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Objective: To investigate the response of the somatotrope axis (insulin-like growth factor-1 (IGF-1), insulinlike growth factor binding protein-3 (IGFBP-3)) to intense exercise in relation to tiredness. Methods: The study involved 11 rugby players who completed a questionnaire intended to evaluate fitness or, conversely, overtraining and who agreed to plasma samples being taken before and after an international rugby match. Results: The main finding of our study is that we observed strong negative correlations between IGF-1 (r = 0.652) and IGFBP-3 (r = 0.824) levels and the overtraining state estimated using the French Society of Sport Medicine questionnaire. In particular, there was a fall (of up to 25%) in IGFBP-3 levels after the match in the more fatigued subjects compared to an increase (of up to 40%) in fit subjects. Conclusions: A fall in IGFBP-3 in response to an intense bout of exercise may represent an index of tiredness in highly trained sportsmen, as indicated by the scores obtained from the overtraining questionnaire.

Lead is known to induce a broad range of physiological, biochemical, and behavioral dysfunctions in laboratory animals and humans. This includes age-specific variations in absorption, retention, and tissue distribution of lead. This study was carried out to investigate the effects of chronic exposure to lead (50 mg/L) on liver and kidneys of two different age groups of male rats treated with lead from delivery until puberty period (40 days) and postpuberty period (65 days). For this purpose, the concentrations of thiobarbituric acid reactive substance (TBARS), total thiol groups (SH), and superoxide dismutase (SOD) activity were measured in the liver and kidney of rats. Renal function was analyzed by determining creatinine, acid uric, and urea. Plasma activities of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and albumin were determined spectrophotometrically to evaluate hepatic function. These markers of damage were determined to assess the level of toxicity in these animals. Our results clearly show that the administration of lead produces oxidative damage in liver and kidney, as strongly suggested by the significant increase in TBARS, decrease in total SH, and the alteration of SOD activity. In young lead-exposed animals, lead-induced perturbations on the synthetic function of the liver and the kidney were more pronounced. However, nephropathy is evident for adult lead-exposed animals. It is concluded that lead induces severe hepatic and renal toxicity, which depends on the age of the animals and the target organ.

Several studies showed that organophosphorus pesticides disturb glucose homeostasis and can increase incidence of metabolic disorders and diabetes via insulin resistance. The current study investigates the influence of malathion on glucose metabolism regulation, in vivo, during subchronic exposure. Malathion was administered orally (200 mg/kg), once a day for 28 consecutive days. Plasma glucose, insulin and Glycated hemoglobin levels were significantly increased while hepatic glycogen content was decreased in intoxicated animals compared with the control group. Furthermore, there was a significant disturbance of lipid content in subchronic treated and post-treated rats deprived of malathion for one month. In addition, we used the homeostasis model assessment (HOMA) to assess insulin resistance (HOMA-IR) and pancreatic β-cell function (HOMA-β). Our results show that malathion increases insulin resistance biomarkers and decreases insulin sensitivity indices. Statistical analysis demonstrates that there was a positive and strong significant correlation between insulin level and insulin resistance indices, HOMA-IR, HOMA-β. Similarly, a negative and significant correlation was also found between insulin level and insulin sensitivity indices. For the first time, we demonstrate that malathion induces insulin resistance in vivo using homeostasis model assessment and these changes were detectable one month after the end of exposure. To explain insulin resistance induced by malathion we focus on lipid metabolism disturbances and their interaction with many proteins involved in insulin signaling pathways.