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BACKGROUND We aimed to assess the predictive value of circulating levels of des-acyl ghrelin, an abundant form of ghrelin in humans, for the risk of cardiovascular disease (CVD) in older hypertensive patients. We simultaneously evaluated other biomarkers, such as high-molecular-weight (HMW) adiponectin, high-sensitivity C-reactive protein (hs-CRP), and plasminogen activator inhibitor 1 (PAI-1), for their usefulness in risk prediction. METHODS We enrolled 590 older hypertensive patients (mean age = 72.9 years; 41.0% men). The incidences of CVD, including coronary artery disease, stroke, congestive heart failure, and sudden death, were prospectively ascertained. RESULTS During an average duration of 2.8 (SD = 0.7) years (1,653 person-years), there were 42 CVD events. Patients with CVD events had lower levels of des-acyl ghrelin at baseline than those without CVD events (median = 78.2 vs. 114.7fmol/ml; P < 0.001). No difference was found among other biomarkers between the patients with CVD events and those without such events. The Cox proportional hazards model adjusted by covariables revealed that the hazard ratio for CVD events in patients with a 1-SD decrease of log des-acyl ghrelin was 1.8 (95% confidence interval = 1.3−2.4). Incorporation of des-acyl ghrelin in the risk model (including age, current smoking, 24-hour systolic blood pressure, preexisting CVD, and carotid intima-media thickness) improved the C statistics (from 0.683 to 0.721; P = 0.22) and resulted in a net reclassification improvement of 20.5% (P = 0.02). In contrast, HMW adiponectin, hs-CRP, and PAI-1 provided no improvement in risk prediction. CONCLUSIONS Des-acyl ghrelin improved the prediction of CVD events in older hypertensive patients. [ABSTRACT FROM AUTHOR]

An abstract of the study "Ghrelin prevents and facilitates recovery of muscle atrophy in mice underwent hind limb suspension," by Keiichi Koshinaka and Koji Toshinai is presented.

Age-related decreases in energy expenditure and physical activity have been associated with the loss of skeletal muscle and decline of food intake, possibly through a mechanism involving changes of growth hormone secretion and feeding behavior. Age-related declines of growth hormone secretion and food intake have been termed the somatopause and anorexia of aging, respectively. Ghrelin was isolated from human and rat stomachs as an endogenous ligand of growth hormone secretagogue receptor. Ghrelin stimulates growth hormone release and food intake when peripherally administered to humans. Plasma ghrelin concentration is decreased with age. Therefore, age-related decline of ghrelin secretion may cause the somatopause and anorexia of aging. Ghrelin replacement may suppress these aging processes.

The molecular mechanisms mediating the cellular adaptations to exercise training in human skeletal muscle are very poorly understood. To investigate the effect of endurance training on the expression of various genes at the mRNA levels in human skeletal muscle, focusing on angiogeneic factors, antioxidant enzymes, and uncoupling proteins (UCPs), seven untrained male students underwent an intensive swimming training five times a week for 3 months and two male students an intensive running training, respectively. Muscle biopsies were taken before training and about 48 h after the last session. All the subjects markedly increased their maximal oxygen uptake levels due to training (P < 0.001), indicating an improvement in aerobic capacity. After training, there were significant (P < 0.04) decreases in the expression of mRNAs for heat shock protein 70, Cu,Zn-superoxide dismutase (Cu,Zn-SOD), and Mn-SOD but a significant (P < 0.02) increase in UCP2 mRNA expression, whereas no definite changes were observed in the levels of mRNAs for vascular endothelial growth factor (VEGF), basic fibroblast growth factor, hypoxia-inducible factor-1alpha (HIF1alpha), myoglobin, or UCP3. The changes in HIF1alpha mRNA expression correlated well with those in VEGF mRNA expression after training (r=0.875, P < 0.01), suggesting that HIF1alpha influences the training-induced VEGF gene expression or alternatively that VEGF and HIF1alpha expressions are coregulated at the transcriptional level in human skeletal muscle. Taken together, it is envisioned that cumulative effects of transient changes in transcription during recovery from successive bouts of exercise may represent the underlying kinetic basis for the cellular adaptations associated with endurance training.