In 1994, molecular biologist Jeffrey Friedman, a professor at Rockefeller University, announced the discovery of leptin after experiments on obese mice. Obese mice were found to lack the one and only gene which is needed so as to produce leptin. When they were given leptin, the effect was reversed and the mice began to lose weight.

Leptin has a specific function in the brain (it operates in the hypothalamus), so as to control metabolism and appetite. It manages fat burning, namely whether the amounts of fat will be stored or used directly for energy production.

As fat cells grow, so do leptin levels in the blood. This is because the body tries to instruct the brain to increase metabolism and slow down the appetite, in order to help burn excess fat. While one would expect leptin in people with a lot of weight to intensively promote the return of weight to normal levels for the body, this does not happen. Because while leptin levels are elevated, the brain becomes more leptin tolerant and does not respond to stimuli, as a result, none of its mechanisms of function are activated.

 

Leptin resistance contributes to obesity

Have you tried different diets with reduced calories and do not lose weight?

You can not lose weight no matter how much you exercise?

Are you constantly gaining weight even if you have not changed your exercise or diet?

Do you feel that your metabolism is unusually slow?

If you experience any of the above, you may have experienced so-called leptin resistance.

Friedman expressed the view that obesity may be the result of leptin resistance. The definition is similar to that of insulin resistance where the message of the hormone is ignored. Type II diabetes is due to the fact that insulin, although it can be produced in significant amounts in the body, can not give the hormonal signal of glucose entering muscle cells.

Similarly, obesity is most likely due to inactivation of the leptin receptor in the brain, which does not perceive the presence of leptin in the blood and does not cause the feeling of hunger satiety. In other words, the obese brain is resistant to leptin.

 

What can you do?

There are ways to enhance the action of leptin in your body.

  • Increase fiber intake. The digestive system puts more effort into processing whole grains and thus slows down the digestive process, preventing a sharp rise in blood sugar (glucose) levels.
  • Maintain your blood glucose levels at normal levels. Avoid excessive consumption of simple sugars such as fructose which has been linked to the development of leptin tolerance.
  • Research has linked sleep deprivation to reduced leptin levels, so make sure you get enough rest and at least 8 hours of sleep a night.
  • Manage stress. Elevated stress levels appear to affect leptin levels in the blood.

 

Diagnosis & Treatment

The body’s leptin levels are accurately measured by the corresponding blood test. With the guidance of the treating Doctor, the body’s deficiencies in vitamins and other micronutrients are supplemented.

Leptin resistance is regulated and the body returns to normal function, losing weight permanently and naturally.

References:

1. Pan H, Guo J, Su Z (May 2014). “Advances in understanding the interrelations between leptin resistance and obesity”. Physiology & Behavior. 130: 157–69. doi:10.1016/j.physbeh.2014.04.003. PMID 24726399. S2CID 12502104.
2. Forny-Germano L, De Felice FG, Vieira M (2019). “The Role of Leptin and Adiponectin in Obesity-Associated Cognitive Decline and Alzheimer’s Disease”. Frontiers in Neuroscience. 12: 1027. doi:10.3389/fnins.2018.01027. PMC 6340072. PMID 30692905.
3. Doherty GH, Beccano-Kelly D, Yan SD, Gunn-Moore FJ, Harvey J (January 2013). “Leptin prevents hippocampal synaptic disruption and neuronal cell death induced by amyloid β”. Neurobiol. Aging. 34 (1): 226–37. doi:10.1016/j.neurobiolaging.2012.08.003. PMID 22921154. S2CID 24676545.
4. Ciriello J, Moreau JM (November 2012). “Systemic administration of leptin potentiates the response of neurons in the nucleus of the solitary tract to chemoreceptor activation in the rat”. Journal of Neuroscience. 229: 88–99. doi:10.1016/j.neuroscience.2012.10.065. PMID 23159310. S2CID 22852202.
5. Sanchez-Garrido MA, Tena-Sempere M (2013). “Metabolic control of puberty: roles of leptin and kisspeptins”. Horm Behav. 64 (2): 187–94. doi:10.1016/j.yhbeh.2013.01.014. PMID 23998663. S2CID 27078496.
6. Rőszer T, Józsa T, Kiss-Tóth ED, De Clerck N, Balogh L (April 2014). “Leptin receptor deficient diabetic (db/db) mice are compromised in postnatal bone regeneration”. Cell and Tissue Research. 356 (1): 195–206. doi:10.1007/s00441-013-1768-6. PMID 24343796. S2CID 2422805.
7. Wabitsch M, Funcke JB, Lennerz B, Kuhnle-Krahl U, Lahr G, Debatin KM, Vatter P, Gierschik P, Moepps B, Fischer-Posovszky P (Jan 2015). “Biologically Inactive Leptin and Early-Onset Extreme Obesity”. N. Engl. J. Med. 372 (1): 48–54. doi:10.1056/NEJMoa1406653. PMID 25551525.
8. Zhang L, Lu M, Yuan L, Lai W, Wang Y (2014). “[Association of leptin gene-2548 G/A polymorphism with obesity: a meta-analysis]”. Wei Sheng Yan Jiu (in Chinese). 43 (1): 128–32. PMID 24564125.
9. Ye XL, Lu CF (Oct 2013). “Association of polymorphisms in the leptin and leptin receptor genes with inflammatory mediators in patients with osteoporosis”. Endocrine. 44 (2): 481–88. doi:10.1007/s12020-013-9899-9. PMID 23460508. S2CID 19769251.
10. Veyrat-Durebex C, Poher AL, Caillon A, Somm E, Vallet P, Charnay Y, Rohner-Jeanrenaud F (2013). “Improved leptin sensitivity as a potential candidate responsible for the spontaneous food restriction of the Lou/C rat”. PLOS ONE. 8 (9): e73452. Bibcode:2013PLoSO…873452V. doi:10.1371/journal.pone.0073452. PMC 3765307. PMID 24039946.

 

Read more

Obesity is not a clinical disorder

Ketogenic diet: benefits and potential risks