Leptin is an adipocyte-derived hormone participating in the regulation of food intake and energy balance. Its secretion from fat cells is potentiated by insulin and by substrates providing ATP, whereas factors increasing cAMP level attenuate hormone release stimulated by insulin and glucose. The present experiments were aimed to determine the
effect of cAMP on leptin secretion stimulated by glucose, alanine or leucine in the presence of insulin. Moreover, the effect of protein kinase A inhibition on leptin secretion was tested. To stimulate leptin secretion, isolated rat adipocytes were incubated for 2 h in the buffer containing 5 mmol/l glucose, 10 mmol/l alanine or 10 mmol/l leucine, all in the presence of 10 nmol/l insulin. Inhibition of protein kinase A (PKA) by H-89 (50 μmol/l) slightly enhanced leptin release stimulated by glucose and leucine but not by alanine. Activation of this enzyme by dibutyryl-cAMP (1 mmol/l)
substantially restricted leptin secretion stimulated by glucose, alanine and leucine. The inhibitory influence of dibutyryl-cAMP on leptin secretion was totally (in the case of stimulation induced by glucose) or partially (in the case of stimulation by alanine and leucine) suppressed by H-89. These results demonstrate that leptin secretion induced by glucose, alanine and leucine is profoundly attenuated by cAMP in PKA-dependent manner. Therefore, the action of different stimulators of leptin secretion may be restricted by agents increasing the cAMP content in adipocytes. Moreover, it has also been shown that inhibition of PKA evokes the opposite effect and enhances leptin release.
The purpose of the present study was to investigate the effect of short-term endurance training on plasma total antioxidant status (TAS) and on in vitro platelet aggregation and ATP release. Blood samples were collected from the abdominal aorta of rats following short-term treadmill exercise (25 m/min, 0 % grade, 30 min) for three consecutive days, as well as in non-exercised control group. Platelet aggregation and platelet ATP release were evaluated by impedance and bioluminescence techniques, respectively. Plasma TAS was measured spectrophotometrically. Plasma TAS was higher and ADP-induced platelet ATP release was lower in the short-term training group with respect to the control group (p<0.001). Significant negative correlation (r = -0.56, p<0.05) was found between plasma TAS and ADP-induced platelet ATP release. Neither ADP- and collagen-induced maximum aggregation rate nor collagen-induced platelet ATP release were significantly different between the groups. According to these results, short-term training caused an alteration in platelet functions limited to the secretion response, which may be related to the oxidant/antioxidant balance changes favoring the antioxidants. The improved plasma total antioxidant capacity was possibly sufficient to prevent exercise-induced oxidative damage, and the adaptive response of platelets might be associated with enhanced antioxidant status.