Hőstressz tejelő tehenekben I. A tejtermelés-csökkenés hátterében álló élettani tényezők - Irodalmi összefoglaló
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SUMMARY The present review describes the physiological background of the heat stress related decrease in the milk yield of dairy cows. The biological cost of heat stress has a profound impact on the nutrient supply of the functioning mammary gland, and consequently milk synthesis. Interrelations of cellular and systemic, short-term and long-term adaptive mechanisms and the effects on milk production are described in details. The cellular heat stress response involves the protective action of heat-shock proteins, also known as stress chaperones, which mitigate the damaging effect of heat on the structure and activity of functional proteins. On a systemic level, short-term adaptation includes behavioural (seeking shade, reduced feed consumption) and physiological changes (increased evaporative heat loss, reduced function of the mammary gland) aimed at maintaining homeothermy, regulated mainly by adrenal and thyroid hormones. Longer term adaptation is characterized by changes in fluid regulation and energy metabolism. An increase in prolactin concentration promotes a favourable inner environment for conductive and evaporative heat loss. Basal plasma insulin concentrations increase, while the action of the growth-hormone – insulin-like growth factor axis is reduced. The comparison of the endocrine and metabolic profiles of lactating dairy cows in negative energy balance kept in thermoneutral versus heat stress conditions serves as an illustration of the heat related changes in the fuel preference, carbohydrate and fat metabolism in the body. The phenomenon of glucose sparing in the heat stressed cow is explained, based on thermodynamic effects of nutrients and the “leaky gut syndrome”. The possible causes of increased insulin action and its consequences on milk production are also discussed.