|Protein-Energy Interactions (International Dietary Energy Consultative Group - IDECG, 1991, 437 pages)|
|Effect of different levels of carbohydrate, fat and protein intake on protein metabolism and thermogenesis|
There are important differences in the control of nutrient metabolism and oxidation following food ingestion. The relationships between glucose and fat metabolism have been much studied and a clear concept emerges from recent studies. Shortly after meal ingestion, the carbohydrate content of the meal induces a stimulation of glucose oxidation, whereas fat oxidation is inhibited. Three to four hours later, glucose oxidation decreases with a concomitant rise in fat oxidation. Overall, the intake of dietary carbohydrate has the effect of reducing the rate of fat oxidation (ACHESON, FLATT and JÉQUIER, 1982; ACHESON et al., 1988). De novo lipogenesis from carbohydrate is not an important pathway in man, and dietary carbohydrates do not increase an individual's fat mass by de novo lipogenesis (ACHESON et al. 1988). Since carbohydrate stores are small compared to fat stores and usually do not vary from day to day, carbohydrate oxidation is adjusted to carbohydrate intake over a 24-hour period (FLATT, 1988).
After a meal, the increase in plasma insulin levels stimulates glucose uptake in muscle and other tissues, which induces a rise in glucose oxidation. The inhibitory effect of insulin on lipolysis in adipose tissue, and the subsequent decline in plasma free fatty acid levels leads to the postprandial inhibition of fat oxidation. This is a consequence of the glucose-fatty acid cycle described by RANDLE et al. (1963).
From our laboratory, FLATT et al. (1985) reported that fat intake did not promote fat oxidation over a period of nine hours following a meal. Neither did a fat supplement (106 ± 6 g fat) stimulate fat oxidation over 24 hours (SCHUTZ, FLATT and JÉQUIER, 1989). Thus, there is no metabolic response increasing fat oxidation to correct a surfeit of fat. It can be concluded that fat balance differs markedly from the regulation of carbohydrate balance: the latter is adjusted by an increased oxidation of glucose after meal ingestion, whereas no stimulation of fat oxidation occurs, even after a meal with a high fat content. Carbohydrate intake is therefore the main regulator of non-protein energy expenditure (FLATT, 1988). By contrast, fat oxidation is regulated by energy needs rather than by fat intake (FLATT et al., 1985).
The maintenance of nitrogen balance depends on both protein and energy intakes (MUNRO, 1964; CALLOWAY and SPECTOR, 1954; SCRIMSHAW et al., 1972; INOUE, FUJITA and NIIYAMA, 1973; GARZA, SCRIMSHAW and YOUNG, 1976; 1978). In the adult human subject who maintains energy balance for prolonged periods, increasing N intake above requirements only causes a transient positive N balance. The ability to achieve protein balance over a wide range of intake is well documented in humans, although the mechanisms, which account for an increased rate of protein oxidation when protein intake is increased above requirements, are complex and poorly understood.
The relationships between energy and protein intakes on protein metabolism depend on the nutritional and clinical state of the patient. The efficiency with which protein retention occurs is greater in depleted or starved patients than in patients suffering from accidental trauma, acute infection or burns (SHENKIN et al., 1980). The latter patients are often hypermetabolic with a decrease in lean tissues and a net loss of proteins from the body. It is therefore important to identify the nutritional and clinical conditions of the patients when one deals with the complex problem of energy-protein relationships (ELIA, 1982).
In studies of N balance, it would be desirable to know the independent effects of changes in N or in energy intakes. To do so is difficult, since the minimal requirement of protein intake to obtain N balance depends on the state of the subject's energy balance.