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Leptin Hormone


This article deals with a role of leptin in regulating energy metabolism. Leptin is a hormone that is structurally close to the first class of cytokines is secreted by fatty cells. The synthesis of leptin is determined by the amount of consumed food. Its leptin decreases at fasting and increased at overconsumption. Most investigators point out that leptin plays the leading role in the development of obesity. However, studies suggest that this hormone is involved in the metabolic and neuroendocrine processes that are characteristic of cachexia, anorexia nervosa, and nonspecific appetite disorders.
   Leptin is a hormone (molecular mass 16 kDa), secreted by fat cells circulating in the blood in the free and bound forms. Its structure is similar to the first class of cytokines. Leptin in the general circulation is subject to daily rhythm with nocturnal rise, and its secretion is pulsed in nature [1]. The synthesis of this hormone is controlled ob-gene, obesity gene, which was discovered by cloning using a model of obesity in mice homozygous line ob / ob [2].
   Basic actions of leptin:
   - Increase hepatic glucose uptake glyukogenoliza and skeletal muscles;
   - Increase in the rate of lipolysis and a decrease in triglycerides in white adipose tissue;
   - Increased thermogenesis;
   - Stimulation of the central nervous system;
   - Reduction of triglycerides in the liver, skeletal muscle and pancreas without increasing plasma NEZHK.
   Most researchers assign leptin leading role in the development of obesity (Figure 1). However, recent studies suggest involvement of leptin in the neuroendocrine and metabolic processes characteristic of cachexia, anorexia nervosa and non-specific eating disorders.
   According to modern concepts leptin signals to the hypothalamus via activation of specific leptin receptor, which manifests a decrease in food intake and increase energy expenditure. At the same time, through specific receptors in the hypothalamus suppresses the synthesis of neuropeptide Y (NPY), produced by arcuate nucleus, which leads to decreased appetite, increased sympathetic tone, and power consumption, as well as changes in metabolism in the peripheral organs and tissues [2, 3 ] (Fig. 2).
   As a result, limiting the consumption of food in the serum concentration of leptin decreases [7]. At the level of the hypothalamus, leptin influences the production of neuropeptides with anorectic action (melaninostimuliruyuschy hormone, corticotropin releasing hormone) and the level of peptides that stimulate food intake. Found that leptin regulation of energy homeostasis pathway is independent of the path of serotonin, which is activated when taking drugs such as fenfluramine and dexfenfluramine. [4] Leptin receptor is also detected in peripheral tissues, including the lungs, kidneys, liver, pancreas, adrenal glands, ovaries, gemipoeza stem cells, skeletal muscle. So widespread leptin receptors in the body may indicate that leptin not only regulates satiety. However, the full range of its effects associated with activation of leptin receptor, has been studied so far is not enough. Also, further studies are needed to clarify the mechanisms of transmission postreceptor leptin signal for the development of therapies that could contribute to an increase in sensitivity to leptin. Apparently, the leptin receptor, located in the capillary endothelium and choroid plexus of the brain, provide the transport of leptin from the blood into the interstitial tissue of the brain and the spinal fluid through the blood-brain barrier. At a certain concentration of leptin in serum (25-30 ng / ml), its further increase is not accompanied by a parallel increase in the concentration of leptin in the brain tissue and cerebrospinal fluid. This phenomenon may play a role in the development of resistance to leptin and obesity [2, 5].
   Serum leptin concentrations increased with an increase in fat mass, and its production in subcutaneous fat than in visceral fat depots. Leptin levels reflect not only the amount of stored fat, but also violations of energy metabolism: the fasting is significantly reduced, with overeating - increases. The composition of the food consumed (especially its content of macro-and micronutrients, such as zinc) and various hormonal factors also affect the level of leptin [2, 6]. Smoking, which is accompanied by the development giperadrenergicheskogo state also reduces the level of leptin [6]. Several studies have shown that some cytokines, such as tumor necrosis factor - D, interleukin-1 and interleukin-6 reduces leptin levels [7]. Another interesting is the fact that leptin levels were higher in women than in men [2, 6, 7], which may be associated with different types of fat distribution, and the stimulating effect of estrogen and progesterone, on the one hand, and the suppressive effect androgens - the other.

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