Heat stress effects on livestock: molecular, cellular and metabolic aspects, a review

Abstract

SummaryElevated ambient temperatures affect animal production and welfare. Animal's reduced production performances during heat stress were traditionally thought to result from the decreased feed intake. However, it has recently been shown that heat stress disturbs the steady state concentrations of free radicals, resulting in both cellular and mitochondrial oxidative damage. Indeed, heat stress reorganizes the use of the body resources including fat, protein and energy. Heat stress reduces the metabolic rates and alters post-absorptive metabolism, regardless of the decreased feed intake. Consequently, growth, production, reproduction and health are not priorities any more in the metabolism of heat-stressed animals. The drastic effects of heat stress depend on its duration and severity. This review clearly describes about biochemical, cellular and metabolic changes that occur during thermal stress in farm animals.

A conceptual model to describe heat stress in dairy cows from actual to questionable loops

“…With high availability of drinking water, satiety by copious liquid intake causes increases of rumen fill which slightly inhibit feed intake, as reported in the loop B3 (Pejman & Shahryar, 2012). Furthermore, heat stress induces hypersensitivity to insulin (Belhadj, Najar, Ghram, & Abdrrabba, 2015), decreasing body fat mobilization for gluconeogenesis and decreasing the metabolic heat production (B4). Figure 2, can be argue that involves three short routes and a long route.…”

“…Figure 2, can be argue that involves three short routes and a long route. Short routes are shown with red arrows and are described as follows: i) increasing respiratory and heart rates as defense mechanisms against an increasing in temperature; which increases maintenance energy requirements and had achieved a decreasing in glucose content available for mammary gland (Collier et al, 2011), ii) increasing blood supplying to periphery tissues, which causes fewer transport of nutrients to organs, especially less glucose to mammary gland (Barrera et al, 2015); iii) hypersensitivity to insulin (Belhadj, Najar, Ghram & Abdrrabba, 2015), which causes greater glucose uptake by adipose tissues (insulin dependent), and had achieved a decreasing in the amount of available glucose for mammary gland (insulin independent).…”

“…Some literature citations on the influence of physiological mechanism that regulates the animal strain to thermal stress (Barragan, Mahecha & Cajas, 2015;Barrera, Angeli, Machado, Cardoso & Gonzalez, 2015;Belhadj, Najar, Ghram & Abdrrabba, 2015;Collier,Zimbelman, Rhoads, Rhoads & Baumgard, 2011;Dunshea et al, 2013;Molina, Silva, Perílla & Sánchez, 2016;Pejman & Shahryar, 2012). …”

Role of Heat Shock Proteins in Livestock Adaptation to Heat Stress

“…11,14 Increase in ROS production, especially the superoxide anion (O 2 _ ) is observed during HS. 11,18 HS was shown to raise both of Thiobarbituric acid-reactive species (TBARS) and malondialdehyde (MDA) levels in broilers, buffalos and dairy cows which are the major products of lipid peroxidation.…”

“…[45][46][47][48] In farm animals, elevation in HSP70 and HSP90 was observed in sheep, buffalo, cattle, broilers and goats. 11,49,50 The highest level of plasma HSP70 and PBMC HSP70 mRNA transcript expression was reported in Osamanabadi goats exposed to heat and nutritional stress as compared to the control goat which was maintained in the shed and fed ad libitum. 50 The HSP70 along with HSP27 and HSP90 proteins is observed to be anti-apoptotic in mammalian cells.…”