To study the effects of regular football training on basal and exercise induced levels of growth hormone (GH) and insulin-like growth factor (IGF-1), 13 young football players were investigated by a submaximal exercise at the beginning of the sporting season in October (S1), at the middle of the season in January (S2) and at the end in May (S3). At each session, an exercise test on an ergogycle was performed for 25 min, beginning with an incremental exercise to reach 90% of theoretical maximal heart, which was maintained for the last 10 min of the test. Venous blood samples were collected at rest, at the end of the exercise and at 30 and 60 min during the recovery period. Plasma lactate and glucose concentrations increased during exercise with no difference found between sessions. GH level increased with exercise at each session but the response was significantly higher in S1 than in S2 and S3 (P<0.01). The GH area under the curve decreased significantly all along the football season (P<0.01); the IGF-1 level did not significantly change during exercise nor with training. Basal insulin-like growth factor binding protein-3 (IGFBP3) remained stable during the three sessions. Football training decreased significantly the exercise-stimulated GH levels all along the football season but did not have any significant effect on IGF-1 levels or on basal IGFBP3 levels.

Cellular resistance to insulin caused by reduced glucose transport and metabolism is a primary defect leading to the development of metabolic disease. While the etiology of insulin resistance is multifactorial, reduced insulin action is associated with impaired activity of the glucose transporter GLUT4 in insulin-sensitive tissues. Yet, the role of adipose tissue GLUT4 deregulation in the pathogenesis of insulin resistance, obesity, and diabetes is still unclear. In this study, we assessed the relative GLUT4 level in human subcutaneous adipose tissue from obese, diabetic, and diabetic obese versus control subjects, using a real-time PCR method. GLUT4 mRNA levels were considerably decreased among type 2 diabetic patients compared with those of the controls (P < 0.01), whereas no such difference was found between obese and normal-weight controls. Multiple linear regressions analysis in both diabetic non-obese and diabetic obese groups showed a negative correlation between GLUT4 mRNA expression and both markers of obesity or insulin resistance (P < 0.01). However, in obese group, GLUT4 was inversely associated only with HOMA-IR (P < 0.01). Our findings showed that adipose GLUT4 gene expression changes were more related to insulin resistance and type 2 diabetes rather than to obesity.

Our data strongly support that the changes of thyroid hormones may be influenced by adiposity and its metabolic consequences, such as insulin resistance. This relationship can be explained by a cross talk between adipose tissue release and thyroid function. Nevertheless, metformin treatment seems to affect thyroid function in diabetic patients by maintaining plasma thyrotropin levels to subnormal levels.

Our study on Tunisian patients shows impaired regulation of circulating and mRNA adiponectin levels dependent of metabolic disorders in obesity and Type 2 diabetes. The data suggest that subcutaneous adipose tissue may play an important role in modulating adiponectin expression in diabetes and obesity. Moreover, adiponectin mRNA could be potentially regulated by endogenous PPARγ/RXRα-dependent pathways.

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