Cortisol: A Short Review

Maigan Espinili Maruquin

The well- being of animal can be monitored from stress levels, which is related to the hypothalamic-pituitary-adrenocortical (HPA) axis activity (Möstl and Palme 2002, Salaberger, Millard et al. 2016). Elevation of glucocorticoid concentrations are observed in stressful situations (Salaberger, Millard et al. 2016).

Fig. 01. Location of Adrenal glands which produces glucocorticoids

Cortisol is known to play an important role in the interconnected responses on physiological, behavioral, and developmental functions (Bennett and Hayssen 2010). As an adrenal glucocorticoid, acute stress response result to rapid release of glucose from energy stores, suppresses inflammation, and promotes immune cell proliferation (Sapolsky, Romero et al. 2000, Charmandari, Tsigos et al. 2005, Mack and Fokidis 2017). Although measuring cortisol used to require significant disruption in behavior, different non- invasive sample collection methods for cortisol is now being used (Bennett and Hayssen 2010).

Cortisol Concentration at Different Tissues

In humans, salivary cortisol concentration for measurement is popular due to its straightforwardness and minimal invasive effect, including the fact that the storage is easy (Chen, Cintrón et al. 1992, Wenger-Riggenbach, Boretti et al. 2010). For healthy dogs, cortisol is unbound and passively diffuses from blood to saliva (Kirschbaum, C., et al, 1992) (Vincent and Michell 1992, Cobb, Iskandarani et al. 2016). Within 5 minutes, concentration of free cortisol in saliva and plasma sets at an equilibrium (Tunn, Möllmann et al. 1992, Wenger-Riggenbach, Boretti et al. 2010). Although blood and saliva can provide immediate view of cortisol concentrations, blood collection can be stressful, causing elevated concentrations. On the other hand, saliva absorption materials cause inconsistent results (Dreschel and Granger 2009, Bennett and Hayssen 2010).

Cortisol concentrations can be measured for a short time in urine and fecal samples (Bennett and Hayssen 2010). In urine, maximum concentration can be reached at approximately 3 hours (Rooney, Gaines et al. 2007, Bennett and Hayssen 2010) and longer in fecal samples (Bennett and Hayssen 2010). Aside from daily fluctuation of cortisol concentrations in saliva, blood, and urine (van Vonderen, Kooistra et al. 1998), it can also be influenced by any stress of the animal (Kobelt, Hemsworth et al. 2003, Mack and Fokidis 2017).

A lot of keratinized tissues contain glucocorticoids (Mack and Fokidis 2017). Concentration in the hair provides a long- term information on glucocorticoid production compared to the concentrations during sample collection (Ouschan, Kuchar et al. 2013). However, based on the effects of hair sampling, analysis of long-term cortisol secretion may be complicated (Mack and Fokidis 2017). Hair may also serve as cortisol storage area, however, validation for every species may be required due to difference in cortisol rhythms, secretions and stress response (Bennett and Hayssen 2010). On the other hand, a study was conducted using dog nails to assess cortisol concentration, wherein nail accumulates cortisol passively from the bloodstream (Mack and Fokidis 2017).

Hyperadrenocorticism and Hypoadrenocorticism

The chronic overexposure to glucocorticoids like cortisol can result to a complex physical and biochemical changes, referred to as hyperadrenocorticism (HAC) (Ouschan, Kuchar et al. 2013). Clinical signs of an affected dog show polyuria, polydipsia, polyphagia, pot-bellied appearance and typical skin and hair changes (Ouschan, Kuchar et al. 2013) (Feldman EC & Nelson RW, 2004). A tumor in the pituitary gland is usually the cause of this disease, wherein it secretes adrenocorticotrophic hormone (ACTH) and stimulates adrenal glands, resulting to glucocorticoids production (Ouschan, Kuchar et al. 2013).

For humans, diagnosis of hypercortisolism and hypocortisolism through the late-night and morning salivary cortisol concentrations is the established screening test (Viardot, Huber et al. 2005, Nieman, Biller et al. 2008, Restituto, Galofré et al. 2008, Wenger-Riggenbach, Boretti et al. 2010).

On the other hand, glucocorticoid deficiency is termed to as hypoadrenocorticism (Peterson, Kintzer et al. 1996), wherein, primary adrenal gland failure is the cause of most cases in dogs (Peterson, Kintzer et al. 1996, Gold, Langlois et al. 2016) (Scott-Moncrieff JC, 2010). Due to general and non- specific clinicopathologic signs, it is confused with primary gastrointestinal, renal, or cardiovascular disease. On-time and accurate diagnosis is important because it is a life-threatening disease if it goes without appropriate treatment (Gold, Langlois et al. 2016).

References:

Addison’s Disease in Dogs

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