Substrate oxidation

One reason given for the preferential use of fatty emulsions in critically ill patients is the belief that they are easily utilized for energy and therefore could spare the energy drawn from endogenous fat fuels during fasting. In hypermetabolic fasting patients, as in fasting volunteers, endogenous fats are extensively oxidized. Moreover, in normal and stressed patients, the rate of oxidation of exogenous glucose (given without fat) increases with the load and the period of infusion. The oxidation of endogenous lipid is progressively reduced even if endogenous fat continues to be oxidized when glucose intake meets energy needs (non-protein respiratory quotient RQnp £ 1).

When glucose intake exceeds energy expenditure, the patient produces more energy (up to 100 per cent (RQ > 1)) from the glucose. However, when both carbohydrates and lipids (long-chain fatty triglycerides) are given, RQ np (i.e. the proportion of glucose and fat oxidized) seems to be determined by the carbohydrate load. The energy not drawn by the carbohydrate load to reach the energy balance is derived from fat. Indirect calorimetry does not separate exogenous from endogenous fat.

The exogenous lipid load neither induces further lipid oxidation nor results in a decrease in carbohydrate oxidation (lower RQ ) compared with that oxidized during the supply of the same amount of carbohydrate without lipid. After a meal or during continuous parenteral nutrition, oxidized lipid is largely derived from endogenous stores; dietary fat is mainly stored and probably oxidized later.

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