Clinical significance of adaptive thermogenesis

Abstract

The epidemic of obesity is developing faster than the scientific understanding of an efficient way to overcome it, as reflected by the low success rate of short-and long-term weight loss interventions. From a clinical standpoint, this suggests that the body tends to defend a set point of possible genetic origin in the context of a weight-reducing program. As described in this paper, this limited therapeutic success may depend on adaptive thermogenesis, which represents in this case the decrease in energy expenditure (EE) beyond what could be predicted from the changes in fat mass or fat-free mass under conditions of standardized physical activity in response to a decrease in energy intake. This issue has been documented in recent studies that have shown in obese individuals adhering to a weight reduction program a greater than predicted decrease in EE, which in some cases was quantitatively sufficient to overcome the prescribed energy restriction, suggesting a role for adaptive thermogenesis in unsuccessful weight loss interventions and reduced body weight maintenance. As also discussed in this paper, this 'adaptive thermogenesis' can be influenced by environmental factors, which have not been frequently considered up to now. This is potentially the case for plasma organochlorine concentration and oxygen desaturation in obstructive sleep apnea syndrome. It is concluded that health professionals should be aware that in some vulnerable individuals, adaptive thermogenesis can be multicausal, and has the capacity to compensate, at least partly, for the prescribed energy deficit, possibly going beyond any good compliance of some patients.

Several obesity- and nutrient-related gene polymorphisms but not FTO and UCP variants modulate postabsorptive resting energy expenditure and fat-induced thermogenesis in obese individuals: the NUGENOB Study

“…These data indicate that CART À1336 delA, PPARG2 1431 C4T and IGF2 Apal A4G may be involved in adaptations in thermogenesis independent of body composition. 7 The present finding that PPARG2 1431 C4T increased postprandial REE, together with an earlier report showing that individuals with the Pro12Ala polymorphism of PPARG2 had an increased postprandial REE and higher satiety, 26 suggest that PPARG2 polymorphisms may play a role in postprandial REE. The association between IGF2 Apal A4G and postprandial REE became statistically nonsignificant when further adjusted for postprandial plasma insulin concentration.…”

“…When, in addition to FFM, age, sex and research centre, postabsorptive REE was adjusted for FM, HSD11B1 G4A, GAD2 À243 A4G and LIPC 644 A4G remained significantly Genetics and energy expenditure GH Goossens et al associated with postabsorptive REE. These data suggest that HSD11B1 G4A, GAD2 À243 A4G and LIPC 644 A4G may influence postabsorptive REE independent of changes in body composition, indicating an effect on adaptive thermogenesis 7 Conflicting data have been reported with respect to associations between SNPs in GAD2 and CART and obesity. [18][19][20][21] These opposing findings may partly be due to effects of GAD2 À243 A4G on both energy intake (higher hunger and disinhibition scores) 19 and, based on the present data, increased postabsorptive REE.…”

“…5 Perhaps the best documented obesity gene polymorphism is in the FTO gene. 6 An altered efficiency of cellular energy metabolism (reduced adaptive thermogenesis) 7 and/or thermogenic response to food intake 3 may be important factors that could contribute to the heterogeneity of the obesity phenotype. Until now, however, no large-scale studies have been performed that have addressed the importance of genetic background in inter-individual variance in EE in obese individuals who have been phenotyped in detail, especially regarding EE components.…”

How dieting makes some fatter: from a perspective of human body composition autoregulation

“…This reduction in the energy cost of maintenance is adaptive in that it reduces the rate at which body's tissues are being depleted, and has been demonstrated both in normal-weight subjects (35,(48)(49)(50) as well as in obese individuals (48)(49)(50) . In order to determine whether this adaptive reduction in thermogenesis during weight loss persists during weight recovery, and underlies the disproportionately greater rate of recovery of fat mass relative to FFM, the dynamic changes in body composition and BMR of the thirty-two Minnesota men who completed the 24 weeks of semi-starvation and first 12 weeks of restricted refeeding were re-analysed.…”

Control of energy expenditure in humans

“…Energy restriction induces a reduction in REE below predicted values, as based on the new body composition reached after underfeeding-induced weight loss. [16][17][18][19] The REE reduction in obese subjects losing 10-20% of initial weight, adjusted for changes in body composition, ranges between 3 and 6% of the initial TEE value. Van Gemert et al 20 observed in morbid obese subjects losing on average one-third of initial weight, an average reduction of 7% at 1 year after the start of weight loss and of 4% when weight loss was maintained for more than 3 years.…”