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Technical Report #4 – Cellular Energy Production: Thermogenesis and Metabolic Rate

Even during rest the human body is constantly metaboliz-ing energy to maintain itself. The rate at which energy is expended by the body, expressed in calories per hour (or more rigorously normalized to calories expended per kg body mass per hour), is known as the metabolic rate. The basal metabolic rate (BMR) is the body’s rate of energy expenditure while at rest. This represents just the energy requirements of maintaining life, consisting mostly of maintenance of body temperature, heart rate, breathing, nerve transmission, and electrochemical gra-dients across cell membranes. The basal metabolic rate accounts for 65-75% of daily energy requirements (Van Zant, 1992). Other components of metabolic rate include the thermic effect of feeding (TEF; also referred to as diet-induced thermogenesis, or DIT), the thermic effect of activity (TEA), and adaptive thermogenesis (AT); Van Zant (1992).

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The components of energy expenditure are illustrated in figure 1. Metabolic rate is affected by many parameters such as eating (caloric consumption as well as dietary com-position), activity (dependent on type, intensity, and duration of activity), lean body mass, age, sex, hor-mones, and drugs .Since all of the energy expended by the body is ultimately converted to heat (except when work is performed outside the body), metabolic rate can be determined by the amount of heat energy liberated by the body (Guyton, 1976). A calorimeter can be used to directly measure the heat given off by the body. However, since greater than 95% of the energy lib-erated by the body is derived from the reaction of foods with oxygen, the metabolic rate can also be calculated from the rate of oxygen consumption (Guyton, 1976). In many studies metabolic rate, or energy expenditure, is expressed in terms of oxygen consumption.Thermic Effect of Feeding Medium Chain TriglyceridesAfter consuming a meal the food is digested, released into the bloodstream, and transported to all the cells of the body. There, it reacts with oxygen to produce en-ergy. Some of the energy is captured in ATP, the energy source used directly by cellular machinery performing work.

Calories consumed in excess of energy require-ments will be stored as body weight. About 55% of the energy contained in food is liberated as heat during the process of ATP formation (Guyton, 1976). This release of heat energy from the oxidation of foods rep-resents an increase in metabolic rate and is accompanied by increased oxygen consumption .Feeding different dietary items while maintaining caloric intake affects oxygen consumption (Baba, Bracco, and Hashim, 1982). That different foods, normalized for energy content, increase the metabolic rate to different extents probably reflects the tendency of a particular food to be burned for energy versus being stored as body weight, as well as its extent of digestion and absorption. That protein increases the metabolic rate more than carbohydrate and conventional fat sug-gests that certain amino acids may directly stimulate thermogenesis (Guyton, 1976). The increase in energy expenditure caused by feeding is known as diet-induced thermogenesis or the thermic effect of feeding (Van Zant, 1992). MCTs cause profound postprandial thermogen-esis because they are very caloric dense and are absorbed and metabolized very rapidly.

The rapid oxidation of MCFAs in the liver causes an increase in postprandial oxygen consumption, i.e. metabolic rate. The increase in metabolic rate resulting from MCT ingestion has been measured in humans as well as in rats, using LCTs as con-trols (Seaton et al, 1986; Hill et al, 1989; Baba, Bracco, and Hashim, 1982). The data seem straight forward, well controlled, and statistically significant. Baba, Bracco, and Hashim (1982) observed that rats overfed MCT gained significantly less fat than rats fed an isocaloric diet containing LCT as the fat source. This was attributed to higher resting oxygen consumption (metabolic rate) in the MCT group. The authors ex-plained this by pointing out that while conventional fats are transported as chylomicrons and are largely stored as body fat, MCTs are transported directly to the liver where they are oxidized extensively to produce energy. The rapid oxidation of MCTs results in increased oxygen consumption, increased heat generation, and increased metabolic rate. In 1986 Seaton and colleagues demonstrated in humans that a meal containing MCTs increased oxygen consump-tion 12% above basal levels for 6 hours following the meal, while the LCT-containing meal increased oxygen consumption by only 4%. This indicates that MCTs are burned faster than conventional fats and increase the metabolic rate more. The increase in energy expenditure accounted for 13% of the energy contained in the MCT meal and 4% of the energy contained in the LCT meal. Hill and coworkers (1989) also compared the thermo-genic effect of medium chain triglycerides with that of long chain triglycerides.

Ten male volunteers were hospitalized and fed diets containing 30% of calories from either MCT or LCT. Metabolic rate was measured before, during, and after the experiment. Each subject was studied for one week on each diet in a double-blind crossover design. The thermic effect of food (TEF) is defined as the difference between metabolic rate during a six hour period after eating and the resting metabolic rate. That is, it is a measure of the increase in metabolic rate caused by eating the test meal. On day one of the experiment, the TEF of the meal containing MCT ac-counted for 8% of the ingested energy, while the TEF of the LCT meal accounted for 5.5% of the ingested energy. On day six of the experiment, the TEF of the MCT meal had increased to 12% of ingested energy, and the TEF of the LCT meal was 6.6% of ingested energy (figure 2). This means that the MCT-enhancement of the metabolic rate increased during the course of the experiment as the subjects became acclimated to the MCTs. On the last day of the trial the subjects were fed a liquid diet by continuous tube feeding.

During this experiment it was found that the TEF of the MCT meal increased to 15.7% of ingested energy, and the TEF of the LCT meal was 7.3% of ingested energy. So the increase in metabolic rate was even greater when MCT was administered continually .Mechanisms of ThermogenesisThe chemical mechanism underlying this thermogenic effect is unknown at present, but several suggestions have been advanced. Hill and coworkers (1989 and 1990) demon-strated that MCT overfeeding results in in-creased hepatic de novo fatty acid synthesis in man. This process is energetically costly and could account for the lesser efficiency of storage of MCT-derived energy. The observed increase in thermogenesis agrees well with the energy cost associated with de novo lipogenesis (Hill et al, 1990). This observation was corroborated by Crozier (1988) working with isolated rat hepatocytes.Alternatively, if electron transport is uncoupled from oxidative phosphorylation the energy spent to es-tablish an electrochemical potential gradient across the mitochondrial membrane is dissipated as heat instead of being conserved as ATP (Baba, Bracco, and Hashim, 1987).

For example, in brown adipose tissue a pathway exists allowing proton leakage across the mitochondrial membrane (Nicholls, 1979).Another means of dissipating energy as heat, believed to occur in liver mitochondria, is redox cycling involv-ing the glycerophosphate and malate shuttles (Berry et al, 1985; Crozier et al, 1987). In the glycerophosphate shuttle, energy is spent to pump reducing equivalents outside the mitochondria to drive the reduction of di-hydroxyacetone phosphate to glycerol-3-phosphate in the cytoplasm. The glycerol-3-phosphate then diffuses into the mitochondria and is oxidized to reform dihy-droxyacetone phosphate, which then diffuses out of the mitochondria to complete the cycle . The net result is the shuttle of glycerol-3-phosphate and dihydroxyacetone phosphate across the mitochondrial membrane (Berry et al, 1985; Crozier et al, 1987; Zubay, 1983, p. 401). Free energy is consumed to drive the cycle, but since no net work is performed the energy ultimately appears as heat (Berry et al, 1985).

The malate/aspartate shuttle is analogous .  Finally, increased activity of Na-K ATPase has also been suggested as a thermogenic mechanism for wasting en-ergy as heat (Levin and Sullivan, 1985). It is estimated that 10-40% of the total energy expended by the cell is used to maintain the concentration gradient of sodium and potassium ions across the cell membrane (Vander, Sherman, and Luciano, 1980). Since these ions also can cross the membrane by passive diffusion, an increase in the activity of the enzyme could be a mechanism for spending ATP.In all of the models de novo fatty acid synthesis, proton leakage, redox cycling (or other futile cycles), and Na-K ATPase the MCFAs are rapidly oxidized (explaining increased oxygen consumption), energy is consumed (explaining the low efficiency of storage of MCT-derived energy) and heat is produced as a by-prod-uct (explaining the thermogenic effect). Considerable evidence exists to support the involvement of de novo fatty acid synthesis as a mechanism for MCT-induced thermogenesis (Hill et al, 1989; Hill et al, 1990; Crozier, 1988) but other mechanisms may be involved as well. The reader is referred to Levin and Sullivan (1985) and Van Zant (1992) for reviews on thermogenesis and en-ergy balance.


1. Baba, Bracco, and Hashim, Enhanced thermogen-esis and diminished deposition of fat in response to over-feeding with diet containing medium chain triglyceride. Am. J. Clin. Nutr. 35: 678-682 (1982).

2. Baba, Bracco, and Hashim, Role of brown adipose tissue in thermogenesis induced by overfeeding a diet containing medium chain triglyceride . Lipids 22: 442-444 (1987).

3. Berry, Clark, Grivell, and Wallace, The contribu-tion of hepatic metabolism to diet-induced thermogenesis . Metab. 34: 141-147 (1985).

4. Crozier, Medium chain triglyceride feeding over the long term: the metabolic fate of C-14 octanoate and C-14 oleate in isolated rat hepatocytes. J. Nutr. 118: 297-304 (1988).

5. Crozier, Bois-Joyeux, Chanez, Girard, and Peret, Metabolic effects induced by long-term feeding of medium chain triglycerides in the rat. Metabolism 36: 807-814 (1987).

6. Guyton, Textbook of Medical Physiology. Pub-lished by W.B. Saunders, chapter 71 (1976).

7. Hill, Peters, Yang, Sharp, Kaler, Abumrad, and Greene, Thermogenesis in humans during overfeeding with medium chain triglycerides. Metabolism 38: 641-648 (1989).

8. Hill, Peters, Swift, Yang, Sharp, Abumrad, and Greene, Changes in blood lipids during six days of over- feeding with medium or long chain tri-glycerides. J. Lipid Res. 31: 407-416 (1990).

9. Levin and Sullivan, Regulation of thermogenesis in obesity. In: Novel Approaches and Drugs for Obesity, eds. Sullivan and Garattini, John Libbey and Co. Ltd. (1985).

10. Nicholls, Brown adipose tissue mitochondria. Bio-chim. Biophys. Acta 549: 1-29 (1979).

11. Seaton, Welle, Warenko, and Campbell, Thermic effect of medium chain and long chain triglycerides in man. Am. J. Clin. Nutr. 44: 630-634 (1986).

12. Vander, Sherman, and Luciano, Human Physiology The Mechanisms of Body Function, p. 236. Published by McGraw-Hill Book Company, 1980 .

2018-03-13T11:10:22+00:00 August 27th, 2009|Medium Chain Triglyceride Technical Reports|

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