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.

Effects of dietary fat on postprandial substrate oxidation and on carbohydrate and fat balances.

To study the effect of dietary fat on postprandial substrate utilization and nutrient balance, respiratory exchange was determined in seven young men for 1 h before and 9 h after the ingestion of one of three different breakfasts: i.e., bread, jam, and dried meat (482 kcal: 27% protein, 62% carbohydrate, and 11% fat); bread, jam, and dried meat plus 50 g of margarine containing long-chain triglycerides (LCT); or bread, jam, and dried meat plus 40 g medium-chain triglycerides (MCT) and 10 g LCT margarine (858 kcal: 15% protein, 35% carbohydrate, and 50% fat). Plasma glucose concentrations peaked 45 min after the start of the meals. When compared with the low fat meal, the LCT margarine supplement had no effect at any time on circulating glucose and insulin concentrations, nor on the respiratory quotient. When MCTs were consumed, plasma glucose and insulin concentrations remained lower and plasma FFA concentrations higher during the first 2 h. 9 h after the breakfasts, the amounts of substrates oxidized were similar in each case, i.e., approximately 320, 355, and 125 kcal for carbohydrate, fat, and protein, respectively. This resulted in comparable carbohydrate (mean +/- SD = -22 +/- 32, -22 +/- 37, and -24 +/- 22 kcal) and protein balances (-7 +/- 9, +7 +/- 7, and -8 +/- 11 kcal) after the low fat, LCT- and MCT-supplemented test meals, respectively. However, after the low fat meal, the lipid balance was negative (-287 +/- 60 kcal), which differed significantly (P less than 0.001) from the fat balances after the LCT- and MCT-supplemented meals, i.e., +60 +/- 33 and +57 +/- 25 kcal, respectively. The results demonstrate that the rates of fat and of carbohydrate oxidation are not influenced by the fat content of a meal.

Evidence that insulin resistance is responsible for the decreased thermic effect of glucose in human obesity.

The thermic effect of glucose was investigated in nine obese and six lean subjects in whom the same rate of glucose uptake was imposed. Continuous indirect calorimetry was performed for 240 min on the supine subject. After 45 min, 20% glucose was infused (609 mg/min) for 195 min and normoglycemia was maintained by adjusting the insulin infusion rate. At 2 h, propranolol was infused (bolus 100 micrograms/kg; 1 microgram/kg X min) for the remaining 75 min. To maintain the same glucose uptake (0.624 g/min), it was necessary to infuse insulin at 3.0 +/- 0.6 (leans) and 6.6 +/- 1.2 mU/kg X min (obese) (P less than 0.02). At this time, glucose oxidation was 0.248 +/- 0.019 (leans) and 0.253 +/- 0.022 g/min (obese) (NS), and nonoxidative glucose disposal was 0.375 +/- 0.011 and 0.372 +/- 0.029 g/min, respectively. Resting metabolic rate (RMR) rose significantly by 0.13 +/- 0.02 kcal/min in both groups, resulting in similar thermic effects, i.e., 5.5 +/- 0.7% (leans) 5.4 +/- 0.9% (obese) (NS) and energy costs of glucose storage 0.35 +/- 0.06 and 0.39 +/- 0.09 kcal/g (NS), respectively. With propranolol, glucose uptake and storage remained the same, while RMR fell significantly in both groups, with corresponding decreases (P less than 0.05) in the thermic effects of glucose to 3.7 +/- 0.6% and 2.9 +/- 0.8% (NS) and the energy costs of glucose storage 0.23 +/- 0.04 and 0.17 +/- 0.05 kcal/g (NS) in the lean and obese subjects, respectively. These results suggest that the defect in the thermic effect of glucose observed in obese subjects is due to their insulin resistance, which is responsible for a lower rate of glucose uptake and hence decreased rate of glucose storage, which is an energy-requiring process.

Insulin. Its role in the thermic effect of glucose.

To investigate the possible role of insulin per se in the thermic response to glucose/insulin infusions, respiratory exchange measurements were performed on eight healthy young men for 45 min before and 210 min after somatostatin infusion. Two tests were performed on separate days and each had two consecutive phases of 90 min each. Test 1. Two different rates of glucose uptake were imposed, one at euglycemia (phase 1) and the other at hyperglycemia (phase 2) while insulinemia was maintained constant throughout. Test 2. Glucose uptake was maintained constant throughout while insulin was infused at two different rates: 1 mU/kg per min with hyperglycemia (phase 1) and 6.45 mU/kg per min with "euglycemia" (phase 2). The thermic effect of glucose and insulin, obtained from phase 1 in both tests, was 5.9 +/- 1.2 and 5.8 +/- 0.5% (NS) of the energy infused, respectively. A step increase in glucose uptake alone, test 1, phase 2, (0.469 +/- 0.039 to 1.069 +/- 0.094 g/min) caused an increase in energy expenditure of 0.14 +/- 0.03 kcal/min (thermic effect 5.9 +/- 1.1%). When insulin was increased by 752 +/- 115 microU/ml, with no change in glucose uptake, energy expenditure rose by 0.05 +/- 0.02 kcal/min, which correlated with the increase in plasma catecholamines. It is concluded that a large proportion of the thermic response to glucose/insulin infusions is due to glucose metabolism alone. The thermic effect of insulin is small and appears to be mediated by the sympathetic nervous system; thus at physiological insulin concentrations, the thermic effect of insulin per se is negligible.

Changes of gut microbiota and immune markers during the complementary feeding period in healthy breast-fed infants.

INTRODUCTION: Little is known about changes in intestinal microbiota during the important period of complementary feeding (weaning). This descriptive study investigated changes of selected gut microbiota and markers of gut permeability and the immune system in breast fed infants during the complementary feeding period. METHODS: 22 healthy, exclusively breast fed infants (from birth to 4 months) with no antibiotic intake during the month prior to the study, were followed from 4 to 9 months of age. Faecal and saliva samples were collected at the start of the study (V0) and at monthly intervals (V1-V5) for measurement of selective gut microbiota (bifidobacteria, lactobacilli, vancomycin-insensitive lactobacilli, enterobacteria, enterococci, Clostridium perfringens) using semi-selective media. Immune markers (alpha-1-antitrypsin, eosinophil cationic protein (ECP), secretory IgA and TNF-alpha were measured in saliva and secretory IgA and TNF-alpha in faecal samples. RESULTS: High stool bifidobacteria counts at the start of the study (7.99 1 1.95 log10 CFU/g faeces) remained stable throughout the 5 months of complementary feeding while counts of enterobacteria and enterococci increased with age (P < 0.05 and P = 0.02 respectively). Vancomycin-insensitive lactobacilli increased significantly during weaning for V0 to V3 (P < 0.01), and then decreased slightly (V4). Faecal Clostridium perfringens remained below the detection limit during the study and parameters measured in saliva did not change. Faecal ECP decreased significantly from 1.011.4 (V0) to 0.510.9 mg/mg protein (V5) P = 0.03. CONCLUSION: Age and/or diet modifications during complementary feeding had no impact on faecal bifidobacteria counts but increased those of enterobacteria and enterococci. Transient increases in faecal lactobacilli and vancomycin-insensitive lactobacilli counts were observed. The reduction in faecal ECP may indicate a decrease in gut permeability (reinforcement of gut mucosa integrity) during the weaning period with age [corrected]

A study of the relationship between thermogenesis and thyroid hormones.

To investigate the relationship between serum T3 levels and thermogenesis in euthyroid subjects, the conversion of T4 to T3 was partially blocked over a period of 3 weeks by weekly ingestion of 2 g iopanoic acid. Serum T3 decreased by 56 +/- 6 ng/100 ml without affecting the metabolic rate or total heat loss. Because an increase in serum T4 levels was observed (3.70 +/- 0.2 microgram/100 ml), the experiment was repeated in T4-substituted subjects. Serum T3 decreased even more in these subjects, (by 85 +/- 12 ng/100 ml), and the increase of serum T4 was also larger (4.6 +/- 0.7 microgram/100 ml). Again, the metabolic rate did not change. Experiments performed on hypothyroid patients and T3-substituted subjects demonstrated that iopanoic acid alone was without effect on the metabolic rate. Furthermore, the effect of a low energy, high protein diet (1672 kilojoules or 400 Cal) on the metabolic rate was confirmed. These results show that the decrease in magnitude of serum T3 seen with iopanoic acid is not sufficient by itself to reduce the metabolic rate.

The measurement of food and energy intake in man-an evaluation of some techniques.

A dietary survey was carried out on an Antarctic base over a period of 6 to 12 months on twelve individuals. Three methods of determining individual food and energy intake were used-weighing and recording of food as eaten in combination with food tables, dietary recall, and bomb calorimetry of duplicate meals. Use of weighed food intakes and food composition tables underestimated energy intake by 7% when compared to analysis of duplicate meals by bomb calorimetry. One week was found to be the most practical period over which intake should be measured to determine "habitual" food intake.

The measurement of daily energy expenditure--an evaluation of some techniques.

An energy balance survey was conducted on an Antarctic base on 12 individuals for periods varying between 6 and 12 months. Energy expenditure was estimated using two activity/dairy card techniques and mean 24-hr heart rate used in conjunction with a variety of derived heart rate/energy expenditure regression equations. The accuracy of the various techniques was determined by comparison with estimates obtained using energy intakes and changes in body fat. No method of measuring energy expenditure was accurate enough to predict fat gain or loss. Errors in individuals were large and random but the mean error in the estimation of energy expenditure of the community was reasonable. When using the dairy card there was no difference between using measured values for energy costs of specific activities and using values taken from the literature. Using heart rate was no less accurate than the diary card if energy expenditure was predicted from a regression line derived from heart rate and log energy expenditure, and the technique was more acceptable to the subjects.

A longitudinal study of body weight and body fat changes in Antarctica.

Body weight and body fat changes (calculated from skinfold thickness) that occurred in a male population spending a year on an Antarctic base are described. There was a marked individual variation in patterns of weight and fat changes between seasons but mean values for the whole community showed little change over the year. Combining skinfold and body weight measurements revealed probable individual differences in fat gain or loss with weight gain and loss, but the role of changes in total body water or fat-free mass could not be determined. The possibility of combining long-term measurements of body fat and energy intake to provide an estimate of energy expenditure is discussed.

Caffeine and coffee: their influence on metabolic rate and substrate utilization in normal weight and obese individuals.

A series of four trials was carried out to investigate the effects of caffeine and coffee on the metabolic rate and substrate utilization in normal weight and obese individuals. In the first trial 8 mg/kg caffeine was compared with a placebo in normal weight subjects. Metabolic rate increased significantly during the 3 hr after caffeine ingestion. While plasma glucose, insulin, and carbohydrate oxidation did not change significantly, plasma free fatty acid levels rose from 432 +/- 31 to 848 +/- 135 muEq/liter and were accompanied by significant increases in fat oxidation during the last hour of the test. In the second and third trials the effects of coffee providing 4 mg/kg caffeine were studied in control and obese subjects. Metabolic rate increased significantly in both groups; however, significant increases in fat oxidation were only observed in the control group. Plasma free fatty acids did not change in the obese. In the fourth trial, coffee was taken with a 3080 kJ meal. The thermic effect of the meal was significantly greater after coffee than after decaffeinated coffee and again fat oxidation was significantly greater after coffee. In conclusion caffeine/coffee stimulates the metabolic rate in both control and obese individuals; however, this is accompanied by greater oxidation of fat in normal weight subjects.

Contribution of 500 g naturally labeled 13C dextrin maltose to total carbohydrate utilization and the effect of the antecedent diet, in man.

Exogenous carbohydrate oxidation was studied for 24 h in 14 healthy young male volunteers after ingestion of 500 g naturally labeled 13C carbohydrate. Prior to the test, the antecedent diet was high in fat (4 subjects), mixed (4 subjects), or high in carbohydrate (6 subjects). The rate of exogenous carbohydrate oxidation was greater in the high carbohydrate and mixed diet groups than in the high fat group and endogenous carbohydrate continued to contribute to total carbohydrate oxidation for approximately 10 h after ingestion of the carbohydrate load in all groups. After 14 h, 178 +/- 5 g, 241 +/- 11 g and 260 +/- 9 g carbohydrate had been utilized of which 130 +/- 8 g, 155 +/- 6 g and 180 +/- 7 g was of exogenous origin in the high fat, mixed and high carbohydrate groups respectively. At the end of the test, postabsorptive glucose oxidation was of exogenous origin whatever the antecedent diet indicating that much of basal hepatic glucose production was covered by glycogenolysis of recently synthesized labeled glycogen.

Carbohydrate metabolism and de novo lipogenesis in human obesity.

Respiratory exchange was measured during 14 consecutive hours in six lean and six obese individuals after ingestion of 500 g of dextrin maltose to investigate and compare their capacity for net de novo lipogenesis. After ingestion of the carbohydrate load, metabolic rates rose similarly in both groups but fell earlier and more rapidly in the obese. RQs also rose rapidly and remained in the range of 0.95 to 1.00 for approximately 8 h in both groups. During this time, RQ exceeded 1.00 for only short periods of time with the result that 4 +/- 1 g and 5 +/- 3 g (NS) of fat were synthesized via de novo lipogenesis in excess of concomitant fat oxidation in the lean and obese subjects, respectively. Results demonstrate that net de novo lipid synthesis from an unusually large carbohydrate load is not greater in obese than in lean individuals.

Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man.

The metabolic balance method was performed on three men to investigate the fate of large excesses of carbohydrate. Glycogen stores, which were first depleted by diet (3 d, 8.35 +/- 0.27 MJ [1994 +/- 65 kcal] decreasing to 5.70 +/- 1.03 MJ [1361 +/- 247 kcal], 15% protein, 75% fat, 10% carbohydrate) and exercise, were repleted during 7 d carbohydrate overfeeding (11% protein, 3% fat, and 86% carbohydrate) providing 15.25 +/- 1.10 MJ (3642 +/- 263 kcal) on the first day, increasing progressively to 20.64 +/- 1.30 MJ (4930 +/- 311 kcal) on the last day of overfeeding. Glycogen depletion was again accomplished with 2 d of carbohydrate restriction (2.52 MJ/d [602 kcal/d], 85% protein, and 15% fat). Glycogen storage capacity in man is approximately 15 g/kg body weight and can accommodate a gain of approximately 500 g before net lipid synthesis contributes to increasing body fat mass. When the glycogen stores are saturated, massive intakes of carbohydrate are disposed of by high carbohydrate-oxidation rates and substantial de novo lipid synthesis (150 g lipid/d using approximately 475 g CHO/d) without postabsorptive hyperglycemia.

Energy expenditure of Chinese infants in Guangdong Province, south China, determined with use of the doubly labeled water method.

The doubly labeled water method was used to measure the energy expenditure of a group of 41, 4- or 6-mo-old infants with a cross-sectional design. The infants were divided into two groups according to whether they were breast-fed (11 at 4 mo, 9 at 6 mo) or formula fed (11 at 4 mo, 10 at 6 mo). Anthropometric measurements were recorded at birth and at the beginning and end of the 8-d study. Anthropometric data, which were supported by the food intake and energy expenditure results, indicated that the infants were within the norms for European and American infants of the same age. Mean energy intakes of 352 kJ (84 kcal) kg(-1) x d(-1) at 4 and 6 mo were lower than the FAO/WHO/UNU recommended value of 452 kJ (108 kcal) x kg(-1) x d(-1)) and Chinese recommendations of 502 kJ (120 kcal) kg(-1) x d(-1). However, some authors believe that values of 398 kJ (95 kcal) kg(-1) x d(-1) at 4 mo and 356 kJ (85 kcal) kg(-1) x d(-1) at 6 mo are more appropriate. At 6 mo the infants' length-for-age and weight-for-age were at the National Center for Health Statistics 55th and 47th percentiles, respectively, whereas 58% were below the 50th percentile for weight-for-length. We conclude that at 4 mo infants receive sufficient energy for their requirements. However, at 6 mo energy requirements might well be greater than the revised recommendations, when infants are being weaned to alternative foods and are more prone to the influence of diet on their growth and development.

PIP: This cross-sectional study uses the doubly labeled water method to measure energy intake, energy expenditure, and energy used for growth in groups of 4- and 6-month old Chinese infants who were predominantly either breast-fed or formula fed. Anthropometric measurements were recorded at birth and at the beginning and end of the 8-day study. Anthropometric data, which were supported by the food intake and energy expenditure results, indicated that the infants were within the norms for European and American infants of the same age. Mean energy intakes were lower than the WHO recommended value. However, some authors believe that values of 398 kilojoule (kJ) at 4 months and 356 kJ at 6 months were more appropriate. At 6 months old, the infants¿ length-for-age and weight-for-age were at the National Center for Health Statistics 55% and 47%, respectively, whereas 58% were below the 50% for weight-for-length. Therefore, infants at 4 months were able to receive sufficient energy for their requirements. However, at 6 months energy requirements might be greater than the revised recommendations, when infants were being weaned to alternative foods and were more prone to the influence of diet on their growth and development.

Thermogenesis in men and women induced by fructose vs glucose added to a meal.

Energy expenditure (EE) was measured by indirect calorimetry in 20 subjects (10 men and 10 women) for 30 min before and 6 h after the ingestion of a mixed meal containing 20% protein, 33% fat, and either 75 g glucose or 75 g fructose as carbohydrate source (47%). Diet-induced thermogenesis (DIT) and the rate of carbohydrate oxidation were significantly greater with fructose (12.4 +/- 0.6% and 54.8 +/- 2.1 g/6 h, respectively) than with glucose (10.7 +/- 0.7%, p less than 0.01, and 48.3 +/- 2.4 g/6 h, p less than 0.01, respectively). The DIT of male (12.1 +/- 1% and 13.9 +/- 0.8% with glucose and fructose, respectively) was greater than that of female subjects (9.2 +/- 0.7%, p less than 0.05, and 11.0 +/- 0.7%, p less than 0.05, respectively). In contrast to the glucose meal, negligible changes in plasma levels of glucose and insulin were observed with the fructose meal but plasma levels of lactate increased more with fructose than with glucose (peak values: 3.3 +/- 0.6 vs 1.5 +/- 0.1 mmol/L, respectively). When fructose provides the only carbohydrate source of a mixed meal, it induces a larger increase in carbohydrate oxidation and thermogenesis than when glucose is the carbohydrate source.

Glycogen synthesis versus lipogenesis after a 500 gram carbohydrate meal in man.

The respiratory exchange and urinary nitrogen excretion of 6 healthy male subjects (age 21 +/- 1 yr; body weight 70 +/- 2 kg; means +/- SD) were followed for 10 hr after ingestion of a large amount of carbohydrates (CHO) in the form of bread, jam, and fruit juice, equivalent to 479 g of starch. Peak values for blood glucose (6.6 +/- 0.6 mM; mean +/- SEM) and plasma insulin (139 +/- 26 microU/ml) were reached after 90 min at which time the nonprotein respiratory quotient (NP-RQ) had risen to 0.97. During the next 8 hr glucose levels remained near 5.5 mM while insulin declined gradually to 22 +/- 7 microU/ml. The average NP-RQ remained in the range of 0.91 to 0.98, though individual values exceeding 1.0 for very short periods were observed. The increase in energy expenditure above basal rates corresponded to a specific dynamic action (SDA) of 5.9 +/- 0.6%. Assuming the CHO load to be completely absorbed after 5 hr, and allowing for glucose oxidation calculated from the gas exchange data, the glycogen content of the subject's body tissue had then increased by 408 +/- 19 g. During the 10 hr after the meal, 133 g CHO, 17 g fat and 29 g protein were oxidized, providing respectively 66%, 19% and 15% of caloric expenditure, and leaving a gain in glycogen stores estimated at 346 +/- 12 g. The data imply that: (1) The capacity for glycogen storage in man in larger than generally believed, and (2) Fat synthesis from CHO will not exceed fat oxidation after one high-carbohydrate meal, even if it is uncommonly large. When a single high-carbohydrate meal is consumed, dietary CHO merely has the effect of reducing the rate of fat oxidation. These findings challenge the common perception that conversion of CHO to fat is an important pathway for the retention of dietary energy and for the accumulation of body fat.

Thyroid hormone action on lipid metabolism in humans: a role for endogenous insulin.

The effects of moderate hyperthyroidism on lipid metabolism were investigated in six healthy subjects before and after thyroxine treatment (300 micrograms/d). T4-treatment increased basal metabolic rate (+8%) and glucose oxidation (+87%), without affecting lipid oxidation, plasma free fatty acids, glycerol, and beta-hydroxybutyrate. During euthyroidism, a hypoinsulinaemic-euglycaemic 150-minute clamp protocol increased energy expenditure (+3%), lipid oxidation (+42%), plasma free fatty acids (+254%), glycerol (+232%), and beta-hydroxybutyrate (+343%), but decreased glucose oxidation (-20%). Similar effects were observed after T4-treatment, but hyperthyroidism induced disproportionate increases in energy expenditure (+7%), plasma glycerol (+310%), and ketone body levels (+436%). We conclude that moderate hyperthyroidism enhances hypoinsulinemia-induced increases in lipolysis, free fatty acid recycling, and ketogenesis without affecting lipid oxidation. Thus basal insulin may camouflage some of thyroid hormone action on lipid metabolism.

The parasympathetic nervous system and the thermic effect of glucose/insulin infusions in humans.

The thermic effect of glucose/insulin infusions was investigated in seven healthy young men before and during either inhibition (atropine sulphate 10 micrograms/kg bolus; 10 micrograms/kg/h) or stimulation (edrophonium chloride, 10 mg bolus; 0.75 mg/min starting rate) of the parasympathetic nervous system. The thermic effects of glucose/insulin were 6.2% +/- 0.4% and 5.6% +/- 0.7% before atropine and edrophonium, respectively, and increased to 7.1% +/- 0.5% (NS) with atropine and 7.5% +/- 1.2% (P less than .05) with edrophonium. In four subjects atropine or edrophonium was infused before the hyperinsulinemic, euglycemic clamp. A significant increase in resting metabolic rate and plasma norepinephrine concentrations was observed with edrophonium alone. When the thermic effects of glucose/insulin were calculated with respect to the metabolic rates observed during the drug infusions alone, they were 5.9% +/- 1.4% and 3.6% +/- 0.6% (NS) for the clamp + atropine and clamp + edrophonium, respectively. These results demonstrate that the increases in the thermic effect of glucose/insulin infusions observed during inhibition or stimulation of the parasympathetic nervous system were due to atropine or edrophonium increasing the resting metabolic rate rather than increasing the thermic response to glucose-insulin infusions. However, because it has been shown that atropine can decrease the thermic effect of an orally administered meal by approximately 60%, it would appear that the parasympathetic nervous system can influence the thermic effect of food by affecting the rate of digestion, absorption and storage of the ingested nutrients.

Thermic effect of epinephrine: a role for endogenous insulin.

The contribution of the basal insulin concentration to the metabolic response to epinephrine was measured in eight, postabsorptive, healthy volunteers before and during epinephrine (0.05 micrograms/kg fat-free mass [FFM] x min) and somatostatin (500 micrograms/h) infusion with and without insulin (0.1 mU/kg body weight [BW] x min) replacement. At basal plasma insulin concentrations, epinephrine increased oxygen consumption, heart rate, heart work, hepatic glucose production, glycogen breakdown in liver and muscle, and glucose oxidation, and the arterial plasma concentrations of glucose, lactate, and free fatty acids. Similar effects were observed during hypoinsulinemia, but epinephrine's actions on oxygen consumption and plasma concentrations of free fatty acids were disproportionally enhanced. We conclude that epinephrine-induced thermogenesis is partially inhibited by basal plasma insulin concentrations.

Two-week stimulation or blockade of the sympathetic nervous system in man: influence on body weight, body composition, and twenty four-hour energy expenditure.

Seven lean healthy young men were studied for 6 weeks during exposure to pharmacologic inhibition or stimulation of the sympathetic nervous system. For a period of 2 weeks their beta-adrenergic receptors were either blocked with propranolol hydrochloride (160 mg/d) or stimulated with terbutaline sulphate (15 mg/d). After a further 2 weeks of placebo administration (500 mg lactose/d), the subjects crossed over to the drug they had not been taking at the beginning of the experiment for another 14 days. During the last five days of each 2-week period, the subjects consumed a weight-maintaining diet, composed of 12% protein, 48% carbohydrate, and 40% fat. They consumed exactly the same menus on the same days during the subsequent study periods. Body weight and physical activity were measured every day for 6 weeks. Daily heart rate and nitrogen excretion were measured continuously for days at the end of each 2-week period, the last two days of which were spent in a respiration chamber where energy expenditure and a variety of metabolic parameters were measured. In the respiration chamber on the propranolol, placebo, and terbutaline treatments, respectively, significant differences were observed in mean daily heart rate (65 +/- 3, 75 +/- 4, and 84 +/- 4 beats/min), mean sleeping heart rate (51 +/- 2, 56 +/- 3, and 62 +/- 3 beats/min), nitrogen excretion (13.6 +/- 0.7, 12.6 +/- 0.6, and 11.9 +/- 0.6 g/d), fat oxidation (+1,045 +/- 95, +1,243 +/- 148, and +1,278 +/- 84 kcal/d) and thyroid hormones (12.0 +/- 0.7, 15.7 +/- 0.9, and 17.2 +/- 1.0 T3/T4 ratio).(ABSTRACT TRUNCATED AT 250 WORDS)