Energy Compensation Following a Supervised Exercise Intervention in Women Living With Overweight/Obesity Is Accompanied by an Early and Sustained Decrease in Non-structured Physical Activity

Background/Objectives: Body composition (BC) does not always vary as a function of exercise induced energy expenditure (exercise EE – resting EE). Energy balance variables were measured to understand energy compensation (EC) in response to an exercise intervention performed at low (LOW) or moderate (MOD) intensity. Subjects/Methods: Twenty-one women with overweight/obesity (33 ± 5 kg/m2; 29 ± 10 yrs; 31 ± 4 ml O2/kg/min) were randomized to a 3-month LOW or MOD (40 or 60% of VȮ2reserve, respectively) matched to expend 1500 kcal/week (compliance = 97 ± 5%). Body energy stores (DXA), energy intake (EI) (food menu and food diaries), resting EE (indirect calorimetry), total EE (doubly-labeled water), time spent in different activities (accelerometers), appetite (visual analog scale), eating behavior traits and food reward (liking and wanting) were assessed at baseline, after weeks 1 and 2 and at the end of the 3-month exercise intervention. Results: EC based on BC changes (fat mass and fat-free mass) was 49 ± 79% and 161 ± 88% in LOW and MOD groups, respectively (p = 0.010). EI did not change significantly during the intervention. However, eating behavior traits and food reward had changed by the end of the 3-month supervised exercise. Non-structured physical activity (NSPA) decreased across the intervention (p < 0.002), independent of the intensity of the exercise training. Conclusion: Women with overweight/obesity training at LOW presented lower EC for a given energy cost of exercise. Our results strongly suggest that NSPA plays a major role in mediating the effects of exercise on energy balance and ultimately on changes in BC

Age-dependent effects of protein restriction on dopamine release

FUNDING AND DISCLOSURE This work was supported by the Biotechnology and Biological Sciences Research Council [grant # BB/M007391/1 to J.E.M.], the European Commission [grant # GA 631404 to J.E.M.], The Leverhulme Trust [grant # RPG-2017-417 to J.E.M.] and the Tromsø Research Foundation [grant # 19-SG-JMcC to J. E. M.). The authors declare no conflict of interest. ACKNOWLEDGEMENTS The authors would like to acknowledge the help and support from the staff of the Division of Biomedical Services, Preclinical Research Facility, University of Leicester, for technical support and the care of experimental animals.Peer reviewedPublisher PD

GLP-1/dexamethasone inhibits food reward without inducing mood and memory deficits in mice.

Background: Pharmacotherapies targeting motivational aspects of feeding and palatable food reward, while sparing mood and cognitive function, represent an alluring approach to reverse obesity and maintain weight loss in an obesogenic environment. A novel glucagon-like peptide-1/dexamethasone (GLP-1/Dexa) conjugate, developed to selectively activate glucocorticoid receptors in GLP-1 receptor-expressing cells was shown to decrease food intake and lower body weight in obese mice. Here, we investigate if this novel drug candidate modulates the rewarding properties of food and if it affects behavioral indices of mood and memory. Methods: C57Bl6 mice treated with the GLP-1/Dexa conjugate, GLP-1 or vehicle lever-pressed for high-fat, high sugar (HFHS) food rewards in an operant task. Alterations in food-motivated behavior were also assessed following a HFHS diet withdrawal manipulation (switch to chow). The effects of repeated GLP-1/Dexa conjugate, GLP-1 or vehicle on free-feeding intake, body weight, anxiodepressive behaviors (elevated-plus maze, open field test &amp; forced swim test), memory (novel object recognition) and mRNA expression of reward-relevant markers in the nucleus accumbens were also evaluated in mice fed a HFHS diet for 12 weeks. Results: Mice treated with a GLP-1 analogue displayed a transient (4 h) reduction in their motivation to lever press for HFHS reward, whereas treatment with equimolar doses of GLP-1/Dexa delivered a superior and sustained (20 h) suppression of food-motivated behavior. GLP-1/Dexa also inhibited food reward following withdrawal from the HFHS diet. These benefits coincided with related transcriptional changes of dopaminergic markers in the nucleus accumbens. Importantly, repeated GLP-1/Dexa treatment during a HFHS diet caused weight loss without affecting anxiodepressive behavior and memory. Conclusion: Via its actions to blunt the rewarding effects of palatable food without affecting mood and recognition memory, GLP-1-directed targeting of dexamethasone may serve as a promising and safe anti-obesity strategy