Title:
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Human information processing during acute insulin-induced hypoglycaemia
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The research described in this thesis includes studies involving experimentally induced hypoglycaemia, and a clinical study of children with insulin-dependent diabetes mellitus. The effect of acute insulin-induced hypoglycaemia on basic sensory information processing was examined. The principal studies performed were: Study 1 - an examination of the effect of acute hypoglycaemia on visual information processing, and; Study 2 - an examination of the effect of acute hypoglycaemia on auditory information processing. During 60 minutes of exposure to moderate hypoglycaemia significant impairments of both visual and auditory information processing were documented. It was also noted that hypoglycaemia did not significantly impair visual acuity for high contrast visual images but did disrupt ability to distinguish between low contrast visual images. Acute hypoglycaemia effects, in general, a negative mood state. The effect of hypoglycaemia on mood and emotion in human subjects was further explored. Hypoglycaemia was found to induce a small, but significant increase in anger-state that could not be predicted from anger-trait or general anger-expression, measures (Study 3). Hypoglycaemia also induced a negative mood-state characterised by increased tension and decreased happiness, lead to more negative appraisals of a life event, but did not effect a change in personality trait measures (Study 4). In addition, studies of were performed on different aspects of the symptomatic response to hypoglycaemia. These included: the symptoms of hypoglycaemia induced by a human insulin analogue in comparison with human soluble insulin (Study 5); the symptoms of hypoglycaemia induced by different experimental models of hypoglycaemia (Study 6); and the symptoms of hypoglycaemia reported by insulin-dependent diabetic children (Study 7). Insulin-dependent subjects do not show a different symptomatic, physiological or counterregulatory hormone response to hypoglycaemia when it is induced experimentally by either human soluble insulin or the human insulin analogue Lispro-insulin.
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