Abstract

Any discussion of carbohydrate metabolism during the 20 years of ESPEN primarily related to glucose and insulin. A brief mention is needed of the events between the discovery of insulin in the 1920s and the introduction of TPN in the 1960s. By 1960, the enzymatic steps in glycolysis and the oxidation of two-carbon fragments in the TCA cycle had established the major pathways for glucose as fuel. The intravenous use of glucose had been accepted for the treatment of hypoglycemia of insulin reactions as well as for limited nutrition and as a source of sodium-free water. This was not so for protein hydrolyzates or fat. Surgical patients who exhibited a negative nitrogen balance often had some degree of hyperglycemia, termed the ‘diabetes of injury’. Successive hormones, which were considered to oppose insulin action, appeared in roughly 20-year intervals: the catecholamines in the 1920s, the corticosteroids in the 1940s and glucagon in the 1960s. Felig, Wahren and coworkers then demonstrated that the three catabolic hormones together appeared to reproduce the metabolic response to injury, including hyperglycemia. Isotopic studies indicated that the hyperglycemia of stress was not due to lack of oxidation but rather to an increased production (1).

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