Rodents with mutations in the leptin, or leptin receptor, genes have been extensively used to investigate the regulation of energy balance and the factors that underlie the development of obesity. The excess energy gain of these mutants has long been considered as being due in part to increased metabolic efficiency, consequent to reduced energy expenditure, but this view has recently been challenged. We argue, particularly though not exclusively, from data on ob/ob mice, that three lines of evidence support the proposition that reduced expenditure is important in the aetiology of obesity in leptin pathway mutants (irrespective of the genetic background): (i) milk intake is similar in suckling ob/ob and +/? mice; (ii) ob/ob mice deposit excess energy when pair-fed to the ad libitum food intake of lean siblings; (iii) in several studies mutant mice have been shown to exhibit a lower RMR ‘per animal’ at temperatures below thermoneutrality. When metabolic rate is expressed ‘per unit body weight’ (inappropriately, because of body composition differences), then it is invariably lower in the obese than the lean. It is important to differentiate the causes from the consequences of obesity. Hyperphagic, mature obese animals weighing 2–3 times their lean siblings may well have higher expenditure ‘per animal’, reflecting the costs of being larger and of enhanced obligatory diet-induced thermogenesis resulting from the increased food intake. This cannot, however, be used to inform the aetiology of their obesity.

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.

Circumstantial evidence suggests that substitution of glucose or sucrose by the low-glycaemic index sugar galactose in the diet may lead to greater thermogenesis and/or fat oxidation. Using ventilated hood indirect calorimetry, we investigated, in twelve overnight-fasted adults, the resting energy expenditure (REE) and respiratory quotient (RQ) for 30 min before and 150 min after ingestion of 500 ml of water containing 60 g of glucose, fructose or galactose in a randomised cross-over design. REE increased similarly with all three sugars, reaching peak values after 50–60 min, but its subsequent fall towards baseline values was faster with galactose and glucose than with fructose (P < 0·001). RQ increased with all three sugars, but to a much greater extent with galactose and fructose than with glucose, particularly after 1 h post-ingestion. When ingested as a sugary drink, postprandial thermogenesis and utilisation of fat after galactose are not higher than after glucose or fructose.

For an adult in N balance, apart from small amounts of amino acids required for the synthesis of neurotransmitters, hormones, etc, an amount of amino acids almost equal to that absorbed from the diet can be considered to be “surplus” in that it will be catabolized. The higher diet-induced thermogenesis from protein than from carbohydrate or fat has generally been assumed to be due to increased protein synthesis, which is ATP expensive. To this must be added the ATP cost of protein catabolism through the ubiquitin-proteasome pathway. Amino acid catabolism will add to thermogenesis. Deamination results in net ATP formation except when serine and threonine deaminases are used, but there is the energy cost of synthesizing glutamine in extra-hepatic tissues. The synthesis of urea has a net cost of only 1·5 × ATP when the ATP yield from fumarate metabolism is offset against the ATP cost of the urea cycle, but this offset is thermogenic. In fasting and on a low carbohydrate diet as much of the amino acid carbon as possible will be used for gluconeogenesis – an ATP-expensive, and hence thermogenic, process. Complete oxidation of most amino acid carbon skeletons also involves a number of thermogenic steps in which ATP (or GTP) or reduced coenzymes are utilized. There are no such thermogenic steps in the metabolism of pyruvate, acetyl CoA or acetoacetate, but for amino acids that are metabolized by way of the citric acid cycle intermediates there is thermogenesis ranging from 1 up to 7 × ATP equivalent per mol.

The present study investigates whether excessive fat accumulation and hyperinsulinaemia during catch-up growth on high-fat diets are altered by n-6 and n-3 PUFA derived from oils rich in either linoleic acid (LA), α-linolenic acid (ALA), arachidonic acid (AA) or DHA. It has been shown that, compared with food-restricted rats refed a high-fat (lard) diet low in PUFA, those refed isoenergetically on diets enriched in LA or ALA, independently of the n-6:n-3 ratio, show improved insulin sensitivity, lower fat mass and higher lean mass, the magnitude of which is related to the proportion of total PUFA precursors (LA+ALA) consumed. These relationships are best fitted by quadratic regression models (r2>0·8, P < 0·001), with threshold values for an impact on body composition corresponding to PUFA precursors contributing 25–30 % of energy intake. Isoenergetic refeeding on high-fat diets enriched in AA or DHA also led to improved body composition, with increases in lean mass as predicted by the quadratic model for PUFA precursors, but decreases in fat mass, which are disproportionately greater than predicted values; insulin sensitivity, however, was not improved. These findings pertaining to the impact of dietary intake of PUFA precursors (LA and ALA) and their elongated–desaturated products (AA and DHA), on body composition and insulin sensitivity, provide important insights into the search for diets aimed at counteracting the pathophysiological consequences of catch-up growth. In particular, diets enriched in essential fatty acids (LA and/or ALA) markedly improve insulin sensitivity and composition of weight regained, independently of the n-6:n-3 fatty acid ratio.

According to the adipostat hypothesis for body-weight control, alterations in body weight should always be compensated by adequate alterations in food intake and thermogenesis. Thus, increased thermogenesis should not be able to counteract obesity because food intake would be increased. However evidence is presented here that thermogenesis in different forms (through artificial uncouplers, exercise, cold exposure) may counteract obesity and is not always fully compensated by increased food intake. Correspondingly, a decreased capacity for metaboloregulatory thermogenesis (i.e. non-functional brown adipose tissue) may in itself lead to obesity. This is evident in mice and may be valid for human subjects, as a substantial proportion of adults possess brown adipose tissue, and those with less or without brown adipose tissue would seem to be more prone to obesity. Thus, increased thermogenesis may counteract obesity, without dietary intervention.

Capsinoids are non-pungent compounds with molecular structures similar to capsaicin, which has accepted thermogenic properties. To assess the acute effect of a plant-derived preparation of capsinoids on energy metabolism, we determined RMR and non-protein respiratory quotient (NPRQ) after ingestion of different doses of the capsinoids. Thirteen healthy subjects received four doses of the capsinoids (1, 3, 6 and 12 mg) and placebo using a crossover, randomised, double-blind trial. After a 10 h overnight fast as inpatients, RMR was measured by indirect calorimetry for 45 min before and 120 min after ingesting capsinoids or placebo. Blood pressure and axillary temperature were measured before ( − 55 and − 5 min) and after (60 and 120 min) dosing. Before dosing, mean RMR was 6247 (se 92) kJ/d and NPRQ was 0·86 (se 0·01). At 120 min after dosing, metabolic rate and NPRQ remained similar across the four capsinoids and placebo doses. Capsinoids also had no influence on blood pressure or axillary temperature. Capsinoids provided in four doses did not affect metabolic rate and fuel partitioning in human subjects when measured 2 h after exposure. Longer exposure and higher capsinoids doses may be required to cause meaningful acute effects on energy metabolism.

General anaesthesia causes hypothermia due to decreased metabolic rate and impaired thermoregulation. Many warming devices are in use to prevent heat loss, but little attention has been paid to stimulating the body's own heat generation. All nutrients raise energy expenditure, and the highest thermic effect is ascribed to amino acids and proteins, 30–40% in the awake state. Amino acids infused during general anaesthesia exert a thermic effect that is enhanced compared with that in the awake state. At awakening from anaesthesia, post-operative hypothermia may be prevented without shivering. The tissues involved and the mechanisms by which nutrients stimulate heat production are still not completely understood. However, these findings support the existence of an inhibitory action normally exerted by central thermosensors, in order to maintain oxidative metabolism within certain limits, to prevent hyperthermia. During anaesthesia central thermosensors are silenced and, hence, amino acid thermogenesis is exaggerated. The amino acid-induced heat generation during anaesthesia predominantly occurs in extra-splanchnic tissues, most probably in skeletal muscle. It may reflect an increased protein turnover, as both protein breakdown and synthesis are energy-consuming processes known to generate heat. Possibly, amino acid infusion provides substrates, otherwise mobilized from the body's own tissues, needed for wound healing and immunological function. However, other cellular mechanisms may also contribute to this non-shivering thermogenesis.

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.

Data on pollination ecology of Araceae are still scarce and most concern species belonging to the subfamily Aroideae (García-Robledo et al. 2004, Gibernau 2003, Ivancic et al. 2004, 2005; Maia & Schlindwein 2006). In this subfamily, inflorescences consist of unisexual flowers: female flowers are located in the lower portion and the male flowers are in the upper portion of the inflorescence (Mayo et al. 1997). In the documented neotropical Aroideae, pollinators are nocturnal beetles and pollination mechanisms take place within a floral chamber during a short flowering cycle (generally 24–48 h) with floral rewards (sterile flowers rich in proteins and/or lipids) for the beetle pollinators, the secretion of resin to secure pollen on the pollinator, and the production of heat and odours (Chouteau et al. 2007, García-Robledo et al. 2004, Gibernau & Barabé 2002, Gibernau et al. 1999, 2000, 2003; Maia & Schlindwein 2006, Young 1986).

Alcohol (ethanol; EtOH) provides fuel energy to the body (29·7 kJ (7·1 kcal)/g, 23·4 kJ (5·6 kcal)/ml), as do other macronutrients, but no associated essential nutrients. The thermogenic effect of EtOH (on average 15 % of its metabolizable value) is much greater than that of the main substrates utilized by the body, i.e. fat and carbohydrates (CHO), suggesting a lower net efficiency of energy utilization for EtOH than for fat and CHO. EtOH cannot be stored in the body and is toxic, so that there is an obligatory continuous oxidation of EtOH and it becomes the priority fuel to be metabolized. In contrast to CHO, its rate of oxidation does not depend on the dose ingested. As with CHO intake, it engenders a shift in postprandial substrate utilization (decrease in fat oxidation), but by a non-insulin-mediated mechanism. A limited amount of EtOH can be converted to fatty acids by hepatic de novo lipogenesis (as occurs with high levels of CHO feeding) from acetate production, which inhibits lipolysis in peripheral tissues. There is no evidence that EtOH consumed under normoenergetic conditions (i.e. isoenergetically replacing CHO or fat) leads to greater body fat storage than fat or CHO. However, there is still a lack of experimental studies on the influence of EtOH on the level of spontaneous physical activity in man. This effect may well depend on the dose of EtOH consumed as well as other intrinsic factors.

This paper discusses possible consequences of energy excess throughout the life cycle. Firstly we consider the effects of foods on hunger, satiety and satiation. Also, the changes in food availability and consumption in relation to changes in social and economic determinants of energy excess. The relationship between physical activity and energy intake (EI) is also considered. Secondly we explore the definition of energy excess and the metabolic effects of macronutrients (mainly in relation to fuel partitioning oxidation/storage) on energy balance. The cellular and molecular regulation determined by specific genes involved in lipogenesis, fuel partitioning and/or in energy dissipation are explored. Thirdly, we examine the main consequences induced by energy excess and positive energy balance, starting with the alterations in glucose utilisation (insulin resistance) leading to type 2 diabetes and the linkage of energy excess with other non-communicable diseases (NCDs). Biological, social and psychological consequences during perinatal, childhood and adolescence periods are specifically analysed. Fourthly, the transition from energy deficit to excess, under the optic of a developing country is analysed with country examples drawn from Latin America. The possible role of supplementary food programmes in determining positive energy balance is discussed especially in relation to pre-school and school feeding programmes. Fifthly, we deal with the economic costs of energy excess and obesity related diseases. Finally, some areas where further research is needed are described; biological and genetic determinants of individual and population energy requirements, foods and food preparations as actually consumed, consumer education and research needs on social determinants of energy imbalances.

Measurement of energy expenditure in humans is required to assess metabolic needs, fuel utilisation, and the relative thermic effect of different food, drink, drug and emotional components. Indirect and direct calorimetric and non-calorimetric methods for measuring energy expenditure are reviewed, and their relative value for measurement in the laboratory and field settings is assessed. Where high accuracy is required and sufficient resources are available, an open-circuit indirect calorimeter can be used. Open-circuit indirect calorimeters can employ a mask, hood, canopy or room/chamber for collection of expired air. For short-term measurements, mask, hood or canopy systems suffice. Chamber-based systems are more accurate for the long-term measurement of specified activity patterns but behaviour constraints mean they do not reflect real life. Where resources are limited and/or optimum precision can be sacrificed, flexible total collection systems and non-calorimetric methods are potentially useful if the limitations of these methods are appreciated. The use of the stable isotope technique, doubly labelled water, enables total daily energy expenditure to be measured accurately in free-living subjects. The factorial method for combining activity logs and data on the energy costs of activities can also provide detailed information on free-living subjects.

Dairy Ca intake has been shown to be superior to elemental Ca in increasing the loss of body fat during energy restriction. We questioned whether the mechanisms involved an increase in postprandial energy expenditure, fat oxidation and/or a greater lipolysis. The acute effects of different sources of Ca were examined in eight subjects, aged 47–66 years and BMI 27·6–36·1kg/m2, in a three-way cross-over study. Subjects were randomly provided breakfast meals either low in dairy Ca and vitamin D (LD; control), high in non-dairy Ca (calcium citrate) but low in vitamin D (HC) or high in dairy Ca and vitamin D (HD). Diet-induced thermogenesis, fat oxidation rates (FOR), carbohydrate oxidation rates (COR), insulin, glucose, ΔNEFA and glycerol were measured hourly over a 6h postprandial period. Postprandial data were calculated as a change (Δ) from the fasting value. Results showed that ΔNEFA was significantly different between meals (LD −1·50 (sem 0·26), HC −1·22 (sem 0·32), HD −0·94 (sem 0·27) mmol/l×6h; P=0·035), with a lesser suppression following both high-Ca meals. ΔFOR was significantly higher following the two high-Ca meals (LD −6·5 (sem 2·2), HC 2·93 (sem 2·34), HD 3·3 (sem 2·5) g×6;h; P=0·005), while reciprocally ΔCOR was significantly lower. ΔGlycerol was less suppressed following the high-Ca meals but statistical significance was not achieved. No differences in diet-induced thermogenesis, insulin or glucose were observed. Regardless of source, Ca intake acutely stimulated postprandial fat oxidation; and there was a lesser suppression of NEFA following these meals.

The influence of the source of dietary fat on postprandial thermogenesis and substrate oxidation rates, was examined in twelve postmenopausal women aged 57–73 years, with BMI 21·9–38·3 kg/m2. A single blind, randomised, paired comparison of two high-fat, isoenergetic, mixed test meals was conducted. The major source of fat was either cream (CREAM) or extra virgin olive oil (EVOO). RMR, diet-induced thermogenesis (DIT) and substrate oxidation rates over 5 h were measured by indirect calorimetry. There were no differences in body weight, RMR, fasting carbohydrate or fat oxidation rates between the two occasions. DIT (EVOO 97 (sd 46) v. CREAM 76 (sd 69) kJ/5 h and EVOO 5·2 (sd 2·5) v. CREAM 4·1 (sd 3·7)% energy) did not differ between the two test meals. The postprandial increase in carbohydrate oxidation rates, relative to their respective fasting values (ΔCOX), was significantly lower following the EVOO meal (EVOO 10·6 (sd 8·3) v. CREAM 17·5 (sd 10) g/5 h; paired t test, P=0·023), while postprandial fat oxidation rates (ΔFOX) were significantly higher (EVOO 0·0 (sd 4·4) v. CREAM -3·6 (sd 4·0) g/5 h; P=0·028). In the eight obese subjects, however, DIT was significantly higher following the EVOO meal (EVOO 5·1 (sd 2·0) v. CREAM 2·5 (sd 2·9) %; P=0·01). This was accompanied by a significantly lower ΔCOX (EVOO 10·9 (sd 9·9) v. CREAM 17·3 (sd 10·5) g/5 h; P=0·03) and significantly higher ΔFOX (EVOO 0·11 (sd 4·4) v. CREAM −4·1 (sd 4·5) g/5 h, P=0·034). The present study showed that olive oil significantly promoted postprandial fat oxidation and stimulated DIT in abdominally obese postmenopausal women.

Although the rapid increase in the prevalence of obesity in many countries suggests that environmental factors (mainly overeating and physical inactivity) play the most important role in the development of overweight, it is very likely that genetic factors also contribute. It appears that one major gene in combination with one or several minor genes constitute the genetic components behind excess accumulation of body fat in most obese individuals. However, monogenic obesity has been described in a few families due to changes in leptin, leptin receptor, prohormone convertase, pro-opiomelanocortin or melanocortin-4 receptor. None of the monogenic variants is of great importance for common human obesity; the latter genes are unknown so far. Results from genomic scans suggest that major obesity genes are located on chromosomes 2, 10, 11 and 20. Studies of candidate genes indicate that the minor obesity genes control important functions of adipose tissue, and that structural variance in these genes may alter adipose tissue function in a way that promotes obesity. Such genes are β2- and β3-adrenoceptors, hormone-sensitive lipase, tumour necrosis factor alpha, uncoupling protein-1, low-density lipoprotein receptor, and peroxisome proliferator activator receptor gamma-2. Some of these genes may promote obesity by gene–gene interactions (for example β3-adrenoceptors and uncoupling protein-1) or gene–environment interactions (for example β2-adrenoceptors and physical activity). Some are important for obesity only among women (for example β2- and β3-adrenoceptors, low-density lipoprotein receptor and tumour necrosis factor alpha). Few ‘non-adipose’ genes have so far shown a firm association to common human obesity, which could suggest that the important genes for the development of excess body fat also control adipose tissue function.

The thermogenic potential of the interscapular brown fat pad in the naked mole-rat Heterocephalus glaber, that exhibits poikilothermic thermal responses to changing temperatures is reported. Histological and ultrastructural study of the brown fat pad showed that it consists of layers of skeletal muscle interposed between the layers of brown adipose tissue with both unilocular and multilocular adipocytes. Large numbers of mitochondria were present between and around the lipid droplets of these cells. Glyoxylic acid condensation, used to demonstrate catecholaminergic nerves, was evident in low concentrations in the connective tissue between the brown adipocytes. A 3-dimensional computer-aided reconstruction of the fat pad showed the extent and ramification of nerves and blood vessels between the adipocytes. These findings show that although the naked mole-rat is regarded as an endothermic poikilotherm, it possesses anatomical features usually found in homeothermic mammals, which are essential for thermogenesis.

A defective thermic response to food may be an energy-sparing adaptation in both obesity and pregnancy. To evaluate the combined effect of obesity and pregnancy on postprandial thermogenesis, the thermic effect of food was assessed for a 240 min period following a high-carbohydrate meal and a typical mixed meal in nine normal-weight non-pregnant, eight overweight non-pregnant, eight normal-weight pregnant and six overweight pregnant women using indirect calorimetry. A test meal that provided 60% of each subject's measured daily requirement for basal metabolism was used. Pregnant women were studied during weeks 30–35 of gestation. Neither obesity nor pregnancy altered the thermic effect of food, although the response to the mixed meal was greater (P <0·01) than that to the high-carbohydrate meal in all cases. The mean responses for the high-carbohydrate and mixed meals were 26·9 (SD 6·0) and 30·1 (SD 6·2)% baseline energy expenditure respectively, and 7·4 (SD 1·6) and 8·3 (SD 1·6)% of the meal energy load respectively. Obesity and pregnancy were associated with hyperinsulinaemia (P <0·005) following both test meals, suggesting that postprandial thermogenesis was not altered by insulin resistance in this group. The incremental glucose response was elevated (P <0·001) in the pregnant women following both test meals; overweight women tended to have a greater incremental glucose response following the high-carbohydrate meal, but it was not significant (P = 0·065). These results do not provide evidence of an impaired thermic response to food in either overweight or third trimester pregnant women.

Heat production (HP) and the intake and retention of energy and nitrogen were measured at 20° in growing female broiler fowl given diets with metabolizable energy (ME) contents ranging from 8 to 15 MJ/kg at each of two crude protein (nitrogen × 6.25; CP) contents (130 and 210 g/kg). ME intake was partially controlled by the birds, but increased by 30% over the range of dietary ME concentration. CP intake varied directly with dietary CP:ME ratio, indicating that control of energy intake took priority and that food intake did not increase in order to enhance amino acid intake on low-CP diets. Maintenance energy requirement and fasting HP were not affected by diet. Although the HP of fed birds was significantly affected by dietary energy source, there was no evidence for regulatory diet-induced thermogenesis as energy intake increased. Total energy retention doubled on the higher-energy diets as a result of increased intake and retention efficiency in the absence of any compensation by diet-induced thermogenesis. The proportion of energy retained as fat was negatively correlated with dietary CP:ME ratio. It was concluded that the growing female broiler fowl responded to large differences in energy intake and dietary CP concentration not by changes in rate of energy dissipation as heat but by changes in the quantity of energy retained and in the partition of retained energy between body protein and body fat.

The effect of underfeeding for 7 d (at 60 kJ/kg ideal body-weight) on the thermic and physiological responses to glucose and insulin infusions (hyperinsulinaemic euglycaemic clamp) was studied in six healthy women. Underfeeding had no significant effect on baseline metabolic rate, heart rate, forearm blood flow, diastolic blood pressure, blood intermediary metabolites, plasma insulin or catecholamines, but reduced both respiratory exchange ratio (RER; control (C) 0.86 (SE 0.02), underfed (U) 0.75 (SE 0.01) P < 0.01) and systolic blood pressure (by approximately 10 mmHg, P < 0.01). Baseline forearm glucose uptake and oxygen consumption were similar in both states. During the final 30 min of the glucose and insulin infusion, metabolic rate rose by 0.43 (SE 0.05) kJ/min in the C state, but no rise was seen in the U state (P < 0.01). Glucose disposal rate (C 47.9 (SE 1.8), U 47.3 (SE 4.1) μmol/kg per min) and storage rate (C 27.5 (SE 2.4), U 31.6 (SE 3.6) μmol/kg per min) were similar in both states, but glucose oxidation rate was reduced in the U state (C 20.5 (SE 1.7), U 15.4 (SE 0.7) μmol/kg per min; P < 0.05). RER rose to a higher value in the C state than in the U state (C 0.97 (SE 0.2), U 0.80 (SE 0.01); P < 0.01). During hyperinsulinaemia, the forearm glucose uptake and O2 consumption rose in both states. No significant differences were seen in the cardiovascular responses to hyperinsulinaemia in either state. Thus underfeeding abolishes the rise in thermogenesis and reduces glucose oxidation during glucose and insulin infusions in healthy women, but does not affect the glucose disposal or storage rates or the other measured responses.