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The Journal of Nutrition Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

Reduction of Dietary Energy Density Reduces Body Mass Regain Following Energy Restriction in Female Mice1,2 Kerry M. Cameron* and John R. Speakman Institute of Biological and Environmental Sciences, University of Aberdeen, Aberdeen, UK AB24 2TZ

Abstract Restriction of energy intake induces a loss of body mass that is often regained when the restriction ends. We aimed to determine whether dietary energy density (independent of macronutrient composition) modulates postrestriction regain then subjected to a 20% energy restriction on this diet for 10 d. Following restriction, mice consumed ad libitum the same diet with either 0 or 40% added cellulose. The study utilized a crossover design so all mice consumed both diets. Body temperature, physical activity, and digestibility were all lower when consuming the 40% cellulose diet (P , 0.001). Mice regained less mass (9%) when consuming the 40% than the 0% cellulose diet, because net energy intake was reduced by 26% (P , 0.001), despite having a greater gross energy intake (P , 0.001) (29%). To test whether there might be a constraint on intake and digestibility of the 40% cellulose diet, 20 different female mice consumed this diet at room temperature and were then transferred to the cold (78C) to determine whether they would increase intake of this diet in response to increased energy demands. It took up to 5 d after transfer for body mass, food intake, and digestibility to increase. This suggests a digestion constraint might have limited intake of the low-energy density diet immediately following restriction. Modulation of dietary energy density in the postrestriction phase may be a valuable strategy for maintaining mass loss achieved on energy-restricted diets. J. Nutr. 141: 182–188, 2011.

Introduction The most commonly used intervention to lose body mass in humans is restriction of energy intake. However, this approach is rarely successful in the long-term and the lost mass is often regained (1–3). During energy restriction, mice (3) and humans (4) show sustained reductions in energy expenditure, which may predispose subjects to a positive energy balance when food is made available postrestriction. Moreover, sustained restriction is associated with neuroendocrine changes promoting hunger, leading to hyperphagia (5), thus making mass regain even more likely. Given the global problem of obesity and associated comorbidities in humans (6), there is a need to find ways in which mass loss can be maintained. Accordingly, many behavioral strategies have been identified (7–9), including the amount of physical activity required to maintain mass loss (8,10). Consumption of low-energy–dense foods is often promoted as a method of weight loss, because for the same amount of energy, a greater mass of low-energy–dense food can be consumed (11– 15). Typically, these diets contain water-rich fruits and vegeta-

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Supported by a PhD studentship partially funded by the University of Aberdeen. Author disclosures: K. M. Cameron and J. R. Speakman, no conflicts of interest. * To whom correspondence should be addressed. E-mail: kerry.cameron@ newcastle.ac.uk.

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bles and reduced dietary fat (14). Usually, diluting dietary energy density results in a reduction in energy intake (13,15– 18) via a promotion of satiety and a reduction in hunger (16). The effects of dietary energy density on body mass are less clear (19,20), but there is some evidence to suggest that sustained intake of low-energy–dense foods induces long-term weight loss (15). This is often ascribed to the suggestion that people eat a constant weight of food (21). This suggestion has been reinforced in other species such as cats (22), voles (23), and rats (24). It might be expected that because low-energy–dense diets can be used to lose body mass that they might also be used to maintain the mass loss following restriction. Indeed, one study has shown that consumption of foods low in energy density was important in the maintenance of weight loss in free-living individuals for up to 2.2 y (12). However, both macronutrients and energy density affect energy intake (25) (and therefore ultimately body mass), so to determine their effects, the 2 variables must be independently manipulated (14,26). Here, we restricted the energy intake of laboratory mice to induce weight loss and then allowed them ad libitum intake. We aimed to separate the effects of macronutrient and energy density on postrestriction body mass by manipulating only the energy density component of the reintroduced diet, using cellulose. Changes in cellulose content have commonly been

ã 2011 American Society for Nutrition. Manuscript received July 12, 2010. Initial review completed August 23, 2010. Revision accepted October 28, 2010. First published online December 15, 2010; doi:10.3945/jn.110.129056.

Downloaded from jn.nutrition.org at University of Aberdeen on May 16, 2011

of body mass. Fifteen female mice consumed ad libitum a standard rodent diet (with 20% added cellulose). They were

used to alter the energy density of rodent diets (23,27–33), although not in the context of examining postrestriction changes in energy intake and body mass. This could lead to important consequences for humans, whereby changes in dietary energy density may be a valuable strategy for maintaining mass loss achieved on energy-restricted diets.

Materials and Methods

Body mass and food intake. The body mass and food intake of each mouse were measured daily between 0800 and 1000 h (60.01 g; Sartorius top-pan balance). Mice consumed food ad libitum from a hopper. When restricted, the entire ration was given at ;0900 h, but body mass was always recorded before food was given. All large pieces of uneaten food found in the cage were returned to the hopper and food intake was calculated as the mass of food missing from the hopper each day. A sample of each diet was dried at 608C for 14 d (Gallenkamp) to determine hydration. The mice varied in the extent to which they ground the diets, resulting in crumbs of uneaten food discarded on the bottom of the cage (orts). In addition, the diets differed in the degree to which they were ground by the mice. Failure to account for such losses can compromise estimates of energy intake (37). Therefore, any food that was ground was collected, weighed and dried. Food intake measurements were therefore corrected for both orts and hydration by using calculations previously detailed (35). Digestive efficiency. A subset of 8 of 15 mice was selected for digestive efficiency analysis. Feces were collected for 24 h during the period when the mice were consuming the 0 and 40% cellulose diets. Feces were weighed (Ohaus analytical balance, 6 0.0001 g) and dried in an oven at 608C until a constant mass (Gallenkamp). The gross energy (GE)3 of the diets and feces were determined using adiabatic bomb calorimetry (Parr). Three replicates of each fecal sample and 5 replicates of the food and cellulose samples were used to calculate the mean GE of each. Daily GE intake and energy lost through defection were calculated as previously

Nutritional composition of the 3 experimental diets

Purina 5001, g/kg Solka-Floc (cellulose), g/kg Protein, g/kg kJ/kg % of total energy Carbohydrate, g/kg kJ/kg % of total energy Fat, g/kg kJ/kg % of total energy Nutrients Cholesterol, mg/g Linoleic acid, g/kg Linolenic acid, g/kg Arachidonic acid, g/kg (n-3) fatty acids, g/kg Total SFA, g/kg Total MUFA, g/kg Crude fiber, g/kg Neutral detergent fiber, g/kg Acid detergent fiber, g/kg Starch, g/kg Glucose, g/kg Fructose, g/kg Sucrose, g/kg Lactose, g/kg Minerals Ash, g/kg Calcium, g/kg Phosphorus, g/kg Phosphorus (nonphytate), g/kg Potassium, g/kg Magnesium, g/kg Sulfur, g/kg Sodium, g/kg Chlorine, g/kg Fluorine, mg/g Iron, mg/g Zinc, mg/g Manganese, mg/g Copper, mg/g Cobalt, mg/g Iodine, mg/g Chromium, mg/g Selenium, mg/g Vitamins, mg/g Carotene Vitamin K Thiamin hydrochloride Riboflavin Niacin Pantothenic acid Choline chloride Folic acid Pyridoxine Biotin Vitamin B-12

0% Cellulose

20% Cellulose

40% Cellulose

1000 0 234 39 28 499 84 60 45 17 12

800 200 187 31 28 399 67 60 36 13 12

600 400 140 24 28 299 50 60 27 10 12

200 1.2 0.1 ,0.01 0.2 1.6 1.6 5.1 15.6 6.7 31.9 0.2 0.3 3.7 2.0

160 1.0 0.1 ,0.01 0.2 0.3 1.3 4.1 12.5 5.4 25.5 0.2 0.2 3.0 1.6

120 0.7 0.1 ,0.01 0.1 0.9 1.0 3.1 9.4 4.0 19.1 0.1 0.2 2.2 1.2

7.0 1.0 0.7 0.4 1.2 0.2 0.4 0.4 0.7 16.0 270.0 79.0 70.0 13.0 0.9 1.0 1.2 0.3

5.6 0.8 0.5 0.3 0.9 0.5 0.3 0.3 0.5 12.8 216.0 63.2 56.0 10.4 0.7 0.8 1.0 0.2

4.2 0.6 0.4 0.2 0.7 0.1 0.2 0.2 0.4 9.6 162.0 47.4 42.0 7.8 0.5 0.6 0.7 0.2

2.3 1.3 16.0 4.5 120.0 24.0 2250.0 7.1 6.0 0.3 50.0

1.8 1.0 12.8 3.6 96.0 19.2 1800.0 5.7 4.8 0.2 40.0

1.4 0.8 9.6 2.7 72.0 14.4 1350.0 4.3 3.6 0.2 30.0


Crossover experiment Mice and study design. Fifteen 4.5-mo-old female laboratory mice (Mus musculus) were used [MF1: outbred strain, selected due to its extensive use in studies of food intake (34,35), sourced from Charles River]. All procedures were licensed under the UK Animals (Scientific Procedures) Act of 1986 and received approval from the University of Aberdeen Ethical Review Committee. Mice were individually caged (NKP; 48 3 15 3 13 cm) at 20 6 28C (room temperature) with free access to water. The environment was on a controlled 12-h-light/-dark cycle, with lights on at 0700 h. Experimental diets of 3 different energy densities were created, consisting of standard pelleted rodent diet (Purina Mills no. 5001) (36) with 0, 20, or 40% cellulose (Solka-Floc) added by weight (specialized diets produced by Research Diets). As cellulose content increased, the absolute macro- and micronutrient content decreased, although the relative percentage of each was kept constant (Table 1). The experiment utilized a crossover design divided into 6 phases. Phase 1 was a baseline monitoring period lasting 5 d where all mice consumed ad libitum the 20% cellulose diet. Mice were divided into 2 groups matched for body mass and food intake (n = 8 mice in group 1 and n = 7 in group 2). In phase 2, all mice consumed the 20% cellulose diet but received a 20% restriction by weight relative to their own baseline food intake for 10 d. In the 3rd phase, groups 1 and 2 consumed ad libitum the 0 and 40% cellulose diets, respectively, for 10 d. Phase 4 was a washout phase where all mice consumed ad libitum the 20% cellulose diet for 5 d. Phase 5 was a second restriction and an exact replicate of phase 2. In phase 6, the treatments were crossed over; groups 1 and 2 consumed ad libitum the 40 and 0% cellulose diets, respectively, for 10 d.

TABLE 1

3 Abbreviations used: AEAE, apparent energy assimilation efficiency; EA, energy assimilation; GE, gross energy, GLM, general linear model.

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detailed, accounting for orts (35). The apparent energy absorption efficiency (AEAE) and net energy assimilation (EA) were calculated as: AEAE ð%Þ ¼ ½dry mass food intake ðgÞ 3 GE food 2½dry mass feces ðgÞ 3 GE feces ½dry mass food intake ðgÞ 3 GE food EA ðkJ=gÞ ¼ energy consumed 3 AEAE: Physical activity and core body temperature. One month prior to the start of the experiment, mice were implanted with a wireless E-mitter (Model PDT-4000 E-Mitter, Mini-Mitter). Mice were sedated (isoflurane), the E-mitter was i.p. inserted, and the mice were allowed to recover before the start of the experiment and any measurements taken. The E-mitter continuously monitored body temperature and activity in vivo. Data from the implant was transmitted by a radio frequency field to a receiver pad under the cage. One measurement was collected from each implant every second and a mean recorded each minute by the Windows PC-based data acquisition system VitalView (Mini-Mitter).

Statistics The order in which each group entered the crossover design was tested for possible residual dietary effects using general linear models (GLM). The data were pooled from each group receiving the same treatment when order effects during the regain phase were nonsignificant (P , 0.05). In the crossover experiment, mean food intake and body mass were calculated each day during each phase. Mean activity and body temperature were also calculated for each day and also for each hour of the day. To test the difference in these means between the same mice in different phases, a paired Student’s t test was used. A 1-way repeatedmeasures ANOVA was used to determine changes in activity and body temperature across days and between groups. For all the digestive efficiency calculations, a mean was calculated for each variable and a paired Student’s t test was used to determine differences between the 0 and 40% diets, or differences between room temperature and cold temperature in the same mice. A GLM was used to determine whether body mass gain during the postrestriction regain phase was related to the net EA and to determine the independent effect of diet. In all GLM analyses, all nonsignificant interaction effects (P . 0.05) were removed to find the best-fitted model and only significant interactions were reported. In the cold experiment, a 1-way repeated-measures ANOVA was used to determine changes over time between the same mice housed at room temperature and then in the cold using Tukey’s tests for comparisons between days. Data are expressed as means 6 SD. Differences were considered significant when P , 0.05. All statistical analyses were performed with MINITAB version 13.1.

Digestive efficiency. AEAE was 41% lower when consuming the 40% cellulose diet than the 0% cellulose diet, which resulted in a significant reduction in the net EA (Table 2). Body mass gain during the postrestriction regain phase was positively related to the net EA (r = 0.67; P , 0.001), with no independent effect of diet (P , 0.05). This indicated that although GE intake increased when mice consumed the less energy-dense diet, they gained less mass because their net energy intake was reduced. Physical activity and core body temperature. During the energy restriction phases, physical activity tended to be 12% lower than baseline (P = 0.13) (Fig. 2A). The activity levels of mice consuming the 0% cellulose diet during the regain phase did not differ from those during the baseline phase (P = 0.52) but were higher than during the restriction phase (P , 0.05). When consuming the 40% cellulose diet, activity levels were lower than during the baseline phase (P , 0.05) but did not differ from the restriction phase (P = 0.20). During the regain phases,

Results Crossover experiment There were no significant residual dietary effects as a result of the crossover design, so the data were pooled from mice on the same treatment. 184

Cameron and Speakman

FIGURE 1 Changes from baseline in food intake (A) and body mass (B) during each day of the crossover experiment. Means were calculated during the baseline phase: data are the difference from this mean. Data are mean 6 SD, n = 15.


Cold exposure experiment To evaluate whether any impact of the 40% cellulose diet in the crossover experiment was due to a digestion constraint in the gut, we used a second cohort of twenty 3.5-mo-old mice of the same sex and strain. We previously showed that in female MF1 mice, intake of a standard rodent diet (0% cellulose) increased as soon as mice were put in the cold, probably to meet the increased thermogenic demands (34). Therefore, to test if the same response was observed when consuming the 40% cellulose diet, mice were housed at room temperature for 10 d and then moved into a different room regulated at 7 6 28C for 10 d (cold temperature) where they continued to consume ad libitum the 40% cellulose diet. Food intake and body mass were monitored daily as detailed above. Feces were collected from a subset of 5 mice during 24 h in approximately the middle of each phase and GE was measured using calorimetry, as detailed above.

Body mass and food intake. Daily food intake was greater during baseline (6.6 6 0.6 g) than the washout phase (5.9 6 0.9 g; P , 0.05) (Fig. 1A), but this did not result in any difference in body mass during these phases (P = 0.34) (Fig. 1B). During the restriction phases, mean daily food intake was 4.6 6 0.6 g and body mass loss was 4.6 6 1.4 g (12% compared with baseline). During the regain phases, the 0 or 40% diets were consumed ad libitum. Daily intake of the 0% cellulose diet (5.1 6 0.9 g/d) was lower than the 40% cellulose diet (7.2 6 0.1 g/d; 29%) (P , 0.001). However, body mass was greater when mice consumed the 0% cellulose diet (37.5 6 3.2 g) than when they consumed the 40% cellulose diet (34.1 6 2.8 g; 9%) (P , 0.001). Relative to baseline, body mass was 1.3 6 1.0 g less when consuming the 40% cellulose diet (P , 0.001).

TABLE 2

Digestive efficiency data measured in mice consuming the 0 or 40% cellulose diets during the postrestriction, regain phase of the crossover experiment1 0% Cellulose

GE of diet, kJ/g GE of feces, kJ/g Dry fecal deposits, g/d Energy in feces, kJ/g Food intake, g/d Energy intake, kJ/d AEAE, % EA, kJ/d

18.5 16.1 1.2 19.6 5.0 93 77.7 72.1

6 0.1 6 0.4 6 0.4 6 6.0 6 0.9 6 17.2 6 9.2 6 12.1

TABLE 3

Digestive efficiency data from mice housed at room temperature (208C) and then at cold temperature (78C) when consuming the 40% cellulose diet1

40% Cellulose 17.1 6 16.7 6 4.0 6 66.9 6 7.0 6 125 6 46.0 6 58.7 6

0.1* 0.2* 0.6* 9.2* 0.9* 16.7** 8.6* 8.1**

Values are means 6 SD, n = 8. Asterisks indicated different from 0% cellulose: *P # 0.001, **P , 0.05. 1

FIGURE 2 Physical activity levels (A) and body temperature (B) for each hour of the day of the crossover experiment. A mean was calculated for each hour for every day during each phase. A mean was also calculated from the 2 restriction phases, because there were no significant differences between them. Arrows represent the time points in which mice were disturbed by feeding, weighing, and cage cleaning. Pooled SD for the baseline, restriction, 0% cellulose, and 40% cellulose diets are 6 0.2, 0.4, 0.3, and 0.28C, respectively. The same data are plotted twice to show daily patterns, n = 15.

GE of feces, kJ/g Dry fecal deposits, g/d Energy in feces, kJ/g Food intake, g/d Energy intake, kJ/d AEAE, % EA, kJ/d

16.7 5.1 84.5 7.7 143 40.3 58.0

6 0.2 6 0.8 6 12.2 6 1.2 6 22.7 6 7.4 6 16.6

78C 16.7 5.5 92.9 11.0 200 53.3 107.3

6 0.2 6 0.7* 6 11.5 6 1.6 6 28.4* 6 5.6 6 22.8**

Difference (cold 2 room temp) 20.0 0.4 8.4 3.3 57.7 13.0 49.3

Values are means 6 SD, n = 5. Asterisks indicate different from room temperature: *P # 0.001, **P , 0.05.

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was higher than when consuming the 40% cellulose diet (P , 0.001). When mice consumed either the 0 or 40% cellulose diet, body temperature did not differ from the baseline phase but was higher than during the restriction phase (P , 0.001). Cold exposure experiment Body mass was 33.1 6 2.2 g at room temperature and 33.3 6 2.7 g in the cold (Fig. 3A). Daily food intake increased by 31% in the cold (P , 0.001) (Fig. 3B). Body mass gain was 2.1 6 1.4 g (6.7%) at room temperature (P , 0.001) and food intake increased by 1.8 6 1.3 g (49%) (P , 0.001). On the first day in the cold, body mass and food intake significantly dropped, contrary to expectations. During the cold phase, body mass did not change (P = 0.35). Food intake increased over time (P , 0.001), but daily intake during the first 5 d in the cold was less

FIGURE 3 Body mass (A) and food intake (B) in the cold exposure experiment. Days 1–10 represent mice housed at room temperature (208C) and d 11–20 represent the same mice housed in the cold (78C). The phases are separated by a dashed line. Means without a common letter differed (P , 0.05). Data are mean 6 SD, n = 20. Postrestriction body mass regain in mice

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activity was 13.1% higher when mice were consuming the 0% cellulose diet than when consuming the 40% cellulose diet (P , 0.05). During the restriction phase, body temperature was 1.7% lower than the baseline phase (P , 0.001) (Fig. 2B). The body temperature decrease during energy restriction was 0.9 6 0.48C (P , 0.001) and the daily decline was 0.18C/d. During the regain phases, body temperature when consuming the 0% cellulose diet

208C

(8.9 6 1.3 g/d) than during the final 5 d (12.4 6 1.2 g/d) (P , 0.001). The GE of feces was not different at room temperature and in the cold (Table 3). AEAE increased by 13% in the cold (P = 0.05), resulting in a 46% increase in the net energy assimilated (P = 0.003).

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Acknowledgments J.R.S. designed the research and study oversight; K.M.C. conducted experiments. Both authors analyzed the data, wrote the paper, and read and approved the final manuscript.

Literature Cited 1.

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We have shown that dietary energy density significantly affected postrestriction body mass regain in laboratory mice. When consuming the 40% cellulose diet, body mass regain was less, primarily due to an effect on net energy intake. Although mice consuming the 40% cellulose diet increased their GE intake relative to the restriction period, net energy intake was far less, which may also have resulted in reduced macro- and micronutrient intakes. Moreover, mice consuming the 0% cellulose diet increased both physical activity and body temperature postrestriction, whereas physical activity when they consumed the 40% cellulose diet did not increase. This may suggest that mice were in a perceived state of energy restriction when consuming the less energy-dense diet. Often, hyperphagia is exhibited following energy restriction, as observed in rats (38,39), mice (40), and in other studies using this strain (5). In this case, postrestriction hyperphagia was not exhibited to a high degree (or at all when consuming the 0% cellulose diet), which agrees with other data from rats (41), although this has been shown to be highly strain dependent (42). Recent data have shown that 1 d of food restriction did not result in an increase in food intake in humans (43). However, the length of time under restriction is very likely to influence this response. Because overeating following energy restriction did not occur when consuming diets of altered energy density containing cellulose, this ensured that body mass did not overshoot baseline levels when consuming the 0% cellulose diet and challenges the conventional idea that hyperphagia is a natural consequence of release from energy restriction (43). The response of activity and body temperature to energy restriction have been shown to strongly depend on the strain of mouse (44–46) and the duration and severity of the restriction (3). Physical activity data during energy restriction are inconclusive, with some showing an increase (3,47), but agree with data from this strain that activity actually decreased (3), probably as an energy-saving mechanism. This may also depend on the presence of a running wheel, whereby energy-restricted mice will run more (48). Additionally, body temperature decreased, probably to reduce thermoregulatory costs (45,49). Although some strains of mice respond to restriction by using torpor (44) [defined as a reduction in internal body temperature below 318C (50)], the mice in this experiment did not, consistent with previous observations for this strain (3). Body temperature progressively declined each day but returned to baseline within the first day of ad libitum intake, as also shown in refed rats following food deprivation (49). Less than one-half of the digestible energy in the 40% cellulose diet was assimilated, suggesting that energy uptake was limited by the time required for the food to be held in the gut to absorb sufficient energy (23). To explore this idea further, mice consuming the 40% cellulose diet were exposed to the cold where body mass and food intake were expected to increase because energetic demands increased (34). Contrary to expectations, food intake and body mass both decreased the first day mice were exposed to the cold. Also, the significant increase in body mass during the room temperature phase was blunted by the cold and it took up to

5 d for food intake to increase. Daily food intake was also more variable during the cold phase; e.g. there was no notable experimental reason for the sudden decrease on d 15. Digestive efficiency tended to increase (P = 0.05), in agreement with data from deer mice (Peromyscus maniculatus) housed in the cold (30). This suggests that a period of up to 5 d was required for adjustments in digestive capacity to be made. These adjustments are likely to involve changes to gut morphology (29,30,51). The digestion limitation when consuming the 40% cellulose diet may therefore have restricted the level to which food intake could be increased during the postrestriction phase described above. A reduction in digestive efficiency with increasing dietary fiber content has also been observed in rats (28), humans (52), dogs (53), and cats (54). The presence of fiber in the diet has also been shown to have a variety of interacting effects with common physiological functions such as obstructing access of digestive enzymes (55), altering enzyme activity of gastrointestinal microorganisms (31), varying nitrogen fecal and urinal output (32), and modifying the digestibility of other macronutrients (52). This suggests there is a limit to how much rodent diets can be diluted with fiber, which is also likely to be different between species depending on gut morphology, such as the presence of a large cecum. For example, prairie voles (Microtus ochrogaster) can process large amounts of cellulose (84%) and still maintain a stable body mass (27). There may also be differences between male and female mice in their ability to digest high-fiber diets, which, to our knowledge, has not previously been investigated. Fiber has been implicated as a key component of humans diets for weight loss (56), primarily because it increases feelings of satiation (57) and therefore energy intake is reduced. Fiber has also been shown to decrease digestibility (52) and increase fecal bulking (58) in humans, suggesting that results may be similar to those presented here. Additionally, epidemiological studies support a negative association between dietary fiber intake and risk of coronary heart disease (59); thus, there may be additional beneficial health effects of adding fiber to the diet. There will be a limit as to how much fiber can be incorporated into humans diets (14). However, perhaps more importantly, the effects of fiber on its own (as would probably be the case in humans) compared with integrated into the food (as in this case in rodents) needs investigation. Importantly, although high-fiber/low-energy diets are often prescribed to lose or maintain mass loss in a clinical setting, the effects of manipulation of energy density and macronutrient composition are often confounded by the nature of the varied human diet. Here, we have shown that low-energy– dense foods, without changes in macronutrient composition, may reduce mass gain exhibited after energy restriction via a reduction in net energy intake and possible digestive limitations. In conclusion, we suggest that modulation of energy density alone in the postrestriction phase may be a valuable strategy for maintaining mass loss achieved with energy-restricted diets, and more work is required to determine whether this is a viable option for humans.

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