Talk:Leptin

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. todd-burstain@uiowa.edu

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

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)[reply]

References

This page sure could use some sources...

-Ryan Bibler, UCHSC

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)[reply]

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)[reply]

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)[reply]

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)[reply]

hello

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?

I was reading this article... http://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)[reply]

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)[reply]

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

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)[reply]

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)[reply]

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)[reply]

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!

Remove the BS about giving monkeys keyboards!