and Dr. Mady Hornig found clear evidence of downnregulation of leptin in chronic fatigue syndrome, please add this to the article, I think its a breakthrough and a very important information about the subject of this article. The transcript of the conference detailing the finding is here: https://docs.google.com/file/d/0B-NT-7M70igudmZVSVJUTnZVclU/edit?pli=1 — Preceding unsigned comment added by 190.97.58.115 (talk) 22:54, 12 September 2013 (UTC)

EDITS
I have retitled most sections; moved sentences and paragraphs to under proper title; rewritten the intro in a more plain English style. Anyone should feel free to continue to edit/merge/delete as they see fit. I believe the whole external reading section serves no purpose and to should be deleted, but I'll leave it anyone else who agrees to do it. Go to History of edits/15:22 27 April 2014, click on cur, if you care to compare all the changes I made to before I started.IiKkEe (talk) 05:41, 28 April 2014 (UTC)

Someone reverted the two new headings I put in: for some reason I can't track down when or who in the history: I'll keep looking. I'm going to put back the changes I made. If anyone would like to discuss why they prefer the former titles, I'm sure open to hearing their logic: let's "Talk".

IiKkEe (talk) 16:24, 28 April 2014 (UTC)

First paragraph genetics defects section
First paragraph is supported by six references ten to 19 years old. Section is obsolete, needs rewrite;(written 4/29, signed 5/2)IiKkEe (talk) 21:07, 2 May 2014 (UTC)


 * I have completely rewritten this section. I looked for anything I could salvage but most of it was not relevant to a section on genetic mutations. This sources are more up to date now, there are a few older ones but having reviewed the literature I am confident that they are still relevant and have not been contradicted by newer studies. There is probably more that can be added to the section but I'm going to leave it as it is for now. Sarahj2107 (talk) 13:32, 30 April 2014 (UTC)


 * Just saw your above response today, and really like what you did to fix the problem.IiKkEe (talk) 21:06, 2 May 2014 (UTC)

Leptin resistance reference 125 faulty
Reference 125 is from an online source which no longer exists. (written 4/29, signed 5/2)

IiKkEe (talk) 21:12, 2 May 2014 (UTC)

Leptin and Bone rewording
I reworded the entire Bone section with no deletions or additions of references, change in order of sentences, or hopefully change in meaning - just clarity. Feel free to change my changes.

IiKkEe (talk) 13:44, 30 April 2014 (UTC)

Template content input is causing PDF printing output issues
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Correlation with Estrogen levels
The page lists positive correlations with estrogen and negative with testosterone, though source does not mention estrogen. Another source claims no correlation: Castracane VD, Kraemer RR, Franken MA, Kraemer GR, Gimpel T. Serum leptin concentration in women: effect of age, obesity, and estrogen administration. Fertility and Sterility. 1998 Sep;70(3):472-477. DOI: 10.1016/s0015-0282(98)00187-3. PMID: 9757875. 2601:204:EF02:2440:F9D9:ABA8:B5A0:2725 (talk) 22:45, 29 March 2024 (UTC)