Does diet and activity lead to difference in resting energy expenditure in obese women? | BMC Women’s Health

The objectives of this study were to investigate REE differences between obese people, confirm low REE in some obese subjects, and determine differences in dietary, biochemical, anthropometric, and body composition parameters and physical activity in obese women with normal and low resting energy expenditure. We achieved exciting results, although REE was different among obese people in this study, no significant difference was observed in the body composition, physical activity level and dietary intake of these people, so the role of other effective factors in metabolism is raised.

REE is the energy required to maintain body at rest [7]. One of the most effective factors in REE is body composition. Fat-free mass consists of water, protein, and minerals and is the major determinant of REE that explains 60–80% of the inter-individual variance in REE. Fat mass, comprising all body lipids, also contributes to REE variance, especially when subjects with a large range of body mass index (BMI) are investigated [8]. Some studies have showed that since obese subjects have more fat-free mass (FFM) and fat mass (FM) than normal weight subjects, REE is typically higher in obesity [9]. However, other studies such as an investigation by Johannsen et al. have shown that the resting energy expenditure (adjusted for fat- free mass and fat mass) of obese women is similar to lean women [3].

We found a significant difference in the measured REE between two obese groups although there was no difference in their body composition. These results highlight the role of other factors that may be involved in energy metabolism.

Similar to our findings, Rosales-Velderrain et al. reported that the measured resting energy expenditure is much lower than the predicted resting energy expenditure in some obese people [4].

Additionally, a meta-analysis about REE was showed that in obese subjects REE was 3–5% lower than normal weight subjects [10].

Some studies have concluded that increased REE in obesity may be due to obesity-related metabolic risk factors. Insulin resistance and hypertension as a consequence of obesity may lead to a higher REE; these may mask the lower metabolic rate that initially contributes to weight gain [11].

Some mechanisms have been suggested for decreasing REE in obese people. Since mitochondria are essential for energy production at the cellular level, differences in energy expenditure and basal metabolism may be attributed to mitochondrial functions [12].

Similarly, we showed an association between UCP2 protein and resting energy expenditure in another study. We demonstrated an increased risk of reduced resting energy expenditure in obese subjects with low levels of UCP2 protein [13, 14]. Uncoupling proteins (UCPs) are a group of mitochondrial proteins which dissipate proton electrochemical gradient across the mitochondrial membrane. By this mechanism, UCPs may uncouple substrate oxidation from conversion of ADP to ATP, leading to generation of heat and thus increased EE [15]. Moreover, some studies have shown that mitochondrial dysfunction, reduced activity of marker enzymes of oxidative pathways, mitochondrial degeneration, and reduced respiratory capacity in obese people [16, 17]. Furthermore, it has been suggested some adipokines and hormones produced by the adipose tissue may effect the mitochondrial function and energy haemostasis [18].

Some studies have revealed down-regulation of metabolism genes in obese subjects [19]. There are reports of gene repression of fat cell metabolism and decreased fatty acid and triacylglycerol synthesis, insulin-stimulated glucose uptake, and mitochondrial energy metabolism pathways, especially tricarboxylic acid cycle and electron transport chain, in the adipose tissue of obese people [20].

Some other studies have suggested a strong genetic component to REE and have implicated low REE as a predictor of weight gain. Based on these finding, ≥40% of variance in REE (adjusted for age, sex, body mass, and body composition) is estimated to be genetic [17].

In our study, the predicted resting energy expenditure was measured using the Harris-Benedict Eq. [6]. Shaneshin et al. showed the Harris-Benedict formula provides a valid estimate of REE at the group level in a range of normal-weight to morbidly obese Iranians [21].

It is known that body weight depends on the balance between energy intake and energy expenditure in such a way that a positive energy balance results in body mass gain [7]. We noted that energy intake was 300 kcal more than energy expenditure in obese group with low REE; therefore, weight gain is expected. However, in the obese group with normal REE, energy intake was 200 kcal less than energy expenditure, which may refer to under-eating and under-recording of habitual food intake in obese people. It has been shown obese subjects underreport what they consume, specially fat and carbohydrate-rich foods [22]. Moreover, it has been reported that obese people change their food patterns during the recording period [23].

Since diet composition may affect resting energy expenditure and there is no significant difference in dietary intake between obese women with normal REE compared to obese women with low REE, the difference in their REE may not be related to their diet.

We found no significant difference in the lipid profile between obese women with normal and low REE. According to our findings, differences in REE or metabolism in obese subjects are not associated with and do not cause lipid profile changes, although there was a significant difference in lipid profile between obese groups and normal weight subjects.

Our finding showed no difference in physical activity between three groups. Physical activity improves weight loss and is also a good predictor of long-term weight loss maintenance [24]. Some studies have shown that obese women spend significantly more time on resting or sedentary behaviors than lean women every day [25]. Moreover, it has been reported that obese women spend less time being active than lean women, including light, moderate, and vigorous activities. It has been suggested that the minimal amount of energy expenditure by physical activity required for protection against body fat gain is ~ 12 kcal/kg body weight per day [26].

Our findings showed a significant difference in T3 between the two obese groups. We believe that the differences in resting energy expenditure between the two obese groups may be related to the level of T3. However, the level of thyroid hormones (T3, T4 and TSH) was within the normal range in all obese subjects.

It should also be considered several limitations of the current study. The first limitation of our study is the small sample size; more studies with more prominent participants are needed. Second, underreporting and under-recording habitual food intakes, typically seen in people with obesity, may contribute to biased findings. However, subjects with extreme dietary intake values were excluded. Another research limitation was possible errors related to measuring REE and body composition due to measurement errors or participant preparation. Despite the abovementioned limitations, this is the first attempt to study external factors such as diet and physical activity and internal factors such as body composition, metabolism, and biochemical factors in participants with different metabolism.

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