Rise In Energy Expenditure Research Articles

Correlation between amino acid induced changes in energy expenditure and protein metabolism in humans.

The relationship between energy expenditure and protein metabolism during amino acid (AA) administration was evaluated in normal humans. A balanced AA solution was infused for 180 min at five different rates: 20 (study I), 40 (study II), 80 (study III), 160 (study IV), and 240 mg.m2(-1).min-1 (study V), on separate days, in seven normal, overnight-fasted subjects (age 25 +/- 2 y; height 172 +/- 5 cm; weight 68 +/- 4 kg). Indirect calorimetry and [1-14C] leucine infusion techniques were employed. Basal total plasma AA concentration averaged 1827 +/- 121 mumol/L and increased to 2192 +/- 142, 2576 +/- 158, 3677 +/- 195, 5638 +/- 237, and 7185 +/- 261 mumol/L in studies I-V, respectively. Basal energy expenditure averaged 0.60 +/- 0.02 kcal.m2(-1).min-1 and increased slightly in studies I and II (to 0.62 +/- 0.03, 0.63 +/- 0.02, respectively), and significantly in studies III-V (to 0.65 +/- 0.03, 0.70 +/- 0.04, and 0.77 +/- 0.05 kcal.m2(-1).min-1, respectively, all P < 0.01 versus basal; P < 0.05-0.01 for each study versus preceding study). Basal nonoxidative leucine disposal (NOLD), an index of protein synthesis, averaged 73 +/- 3 mumol.m2(-1).min-1 and increased, albeit not significantly, in studies I and II (to 75 +/- 5, 76 +/- 4, respectively). In contrast, a significant increase in NOLD was observed in studies III-V (to 87 +/- 7, 103 +/- 7, and 127 +/- 9 mumol.m2(-1).min-1, respectively; all P < 0.01 versus basal; P < 0.05-0.01 for each study versus preceding study). Basal respiratory quotient averaged 0.81 +/- 0.02 and did not change significantly in studies I-V (0.80 +/- 0.02, 0.79 +/- 0.02, 0.80 +/- 0.03, 0.82 +/- 0.02 and 0.82 +/- 0.03, respectively). The thermic effect of AA administration, calculated as percent of the AA energy infused, was constant and averaged 24 +/- 4, 19 +/- 3, 17 +/- 4, 17 +/- 3, and 18 +/- 3% in studies I-V, respectively. When AA-induced increase in protein synthesis was plotted with the increment in energy expenditure, a positive correlation was obtained (r = 0.792, P < 0.001). In summary, during AA administration (1) the absolute rise in energy expenditure is dose-dependent and does not show evidence of achieving a plateau; (2) it is positively correlated with AA-induced protein synthesis; and (3) the thermic effect is not dependent upon the AA dose administered. The data provide a quantitative assessment of AA-induced thermogenesis in normal humans and the energy needs associated with an acute stimulation of protein synthesis.

Energy metabolism and substrate oxidation in acromegaly.

Short term GH administration increases lipid breakdown and oxidation (lipidox) and reduces glucose uptake and carbohydrate oxidation (CHOox). It is not clear whether similar shifts in substrate oxidation occur in acromegaly, and our aim was to investigate this. Using indirect calorimetry, we compared energy expenditure, CHOox, and lipidox in 20 acromegalic patients and 20 normal subjects pair-matched for sex, age, height, and weight. Investigations were performed in the basal state (12-h fast) and during a 75-g oral glucose tolerance test (OGTT). Acromegalic patients had significantly higher fasting glucose levels and greater glucose and insulin responses during an OGTT than normal subjects. Fasting nonesterified free fatty acid and insulin-like growth factor (IGF)-binding protein-1 levels were similar in the two groups, and both were acutely suppressed by oral glucose to the same degree. Basal energy expenditure was significantly greater in the acromegalic patients (1682 +/- 49 vs. 1540 +/- 45 Cal/24 h; P < 0.05), who showed a trend toward higher basal CHOox. Oral glucose resulted in a significantly higher rise in energy expenditure in the normal compared to the acromegalic subjects. During the OGTT, CHOox significantly increased in both groups, but rose to a higher level in the acromegalic patients (177 +/- 10 vs. 138 +/- 9 mg/min; P = 0.004). Oral glucose significantly reduced lipidox in both groups, but lipidox was reduced to a significantly lower level in the acromegalic patients (32 +/- 4 vs. 46 +/- 3 mg/min; P = 0.004). In acromegaly, basal CHOox (r = 0.56; P = 0.01) and postglucose CHOox (r = 0.79; P = 0.0001) were both positively correlated to IGF-I, but not to insulin and/or glucose. In normal subjects, postglucose CHOox was positively correlated to IGF-I. In summary, hyperinsulinemia in acromegaly was associated with higher glucose levels and a blunted thermogenic response to glucose, and displayed no relationship to the pattern of substrate oxidation. CHOox was increased, and lipidox was reduced in acromegaly, and the extent of IGF-I elevation was related to CHOox in the basal and postglucose states. We conclude that 1) the chronic effects of GH excess on substrate oxidation differ from the short term effects of GH administration; 2) impaired insulin action in acromegaly extends to effects on energy expenditure; and 3) IGF-I may be an important regulator of substrate oxidation in acromegaly.

Thermogenic response to total parenteral nutrition in depleted patients with multiple organ failure

Nutrient-induced thermogenesis was studied in eight patients with severe nutritional depletion and multiple organ failure after abdominal surgery. Energy expenditure (EE) and RQ were recorded continuously over a period of 4 days. On each study day balanced total parenteral nutrition was administered during a period of approximately 16 h, followed by a period of low-energy glucose infusion. The total energy supply was in the order of 110% of the measured EE and the supply of glucose, fat and amino-acids was 2.6 ± 0.4, 2.6 ± 0.2 and 0.84 ± 0.2 kJ × kg BW −1 × h −1 (mean ± SD), respectively. The nutrient-induced thermogenesis, expressed as the rise in EE in percent of the energy content of the administered nutrients, was approximately 5%, which appears to be lower than previously observed in healthy individuals. A plateau in energy expenditure was reached after 6–8 h in response to parenteral nutrition. It is hypothesized that this plateau reflects the oxidative capacity and thus may be used as a guideline for nutritional therapy.

Meal-induced rise in resting energy expenditure in patients with complete cervical spinal cord lesions.

Central activation of the sympathoadrenal system is generally considered to be an essential component of the mechanisms whereby food ingestion stimulates resting energy expenditure. The functional importance of such sympathoadrenal stimulation has been demonstrated primarily in animals. To the extent that central sympathoadrenal stimulation is required for normal human nutrient-induced thermogenesis, this process should be defective in patients with complete cervical spinal cord lesion and severed connection between the central nervous system and the peripheral sympathetic nerves. Consequently, respiratory gas exchange was measured by indirect calorimetry in 9 tetraplegic patients and in 6 healthy individuals. Measurements were performed before and 2 hours after ingestion of a standardised mixed meal (40% of basal 24 h energy requirements). The basal energy expenditure was 64 +/- 4 watts in the tetraplegic patients and 79 +/- 6 watts in the controls. After the meal, energy expenditure increased on average by 17 +/- 2 watts or 26 +/- 3% of the basal values in the patients and by 14 +/- 2 watts or 19 +/- 3% in the healthy controls (NS). The thermic effect of the meal, ie the rise in energy expenditure expressed in percent of the meal's energy content, was 5.5 +/- 0.7% in the patients and 3.8 +/- 0.6% in the controls (NS). Plasma concentrations of noradrenaline were low in the tetraplegic patients (0.3-0.4 nmol/l) compared to the healthy controls (1.1-1.4 nmol/l), p < 0.02. It is concluded that nutrient-induced thermogenesis in tetraplegic patients with low sympathoadrenal activity is not diminished compared to healthy controls. The findings indicate that efferent sympathoadrenal stimulation from the brain is not a causal necessity for nutrient-induced thermogenesis in man.

Metabolic and febrile responses to typhoid vaccine in humans: effect of beta-adrenergic blockade.

Fever and activation of acute phase responses were induced in human volunteers by intramuscular injection of typhoid vaccine. Vaccine injection caused a rapid (within 1 h) and sustained rise in metabolic rate (peak response 16%, 6-8 h), followed by later increases in white blood cell count (3-4 h), skin temperature (4-5 h), oral temperature (5-6 h), heart rate (6-8 h), and plasma cortisol (5-8 h). A peak fever [1.2 +/- 0.2 degree C (SE) rise] was recorded 12 h after vaccine injection. The involvement of the sympathetic nervous system in the development of these responses was investigated by the oral administration of propranolol before (80 mg) and 3 h after (40 mg) vaccine injection. Propranolol prevented the increases in metabolic rate, heart rate, and skin temperature but did not inhibit the rise in oral temperature or white cell count after vaccine administration. These data indicate that the sympathetic nervous system is responsible for the rise in energy expenditure associated with fever in humans. However, the rise in body temperature can develop in the absence of this increase in metabolic rate possibly by changes in heat loss.

Thermogenic response to intravenous nutrition in patients with cirrhosis

Energy expenditure was determined using continuous indirect calorimetry in the basal state and during 3 h of total parenteral nutrition (TPN) in 8 patients with cirrhosis and 8 healthy volunteers. TPN consisted of glucose, fat and amino acids and had a glucose/fat ratio of 50:50. The infusion rate was set to provide energy corresponding to 62.5% of the individually measured 24-h resting energy expenditure. In the basal state energy expenditure was similar in patients and controls while the respiratory quotient (RQ) was lower in the patients (0.78 +/- 0.01 vs. 0.82 +/- 0.01, mean +/- SEM, p < 0.05). During TPN, energy expenditure increased progressively during the 3-h infusion period. The average rise in energy expenditure was similar in patients (19.1 +/- 1.2%) and in controls (21.4 +/- 1.6%, n.s.). The RQ rose in both groups, but more in the patients with cirrhosis. At the end of the study, RQ was higher in patients (0.89 +/- 0.01) than in controls (0.85 +/- 0.01, p < 0.05). It is concluded that the nutrient-induced rise in energy expenditure during TPN is not significantly different in patients with cirrhosis and control subjects. Furthermore, the results indicate that the increased fat utilization in overnight fasting cirrhotic patients is rapidly shifted to an augmented carbohydrate oxidation during TPN, possibly as a consequence of marked hyperinsulinemia.

Sleep Deprivation in the Rat:XII. Effect on Ambient Temperature Choice

Previous studies of total sleep deprivation in the rat by the disk-over-water method had shown an initial rise in body temperature (Tb), a later decline to below baseline levels, and a progressive rise in energy expenditure (EE). To evaluate the role of changes in temperature setpoint in these results, the ambient temperature choices (Tc) of six totally sleep-deprived (TSD) rats and their yoked control (TSC) rats were determined by the position in a thermally graded alley at which they chose to fall asleep. (Rats were removed from the alley and returned to the deprivation apparatus 1 min after sleep onset). Sleep deprivation was continued until TSD rats were near death. Tb and EE results were like those of the earlier studies. Tc rose progressively from 26.8 degrees C during baseline to 49.9 degrees C near the end of the deprivation period in TSD rats, whereas TSC rats showed only modest, nonsignificant increases. The attempt by TSD rats to get warmer, in spite of an elevated Tb, indicates a raised setpoint for behavioral thermoregulation and suggests that the increase in EE was also, at least in part, an attempt to reach an elevated setpoint. The progressively raised Tc also indicates that the late decline in Tb was a decline below setpoint rather than a response to a lower setpoint. Because EE increased, Tb decline must have resulted from excessive heat loss. Thus, TSD in the rat produced two thermoregulatory deficits-increased setpoint and excessive heat loss.(ABSTRACT TRUNCATED AT 250 WORDS)

Metabolic and thermoregulatory responses to burn wound colonization.

This study was designed to determine whether there is a relationship between bacterial colonization of the burn wound and resting oxygen consumption (VO2) and colonic temperature (Tc) in burned rats. Resting VO2, Tc, and blood, spleen, and wound cultures were monitored for 2 weeks after 30% total body surface full-thickness burns. The wounds of 53 animals were seeded with 10(8) nonvirulent P. aeruginosa (NVP) at the time of injury, while the wounds of 33 rats were allowed to colonize spontaneously. The seeded wounds contained 10(6) colony forming units/gm (CFU/gm) by the fourth postburn day (PBD), while the unseeded wounds did not reach this level of colonization until after the first week postinjury. Wound seeding accelerated the metabolic and thermoregulatory responses to injury. Average VO2 and Tc of the seeded group were above the unseeded group on PBD's 3-4 and 7-8, but there were no significant differences between groups on PBD's 14-15. Although the unseeded animals were hypermetabolic during the first week, they remained afebrile. There was a significant correlation between wound bacterial counts and the increase in resting VO2 of 44 nonbacteremic animals, but variations in the data suggest that factors other than number of viable wound bacteria affect this relationship. Changes in Tc were unrelated to wound bacterial count but were correlated with changes in VO2. Taken together, the data suggest that bacteria in the burn wound contribute to the rise in energy expenditure following thermal injury.

A new approach for studying the thermic response to dietary fuels

We describe a new method of studying the thermic response to dietary fuels that involves continuous infusion of a liquid formula diet through a thin nasogastric tube. The data show that the steady inflow of dietary fuel is accompanied by a relatively constant level of energy expenditure, the magnitude of which depends on the rate of fuel inflow. An increase in the rate of fuel infusion above that required for caloric maintenance leads to a rise in energy expenditure. We also give examples, based on preliminary observations, of how the technique can be used to more precisely quantify energy metabolism. The technique may prove useful in the studying efficiency of energy utilization and in examining the extent to which individuals differ in energy efficiency.

Thermic effect of glucose in man. Obligatory and facultative thermogenesis.

The contribution of the sympathetic nervous system to the thermic effect of intravenously infused glucose and insulin was studied in 10 healthy young men before and after beta-adrenergic receptor blockade with propranolol during conditions of normoglycemia (90 mg/dl) at two levels of hyperinsulinemia (approximately 90 microU/ml and approximately 620 microU/ml). During steady state conditions of glucose uptake (0.515 +/- 0.046 and 0.754 +/- 0.056 g/min), significant increases were observed in energy expenditure (0.10 +/- 0.02 kcal/min, P less than 0.001, and 0.21 +/- 0.02 kcal/min, P less than 0.01, respectively). Similarly, glucose oxidation increased from 0.100 +/- 0.015 to 0.266 +/- 0.022 g/min (P less than 0.001) at approximately microU/ml insulin and from 0.082 +/- 0.013 to 0.295 +/- 0.018 g/min (P less than 0.001) at approximately 620 microU/ml insulin. Concomitantly, the rate of nonoxidative glucose disposal or "glucose storage" was 0.249 +/- 0.033 and 0.459 +/- 0.048 g/min, respectively. At this time the thermic effect of infused glucose/insulin was 5.3 +/- 0.9 and 7.5 +/- 0.7%, and the energy cost of "glucose storage" was 0.50 +/- 0.16 kcal/g and 0.47 +/- 0.04 kcal/g at the two different levels of glucose uptake. After beta-adrenergic receptor blockade with propranolol, glucose uptake, oxidation, and "storage" were unchanged in both studies, but significant decreases in energy expenditure were observed (1.41 +/- 0.06-1.36 +/- 0.05 kcal/min, P less than 0.01 at approximately 90 microU/ml insulin, and 1.52 +/- 0.07-1.43 +/- 0.05 kcal/min, P less than 0.005 at approximately 620 microU/ml insulin) causing significant falls in both the estimated thermic effect of infused glucose/insulin and the energy cost of "glucose storage". Regression analysis of the results from both studies indicated a mean energy cost for "glucose storage" of 0.36 kcal/g (r = 0.74, P less than 0.001), which fell significantly (P less than 0.005) to 0.21 kcal/g (r = 0.49, P less than 0.05) during beta-adrenergic receptor blockade with propranolol. The latter is in close agreement with that calculated on theoretical grounds for the metabolic cost of glucose storage as glycogen, i.e., obligatory thermogenesis. It is concluded that beta-adrenergically mediated sympathetic nervous activity is responsible for almost the entire rise in energy expenditure in excess of the obligatory requirements for processing and storing glucose during conditions of normoglycemia and hyperinsulinemia in healthy man, and that the energy cost of "glucose storage" is not different at normal (approximately 90 microU/ml) and supraphysiological (approximately 620 microU/ml) plasma insulin concentrations.

Effect of the energy source on changes in energy expenditure and respiratory quotient during total parenteral nutrition.

It has been suggested that malnourished patients respond to glucose intake in excess of energy needs by a rise in respiratory quotient (RQ) above 1.0, indicating net fat synthesis. This would represent inefficient utilization of glucose as an energy source. It is unclear, however, whether this also occurs when some of the energy source is provided as a fat emulsion.Energy expenditure was measured by indirect calorimetry using a canopy hood and RQ, calculated from the analysis of 2 X 5 minute collections of expired air, were measured every 3rd day in two groups of surgical patients who received a 14‐day course of intravenous nutrition [total parenteral nutrition (TPN)]. Group I (mean ± 1 S.D. 57.4 ± 15.4 yers, 9 females, 3 males) received glucose as the only source (46.6 ± 9.2 kilocalories per kilogram per day and group II (55.8 ± 14.2 years, 5 males, 3 females) 60% of their calories as fat (44.0 ± 7.5 kilocalories per kilogram per day). Both groups were given similar amounts of crystalline amino acid solution (0.34 ± 0.007, 0.32 ± 0.005 gram nitrogen per kilogram per day, respectively) and no other intake. There was no significant difference between the groups mean values of body weight (52.3 ± 7.9 versus 57.9 ± 12.5 kilograms) or energy expenditure before TPN commenced (31.3 ± 6.5, 32.3 ± 3.0 kilocalories per square meter per hour). In group I there was a persistent elevation (p &lt; 0.001) of mean RQ above 1.0 from the 9th day of TPN, together with a significant increase (p &lt; 0.001) in mean energy expenditure which attained the value of 38.0 ± 4.8 kilocalories per square meter per hour on the 14th day. In group II, the mean RQ never exceeded 1.0. The rise in the mean expenditure in group II was significantly less (p &lt; 0.02) than that observed in group I.This study shows that the use of glucose as the only energy source during TPN is associated with a greater rise in energy expenditure than is observed with a glucose‐fat regime and a persistent elevation of RQ above 1, indicating net lipogenesis. These results suggest, therefore, that complete oxidation of glucose occurs when it is the only source of nonprotein calories given during TPN.