Controversial data on ghrelin concentration during exercise in human subjects have been published. We tested the hypothesis that exercise could affect acylated ghrelin (AG) and unacylated ghrelin (UAG), which could partly explain the previously reported inconsistent findings on the association of exercise with changes in ghrelin.
A prospective randomized study.
We randomized 17 overweight volunteers (11-year-old boys) to a 12-week combined exercise group (EG, n = 8) or control group (CG, n = 9). At baseline, 1, 4 and 12 weeks, we measured body weight and composition, insulin, leptin, total ghrelin and acylated ghrelin.
Compared with the CG, body weight, percentage body fat and homeostatic model assessment (HOMA) indices were significantly lower throughout the 12 weeks in the EG. Total ghrelin and UAG levels gradually increased to 131.9 +/- 5.2% and 130.4 +/- 5.2% of baseline, respectively, at week 12 in the EG, whereas AG concentration remained unchanged throughout the 12 weeks both within each group and between the groups. At week 12, there were differences in the total ghrelin level and UAG level between the groups.
This study shows an increase in unacylated acylated ghrelin and unchanged acylated ghrelin after a 12-week combined exercise programme in overweight children. These findings provide evidence of favourable effects of exercise on improving energy metabolism.
"However, most studies showed a compensatory increase in fasting ghrelin levels in response to reductions in body weight (Foster-Schubert et al. 2005; Kelishadi et al. 2008; Kim et al. 2008; Konopko-Zubrzycka et al. 2009; Leidy et al. 2004; Martins et al. 2010; Mizia-stec et al. 2008; Santosa et al. 2007). For example, whereas total ghrelin fasting levels were not affected by aerobic exercise training for 5 days without reductions in body weight (Mackelvie et al. 2007), fasting plasma levels gradually increased during 12 weeks of aerobic and resistance exercise with significant decreases in body weight and fat; and such reductions were strongly associated with increased fasting ghrelin levels (Kim et al. 2008; Leidy et al. 2004). For longer term exercise training where weight reductions were achieved over one year without caloric restriction, fasting ghrelin levels increased with weight loss, again suggesting a role for ghrelin in the adaptive response constraining weight loss (Foster-Schubert et al. 2005). "
[Show abstract][Hide abstract] ABSTRACT: The purpose of this study was to investigate the effects of 12 weeks of exercise training on gut hormone levels after a single bout of exercise in middle-aged Japanese women. Twenty healthy middle-aged women were recruited for this study. Several measurements were performed pre and post exercise training, including: body weight and composition, peak oxygen consumption (peak VO2), energy intake after the single bout of exercise, and the release of gut hormones with fasting and after the single bout of exercise. Exercise training resulted in significant increases in acylated ghrelin fasting levels (from 126.6 ± 5.6 to 135.9 ± 5.4 pmol/l, P < 0.01), with no significant changes in GLP-1 (from 0.54 ± 0.04 to 0.55 ± 0.03 pmol/ml) and PYY (from 1.20 ± 0.07 to 1.23 ± 0.06 pmol/ml) fasting levels. GLP-1 levels post exercise training after the single bout of exercise were significantly higher than those pre exercise training (areas under the curve (AUC); from 238.4 ± 65.2 to 286.5 ± 51.2 pmol/ml x 120 min, P < 0.001). There was a tendency for higher AUC for the time courses of PYY post exercise training than for those pre exercise training (AUC; from 519.5 ± 135.5 to 551.4 ± 128.7 pmol/ml x 120 min, P = 0.06). Changes in (delta) GLP-1 AUC were significantly correlated with decreases in body weight (r = -0.743, P < 0.001), body mass index (r = -0.732, P < 0.001), percent body fat (r = -0.731, P < 0.001), and energy intake after a single bout exercise (r = -0.649, P < 0.01) and increases in peak VO2 (r = 0.558, P < 0.05). These results suggest that the ability of exercise training to create a negative energy balance relies not only directly on its impact on energy expenditure, but also indirectly on its potential to modulate energy intake.
"Currently, little is known about the influence of exercise on acylated ghrelin and acylated ghrelin's relationship with appetite and food intake after exercise. The limited number of studies are in contrast with each other and new studies are certainly needed in this field (Broom et al., 2007; 2009; Kim et al., 2008; King et al., 2010a; 2010b; Mackelvie et al., 2007; Marzullo et al., 2008; Unick et al., 2010). "
[Show abstract][Hide abstract] ABSTRACT: This study investigated the effects of a long bout of aerobic exercise on hunger and energy intake and circulating levels of leptin and acylated ghrelin. Ten healthy male subjects undertook two, 4 h trials in a randomized crossover design. In the exercise trial subjects ran for 105 min at 50% of maximal oxygen uptake and the last 15 min at 70% of maximal oxygen uptake followed by a 120 min rest period. In the control trial, subjects rested for 4 h. Subjects consumed a buffet test meal at 180 min during each trial. Hunger ratings, acylated ghrelin, leptin, glucose and insulin concentrations were measured at 0, 1, 2, 3 and 4 h. No differences were found at baseline values for hunger, acylated ghrelin, leptin, insulin and glucose for both trials (p > 0.05). The estimated energy expenditure of the exercise trial was 1550 ± 136 kcal. Exercise did not change subsequent absolute energy intake, but produced a significant decrease (p < 0.05) in relative energy intake. A two-way ANOVA revealed a significant (p <0.05) interaction effect for hunger and acylated ghrelin. In conclusion, this exercise regimen had a positive effect on reducing appetite which is related to reduced acylated ghrelin responses over time. This finding lends support for a role of exercise in weight management.
Journal of sports science & medicine 06/2011; 10(2):283-91. · 1.03 Impact Factor
"So far, the majority of studies have focused on the effects of diet induced or combined exercise/diet weight loss on total ghrelin concentrations [21–28]. These studies are very diverse, with different interventions, intervention periods, age and number of participants, and also inclusion criteria. "
[Show abstract][Hide abstract] ABSTRACT: Metabolic syndrome is a cluster of related risk factors for cardiovascular disease, type 2 diabetes and liver disease. Obesity, which has become a global public health problem, is one of the major risk factors for development of metabolic syndrome and type 2 diabetes. Obesity is a complex disease, caused by the interplay between environmental and genetic factors. Ghrelin is one of the circulating peptides, which stimulates appetite and regulates energy balance, and thus is one of the candidate genes for obesity and T2DM. During the last years both basic research and genetic association studies have revealed association between the ghrelin gene and obesity, metabolic syndrome or type 2 diabetes.
International Journal of Peptides 04/2010; 2010(4). DOI:10.1155/2010/248948
S. Kofuji, M. Warren, K. Sumita, A. Hirayama, A. Ramkissoon, A. Malhotra, H. Yoshino, L. Pater, Y. Gozal, S. Gogela, A. Kendler, T. Wise, R. Curry, R. Warnick, H. Wakimoto, B. DasGupta, L. Chow, T. Soga, C. Horbinski, A. Sasaki,
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