Insulin resistance in catabolic diseases.

With remarkable intuition, John Hunter [1] in 1794 described the response to injury as follows: ‘Impressions are capable of producing or increasing natural actions and are then called stimuli: they are likewise capable of producing too much action as well as depraved, unnatural or what we commonly called diseased actions’. Scientific studies over the last century have lent support to this hypothesis in which the neuroendocrine, cytokine and consequent metabolic responses to injury are essential to survival, but when carried to extreme may put survival in jeopardy.