Effect of an oral glucose load on PTH, 250HD3, calcium, and phosphorus homeostasis in postmenopausal women.

INTRODUCTION. Previous studies particularly in children and neonates have shown that serum calcium declines and parathyroid hormone (PTH) rises during an oral glucose load. However, there is not a general agreement in this regard. This study was carried out to evaluate the effects of an oral glucose load on calcium and phosphorus homeostasis in postmenopausal women along with serum insulin, PTH, and 250HD3 changes. PATIENTS AND METHODS. After an overnight fasting, an oral glucose tolerance test was performed in 50 postmenopausal women; and glucose, insulin, PTH, and D3 were measured at baseline and every 30 min during the 2 hours of the test. RESULTS. Serum glucose and insulin increased as expected and reached their peak values at 60 and 90 min, respectively. PTH and phosphorus decreased significantly and the maximum decline was observed at 30 and 120 min after glucose load (p < 0.0001), respectively. Serum calcium, magnesium, and D3 levels showed no significant changes at any time measured. Serum PTH values had a significant negative correlation with glucose and insulin values (p = 0.026 and p = 0.031, respectively). Serum D3 also correlated negatively with glucose (p = 0.002). CONCLUSION. Our study shows that an oral glucose load induced hyperglycemia/hyperinsulinemia promotes a significant decline in serum PTH and phosphorus levels without changes in calcium or 250HD3 in postmenopausal women.

The effect of lead intoxication on endocrine functions.

Studies on the effects of lead on the endocrine system are mainly based on occupationally lead-exposed workers and experimental animal models. Although evidence is conflicting, it has been reported that accumulation of lead affects the majority of the endocrine glands. In particular, it appears to have an effect on the hypothalamic-pituitary axis causing blunted TSH, GH, and FSH/LH responses to TRH, GHRH, and GnRH stimulation, respectively. Suppressed GH release has been reported, probably caused by reduced synthesis of GHRH, inhibition of GHRH release or reduced somatotrope responsiveness. Higher levels of PRL in lead intoxication have been reported. In short-term lead-exposed individuals, high LH and FSH levels are usually associated to normal testosterone concentrations, whereas in long-term exposed individuals' low testosterone levels do not induce high LH and FSH concentrations. These findings suggest that lead initially causes some subclinical testicular damage, followed by hypothalamic or pituitary disturbance when longer periods of exposure take place. Similarly, lead accumulates in granulosa cells of the ovary, causing delays in growth and pubertal development and reduced fertility in females. In the parenchyma of adrenals histological and cytological changes are demonstrated, causing changes in plasma basal and stress-mediated corticosterone concentrations and reduced cytosolic and nuclear glucocorticoid receptor binding. Thyroid hormone kinetics are also affected. Central defect of the thyroid axis or an alteration in T4 metabolism or binding to proteins may be involved in derangements in thyroid hormone action. Lead toxicity involves alterations on calcitropic hormones' homeostasis, which increase the risk of skeletal disorders.

sRANKL/osteoprotegerin complex and biochemical markers in a cohort of male and female hemodialysis patients.

OBJECTIVE: The processes involved in bone remodeling are under the control of a multitude of systemic and local factors. Receptor activator of nuclear factor-kappaB ligand (RANKL)/osteoprotegerin (OPG) complex seems to be one of the major modulators of bone remodeling. In chronic renal failure, the cytokine systems involved in the regulation of bone turnover may be influenced, and are therefore likely to contribute to the pathogenesis of renal bone disease. The aim of the present study was the evaluation of RANKL/OPG complex in concert with other biochemical parameters in hemodialysis (HD) patients and the investigation of possible correlations between the serum levels of its components and several clinical parameters of these patients. METHODS: We measured serum levels of intact PTH (iPTH), total serum RANKL (sRANKL), osteoprotegerin (OPG), alkaline phosphatase, osteocalcin (OC), and tartrate-resistant acid phosphatase (TRAP) in 104 HD patients and in 40 healthy controls. RESULTS: The average serum OPG level was significantly higher, whereas the average serum concentration of RANKL was nonsignificantly lower in patients on HD therapy than in age-matched healthy controls. Consequently, the mean sRANKL/OPG ratio was significantly lower in patients. Among HD patients, serum level of OPG increased significantly with aging and with a longer duration of hemodialysis. RANKL levels were inversely correlated with age nonsignificantly in the whole group of patients and significantly in the female subgroup (r=-0.322, p=0.035), whereas RANKL/OPG ratio declined significantly with age in the entire cohort of patients (r=-0.259, p=0.008). In addition, iPTH, OC, TRAP were significantly higher in female, whereas RANKL/OPG ratio was significantly higher in male than female patients. CONCLUSIONS: Lower values of sRANKL/OPG ratio in HD patients, as well as the age and duration of HD dependent increase of serum OPG and the age-dependent decrease of sRANKL concentration especially in women cannot be explained by the elimination of renal clearance only. Alterations in sRANKL/OPG ratio might reflect a compensatory mechanism to modulate bone remodeling in these patients.