Obligatory disclaimer: I am not a medical doctor, and the content of this website was created for informational purposes only. Such content is not intended as a substitute for medical advice, treatment or diagnosis.
We’ve previously talked about grhelin, the so called hunger hormone. In this post we’ll talk about another hormone related to our metabolism: leptin. As was the case with grhelin, we’ll learn what leptin is, what our body uses it for, and how it relates to our metabolism, being overweight, and obesity.
What is leptin?
Leptin is a hormone, primarily produced in the adipocytes (fast cells), that helps regulate our metabolism by inhibiting appetite, and making us feel sated. Although leptin is used by our body in a variety of ways, we’ll just stick to those related to metabolic rates, food intake, and obesity.
Leptin and genetics
I know very little of genetics, so please bear with my misuse of the terminology or my misunderstanding of it. In our organism, the gene LEP contains the instructions to produce leptin, so mutations in that gene will have an effect on the production of leptin and our overall metabolism.
Thanks to our parents, we have two copies of the LEP gene, one inherited from each parent. However, this also means that the gene can suffer from several mutations. According to Wikipedia, there are eight of those mutations, and all of them result in obesity with hyperphagia (excessive hunger or eating) in childhood. For the purposes of this post, we’ll just talk about the three possible scenarios that result from LEP mutations that are mentioned in Advanced Nutrition and Dietetics in Obesity:
- Case 1: the LEP copies have no mutations. In this case or bodies response to leptin is the standard one. All is well, and is business as usual.
- Case 2: one of the LEP copies contains a mutation. In this case BMI is skewed towards larger values, but no other problems are present.
- Case 3: both LEP copies contain mutations. In this case both obesity and hyperphagia are present.
Leptin and food intake
Here we will talk about the lipostatic hypothesis. The hypothesis essentially tries to account for the perceived relationship between obesity and food intake by proposing that fat tissue is somehow involved in appetite control. There is also a glucostatic hypothesis, but we’ll talk about it in a later post.
The lipostatic hypothesis seems to make sense, right? The more fat tissue you have, the more leptin is produced. By having greater leptin levels then your appetite would be at a minumum and you would eat less since you’ve got more fat to spare. However, it turns out that the relationship between the amount of fat that we carry and the control of our food intake is neither obvious nor simple. The hypothesis works well for leaner people with more normal weights: fat acts as a regulator of appetite and further food intake is inhibited due to fat reserves. The problem is that as our fat levels increase, so does the level of leptin and, just like it happens with insulin, a resistance to leptin is developed. In other words, as one becomes fatter, leptin becomes less useful and it is more difficult to control our eating.
When it comes to weight loss (focusing specifically on fat loss), studies have shown that dieters who lose weight also have reduced levels of leptin. Such a dramatic decrease in leptin levels is associated with an increase of hunger, which may result in weight regain. If anything, all this should tell you to not get too fat.
We’ve learned that leptin is a hormone that helps us control our appetite and our eating. It is mainly produced in our fat tissues, so being very fat comes along with high leptin levels and the development of leptin resistance. On next week’s post we’ll talk about insulin, then about the glucostatic hypothesis, after that we’ll deal with the satiety cascade.
If you’ve enjoyed this post and would like to see more content like it, check out our page on Rebuttals to Fatlogic. See you next week!