The aim of this article is to review the research into the main peripheral appetite signals altered in human obesity, together with their modifications after body weight loss with diet and exercise and after bariatric surgery, which may be relevant to strategies for obesity treatment. Body weight homeostasis involves the gut–brain axis, a complex and highly coordinated system of peripheral appetite hormones and centrally mediated neuronal regulation. The list of peripheral anorexigenic and orexigenic physiological factors in both animals and humans is intimidating and expanding, but anorexigenic glucagon-like peptide 1 (GLP-1), cholecystokinin (CCK), peptide YY (PYY) and orexigenic ghrelin from the gastrointestinal tract, pancreatic polypeptide (PP) from the pancreas and anorexigenic leptin from adiposites remain the most widely studied hormones. Homeostatic control of food intake occurs in humans, although its relative importance for eating behaviour is uncertain, compared with social and environmental influences. There are perturbations in the gut–brain axis in obese compared with lean individuals, as well as in weight-reduced obese individuals. Fasting and postprandial levels of gut hormones change when obese individuals lose weight, either with surgical or with dietary and/or exercise interventions. Diet-induced weight loss results in long-term changes in appetite gut hormones, postulated to favour increased appetite and weight regain while exercise programmes modify responses in a direction expected to enhance satiety and permit weight loss and/or maintenance. Sustained weight loss achieved by bariatric surgery may in part be mediated via favourable changes to gut hormones. Future work will be necessary to fully elucidate the role of each element of the axis, and whether modifying these signals can reduce the risk of obesity.

Background:The extent to which exercise-induced changes to postprandial metabolism are dependant on the associated energy deficit is not known. Objective: To determine the effects of exercise, with and without energy replacement, on postprandial metabolism. Design: Each subject underwent three 2-day trials in random order. On day 1 of each trial subjects rested (control), walked at 50% maximal oxygen uptake to induce a net energy expenditure of 27 kJ kg À1 body mass (energy-deficit) or completed the same walk with the net energy expended replaced (energy-replacement). On day 2 subjects completed an 8.5-h metabolic assessment. For 3 days prior to day 2, subjects consumed an isocaloric diet, avoided planned exercise (apart from exercise interventions) and alcohol. Subjects: A total of 13 overweight/obese men (age: 40 ± 8 years, body mass index: 31.1 ± 3.0 kg m À2 ). Measurements: Postprandial triglyceride, insulin, glucose, non-esterified fatty acid and 3-hydroxybutyrate concentrations and substrate utilization rates were determined. Results: Energy-deficit lowered postprandial triglyceride concentrations by 14 and 10% compared with control and energyreplacement (Po0.05 for both). Energy-deficit increased postprandial 3-hydroxybutyrate concentrations by 40 and 19% compared with control and energy-replacement (Po0.05 for both). Postprandial insulin concentrations were 18 and 10% lower for energy-deficit and energy-replacement compared with control and 10% lower for energy-deficit than energy-replacement (Po0.05 for all). Postprandial fat oxidation increased by 30 and 14% for energy-deficit and energy-replacement compared to control and was 12% higher for energy-deficit than energy-replacement (Po0.05 for all). Conclusion: Exercise with energy replacement lowered postprandial insulinaemia and increased fat oxidation. However an exercise-induced energy deficit augmented these effects and was necessary to lower postprandial lipaemia.

Prior exercise decreases postprandial plasma triacylglycerol (TG) concentrations, possibly through changes to skeletal muscle TG extraction. We measured postprandial substrate extraction across the leg in eight normolipidemic men aged 21-46 yr. On the afternoon preceding one trial, subjects ran for 2 h at 64 +/- 1% of maximal oxygen uptake (exercise); before the control trial, subjects had refrained from exercise. Samples of femoral arterial and venous blood were obtained, and leg blood flow was measured in the fasting state and for 6 h after a meal (1.2 g fat, 1.2 g carbohydrate/kg body mass). Prior exercise increased time averaged postprandial TG clearance across the leg (total TG: control, 0.079 +/- 0.014 ml.100 ml tissue(-1).min(-1) ; exercise, 0.158 +/- 0.023 ml.100 ml tissue(-1).min(-1), P <0.01), particularly in the chylomicron fraction, so that absolute TG uptake was maintained despite lower plasma TG concentrations (control, 1.53 +/- 0.13 mmol/l; exercise, 1.01 +/- 0.16 mmol/l, P < 0.001). Prior exercise increased postprandial leg blood flow and glucose uptake (both P < 0.05). Mechanisms other than increased leg TG uptake must account for the effect of prior exercise on postprandial lipemia.

There is a considerable body of evidence gathered from studies over the past half a century indicating that a high level of physical activity and a moderately high or high degree of cardiorespiratory fitness reduces the risk of CVD (cardiovascular disease). Recent data suggest that high levels of physical activity or fitness may be particularly beneficial to individuals with insulin-resistant conditions, such as the metabolic syndrome, Type II diabetes or obesity. These individuals, if unfit and sedentary, exhibit increased CVD risk, but their dose-response relationship for physical activity/fitness appears to be particularly steep such that, when they undertake high levels of activity (or have high fitness), their level of risk becomes closer to that of their normal weight or nondiabetic peers. This may be due to effects of physical activity in normalizing the metabolic dysfunction particularly associated with insulin-resistant conditions.

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Purpose: To examine extent to which changes in non-exercise physical activity contribute to individual differences in body fat loss induced by exercise programs. Results: Over the 8-week exercise program net ExEE was 30.2 ± 12.6 MJ and based on this, body fat loss was predicted to be 0.8 ± 0.2 kg. For the group as a whole, change in body fat (-0.0 ± 0.2 kg) was not significant but individual body fat changes ranged from -3.2 kg to +2.6 kg. Eleven participants achieved equal or more than the predicted body fat loss and were classified as 'Responders' and 23 subjects achieved less than the predicted fat loss and were classified as 'Non-responders'. In the group as a whole, daily TEE was increased by 0.62 ± 0.30 MJ (p<0.05) and the change tended to be different between groups (Responders, +1.44 ± 0.49 MJ; Non-responders, +0.29 ± 0.36 MJ, p=0.08). Changes in daily AEE of MethodsResponders and Non-responders differed significantly between groups (Responders, +0.79 ± 0.50 MJ; Non-responders, -0.62 ± 0.39 MJ, p<0.05). There were no differences betweenResponders and Non-responders for changes in SEDEE and SEE or energy intake. Conclusion:Overweight and obese women who during exercise intervention achieve lower than predicted fat loss are compensating by being less active outside exercise sessions.

. (2016) Identification of plasma and urinary metabolites and catabolites derived from orange juice (poly)phenols: analysis by high-performance liquid chromatography-high-resolution mass spectrometry. Journal of Agricultural and Food Chemistry, 64(28)

AimMicroRNAs (miRNAs) are stable in the circulation and are likely to function in inter-organ communication during a variety of metabolic responses that involve changes in gene expression, including exercise training. However, it is unknown whether differences in circulating-miRNA (c-miRNA) levels are characteristic of training modality.MethodsWe investigated whether levels of candidate c-miRNAs differ between elite male athletes of two different training modalities (n = 10 per group) - endurance (END) and strength (STR) - and between these groups and untrained controls (CON; n = 10). Fasted, non-exercised, morning plasma samples were analysed for 14 c-miRNAs (miR-1, miR-16-2, miR-20a-1, miR-21, miR-93, miR-103a, miR-133a, miR-146a, miR-192, miR-206, miR-221, miR-222, miR-451, miR-499). Moreover, we investigated whether c-miRNA levels were associated with quantitative performance-related phenotypes within and between groups.ResultsmiR-222 was present at different levels in the three participant groups (p = 0.028) with the highest levels being observed in END and the lowest in STR. A number of other c-miRNAs were present at higher levels in END than in STR (relative to STR, ± 1 SEM; miR-222: 1.94 fold (1.73-2.18), p = 0.011; miR-21: 1.56 fold (1.39-1.74), p = 0.013; miR-146a: 1.50 fold (1.38-1.64), p = 0.019; miR-221: 1.51 fold (1.34-1.70), p = 0.026). Regression analyses revealed several associations between candidate c-miRNA levels and strength-related performance measures before and after adjustment for muscle or fat mass, but not following adjustment for group.ConclusionCertain c-miRNAs (miR-222, miR-21, miR-146a and miR-221) differ between endurance- and resistance-trained athletes and thus have potential as useful biomarkers of exercise training and / or play a role in exercise mode-specific training adaptations. However, levels of these c-miRNAs are probably unrelated to muscle bulk or fat reserves.