Leptin is a hormone produced primarily in fat cells inside the human body and acts via leptin receptors to regulate body metabolism and play its role in reproduction and immune functions.
It’s not been long since we know leptin as it was discovered in the 1990s. The role of leptin in obesity-related medical conditions is being increasingly recognized.
What does the Leptin hormone do?
It is commonly said in medicine that leptin makes you thin and ghrelin (another hormone) makes you hungry. So, leptin has something to do with satiety and food intake.
Raised levels of this hormone decrease appetite and, in turn, food intake. In other words, when we eat, the levels of this hormone keep on rising gradually along with food intake until peak levels.
It acts in different areas of the brain, like the hypothalamus and brainstem nuclei, to induce satiety, and we no longer feel hungry and stop eating.
So, it’s a satiety-inducing hormone. Several mechanisms have been proposed by which leptin decreases food intake.
Two of the mechanisms are worth mentioning here and are as follows:
- A peptide called neuropeptide Y (NPY) is present in the hypothalamus and is thought to be one of the most potent stimuli for food intake, this is inhibited by leptin.
- Secondly, leptin increases the contents of neuropeptides like proopiomelanocortin (POMC) mRNA that induce anorexia. Post-translational cleavage of POMC produces an alpha-melanocyte-stimulating hormone that also causes inhibition of food intake.
What Increases Leptin production?
Under normal circumstances, leptin production in the human body is strongly affected by both BMI and body fat.
What leptin does under ordinary circumstances is that it communicates with the brain about the body fat content and the energy status and energy reserves of the body to regulate its serum levels.
Studies have concluded that leptin concentration increases by 40% within 12 hours of overeating.
The opposite is true for starvation which reduces leptin concentration by almost 70% within 48 hours and 80% within 3 days.
This effect of starvation or overeating is irrespective of body weight.
Following are some of the other characteristics of leptin:
Leptin Levels increase during childhood and are associated with the earlier onset of puberty. After puberty levels start to decline especially in boys in response to an increase in testosterone levels.
Levels are higher in girls and continue to increase with rising estrogen. So, as opposed to androgens, estrogens increase leptin levels. This explains why women eat less than men.
The placenta and breast milk produce leptin and levels are higher during pregnancy.
Raised insulin levels in type 2 diabetes cause an increase in glucose utilization and leptin formation by fat cells.
Diurnal variation is also seen in leptin concentration with levels 20-40% high during midnight.
How are Leptin and Obesity Linked?
Since leptin is a satiety hormone, it can be one of the game-changing drugs to end the obesity pandemic.
It exerts its major effect by reducing cravings for food especially those that have a high glycemic index.
Who may benefit from exogenous leptin (Metreleptin or Myalept)?
Low Leptin levels caused by leptin gene mutation are a cause of obesity in only a small subset of patients.
These patients do get benefit from exogenous leptin available in the form of metreleptin which help them lose weight.
But quite, unfortunately, a huge majority of obese patients are not at all leptin-deficient, and in fact, they have a raised concentration of leptin which is in direct proportion to their body fat content that is the more fat they have the more leptin in their blood.
This means that they develop resistance to leptin and that is the reason that the levels keep on increasing.
Leptin hormone Resistance . . .
In several studies, no leptin gene mutations have been found in such patients and as the leptin concentrations are already high exogenous leptin is not expected to do any significant benefit.
In one trial higher doses than usual of leptin caused a modest degree of weight loss in some individuals but not all of them.
One study showed that the administration of leptin prevented a decrease in basal metabolic rate and serum concentrations of thyroid hormone and these patients lost weight.
Another question arises as obese people develop resistance to leptin, are there any leptin sensitizers available that can enhance its action just like in the case of insulin?
The answer is No. Leptin sensitizers are not available yet and it is now known even if they become available, would they be effective or not?
Can you boost your leptin levels naturally to induce weight loss?
There are no leptin hormone sensitizers or drugs that may boost its effects. However, the consumption of certain food items may increase leptin levels and reduce resistance to its effects. Food items that have been used to increase the levels of endogenous leptin levels include:
- Increasing the amount of dietary fiber in your diet
- Reducing the consumption of refined sugars and fructose
- Eating complex carbohydrates
- Eating more proteins in your breakfast such as eggwhite, meat, and fish.
- Increasing the intake of Omega-3 fish supplements
- Improving sleep quality and timing
- Performing high-intensity training exercises
- Avoiding severe caloric restriction.
- Eating certain food items such as avocado, coconut, fish, and olive oil, and consuming green tea.
The same factors that may increase the levels of leptin in the blood may also enhance its sensitivity and decrease leptin resistance.
Conclusion:
The major impact on endogenous leptin is food intake. So, to reach that satiety level one must eat food and exogenous leptin would induce satiety in only a small subset of patients who have genetic abnormalities.
The rest of the obese patients cannot get significant benefits from exogenous leptin and control their cravings for fats and carbohydrate-rich foods like burgers, pizzas, etc, with just a pill of leptin.
So, controlling your food cravings along with healthy workouts is the way to weight loss.
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