Energy compensation and adiposity in humans

Careau, Vincent; Halsey, Lewis G.; Pontzer, Herman; Ainslie, Philip N.; Andersen, Lene Frost; Anderson, Liam; Arab, Lenore; Baddou, Issad; Bedu-Addo, Kweku; Blaak, Ellen E.; Blanc, Stéphane; Bonomi, A.; Bouten, Cvc Carlijn; Buchowski, Maciej S.; Butte, Nancy F.; Camps, Stefan Gerardus; Close, Graeme L.; Cooper, Jamie A.; Das, Sai Krupa; Cooper, Richard S.; Dugas, Lara R.; Eaton, Simon; Ekelund, Ulf; Entringer, Sonja; Forrester, Terrence; Fudge, Barry W.; Goris, Annelies H. C.; Gurven, Michael; Hambly, Catherine; Hamdouchi, Asmaa El; Hoos, Marije B.; Hu, Sumei; Joonas, Noorjehan; Joosen, Annemiek M.C.P.; Katzmarzyk, Peter T.; Kempen, Kitty P.; Kimura, Misaka; Kraus, William E.; Kushner, Robert F.; Lambert, Estelle V.; Leonard, William R.; Lessan, Nader; Martin, Corby K.; Medin, Anine Christine; Meijer, Erwin P.; Morehen, James C; Morton, James P.; Neuhouser, Marian L.; Nicklas, Theresa A.; Ojiambo, Robert; Pietiläinen, Kirsi H.; Pitsiladis, Yannis; Plange‐Rhule, Jacob; Plasqui, Guy; Prentice, Ross L.; Rabinovich, Roberto; Racette, Susan B.; Raichlen, David A.; Ravussin, Éric; Reilly, John J.; Reynolds, Rebecca M.; Roberts, Susan B.; Schuit, Albertine J.; Sjödin, Anders; Stice, Eric; Urlacher, Samuel S.; Valenti, Giulio; Etten, Ludo M. Van; Mil, Edgar A. Van; Wells, Jonathan C. K.; Wilson, George; Wood, Brian M.; Yanovski, Jack A.; Yoshida, Tsukasa; Zhang, Xueying; Murphy‐Alford, Alexia J.; Loechl, Cornelia; Luke, Amy; Rood, Jennifer; Sagayama, Hiroyuki; Schoeller, Dale A.; Wong, William W.; Yamada, Yosuke; Speakman, John R.

doi:10.1016/j.cub.2021.08.016

Cited by 84 publications

(69 citation statements)

References 40 publications

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“…Weight-loss therapies have been largely unsuccessful due to low adherence and unwanted side effects ( 70 ). Weight-loss strategies may be less effective in obese individuals due to compensations in energy expenditure resulting from caloric restriction or exercise ( 71 , 72 ). Increasing energy expenditure via β3 agonists has been explored clinically and has shown some positive results in healthy and obese humans ( 58 , 73 – 76 ).…”

Section: Discussionmentioning

confidence: 99%

β3-Adrenergic receptor downregulation leads to adipocyte catecholamine resistance in obesity

Valentine¹,

Ahmadian²,

Keinan³

et al. 2022

Journal of Clinical Investigation

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The dysregulation of energy homeostasis in obesity involves multi-hormone resistance. Although leptin and insulin resistance have been well characterized, catecholamine resistance remains largely unexplored. Murine b3-adrenergic receptor expression in adipocytes is orders of magnitude higher compared to other isoforms.While resistant to classical desensitization pathways, its mRNA (Adrb3) and protein expression are dramatically downregulated after ligand exposure (homologous desensitization). b3-adrenergic receptor downregulation also occurs after high fat diet feeding, concurrent with catecholamine resistance and elevated inflammation. This downregulation is recapitulated in vitro by TNFa treatment (heterologous desensitization). Both homologous and heterologous desensitization of Adrb3 were triggered by induction of the pseudokinase TRIB1 downstream of the EPAC/RAP2A/PI-PLC pathway. TRIB1 in turn degraded the primary transcriptional activator of Adrb3, CEBPa. EPAC/RAP inhibition enhanced catecholamine-stimulated lipolysis and energy expenditure in obese mice. Moreover, adipose tissue expression of genes in this pathway correlated with body weight extremes in a cohort of genetically diverse mice, and with BMI in two independent cohorts of humans. These data implicate a signaling axis that may explain reduced hormone-stimulated lipolysis in obesity and resistance to therapeutic interventions with b3-adrenergic receptor agonists.

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Section: Discussionmentioning

confidence: 99%

β3-Adrenergic receptor downregulation leads to adipocyte catecholamine resistance in obesity

Valentine¹,

Ahmadian²,

Keinan³

et al. 2022

Journal of Clinical Investigation

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“…A greater NetC w/kg therefore represents a potential target for morbid obesity management through the daily total energy expenditure increase (TEE), especially in sedentary people with obesity who are in the so-called "unregulated zone", in which appetite and food intake are not affected by TEE; thus, food intake drives body weight gain [44]. Although increasing physical activity using walking and its associated higher NetC w/kg could be useful to shift individuals with obesity into the "regulated zone", in which appetite and food intake are affected by physical activity [44], the role of the latter in energy balance and weight loss remains controversial [44][45][46]. Nevertheless, decreasing the greater NetC w/kg in adults with obesity may be beneficial to increase non-exercise activity thermogenesis (NEAT) [11], and thus, light physical activity energy expenditure (1.6-2.9 metabolic equivalents; METs), which is inversely related to sedentary time [47] and has complementary effects to improve health [48].…”

Section: Discussionmentioning

confidence: 99%

The Effect of Obesity Class on the Energetics and Mechanics of Walking

et al. 2021

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Higher mass-normalized net energy cost of walking (NetCw/kg) and mechanical pendular recovery are observed in obese compared to lean adults. This study aimed to investigate the effect of different classes of obesity on the energetics and mechanics of walking and to explore the relationships between body mass, NetCw/kg and gait mechanics by using principal component analysis (PCA). NetCw/kg and gait mechanics were computed in severely obese (SOG; n = 18, BMI = 40.1 ± 4.4 kg·m−2), moderately obese (MOG; n = 17, BMI = 32.2 ± 1.5 kg·m−2) and normal-weight (NWG; n = 13, BMI = 22.0 ± 1.5 kg·m−2) adults during five walking trials (0.56, 0.83, 1.11, 1.39, 1.67 m·s−1) on an instrumented treadmill. NetCw/kg was significantly higher in SOG compared to NWG (p = 0.019), with no significant difference between SOG and MOG (p = 0.14), nor between MOG and NWG (p = 0.27). Recovery was significantly higher in SOG than in NWG (p = 0.028), with no significant difference between SOG and MOG (p = 0.13), nor between MOG and NWG (p = 0.35). PCA models explained between 17.0% and 44.2% of the data variance. This study showed that: (1) obesity class influences the gait energetics and mechanics; (2) PCA was able to identify two components, showing that the obesity class is associated with lower walking efficiency and better pendulum-like characteristics.

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“…Previous study demonstrated that participants with obesity but metabolic healthy (MH) were associated with an increased risk for MI [ 24 ] compared with MH-NW, which suggested an important influence of obesity or overweight on CVDs. A possible mechanism also demonstrated that it is difficult to lose fat when we get fatter, because our body makes more strongly energy compensation that burned during PA [ 41 ]. Therefore, it is importance to maintain healthy weight for decreasing CVDs risk.…”

Section: Discussionmentioning

confidence: 99%

Moderate physical activity may not decrease the risk of cardiovascular disease in persistently overweight and obesity adults

et al. 2022

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Background Body mass index (BMI) and physical activity (PA) has been documented to be associated with cardiovascular disease (CVD). However, the evidences regarding joint phenotypes of BMI and PA trajectories with risk for CVD and all-cause mortality are still limited. Methods Participants from the Kailuan Study, followed up during 2006–2019 were included, with primary outcomes of CVDs (myocardial infarction or stroke) and all-cause mortality. BMI and PA were repeatedly measured at least three times, and thus joint phenotypes trajectory groups were identified by group-based trajectory modeling. Cox proportional hazards models were used to examine the associations between trajectory groups and CVDs and all-cause mortality. Results Totally 88,141 (6 trajectories) and 89,736 participants (5 trajectories) were included in the final analyses relating trajectories to CVDs and all-cause mortality, respectively. Compared with persistent normal-weight with moderate PA group, participants were associated with increased risk of CVD in persistent overweight with moderate PA trajectory group (adjusted hazard ratio [aHR]: 1.31, 95% confidence interval [CI]: 1.22–1.41) and persistent obesity with moderate PA trajectory group (aHR: 1.55, 95% CI: 1.41–1.69). While the rising to overweight with moderate PA in normal-weight status with active PA (aHR: 0.72, 95% CI: 0.65–0.79), persistent overweight with moderate PA (aHR: 0.92, 95% CI: 0.87–0.97) and decline to normal-weight in overweight status with moderate PA (aHR: 0.73, 95% CI: 0.67–0.80) trajectories group were significantly associated with decreased all-cause mortality risk. The associations remained robust among stratifying by age and sex individuals and sensitive analysis. Conclusions The long-term trajectories analysis showed that moderate PA may not decrease the risk of CVD in persistently overweight and obesity adults.

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Energy compensation and adiposity in humans

Abstract: Highlights d Energy compensation in humans was analyzed from daily and basal energy expenditure d Reduced BEE results in energy compensation of 28% d Degree of energy compensation varied between people of different body composition

Cited by 84 publications

References 40 publications

β3-Adrenergic receptor downregulation leads to adipocyte catecholamine resistance in obesity

β3-Adrenergic receptor downregulation leads to adipocyte catecholamine resistance in obesity

The Effect of Obesity Class on the Energetics and Mechanics of Walking

Moderate physical activity may not decrease the risk of cardiovascular disease in persistently overweight and obesity adults

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