CHAPTER ONE
1.0 INTRODUCTION
It is estimated that world food consumption will double by 2050 as more
developing nations improve their economic status and per capital meat consumption
increase (Godfray et al., 2010). This
places an increasing pressure on animal producers especially poultry farmers to
maximize output levels of their animals to meet this growing demand.
Physiological stress is one of many concerns facing the modern broiler
producer. The term stress is very familiar to most researchers, but there is no
universal definition for stress. When a stressor is actually causing a negative
impact on the well-being of an animal, this can be defined as distress (Moberg,
2000). Another broader definition states that stress is any biological response
elicited when an animal perceives a threat to its homeostasis (Moberg, 2000).
Extremes of ambient temperature is an important stressor that confronts poultry
in many regions of the world and large economic losses occur because of
mortality and decreased production (Altan et
al., 2000).
The thermoneutral zone for poultry is 18°C–24°C in the tropics and 12°C–26°C in the temperate zones, but this often gets exceeded in the tropics, resulting in heat stress (Holik, 2009; Dei and Bumbie, 2011). When the hypothalamic-pituitary-adrenocortical axis is activated, the hypothalamus produces corticotrophin-releasing factor, which in turn stimulates the pituitary to release adrenocorticotropic hormone (ACTH) (Mormède et al., 2007). Secretion of ACTH causes the cells of the adrenal cortical tissue to proliferate and to secrete corticosteroids. The main active hormone of the axis is cortisol in cattle, sheep, pig, mink, fox and fish, and corticosterone (CS) in birds and rodents (Mormède et al., 2007). These are cholesterol-derived steroids synthesized in the fascicular zone of the adrenal cortex under the control of the pituitary hormone. ACTH is synthesized by specialized cells (corticotrophs) of the anterior pituitary gland (Mormède et al., 2007).The
production of glucocorticoids is increased by stress; therefore, corticosterone
can be used as a biomarker of stress in poultry.
In chickens, adrenal corticosteroids are secreted shortly after exposure to stress and elevated levels of plasma glucocorticoids have been used as an index of the response to stress in poultry (Siegel, 1995). By elevating circulatory corticosteroids and decreasing thyroid activity, heat stress impairs broiler performance, especially adult birds, because the ability to dissipate heat decreases with age (Mahmoud et al., 2014). Drastic decline in feed intake occurring in heat-stressed birds is a physiological response to minimize intrinsic heat production. It is aimed at maintaining thermal homeostasis, thus decreasing feed efficiency, live weight gain, and survival rates (Faria-Filho et al., 2007). Lower breast-meat yield and higher carcass-fat deposition are the other deleterious effects of heat stress that lower the economic value of broiler carcasses (Geraert et al., 1996; Ain-Baziz et al., 1996). Corticosterone has an indirect role in lipid metabolism bycausing the rate of fat deposition to increase in poultry (Jiang et al., 2008; Yuan et al., 2008). Glucocorticoid hormone secretion also has implications for mineral metabolism, thus corticosteroids have been directly implicated in the development of osteoporosis in stressed animals (Siegel and Latimer, 1970). It has also been shown that glucocorticoids support the action of catecholamines, which have been shown to increase urinary calcium and sodium excretion (Fink and Brody, 1978).
Corticosteroids have been shown to inhibit several immune system
functions in various species, as demonstrated in depressed number of circulating
lymphocytes, which results in an increase in the ratio of circulating
heterophils to lymphocytes, the most recognizable symptom of stress in poultry
(Siegel, 1995). Regression of the thymus, bursa, and spleen has also been
demonstrated in chickens after corticosterone or ACTH administration (Puvadolpirod and Thaxton, 2000a).
Similarly, synthetic glucocorticoid dexamethasone administration mimics
the adverse effects of increased corticosterone. Dexamethasone (doses ranging
from 0.2 to 4.0 mg/kg) has been used as an immune suppressive agent (Fowles et al., 1993), mediator of prenatal
stress (Maccari et al., 2003) and to
induce oxidative stress in laying hens (El-Habbak et al. 2005) and cockerels (Eid et
al., 2006). Aengwanich (2007)
demonstrated that synthetic glucocorticoid; dexamethasone indoses of up to 6 mg/kg in their diets
had many effects on broilers like internal glucocorticoid.
Certain feed additives (selenium, vitamins C and E, α-lipoic acid, α-tocopherol, prebiotics and probiotics) enhance performance in heat-stressed broilers (Ghazi Harsini et al., 2012; Hamano, 2012; Imik et al., 2012; Khan et al., 2012; Sandhu et al., 2012; Sohail et al., 2012). Betaine, a methyl group donor, functions in lipid metabolism by stimulating oxidative catabolism of fatty acids through carnitine synthesis. Betaine is also an organic osmolyte and does not interfere with enzyme function or upset metabolism (Simon, 1999). As an osmolyte, betaine may have a stabilizing function on cells subjected to osmotic stressors, such as in the case of coccidiosis infection (Klasing et al., 2002) by regulating the water balance, resulting in the stability of tissue metabolism especially in the gastrointestinal tract (Lipinski et al., 2012). Dietary supplementation of betaine presumably reduces the requirement for other methyl-group donors, such as methionine and choline (Siljander-Rasi et al., 2003). Florou-Paneri et al. (1997) showed that between 30 and 80 percent of supplemental methionine can be substituted by betaine without negative effects on performance. As a feed additive, betaine is most commonly added to animal diets as anhydrous betaine; betaine monohydrate, and betaine hydrochloride (Kidd et al., 1997; Eklund et al., 2005). Within the body, betaine is synthesized from choline (Sakomura et al., 2013).