Abstract
The underlying cause of predisposition to obesity is complex but has measurable physiological and psychological traits. One marker is cortisol responsiveness. Thus, humans with high cortisol response to stress consume more calories than low responders [1]. In sheep with either high (HR) or low (LR) cortisol responses to Synacthen (ACTH), HR are more likely to become obese. This is associated with reduced thermogenesis in HR [2]. Here, we aimed to quantify physiological (n = 5/group) and psychological (n = 10/group) responses to various stressors in HR and LR sheep. Three stressors were applied to LR and HR animals and energy homeostasis (food intake and thermogenesis) was measured. Thermogenesis was recorded with dataloggers implanted into muscle. Stressors were hypoglycaemia (0.125 units/kg insulin, i.v.), a barking dog and immune challenge (200 ng/kg Lipopolysaccharide-LPS, i.v.). LPS induced the greatest overall disturbance in energy homeostasis with reduction (p < 0.01) in food intake in both groups (47± 7% in LR vs 26± 5% in HR); LR showed a greater (p < 0.05) reduction in food intake and greater (p < 0.05) rise in temperature measured by area under the curve (AUC) of temperature× time (LR, 20.4± 2 vs HR, 14.7± 2). Metabolic responses were minimal with the other 2 stressors. The change in energy homestasis was paralleled by cortisol responsiveness to stressors with the greatest effect and difference between HR and LR seen in LPS treatment (AUC 1543± 273 ng/mL, 6 h in HR and 1051± 138 ng/mL, 6 h, p < 0.05). Behavioural responses to (1) isolation in an enclosure (5× 3m), (2) a human intruder and (3) competition for food were analysed. LR had greater (p < 0.05) activity in Test(1) (Activity Score: LR, 6.5± 1.4 vs HR, 2.9± 1.5), spent more (p < 0.05) time (109± 25 s) facing the human (63± 25 s) in Test(2) and competed for food more successfully than HR in Test(3). Greater activity and increased thermogenesis in LR may reduce their propensity to become obese on a high energy diet.
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