Leptin and Obesity: Leptin hormone was initially used for the treatment of obesity because of its capability to effectively reduce food intake and body weight. Recent studies have shown that obese individuals have been found to have high levels of circulating leptin.
The inability of this circulating leptin to exert its anorexigenic effects in obese individuals shows that there is a lack of clinical utility of leptin in obesity.
This is defined as leptin resistance. Although, the phenomenon of leptin resistance has still not been adequately characterized. It is, therefore, important to understand the molecular mechanism of leptin resistance to know its importance as an effective treatment for obesity.
Leptin has to cross the blood brain barrier to reach the hypothalamus and exert its anorexigenic effects. Although, the mechanism of leptin transportation across the blood-brain barrier is unclear and prevents the clinical application of leptin for treating obesity. New strategies have been developed in recent years to recover the response to leptin in obesity1.
Leptin resistance in obesity
Leptin is a polypeptide hormone produced by adipocytes (fat cells) in the body in proportion to the triglyceride content. The hormone binds to and activates the long form of its receptor (LERP-B) in the brain, decreases food intake and increases energy expenditure.
A large body of experimental data has shown that leptin plays a major physiologic role to respond to, as well as, defend against reductions of body fat. A lack of leptin or LERP-B mirror a physiological response of insulin resistance, immune dysfunction, infertility, decreased metabolic rate and hunger.
Therefore, the action of leptin is necessary for energy stores to be sensed in the central nervous system, moreover, is essential for reproduction and homeostasis.
In addition to this, the altered physiology associated with low-leptin states is reversed effectively with leptin replacement. What’s more, a lack of adipose tissues in the body results in a reduction of the circulating leptin, known as lipodystrophic syndromes.
A decrease in fat mass, furthermore, decreases the circulating leptin in otherwise normal weight-reduced humans. Leptin deficiency is, therefore, a key regulator of neuroendocrine and metabolic responses, which is characterized by weight loss and negative energy expenditure2.
Leptin is not an obesity hormone but a starvation hormone. It circulates in the blood stream and goes to the brain. It is a way the fat cells tell the brain that your energy thermostat is at the right setting.
Leptin informs the brain that you have enough stored energy in your fat cells to engage in relative expensive/normal metabolic activity.
In simpler words, when the levels of leptin are at a certain threshold, the brain senses that you have enough energy sufficiency, meaning that you can burn energy at a normal rate, moreover, engage in exercise and eat food at a normal rate.
However, when people diet, the fat cells lose some fat because they eat less, which decreased the production of leptin. As a result, the leptin level goes below the leptin threshold and the brain senses starvation3.
Izquierdo, A. G., Crujeiras, A. B., Casanueva, F. F., & Carreira, M. C. (2019). Leptin, obesity, and leptin resistance: where are we 25 years later?. Nutrients, 11(11), 2704.
Myers Jr, M. G., Leibel, R. L., Seeley, R. J., & Schwartz, M. W. (2010). Obesity and leptin resistance: distinguishing cause from effect. Trends in Endocrinology & Metabolism, 21(11), 643-651.
Myers Jr, M. G., Münzberg, H., Leinninger, G. M., & Leshan, R. L. (2009). The geometry of leptin action in the brain: more complicated than a simple ARC. Cell metabolism, 9(2), 117-123.
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