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The capacity of an organism to cope with harsh conditions is the result of long evolutionary processes and interactions between hormones involved in reproduction (LH, FSH, GnRH), metabolic processes (leptin, prolactin, growth hormone) and seasonality (melatonin). The mechanism through which animals adjust energy intake and expenditure according to the demands of the organism in different physiological status is still unknown. In the literature, information about interaction between leptin and prolactin is scarce and contradictory. Leptin plays a crucial role in the regulation of energy homeostasis or food intake and, as well as prolactin, it is a hormone of importance as an endocrine mediator. Day length and lactation are able to affect leptin and prolactin expression and secretion, but also modulate the correlation between them. The present review summarises research on interaction between leptin and prolactin, starting from the direct effects, through the influence of seasonality and lactation. The complete understanding of mechanisms involved in the interactions may be very useful not only in animal breeding, but also in developing effective therapies in human obesity, eating disorders and infertility.
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Leptin is a hormone of molecular weight of about 16 kDa consisted of 167 amino acids. It is produced mainly by white adipose tissue but its receptors are present also in other tissues and organs. Leptin is recognized as a sensing hormone factor regulating signal responsible for satiety acting as inhibitor of neuropeptide-Y release in hypothalamus generating reduced food intake and thereby a decrease of body weight. Leptin influences the reproductive system and is indispensable in sexual pubescence, its presence is important for proper function of female and male reproductive systems. Concentration of leptin in animal blood is correlated with fat deposition, back fat thickness and intramuscular fat suggesting possibility of its applying as a test of selection in pig, cattle and sheep meat quality evaluation. Leptin is synthesized in mammary gland and its concentration in colostrum and milk depends on the lactation stage. The results of experiments on piglets suggest that the presence of leptin in colostrum and milk influences the development and maturation of digestive tract in suckling piglets.
Leptin is an adipose tissue-derived hormone whose circulating levels correlate with the amount of body fat stores. The main function of this adipokine is to regulate energy metabolism. By modulating the expression of orexigenic and anorexigenic neuropeptides in the hypothalamus, leptin reduces appetite. It also increases energy expenditure, contributing to the decrease of body fat and body weight. Mutations in the leptin receptor gene or prolonged consumption of a high-fat diet may impair leptin action, leading to leptin resistance. Resistance to leptin can also be an adaptive response that occurs in seasonal animals and in pregnant mammals. Reversible insensitivity to the satiety signal of leptin promotes hyperphagia, which is essential for animals living in dynamic environments and experiencing seasonal variation in food availability, since it allows them to forage intensely when food is abundant and accumulate fat reserves necessary to survive periods when food is scarce. Moreover, leptin resistance and subsequent hyperphagia develop during pregnancy in order to meet the energy needs of the growing fetus. Physiological leptin resistance may be due to impaired transport of leptin across the blood-brain barrier and/or to decreased sensitivity of the hypothalamus to this hormone resulting from an inhibition of leptin signalling in hypothalamic neurons. In pregnancy, an increased resistance to leptin action is also mediated by the binding of this adipokine to its placenta-derived soluble receptor. Reduced entry of leptin into the brain as well as alterations in the leptin signalling pathway in the hypothalamus leads to a transient decrease in sensitivity to this hormone preventing appetite suppression.
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