Journal articles: 'Meal induced thermogenesis'

1

Thörne, A., I. Näslund, and J. Wahren. "Meal-induced thermogenesis in previously obese patients." Clinical Physiology 10, no. 1 (January 1990): 99–109. http://dx.doi.org/10.1111/j.1475-097x.1990.tb00087.x.

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Thörne, A., and J. Wahren. "Diminished meal-induced thermogenesis in elderly man." Clinical Physiology 10, no. 5 (September 1990): 427–37. http://dx.doi.org/10.1111/j.1475-097x.1990.tb00823.x.

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Glick, Z., S. Y. Wu, J. Lupien, R. Reggio, G. A. Bray, and D. A. Fisher. "Meal-induced brown fat thermogenesis and thyroid hormone metabolism in rats." American Journal of Physiology-Endocrinology and Metabolism 249, no. 5 (November 1, 1985): E519—E524. http://dx.doi.org/10.1152/ajpendo.1985.249.5.e519.

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The relationship between the meal-induced increase in brown adipose tissue (BAT) thermogenesis, determined by the level of GDP binding to BAT mitochondria, and thyroid hormone metabolism have been examined. A single low-protein, high-carbohydrate meal resulted in a significant increase in the thermogenic activity of BAT. This effect on BAT thermogenesis was accompanied by significant increases in activity of thyroxine 5'-monodeiodinase in the BAT (P less than 0.05) and liver (P less than 0.02) but not with any significant changes in serum concentrations of the thyroid hormones. The stimulatory effects of the meal on BAT thermogenesis and hepatic thyroxine (T4) to triiodothyronine (T3) conversion persisted at least as late as 24 h after meal onset. Food deprivation for 40 h was associated with large reductions in serum concentrations of T3 (P less than 0.01) and T4 (P less than 0.001), but deprivation for 18 h had no significant effect on serum T3 and T4 concentrations. Our data indicate that the meal-induced increase in BAT thermogenesis can be independent from changes in serum concentrations of thyroid hormones and suggest that T3 produced in BAT in response to feeding may play a role in the thermic response of this tissue to meals.

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Yoshioka, Mayumi, Sylvie St-Pierre, Masashige Suzuki, and Angelo Tremblay. "Effects of red pepper added to high-fat and high-carbohydrate meals on energy metabolism and substrate utilization in Japanese women." British Journal of Nutrition 80, no. 6 (December 1998): 503–10. http://dx.doi.org/10.1017/s0007114598001597.

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The effects of dietary red pepper added to high-fat (HF) and high-carbohydrate (HC) meals on energy metabolism were examined in thirteen Japanese female subjects. After ingesting a standardized dinner on the previous evening, the subjects took an experimental breakfast (1883 kJ) under the following four conditions: HF meal, HF and red-pepper (10 g) meal, HC meal, or HC and red-pepper meal. Palatability of the experimental meals was measured immediately after the meals. Expired air was collected before and for 210 min after the meal to determine energy expenditure and macronutrient oxidation. Diet-induced thermogenesis was significantly higher after the HC meals than after the HF meals. Lipid oxidation was significantly lower and carbohydrate oxidation was significantly higher after the HC meals than after the HF meals. Addition of red pepper to the experimental meals significantly increased diet-induced thermogenesis and lipid oxidation, particularly after the HF meal. On the other hand, carbohydrate oxidation was significantly decreased by the addition of red pepper to the experimental meals. Addition of red pepper to the HC meal increased the perceived oiliness of the meal to the same level as that of the HF meals. These results indicate that red pepper increases diet-induced thermogenesis and lipid oxidation. This increase in lipid oxidation is mainly observed when foods have a HF content whereas the increase in the perceived oiliness of the meal was found under the HC meal conditions.

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MCDONALD, ROGER B., STEVE WICKLER, BARBARA HORWITZ, and JUDITH S. STERN. "Meal-induced thermogenesis following exercise training in the rat." Medicine & Science in Sports & Exercise 20, no. 1 (February 1988): 44–49. http://dx.doi.org/10.1249/00005768-198802000-00006.

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Maffeis, C., Y. Schutz, L. Zoccante, R. Micciolo, and L. Pinelli. "Meal-induced thermogenesis in lean and obese prepubertal children." American Journal of Clinical Nutrition 57, no. 4 (April 1, 1993): 481–85. http://dx.doi.org/10.1093/ajcn/57.4.481.

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Oomen, J. M., P. M. C. M. Waijers, C. van Rossum, B. Hoebee, W. H. M. Saris, and M. A. van Baak. "Influence of ß2-adrenoceptor gene polymorphisms on diet-induced thermogenesis." British Journal of Nutrition 94, no. 5 (November 2005): 647–54. http://dx.doi.org/10.1079/bjn20051516.

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The sympathetic nervous system is involved in the control of energy metabolism and expenditure. Diet-induced thermogenesis is mediated partly by the ß-adrenergic component of this system. The aim of the present study was to investigate the role of genetic variation in the ß2-adrenoceptor in diet-induced thermogenesis. Data from twenty-four subjects (fourteen men and ten women; BMI 26·7(sem 0·8) kg/m2; age 45·2(sem1·4) years) with different polymorphisms of the ß2-adrenoceptor at codon 16 (Gly16Gly, Gly16Arg or Arg16Arg) were recruited for this study. Subjects were given a high-carbohydrate liquid meal, and the energy expenditure, respiratory exchange ratio, and plasma concentrations of NEFA, glycerol, glucose, insulin and catecholamines were measured before and over 4 h after the meal. The AUC of energy expenditure (diet-induced thermogenesis) was not significantly different between polymorphism groups, nor was the response of any of the other measured variables to the meal. In a multiple regression model, the only variable that explained a significant proportion (32 %) of the variation in diet-induced thermogenesis was the increase in plasma adrenaline in response to the meal (P<0·05). The ß2-adrenoceptor codon16 polymorphisms did not contribute significantly. In conclusion, an independent contribution of the codon 16 polymorphism of the ß2-adrenoceptor gene to the variation in thermogenic response to a high-carbohydrate meal could not be demonstrated. The interindividual variation in thermogenic response to the meal was correlated with variations in the plasma adrenaline response to the meal.

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LeBlanc, J., and L. Brondel. "Role of palatability on meal-induced thermogenesis in human subjects." American Journal of Physiology-Endocrinology and Metabolism 248, no. 3 (March 1, 1985): E333—E336. http://dx.doi.org/10.1152/ajpendo.1985.248.3.e333.

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To study the possible participation of food-induced sensory stimulation on meal thermogenesis an experiment was performed with eight female subjects. On alternate days subjects were fed either a highly palatable meal (HPM), containing 710 calories, or a nonpalatable meal (NPM). The NPM was prepared by mixing all the ingredients of the HPM and was presented to the subjects as a desiccated biscuit. The subjects were not informed about the composition of the NPM, which they rated as tasteless and unappetizing. The increase in O2 consumption was approximately 20% during the 90 min following the HPM compared with 12% with the NPM (P less than 0.01). With comparable increases in plasma glucose, plasma insulin level was significantly (P less than 0.01) lower following NPM ingestion than with ingestion of the HPM. At that time a significant increase in plasma norepinephrine was also observed but only following ingestion of the HPM. It would appear that both central sensory stimulation or plasma insulin level, as affected by food palatability, could be considered at this time as possible activators of the increased sympathetic activity observed following ingestion of the HPM. It is suggested that a part of meal thermogenesis is due to food palatability and that the concomitant activation of the sympathetic system may be related to this action.

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Ruddick-Collins, Leonie C., Neil A. King, Nuala M. Byrne, and Rachel E. Wood. "Methodological considerations for meal-induced thermogenesis: measurement duration and reproducibility." British Journal of Nutrition 110, no. 11 (May 20, 2013): 1978–86. http://dx.doi.org/10.1017/s0007114513001451.

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Meal-induced thermogenesis (MIT) research findings have been highly inconsistent, in part, due to the variety of durations and protocols used to measure MIT. In the present study, we aimed to determine the following: (1) the proportion of a 6 h MIT response completed at 3, 4 and 5 h; (2) the associations between the shorter durations and the 6 h measures; (3) whether shorter durations improved the reproducibility of the measurement. MIT was measured in response to a 2410 kJ mixed composition meal in ten individuals (five males and five females) on two occasions. Energy expenditure was measured continuously for 6 h post-meal using indirect calorimetry, and MIT was calculated as the increase in energy expenditure above the pre-meal RMR. On average, 76, 89 and 96 % of the 6 h MIT response was completed within 3, 4 and 5 h, respectively, and MIT at each of these time points was strongly correlated with the 6 h MIT response (range for correlations, r 0·990–0·998; P< 0·01). The between-day CV for the 6 h measurement was 33 %, but it was significantly lower after 3 h of measurement (CV 26 %; P= 0·02). Despite variability in the total MIT between days, the proportion of MIT that was completed at 3, 4 and 5 h was reproducible (mean CV: 5 %). While 6 h are typically required to measure the complete MIT response, the 3 h measures provide sufficient information about the magnitude of the MIT response and may be applicable for testing individuals on repeated occasions.

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Weston, P. M. T., R. F. G. J. King, A. W. Goode, and N. S. Williams. "Diet-Induced Thermogenesis in Patients with Gastrointestinal Cancer Cachexia." Clinical Science 77, no. 2 (August 1, 1989): 133–38. http://dx.doi.org/10.1042/cs0770133.

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1. Indirect calorimetry has been used to measure resting energy expenditure (REE) and the thermogenic response to a test meal (diet-induced thermogenesis) in groups of weight-stable and weight-losing patients with gastrointestinal adenocarcinoma. Average daily intakes of energy and protein were computed from dietary assessment for the week before hospitalization. Results were compared with a control group of patients with benign gastrointestinal disease. 2. Weight-losing cancer patients had a significantly reduced mean total energy and protein intake. 3. There was no significant difference in REE between the groups when results were normalized in terms of metabolic body size (kJ/kg 0.75) and lean body mass (kJ/kg). 4. Diet-induced thermogenesis was reduced in weight-losing cancer patients. 5. It is suggested that the reduction of diet-induced thermogenesis in weight-losing cancer patients is another element of starvation adaptation, subsequent to their weight loss, and that altered thermogenesis does not contribute to the weight loss seen in cancer cachexia.

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Ho, Ken K. Y. "Diet-induced thermogenesis: fake friend or foe?" Journal of Endocrinology 238, no. 3 (September 2018): R185—R191. http://dx.doi.org/10.1530/joe-18-0240.

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Diet-induced thermogenesis (DIT) is energy dissipated as heat after a meal, contributing 5–15% to total daily energy expenditure (EE). There has been a long interest in the intriguing possibility that a defect in DIT predisposes to obesity. However, the evidence is conflicting; DIT is usually quantified by indirect calorimetry, which does not measure heat. Using gas exchange, indirect calorimetry measures total post-prandial EE, which comprises heat energy produced from brown adipose tissue (BAT) and energy required for processing and storing nutrients. We questioned whether DIT is reliably quantified by indirect calorimetry by employing infrared thermography to independently assess thermogenesis. Thermogenic activity of BAT was stimulated by cold and by a meal that induced a parallel increase in energy production. These stimulatory effects on BAT thermogenesis were inhibited by glucocorticoids. However, glucocorticoids enhanced postprandial EE in the face of reduced BAT thermogenesis and stimulated lipid synthesis. The increase in EE correlated significantly with the increase in lipogenesis. As energy cannot be destroyed (first law of thermodynamics), the energy that would have been dissipated as heat after a meal is channeled into storage. Post-prandial EE is the sum of heat energy that is lost (true DIT) and chemical energy that is stored. Indirect calorimetry does not reliably quantify DIT. When estimated by indirect calorimetry, assumed DIT can be a friend or foe of energy balance. That gas exchange-derived DIT reflects solely energy dissipation as heat is a false assumption likely to explain the conflicting results on the role of DIT in obesity.

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Scott, Chris B., and Rachel Devore. "Diet-induced thermogenesis: variations among three isocaloric meal-replacement shakes." Nutrition 21, no. 7-8 (July 2005): 874–77. http://dx.doi.org/10.1016/j.nut.2004.12.010.

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13

Thörne, A., D. Hallberg, and J. Wahren. "Meal-induced thermogenesis in obese patients before and after weight reduction." Clinical Physiology 9, no. 5 (October 1989): 481–98. http://dx.doi.org/10.1111/j.1475-097x.1989.tb01002.x.

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14

Peracchi, Maddalena, Alessandra Santangelo, Dario Conte, Mirella Fraquelli, Rosalia Tagliabue, Carlotta Gebbia, and Marisa Porrini. "The physical state of a meal affects hormone release and postprandial thermogenesis." British Journal of Nutrition 83, no. 6 (June 2000): 623–28. http://dx.doi.org/10.1017/s0007114500000799.

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There is evidence that food consistency may influence postprandial physiological responses. Recently we found that homogenization of a vegetable-rich meal significantly delayed the gastric emptying rate and was more satiating than the same meal in solid–liquid form. In this present study we investigated whether homogenization also influences endocrine and metabolic responses to the meal. Eight healthy men, aged 21–28 (mean 24·5) years, were given the meal (cooked vegetables 250 g, cheese 35 g, croutons 50 g and olive oil 25 g, with water 300 ml; total energy 2·6 MJ) in both solid–liquid (SM) and homogenized (HM) form, in random order, at 1-week intervals. Variables assayed were plasma glucose, insulin and glucose-dependent insulinotropic peptide (GIP) levels for 2 h and diet-induced thermogenesis (DIT) for 5 h. Plasma glucose pattern was similar after both meals. However, HM induced significantly greater insulin, GIP and DIT responses than SM. Mean integrated areas under the curves (AUC) were 1·7 (SEM 0·38) V. 1·2 (sem 0·33) U/l per 120 min (P = 0·005) for insulin, 19·9 (sem 2·44) v. 16 (sem 1·92) nmol/l per 120 min (P = 0·042) for GIP, and 237·7 (sem 16·32) v. 126·4 (sem 23·48) kJ/300 min (P = 0·0029) for DIT respectively. Differences between GIP-AUC after HM and SM correlated significantly with differences between insulin-AUC after HM and SM (r2 0·62, P = 0·021). These findings demonstrate that homogenization of a meal results in a coordinated series of changes of physiological gastroentero–pancreatic functions and confirm that the physical state of the meal plays an important role in modulating endocrine and metabolic responses to food.

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Even, Patrick C., Eric Bertin, Marie-Noelle Gangnerau, Suzanne Roseau, Daniel Tomé, and Bernard Portha. "Energy restriction with protein restriction increases basal metabolism and meal-induced thermogenesis in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 3 (March 1, 2003): R751—R759. http://dx.doi.org/10.1152/ajpregu.00268.2002.

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We previously observed an increased sympathetic nervous system (SNS) activity that was partly responsible for a defect in the insulin secretion response to glucose after postweaning protein-energy restriction (PER) in female rats. These results, together with other data on low-protein feeding, suggested that a low protein-to-energy ratio (P/E) in the diet could stimulate energy expenditure (EE), but direct measurements of EE have never been reported under conditions of PER. The goal of the present study was thus to quantify the changes induced by PER to body composition, the various parameters of EE, and plasma triiodothyronine levels. PER induced severe growth retardation, but the subcutaneous white and interscapular brown adipose tissue masses were preserved. Basal metabolism, meal-induced thermogenesis, and triiodothyronine levels were increased, but substrate utilization by the working muscles was unaffected. Meal-induced thermogenesis was increased by spontaneous activity in PER rats only. These results suggest that rats adapt to a low P/E in the diet by burning part of their excess nonprotein energy and storing the remaining excess in subcutaneous adipose tissue.

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Heijnen, Marie-Louise A., Paul Deurenberg, Johan M. M. Van Amelsvoort, and Anton C. Beynen. "Replacement of digestible by resistant starch lowers diet-induced thermogenesis in healthy men." British Journal of Nutrition 73, no. 3 (March 1995): 423–32. http://dx.doi.org/10.1079/bjn19950044.

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The present study describes the effect of replacement of digestible starch by resistant starch (RS) on diet-induced thermogenesis (DIT), postprandial glucose and insulin responses, and colonic fermentation. Ten healthy males consumed three test meals, consisting of diluted, artificially-sweetened fruit syrup and either 50 g raw potato starch (550 g RS/kg), or 50 g pregelatinized potato starch (0 g RS/kg) or 30 g pregelatinized potato starch plus 20 g lactulose (670 g indigestible disaccharide/kg). The meals were served in the morning after an overnight fast. Each volunteer consumed each meal twice on six separate days in random order. Metabolic rate was measured by indirect calorimetry in the fasting state for 15 min and postprandially for 5 h. Shortly before and hourly up to 7 h after consumption of the test meal, end-expiratory breath samples were obtained for H2 and CH4 analysis. Shortly before the meal and 30, 60, 180, and 300 min postprandiaily, blood samples were taken for glucose and insulin analyses. Postprandial increases in glucose and insulin levels were proportional to the amount of digestible carbohydrate in the meal. Breath H2 and CH4 concentrations indicated that the pregelatinized starch was not fermented and that lactulose was fermented rapidly. Fermentation of the raw starch started only 6 to 7 h after consumption, resulting in a rise in breath H2 but not in CH4. The replacement of 27 g digestible starch by RS in a single meal lowered DIT by on average 90 kJ/5 h, as could also be calculated by assuming that RS does not contribute to DIT. The ingestion of lactulose resulted in a substantial rise in DIT which was most probably caused by its fermentation.

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Astrup, A., L. Simonsen, J. Bulow, J. Madsen, and N. J. Christensen. "Epinephrine mediates facultative carbohydrate-induced thermogenesis in human skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 257, no. 3 (September 1, 1989): E340—E345. http://dx.doi.org/10.1152/ajpendo.1989.257.3.e340.

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The thermic effect of carbohydrate has a component mediated by the sympathoadrenal system but of unknown anatomical localization. We have studied the contribution of skeletal muscle to the thermic effect of a carbohydrate-rich natural meal (115 g of carbohydrate, approximately 80% of energy) by means of the forearm technique on two occasions, with and without intravenous beta-blockade with propranolol. The meal-induced thermogenesis was reduced from 9.6 to 7.1% by beta-blockade (P less than 0.04), the major difference was found 90 to 240 min after the meal. The postprandial increments in plasma glucose and lactate did not change by beta-blockade, but there was a trend toward a decreased insulin response (P = 0.06). The carbohydrate-induced increase in forearm oxygen consumption was reduced by 23% after beta-blockade (P less than 0.05), the entire difference being present 90-180 min postprandially and coinciding with the peak in arterial epinephrine. The present study provides evidence of a facultative thermogenic component in skeletal muscle, mediated by epinephrine via beta 2-adrenoreceptors. However, it also points to a nonmuscle component mediated through beta 1-adrenoceptors by norepinephrine released from the sympathetic nervous system. Consequently, the sympathoadrenal system seems to play a physiological role in the daily energy balance.

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Fojt, A., J. S. Keller, J. Bujko, S. Halilu Bawa, and E. Furstenberg. "Dietary-induced thermogenesis as influenced by meal frequency and gender in rats." Zeitschrift für Ernährungswissenschaft 36, no. 4 (December 1997): 323. http://dx.doi.org/10.1007/bf01617810.

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Nguo, Kay, Catherine E. Huggins, Helen Truby, Justin Brown, and Maxine P. Bonham. "Effect of macronutrient composition on meal-induced thermogenesis in adolescents with obesity." European Journal of Nutrition 58, no. 6 (July 20, 2018): 2327–33. http://dx.doi.org/10.1007/s00394-018-1783-1.

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Maffeis, C. "Meal-Induced Thermogenesis and Obesity: Is a Fat Meal a Risk Factor for Fat Gain in Children?" Journal of Clinical Endocrinology & Metabolism 86, no. 1 (January 1, 2001): 214–19. http://dx.doi.org/10.1210/jc.86.1.214.

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Betts, James A., Enhad A. Chowdhury, Javier T. Gonzalez, Judith D. Richardson, Kostas Tsintzas, and Dylan Thompson. "Is breakfast the most important meal of the day?" Proceedings of the Nutrition Society 75, no. 4 (June 13, 2016): 464–74. http://dx.doi.org/10.1017/s0029665116000318.

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The Bath Breakfast Project is a series of randomised controlled trials exploring the effects of extended morning fasting on energy balance and health. These trials were categorically not designed to answer whether or not breakfast is the most important meal of the day. However, this review will philosophise about the meaning of that question and about what questions we should be asking to better understand the effects of breakfast, before summarising how individual components of energy balance and health respond to breakfast v. fasting in lean and obese adults. Current evidence does not support a clear effect of regularly consuming or skipping breakfast on body mass/composition, metabolic rate or diet-induced thermogenesis. Findings regarding energy intake are variable, although the balance of evidence indicates some degree of compensatory feeding later in the day such that overall energy intake is either unaffected or slightly lower when breakfast is omitted from the diet. However, even if net energy intake is reduced, extended morning fasting may not result in expected weight loss due to compensatory adjustments in physical activity thermogenesis. Specifically, we report that both lean and obese adults expended less energy during the morning when remaining in the fasted state than when consuming a prescribed breakfast. Further research is required to examine whether particular health markers may be responsive to breakfast-induced responses of individual components of energy balance irrespective of their net effect on energy balance and therefore body mass.

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Cioffi, Iolanda, Lidia Santarpia, Andrea Vaccaro, Roberto Iacone, Giuseppe Labruna, Maurizio Marra, Franco Contaldo, Mette Kristensen, and Fabrizio Pasanisi. "Whole-grain pasta reduces appetite and meal-induced thermogenesis acutely: a pilot study." Applied Physiology, Nutrition, and Metabolism 41, no. 3 (March 2016): 277–83. http://dx.doi.org/10.1139/apnm-2015-0446.

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In epidemiological studies, the intake of foods rich in dietary fiber is associated with a reduced risk of developing overweight and type 2 diabetes. This work aims to identify acute strategies to regulate appetite and improve glucose control by using different pasta meals. Hence, 4 different isocaloric lunch meals, consisting of (i) refined-grain pasta (RG+T), (ii) whole-grain pasta (WG+T), (iii) lemon juice-supplemented refined-grain pasta (LRG+T), and (iv) refined-grain pasta with legumes (RG+L), were administered to 8 healthy participants in a crossover design. On the test days, participants underwent baseline measurements, including appetite sensation, blood sample, and resting energy expenditure (EE), after which the test lunch was served. Subjective appetite was assessed and a blood sample was taken each hour for 240 min, and postprandial EE was measured for 3 h. In repeated-measures analysis of covariance (ANCOVA), postprandial fullness (p = 0.001) increased and hunger (p = 0.038) decreased. WG+T had a lower EE than did both LGR+T (p = 0.02) and RG+L (p < 0.001). Likewise, meal-induced thermogenesis was lower for WG+T compared with RG+L (58 ± 81 kJ vs 248 ± 188 kJ; p < 0.05). Plasma glucose (p = 0.001) was lower for RG+T, and triacylglycerols (p = 0.02) increased for LRG+T; however, insulin, C-peptide, and ghrelin were comparable in all other meals. In conclusion, our study indicates that acute consumption of whole-grain pasta may promote fullness and reduce hunger, lowering postprandial thermogenesis, and adding lemon juice to the pasta or legumes does not appear to affect appetite. However, none of pasta meal alterations improved the postprandial metabolic profile.

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Kumstát, Michal, and Luboš Hrazdira. "Diet-Induced Thermogenesis: Comparison of Two Isocaloric Meal-Replacement Shakes. A pilot study." Journal of Human Sport and Exercise 7, no. 1Proc (2012): S140—S146. http://dx.doi.org/10.4100/jhse.2012.7.proc1.15.

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Maffeis, C., Y. Schutz, L. Zoccante, and L. Pinelli. "Meal-induced thermogenesis in obese children with or without familial history of obesity." European Journal of Pediatrics 152, no. 2 (February 1993): 128–31. http://dx.doi.org/10.1007/bf02072489.

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Maffeis, Claudio, Yves Schutz, Alessandra Grezzani, Silvia Provera, Giorgio Piacentini, and Luciano Tatò. "Meal-Induced Thermogenesis and Obesity: Is a Fat Meal a Risk Factor for Fat Gain in Children?1." Journal of Clinical Endocrinology & Metabolism 86, no. 1 (January 2001): 214–19. http://dx.doi.org/10.1210/jcem.86.1.7132.

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Khossousi, A., C. W. Binns, S. S. Dhaliwal, and S. Pal. "The acute effects of psyllium on postprandial lipaemia and thermogenesis in overweight and obese men." British Journal of Nutrition 99, no. 5 (May 2008): 1068–75. http://dx.doi.org/10.1017/s0007114507864804.

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Overweight and obesity is one of the risk factors for developing CVD. At present, very little is known about the acute effects of dietary fibre on lipids, glucose and insulin, resting energy expenditure and diet-induced thermogenesis in overweight and obese individuals. This study examined the postprandial metabolic effects of dietary fibre in overweight and obese men. Ten overweight and obese men consumed a mixed meal accompanied by either a high-fibre or low-fibre supplement on two separate visits, in a random order, 1 week apart. Two isoenergetic breakfast meals with similar composition were consumed by ten overweight/obese men. The meals contained either a low (3 g) or high (15 g) amount of fibre, low-fibre meal (LFM) and high-fibre meal (HFM) respectively. Analysis was carried out using paired t test and ANOVA. Serum TAG incremental area under the curve during 6 h of the postprandial period was significantly lower after the consumption of HFM compared with LFM. At the first hour of the postprandial period, plasma apo B48 concentration after consumption of HFM was significantly lower compared with LFM. The resting energy expenditure and diet-induced thermogenesis after both meals was similar during 6 h of the postprandial period. Collectively, these findings suggest that a single acute dose of dietary fibre in the form of psyllium supplement can decrease arterial exposure to TAG and modify chylomicron responses in the postprandial period.

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Schwarz, J. M., Y. Schutz, F. Froidevaux, K. J. Acheson, N. Jeanprêtre, H. Schneider, J. P. Felber, and E. Jéquier. "Thermogenesis in men and women induced by fructose vs glucose added to a meal." American Journal of Clinical Nutrition 49, no. 4 (April 1, 1989): 667–74. http://dx.doi.org/10.1093/ajcn/49.4.667.

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Marques-Lopes, Iva, Luis Forga, and J. Alfredo Martı́nez. "Thermogenesis induced by a high-carbohydrate meal in fasted lean and overweight young men:." Nutrition 19, no. 1 (January 2003): 25–29. http://dx.doi.org/10.1016/s0899-9007(02)00950-4.

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Hamada, Yuka, Hideaki Kashima, and Naoyuki Hayashi. "The number of chews and meal duration affect diet-induced thermogenesis and splanchnic circulation." Obesity 22, no. 5 (May 2014): E62—E69. http://dx.doi.org/10.1002/oby.20715.

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30

Ratcliff, Lance, Sareen S. Gropper, B. Douglas White, David M. Shannon, and Kevin W. Huggins. "The Influence of Habitual Exercise Training and Meal Form on Diet-Induced Thermogenesis in College-Age Men." International Journal of Sport Nutrition and Exercise Metabolism 21, no. 1 (February 2011): 11–18. http://dx.doi.org/10.1123/ijsnem.21.1.11.

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This study compared type of habitual exercise and meal form on diet-induced thermogenesis (DIT) in 29 men age 19–28 yr. Resting metabolic rate (RMR) and DIT response to solid-meal (bar) vs. liquid-meal (shake) ingestion were measured via indirect calorimetry; classifications were sedentary (n = 9), endurance trained (n = 11), or resistance trained (n = 9). Height, weight, and body composition (using bioelectrical impedance) were measured for each subject. Energy expenditure was determined before and every 30 min after meal consumption for 210 min. RMR was significantly (p = .045) higher in the endurance- and resistance-trained groups. However, when expressed per kilogram fat-free mass (FFM; relative RMR), differences were not significant. Both DIT (kcal/min) and relative DIT (kcal · min−1 · kg FFM−1) significantly increased with time (p < .0001) from RMR for each meal form. There was no significant exercise-group effect on DIT or relative DIT. There was a significant (p = .012) effect of meal form on DIT; shakes elicited a higher DIT. This significant difference was not found for relative DIT. There was a significant interaction between group and meal form for DIT (p = .008) and relative DIT (p < .0001). Shakes elicited a significantly greater DIT (p = .0002) and relative DIT (p = .0001) in the resistance-trained group. In the sedentary group, relative DIT from shakes was significantly lower than from bars (p = .019). In conclusion, habitual exercise appears to increase RMR, and meal form may impart changes in relative DIT depending on exercise status.

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Nguo, Kay, Catherine E. Huggins, Helen Truby, Andrew J. Sinclair, Rachel E. Clarke, and Maxine P. Bonham. "No effect of saturated fatty acid chain length on meal-induced thermogenesis in overweight men." Nutrition Research 51 (March 2018): 102–10. http://dx.doi.org/10.1016/j.nutres.2018.01.003.

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Dulloo, A. G., and L. Girardier. "Energy expenditure and diet-induced thermogenesis in presence and absence of hyperphagia induced by insulin." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 4 (October 1, 1989): R717—R725. http://dx.doi.org/10.1152/ajpregu.1989.257.4.r717.

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The influence of experimental hyperinsulinemia on energy intake, energy expenditure, and body composition was investigated in rats treated chronically with high doses of insulin. Energy balance studies, each of 2-wk duration, were conducted with two different long-acting insulins (Protamine and Monotard), administered in the morning (IM), the late afternoon (IA), or both (IMA) and in animals of three different ages, namely in 4-, 8-, and 12-wk-old rats. The results indicate that the level of hyperphagia induced by insulin was markedly influenced by the type of long-acting insulin (P less than 0.001; Protamine greater than Monotard), by age (P less than 0.001; 12 greater than 8 greater than 4 wk), as well as by the timing of insulin administration (P less than 0.002, IMA greater than IM or IA). Body protein deposition was unaltered, but body fat and energy expenditure increased in parallel to the level of hyperphagia. Regression analysis shows a strong linear correlation (r = 0.963) between the change in energy expenditure and the change in energy intake in response to insulin and indicates that approximately 50% of the excess calories consumed was dissipated as heat. In the absence of hyperphagia, however, insulin administration had no effect on energy expenditure nor on energy partitioning. Similarly, the influence of altered meal pattern, induced by administering insulin at different times of the day, was also found to have no impact on energy expenditure. The current investigations therefore refute the notion that high doses of insulin via hyperinsulinemia and/or altered meal pattern have an inhibitory influence on whole body thermogenesis. In contrast, our data demonstrate that the adaptive phenomenon that tends to minimize the accumulation of excess caloric intake, i.e., diet-induced thermogenesis, persists in the hyperinsulinemic state.

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Nagai, Narumi, Naoki Sakane, Linda Massako Ueno, Taku Hamada, and Toshio Moritani. "The −3826 A→G Variant of the Uncoupling Protein-1 Gene Diminishes Postprandial Thermogenesis after a High Fat Meal in Healthy Boys." Journal of Clinical Endocrinology & Metabolism 88, no. 12 (December 1, 2003): 5661–67. http://dx.doi.org/10.1210/jc.2003-030672.

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Abstract This study investigated whether the −3826 A→G nucleotide variant of the uncoupling protein-1 (UCP1) gene is correlated with postprandial thermogenesis after a high fat meal in children. Healthy boys, aged 8–11 yr, were examined for resting energy expenditure and the thermic effect of a meal (TEM), which were measured by indirect calorimetry for 180 min after a high fat (70% fat, 20% carbohydrate, and 10% protein, providing 30% of the daily energy requirement) and a high carbohydrate meal (20% fat, 70% carbohydrate, and 10% protein). The sympatho-vagal activities were assessed by means of spectral analysis of the heart rate variability during the same period. Children were genotyped for UCP1 polymorphism by applying a PCR-restriction fragment length polymorphism using buccal samples. There was no reaction of sympathetic activity to the high carbohydrate meal in eitherthe GG allele or the AA+AG group and no significant difference in TEM. However, after the high fat meal, sympathetic responses were found in both groups; further, the GG allele group showed significantly lower TEM than the AA+AG group. In conclusion, despite fat-induced sympathetic stimulation, GG allele carriers have a lowered capacity of TEM in response to fat intake, suggesting that such impaired UCP1-linked thermogenesis can have adverse effects on the regulation of body weight.

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Tulp, Orien L., Susan P. DeBolt, Aftab R. Awan, and George P. Einstein. "Residual thermic effects of diet induced thermogenesis (RDIT) in aging lean and obese LA/Ntu1//-cp (corpulent) rats." Advances in Obesity, Weight Management & Control 11, no. 4 (August 23, 2021): 120–26. http://dx.doi.org/10.15406/aowmc.2021.11.00345.

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Diet induced thermogenesis has been proposed to account for up to 15% of the caloric content of an ingested meal and to become decreased with aging and in obesity. Genetically obese rodents have been shown to exhibit impairments in the thermic responses to diet and environment, which may partially account for an improved caloric efficiency and to contribute to their increased propensity to become obese. In the present study we sought to determine the thermic responses to diet and environment in aging obese rats when young, middle aged, and aged. Resting oxygen consumption tended to decrease with advancing age and the thermic responses were lower than predicted in obese than in lean rats. This study provides important new insights regarding the thermogenic effects of diet and diet induced thermogenesis and their potential contributions to mechanisms of energy balance across the spectrum of aging in lean and obese LA/Ntul//-cp rats

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Brundin, Tomas, Anders Thörne, and John Wahren. "Heat leakage across the abdominal wall and meal-induced thermogenesis in normal-weight and obese subjects." Metabolism 41, no. 1 (January 1992): 49–55. http://dx.doi.org/10.1016/0026-0495(92)90190-l.

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Tentolouris, Nicholas, Kleopatra Alexiadou, Alexander Kokkinos, Eustathia Koukou, Despoina Perrea, Despoina Kyriaki, and Nicholas Katsilambros. "Meal-induced thermogenesis and macronutrient oxidation in lean and obese women after consumption of carbohydrate-rich and fat-rich meals." Nutrition 27, no. 3 (March 2011): 310–15. http://dx.doi.org/10.1016/j.nut.2010.02.007.

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Weststrate, Jan A., Ingrid Wunnink, Paul Deurenberg, and Joseph G. A. J. Hautvast. "Alcohol and its acute effects on resting metabolic rate and diet-induced thermogenesis." British Journal of Nutrition 64, no. 2 (September 1990): 413–25. http://dx.doi.org/10.1079/bjn19900042.

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The impact of alcohol (ethanol) on resting energy expenditure of male non-obese volunteers was determined in two studies. In the first study the thermic effect of alcohol on resting metabolic rate (RMR) was assessed in ten male non-obese volunteers. In the second study the impact of alcohol on diet-induced thermogenesis (DIT) was determined in twelve male non-obese volunteers. Energy expenditure was measured with a ventilated-hood system. RMR was measured for 60 min with the subjects in a fasting state. In the first study subjects received in random order 20 g alcohol in concentrations of 75, 180 and 300 ml/I water respectively. After measurement of the RMR the thermic effect of alcohol was measured for 90 min. In the second study volunteers received in random order and in duplicate either a meal of food (2 MJ) plus an alcoholic aperitif (20 g alcohol in a 180 ml/1 solution) or an isoenergetic meal of food alone (2.55 MJ) plus a placebo aperitif containing no alcohol. DIT was measured for 240 min. Alcohol induced a significant thermic effect, which varied between 0.22 and 0.30 kJ/min. No systematic difference in DIT was observed among the different concentrations. DIT was not significantly affected by the ingestion of alcohol. Total DIT was 219 (SE 14) kJ for the alcohol treatment and 185 (SE 20) kJ for the control treatment. The results do not support the suggestion that alcohol is less efficiently used as an energy source in comparison with, for example, fats and carbohydrates.

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Chiu, Chih-Hui, Che-Hsiu Chen, Min-Huan Wu, and Yin-Fu Ding. "Nonexercise Activity Thermogenesis-Induced Energy Shortage Improves Postprandial Lipemia and Fat Oxidation." Life 10, no. 9 (August 27, 2020): 166. http://dx.doi.org/10.3390/life10090166.

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(1) Background: This study investigated the effect of nonexercise activity thermogenesis on postprandial triglyceride (TG) concentrations; (2) Methods: Ten healthy males completed a sedentary trial (ST) and a physical activity trial (PA) in a random order separated by at least 7 days. After each intervention on day 1, the participants consumed a high-fat test meal on the next day. The blood samples and gas sample were observed in the fasted state and for 4 h after consuming the oral fat tolerance test; (3) Results: The postprandial TG concentrations of total (AUC) (p = 0.008) and incremental area under the curve (IAUC) (p = 0.023) in the plasma of participants in the PA trial were significantly lower than those in the plasma of participants in the ST trial. The postprandial fat oxidation rate AUC of the PA trial was significantly higher than that of the ST trial (p = 0.009); (4) Conclusions: The results of this study indicated that nonexercise energy expenditure decrease the postprandial TG concentration and increase the fat oxidation the next day.

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Ma, Stephanie W. Y., and David O. Foster. "Brown adipose tissue, liver, and diet-induced thermogenesis in cafeteria diet-fed rats." Canadian Journal of Physiology and Pharmacology 67, no. 4 (April 1, 1989): 376–81. http://dx.doi.org/10.1139/y89-061.

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Diet-induced thermogenesis (DIT) in young rats overeating a "cafeteria" (CAF) diet of palatable human foods is characterized by a chronic, propranolol-inhibitable elevation in resting metabolic rate [Formula: see text] and is associated with various changes in brown adipose tissue (BAT) that have been taken as evidence for BAT as the effector of DIT. But direct evidence for participation of BAT in DIT has been lacking. By employing a nonocclusive cannula to sample the venous effluent of interscapular BAT (IBAT) for analysis of its O2 content and measuring tissue blood flow with microspheres, we accomplished direct determination (Fick principle) of the O2 consumption of BAT in conscious CAF rats. In comparison with normophagic controls fed chow, the CAF rats exhibited a 43% increase in metabolizable energy intake, reduced food efficiency, a 22% elevation in resting [Formula: see text] at 28 °C (thermoneutrality) or 24 °C (housing temperature), and characteristic changes in the properties of their BAT (e.g., increased mass, protein content and mitochondrial GDP binding). They also exhibited the greater metabolic response to exogenous noradrenaline characteristic of CAF rats and the near elimination by propranolol of their elevation in [Formula: see text]. By the criterion of their elevated [Formula: see text], the CAF rats were exhibiting DIT at the time of the measurements of BAT blood flow and blood O2 levels. However, BAT O2 consumption was found to be no greater in the CAF rats than in the controls at either 28 or 24 °C. At 28 °C it accounted for less than 1% of whole body [Formula: see text]; at 24 °C it increased to about 10% of overall [Formula: see text] in both diet groups. Direct measurements of BAT O2 consumption during expression of the thermic response to a tube-fed meal were also made in conscious CAF and control rats. Both diet groups exhibited an approximately 15% increase in whole body [Formula: see text] at 90–120 min after the meal. The contribution by BAT to this increase was only 2–3% and did not differ significantly between groups. Thus, the results of these direct measurements of BAT O2 consumption in vivo do not support the theory that DIT in CAF rats is mainly due to increased BAT thermogenesis occurring either chronically or during assimilation of a meal. In further studies of the effector(s) of DIT in CAF rats, partial hepatectomy (two-thirds of the liver removed) was found to acutely reduce the resting [Formula: see text] of CAF rats by 1.85 mL/min, 2.3 times as much as in chow-fed controls. From this difference in response, it was estimated that in the CAF rats liver O2 consumption before hepatectomy exceeded that of the controls by about 1.5 mL/min, an amount that would be sufficient to fully account for the elevation in resting [Formula: see text] of the former. A major role for the liver in the DIT of CAF rats is thus suggested.Key words: cafeteria feeding, diet-induced thermogenesis, thermic effect of food, brown fat, liver.

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Nielsen, Lone, Signe Nyby, Lars Klingenberg, Christian Ritz, Ulrik Sundekilde, Hanne Bertram, Margriet Westerterp-Plantenga, et al. "Salmon in Combination with High Glycemic Index Carbohydrates Increases Diet-Induced Thermogenesis Compared with Salmon with Low Glycemic Index Carbohydrates–An Acute Randomized Cross-Over Meal Test Study." Nutrients 11, no. 2 (February 10, 2019): 365. http://dx.doi.org/10.3390/nu11020365.

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The study investigated the acute effects of meals containing either salmon or veal in combination with carbohydrates with high or low glycemic index (GI) on diet-induced thermogenesis (DIT) (primary endpoint), appetite sensations, and energy intake (EI). Twenty-five overweight men and women ingested four iso-caloric test meals: salmon with mashed potatoes (high GI) (SM), salmon with wholegrain pasta (low GI) (SP), veal with mashed potatoes (VM) and veal with wholegrain pasta (VP). Energy expenditure was measured in the fasting state and six times postprandially for 25 min with 5-min breaks between each measurement. Appetite sensations were measured every 30 min. Blood samples, from arterialized venous blood, were drawn every 20 min until an ad libitum buffet-style lunch was served 3.5 h later. DIT was 40% higher after the SM meal compared to the SP meal (p = 0.002). Prospective food consumption was lower after the SM meal compared with the VP meal (p = 0.01). There were no differences in satiety, hunger, fullness, or ad libitum EI between the test meals (all p > 0.05). In conclusion, salmon with high GI carbohydrates increased DIT compared to salmon with low GI carbohydrates. This indicates that DIT is sensitive to the GI of the carbohydrates after intake of salmon but not veal.

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Smeets, Astrid J., and Margriet S. Westerterp-Plantenga. "Acute effects on metabolism and appetite profile of one meal difference in the lower range of meal frequency." British Journal of Nutrition 99, no. 6 (June 2008): 1316–21. http://dx.doi.org/10.1017/s0007114507877646.

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A gorging pattern of food intake has been shown to enhance lipogenesis and increase body weight, which may be due to large fluctuations in storage and mobilisation of nutrients. In a state of energy balance, increasing meal frequency, and thereby decreasing inter-meal interval, may prevent large metabolic fluctuations. Our aim was to study the effect of the inter-meal interval by dividing energy intake over two or three meals on energy expenditure, substrate oxidation and 24 h satiety, in healthy, normal-weight women in a state of energy balance. The study was a randomised crossover design with two experimental conditions. During the two experimental conditions subjects (fourteen normal-weight women, aged 24·4 (sd 7·1) years, underwent 36 h sessions in energy balance in a respiration chamber for measurements of energy expenditure and substrate oxidation. The subjects were given two (breakfast, dinner) or three (breakfast, lunch, dinner) meals per d. We chose to omit lunch in the two meals condition, because this resulted in a marked difference in inter-meal-interval after breakfast (8·5 h v. 4 h). Eating three meals compared with two meals had no effects on 24 h energy expenditure, diet-induced thermogenesis, activity-induced energy expenditure and sleeping metabolic rate. Eating three meals compared with two meals increased 24 h fat oxidation, but decreased the amount of fat oxidised from the breakfast. The same amount of energy divided over three meals compared with over two meals increased satiety feelings over 24 h. In healthy, normal-weight women, decreasing the inter-meal interval sustains satiety, particularly during the day, and sustains fat oxidation, particularly during the night.

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Kus, Vladimir, Tomas Prazak, Petr Brauner, Michal Hensler, Ondrej Kuda, Pavel Flachs, Petra Janovska, et al. "Induction of muscle thermogenesis by high-fat diet in mice: association with obesity-resistance." American Journal of Physiology-Endocrinology and Metabolism 295, no. 2 (August 2008): E356—E367. http://dx.doi.org/10.1152/ajpendo.90256.2008.

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The obesogenic effect of a high-fat (HF) diet is counterbalanced by stimulation of energy expenditure and lipid oxidation in response to a meal. The aim of this study was to reveal whether muscle nonshivering thermogenesis could be stimulated by a HF diet, especially in obesity-resistant A/J compared with obesity-prone C57BL/6J (B/6J) mice. Experiments were performed on male mice born and maintained at 30°C. Four-week-old mice were randomly weaned onto a low-fat (LF) or HF diet for 2 wk. In the A/J LF mice, cold exposure (4°C) resulted in hypothermia, whereas the A/J HF, B/6J LF, and B/6J HF mice were cold tolerant. Cold sensitivity of the A/J LF mice was associated with a relatively low whole body energy expenditure under resting conditions, which was normalized by the HF diet. In both strains, the HF diet induced uncoupling protein-1-mediated thermogenesis, with a stronger induction in A/J mice. Only in A/J mice: 1) the HF diet augmented activation of whole body lipid oxidation by cold; and 2) at 30°C, oxygen consumption, total content, and phosphorylation of AMP-activated protein kinase (AMPK), and AICAR-stimulated palmitate oxidation in soleus muscle was increased by the HF diet in parallel with significantly increased leptinemia. Gene expression data in soleus muscle of the A/J HF mice indicated a shift from carbohydrate to fatty acid oxidation. Our results suggest a role for muscle nonshivering thermogenesis and lipid oxidation in the obesity-resistant phenotype of A/J mice and indicate that a HF diet could induce thermogenesis in oxidative muscle, possibly via the leptin-AMPK axis.

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Campbell, K. L., I. W. McIntyre, and R. A. MacArthur. "Postprandial heat increment does not substitute for active thermogenesis in cold-challenged star-nosed moles (Condylura cristata)." Journal of Experimental Biology 203, no. 2 (January 15, 2000): 301–10. http://dx.doi.org/10.1242/jeb.203.2.301.

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The postprandial increase in metabolic rate associated with consuming, assimilating and excreting a meal is often termed the heat increment of feeding (HIF). The metabolic heat production of star-nosed moles, Condylura cristata, held at thermoneutrality was monitored for 4 h following a single 10 min session of feeding on a ration consisting of 0 g (controls), 3.5 g or 10 g of earthworms. Coefficients for metabolizable energy digestibility and digesta passage rate of earthworms fed to C. cristata were also determined. We then tested whether feeding-induced thermogenesis substitutes partially or completely for thermoregulatory heat production in these animals exposed to sub-thermoneutral air temperatures (9–24 degrees C). A single feeding on earthworms had both short- and long-term effects on the metabolic rate and respiratory exchange ratio of C. cristata. The observed short-term (0–65 min) rise in metabolic rate, assumed to be associated primarily with the physical costs of nutrient digestion, absorption and excretion, was similar to the calculated mean retention time (66.7+/−7.8 min; mean +/− s.e. m., N=5) of this species. This component of the HIF represented 2.9 % of the food energy ingested by moles fed a single 3.5 g (13.21 kJ) meal of earthworms and 1.4 % of the food energy ingested by moles fed a single 7.5 g (28.09 kJ) meal of earthworms. At all test temperatures, resting metabolic rate typically remained above fasting levels for 1–4 h following ingestion of the high-protein earthworm diet. This protracted rise in metabolic rate, presumably associated with the biochemical costs of amino acid oxidation/gluconeogenesis and ureagenesis, averaged 12.8 % of the metabolizable energy and 8.7 % of the gross energy intake. Despite the potential thermoregulatory benefit, we found no evidence that biochemical HIF substitutes for facultative thermogenesis in star-nosed moles exposed to low air temperatures.

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Lupien, J. R., Z. Glick, M. Saito, and G. A. Bray. "Guanosine diphosphate binding to brown adipose tissue mitochondria is increased after single meal." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 249, no. 6 (December 1, 1985): R694—R698. http://dx.doi.org/10.1152/ajpregu.1985.249.6.r694.

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A single meal results in an increased thermic activity of brown adipose tissue (BAT). The purpose of the present studies was threefold: 1) to identify major metabolic origins involved in this thermic response, 2) to determine the effect of meal composition on it, and 3) to determine time changes in postprandial brown fat thermogenesis. Wistar rats were trained to eat during 2 feeding sessions/day. On the days of the experiment, rats received a test meal for 2 h, and respective control rats were simultaneously meal deprived. The animals were killed at one or more time points after meal onset, and their BAT was removed for determination of mitochondrial guanosine diphosphate (GDP) binding to indicate rate of uncoupled respiration (expts 1 and 3) or Na+-K+-ATPase activity representing coupled respiration (expt 2). Meal taking was followed by an 85% increase in GDP binding (P less than 0.001). In contrast, Na+-K+-ATPase activity was not altered by a test meal of a similar composition. The largest meal-induced rise in mitochondrial GDP binding was evident during the early postprandial hours, and it was greatly reduced by 10 h after meal onset. Expressed per total interscapular brown fat depot, a high-carbohydrate meal caused a greater increase in GDP binding than an equicaloric high-fat meal. Our data indicate that the BAT proton conductance pathway is activated by a single meal.

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Green, J. H., and M. F. Muers. "Comparisons between basal metabolic rate and diet-induced thermogenesis in different types of chronic obstructive pulmonary disease." Clinical Science 83, no. 1 (July 1, 1992): 109–16. http://dx.doi.org/10.1042/cs0830109.

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1. Some patients with the emphysematous type of tobacco-related chronic obstructive pulmonary disease are hypermetabolic. Since the likely mechanism is the increased work of breathing, other groups of patients with chronic obstructive pulmonary disease should be similar. We have now measured basal metabolic rate and diet-induced thermogenesis in six patients with chronic obstructive pulmonary disease with an arterial partial pressure of CO2 of <5kPa (emphysematous), nine patients with chronic obstructive pulmonary disease with an arterial partial pressure of CO2 of >6kPa (bronchitic), eight patients with chronic obstructive pulmonary disease due to chronic asthma and seven control subjects. Diet-induced thermogenesis was measured for 4h after a meal of 87% carbohydrate, 11% protein and 2% fat as energy, with a total energy content of 40% of basal metabolic rate. 2. There was no difference between measured and predicted basal metabolic rate in the control (5541 ± 272 versus 5881 ± 245 kJ/24h) or emphysematous (5552 ± 370 versus 6239 ± 197 kJ/24 h) groups, but measured basal metabolic rate was significantly higher than predicted in the bronchitic (6126 ± 387 versus 5405 ± 250 kJ/24 h) and asthmatic (6293 ± 197 versus 5701 + 245, mean ± SEM, P<0.01) groups. All the control subjects had measured basal metabolic rates within 10% of predicted, whereas two out of six emphysematous patients, four out of nine bronchitic patients and five out of eight asthmatic patients were hypermetabolic. The contributions of fat, carbohydrate and protein oxidation rates to the overall basal metabolic rate were similar between groups. 3. Diet-induced thermogenesis was similar between groups. The postprandial fuel mix oxidized was also similar between all four groups. 4. Thus, some patients with both types of smoking-related chronic obstructive pulmonary disease and other patients with chronic asthma were hypermetabolic. This could not be predicted from detailed lung function tests, arterial blood gases or anthropometric measurements, and suggests that the increased work of breathing may not be the only cause of the hypermetabolism and weight loss seen in these patients.

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Duhita, Maharani R., Yves Schutz, Jean-Pierre Montani, Abdul G. Dulloo, and Jennifer L. Miles-Chan. "Assessment of the Dose–Response Relationship between Meal Protein Content and Postprandial Thermogenesis: Effect of Sex and the Oral Contraceptive Pill." Nutrients 11, no. 7 (July 15, 2019): 1599. http://dx.doi.org/10.3390/nu11071599.

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Implementation of efficacious dietary interventions to regulate energy balance requires understanding of the determinants of individual response. To date, information regarding individual variability in response to elevated meal protein content is lacking. This study investigates whether sex and/or oral contraceptive pill (OCP) use play a role in the response to elevated meal protein in 21 healthy young adults (seven men, seven women not taking OCP, and seven women who were OCP users). Participants consumed each of three standardized isocaloric (590 kcal) meals of differing protein content (11, 23, 31% kcal protein). Resting energy expenditure (EE), respiratory quotient (RQ), hunger and satiety were measured at baseline (fasting) and during 180 min postprandial. Whilst significant dose–response increases in EE were observed in men, meal protein-induced EE in women without OCP reached a maximum at <23% protein. Women taking OCP reported lower postprandial fullness than women without OCP, despite similar body size, but also, most notably, no significant difference in EE response between any of the meals. Whilst the mechanisms underpinning this thermogenic inflexibility in response across a wide-range (three-fold) of protein meal content require further investigation, this highlights the need for careful consideration of factors that may influence an individual’s metabolic response to dietary interventions aimed at optimising postprandial thermogenesis for body weight regulation.

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Fuller-Jackson, John-Paul, Aimee L. Dordevic, Iain J. Clarke, and Belinda A. Henry. "Effect of sex and sex steroids on brown adipose tissue heat production in humans." European Journal of Endocrinology 183, no. 3 (September 2020): 343–55. http://dx.doi.org/10.1530/eje-20-0184.

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Objective: Retrospective studies suggest that women have more active brown adipose tissue (BAT) than men, but little is known of the effect of fluctuating sex steroids across the menstrual cycle on thermogenesis in women. Design: To characterise the effects of sex and sex steroids on BAT activity we recruited healthy weight men (n = 14) and women at two stages of the menstrual cycle (luteal, n = 9; follicular, n = 11). Methods: Infrared thermography measured supraclavicular temperature to index BAT thermogenesis in response to both cold (immersion of one hand in water at 15°C) and meal (Ensure, 10 kcal/kg body weight) stimuli. Results: Adaptive BAT temperature responses were greater (P < 0.05) in women than men, irrespective of stage of menstrual cycle. Whereas during cold exposure, the increase in BAT temperature was abrogated (P < 0.05) in women during follicular phase compared to men and women during luteal phase. Plasma concentrations of progesterone, 17β-estradiol, testosterone and cortisol were measured. Regression analyses demonstrated that baseline BAT temperature was positively correlated (P < 0.05) with progesterone levels, but was inversely associated (P < 0.05) with cortisol concentration. Both cold- and meal-induced changes in BAT temperature mildly correlated (P = 0.07; P < 0.05) with 17β-estradiol levels, but not with testosterone concentrations. Conclusions: Baseline supraclavicular temperature is elevated in women during the luteal phase of the menstrual cycle, which correlated with elevated progesterone concentrations. Women exhibited greater thermogenic responses than men, irrespective of the state of the menstrual cycle, which was associated with plasma levels of 17β-estradiol. We conclude that sex steroids may regulate BAT thermogenesis in healthy adults.

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Muller, M. J., A. Fenk, H. U. Lautz, O. Selberg, H. Canzler, H. J. Balks, A. von zur Muhlen, E. Schmidt, and F. W. Schmidt. "Energy expenditure and substrate metabolism in ethanol-induced liver cirrhosis." American Journal of Physiology-Endocrinology and Metabolism 260, no. 3 (March 1, 1991): E338—E344. http://dx.doi.org/10.1152/ajpendo.1991.260.3.e338.

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Energy expenditure and substrate metabolism were investigated in 10 patients with alcoholic liver cirrhosis (EtOH-Ci) and 10 healthy controls (C). Resting metabolic rate (RMR) varied from 1,269 to 2,467 kcal/day in C and from 1,228 to 2,098 kcal/day in EtOH-Ci. RMR was significantly related to fat-free mass (FFM) in both groups, but EtOH-Ci decreased FFM and increased RMR when expressed per kilogram FFM (+33%). Glucose intolerance, hyperinsulinemia, and a decreased C-peptide-to-insulin ratio were observed in EtOH-Ci after a test meal. Concomitantly, nonoxidative glucose metabolism was reduced in association with normal increases in glucose oxidation. EtOH-Ci reduced insulin sensitivity (-59%) and maximal insulin-dependent glucose disposal (-40%) during a sequential two-step glucose clamp protocol (phase 1: 1 mU.kg body wt-1.min-1 insulin infusion rate + euglycemia; phase 2: 4 mU.kg body wt-1.min-1 insulin infusion rate + 165 mg/dl plasma glucose concentration). This was explained by reduced glucose storage (-99%, -51%) in association with normal responses in glucose oxidation rate, plasma lactate concentration, lipid oxidation rate, and rate of lipogenesis. Defective glucose storage was independent of reduced FFM. EtOH-Ci increased glucose-induced thermogenesis by 57%. We conclude that increased resting metabolic rate, enhanced thermogenesis, defective glucose storage, and normal glucose oxidation together result in increased energy needs and favor negative energy balance in patients with alcoholic cirrhosis.

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Mähler, Anja, Samuel Klamer, András Maifeld, Hendrik Bartolomaeus, Lajos Markó, Chia-Yu Chen, Sofia K. Forslund, Michael Boschmann, Dominik N. Müller, and Nicola Wilck. "Increased Salt Intake Decreases Diet-Induced Thermogenesis in Healthy Volunteers: A Randomized Placebo-Controlled Study." Nutrients 14, no. 2 (January 7, 2022): 253. http://dx.doi.org/10.3390/nu14020253.

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High salt intake ranks among the most important risk factors for noncommunicable diseases. Western diets, which are typically high in salt, are associated with a high prevalence of obesity. High salt is thought to be a potential risk factor for obesity independent of energy intake, although the underlying mechanisms are insufficiently understood. A high salt diet could influence energy expenditure (EE), specifically diet-induced thermogenesis (DIT), which accounts for about 10% of total EE. We aimed to investigate the influence of high salt on DIT. In a randomized, double-blind, placebo-controlled, parallel-group study, 40 healthy subjects received either 6 g/d salt (NaCl) or placebo in capsules over 2 weeks. Before and after the intervention, resting EE, DIT, body composition, food intake, 24 h urine analysis, and blood pressure were obtained. EE was measured by indirect calorimetry after a 12 h overnight fast and a standardized 440 kcal meal. Thirty-eight subjects completed the study. Salt intake from foods was 6 g/d in both groups, resulting in a total salt intake of 12 g/d in the salt group and 6 g/d in the placebo group. Urine sodium increased by 2.29 g/d (p < 0.0001) in the salt group, indicating overall compliance. The change in DIT differed significantly between groups (placebo vs. salt, p = 0.023). DIT decreased by 1.3% in the salt group (p = 0.048), but increased by 0.6% in the placebo group (NS). Substrate oxidation indicated by respiratory exchange ratio, body composition, resting blood pressure, fluid intake, hydration, and urine volume did not change significantly in either group. A moderate short-term increase in salt intake decreased DIT after a standardized meal. This effect could at least partially contribute to the observed weight gain in populations consuming a Western diet high in salt.

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Heenan, Kelsey A., Andres E. Carrillo, Jacob L. Fulton, Edward J. Ryan, Jason R. Edsall, Dimitrios Rigopoulos, Melissa M. Markofski, Andreas D. Flouris, and Petros C. Dinas. "Effects of Nutrition/Diet on Brown Adipose Tissue in Humans: A Systematic Review and Meta-Analysis." Nutrients 12, no. 9 (September 10, 2020): 2752. http://dx.doi.org/10.3390/nu12092752.

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Background: Brown adipose tissue (BAT) provides a minor contribution to diet-induced thermogenesis (DIT)—the metabolic response to food consumption. Increased BAT activity is generally considered beneficial for mammalian metabolism and has been associated with favorable health outcomes. The aim of the current systematic review was to explore whether nutritional factors and/or diet affect human BAT activity. Methods: We searched PubMed Central, Embase and Cochrane Library (trials) to conduct this systematic review (PROSPERO protocol: CRD42018082323). Results: We included 24 eligible papers that studied a total of 2785 participants. We found no mean differences in standardized uptake value of BAT following a single meal or after 6 weeks of L-Arginine supplementation. Resting energy expenditure (REE), however, was increased following a single meal and after supplementation of capsinoid and catechin when compared to a control condition (Z = 2.41, p = 0.02; mean difference = 102.47 (95% CI = 19.28–185.67)). Conclusions: Human BAT activity was not significantly affected by nutrition/diet. Moreover, REE was only increased in response to a single meal, but it is unlikely that this was due to increased BAT activity. BAT activity assessments in response to the chronic effect of food should be considered along with other factors such as body composition and/or environmental temperature.

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Journal articles on the topic 'Meal induced thermogenesis'

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