Role of resting metabolic rate and energy expenditure in hunger and appetite control: a new formulation

Abstract

A long-running issue in appetite research concerns the influence of energy expenditure on energy intake. More than 50 years ago, Otto G. Edholm proposed that "the differences between the intakes of food [of individuals] must originate in differences in the expenditure of energy". However, a relationship between energy expenditure and energy intake within any one day could not be found, although there was a correlation over 2 weeks. This issue was never resolved before interest in integrative biology was replaced by molecular biochemistry. Using a psychobiological approach, we have studied appetite control in an energy balance framework using a multi-level experimental system on a single cohort of overweight and obese human subjects. This has disclosed relationships between variables in the domains of body composition [fat-free mass (FFM), fat mass (FM)], metabolism, gastrointestinal hormones, hunger and energy intake. In this Commentary, we review our own and other data, and discuss a new formulation whereby appetite control and energy intake are regulated by energy expenditure. Specifically, we propose that FFM (the largest contributor to resting metabolic rate), but not body mass index or FM, is closely associated with self-determined meal size and daily energy intake. This formulation has implications for understanding weight regulation and the management of obesity.

Fig. 1.

Relationship between FFM, daily EI and daily profile of hunger. (A) Scatter plot shows the relationship between FFM and daily EI in a group of 41 overweight or obese men and women. The regression is significant (P<0.001). The values represent the average values from objective measures taken at specific probe days at weeks 0, 6 and 12. (B) Daily hunger profiles for individuals with the highest FFMs (eight women and five men) and those with the lowest FFMs (eight women and five men). The groups were formed by dividing the whole sample into tertiles of FFM and comparing the upper and lower tertiles (but keeping similar numbers of men and women in each tertile). The difference between the area under the curve for the two profiles is significant (P<0.01); asterisks indicate time points at which the profiles are significantly different. The profiles indicate that hunger in the high FFM group is greater before the onset of a meal and in the period leading up to the meal, but not at the end of the meal. This is consistent with the fact that the high FFM individuals eat a larger meal, which would return hunger to a level appropriate for full satiation. Together, data displayed in A and B indicate that FFM is positively associated with daily EI and with daily hunger levels. Additionally, because RMR is highly and significantly correlated with FFM, the relationships between RMR, EI and hunger very closely match those for FFM shown in the figure. Data derived from studies reported by Blundell et al. (Blundell et al., 2012). BF, breakfast. Hunger is measured in units on a 100 unit scale on the screen of a hand-held PDA.

Fig. 2.

A new formulation for appetite control. A proposed tonic signal for the drive to eat that reflects the body’s demand for energy arises (mainly) from FFM and RMR. In turn, this drive is under tonic inhibition from leptin, whose action reflects the amount of stored energy reserves in the body. As the amount of adipose tissue increases, leptin insensitivity occurs and this tonic inhibition is reduced. The drive to eat is periodically interrupted and suppressed by episodic signals in the form of peptides that are released from the GI tract in response to food consumption. The resulting pattern of eating is a consequence of the interactions between tonic and episodic physiological signals. The figure also illustrates the postulated effect of exercise on appetite control. Prolonged exercise displays a dual-process action by stimulating hunger (an effect that is highly variable between individuals) but also by increasing post-prandial satiety signalling (King et al., 2009) through an effect on GI peptides (Martins et al., 2010). See text for further description.