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Biomedical subjects

C di Carlo

Publications and source records attributed to C di Carlo.

4 recordsLinked to original sources
PubMed2003

Leptin induces mitogenic effect on human choriocarcinoma cell line (JAr) via MAP kinase activation in a glucose-dependent fashion.

Leptin and glucose effect on cell growth has been investigated in the JAr human choriocarcinoma cells. When JAr cells were cultured in the presence of 6m M glucose (LG), proliferation and thymidine incorporation were induced by serum but not by leptin. At variance, at 25m M glucose (HG), proliferation and thymidine incorporation were stimulated by leptin and serum to a comparable extent. HG culturing also enhanced leptin-stimulated insulin receptor substrate 1 (IRS1) and MAPK phosphorylation. Blockage of MAPK activity with PD98059 caused an inhibition of glucose- and leptin-dependent thymidine incorporation. At variance with HG conditions no effects were observed in cells cultured in 6m M glucose upon treatment with PD98059. Neither glucose nor leptin determined a modification in leptin receptors total content. In this study, we provide evidence that in placental cells, leptin, similarly to that observed with insulin, stimulates cell proliferation by inducing the IRS1/MAPK pathway in a glucose-dependent fashion.

Cell Division↗
PubMed1996

Changes in bone mineral density and calcium metabolism in breastfeeding women: a one year follow-up study.

The aim of this study was to evaluate bone metabolism in breast-feeding women. Thirty-six healthy women (24-31 yr, mean age 28.1 +/- 1.8 yr) were divided into 2 groups: group A including 18 women that exclusively breast-fed for 6 months, and group B composed of 18 women in whom lactation was inhibited with bromocriptine. Three days and 3, 6, and 12 months after delivery, distal radius, and lumbar spine bone mineral density (BMD) and some of the main biochemical parameters of bone turnover were assessed. In group A, we detected a significant decrease (P < 0.01 vs. basal and group B) in lumbar spine and distal radium BMD during breast-feeding. An incomplete recovery of BMD was detected 6 months after breast-feeding interruption. In group B, no significant changes occurred in BMD. In group A, during lactation, serum osteocalcin and urinary hydroxyproline showed a significant increase (P < 0.01 vs. basal and group B), while parathyroid hormone was significantly decreased (P < 0.02 vs. basal and group B). No significant variations in these parameters occurred in group B throughout the study. Our findings show that a significant decrease of BMD occurs during lactation and that this decrease is only partially recovered 6 months after interrupting breast-feeding.

Adult↗
PubMed1996

Effects of thyroxine therapy on bone metabolism in postmenopausal women with hypothyroidism.

OBJECTIVE: To evaluate whether thyroid stimulating hormone-suppressive thyroxine replacement therapy increases bone loss in postmenopausal women. MATERIALS AND METHOD: The study had a cross-sectional design. Fifty-four postmenopausal women on long-term treatment with thyroxine for primary hypothyroidism, who showed suppressed thyroid stimulating hormone levels were enrolled in our study. In these patients and in a control group of 54 healthy postmenopausal women we evaluated bone mineral density at distal radius and the main biochemical parameters of bone turnover. Student's t test, Wilcoxon signed rank-test, Chi-square test and the univariate linear regression in the statistical analysis of the data were employed. RESULTS: Bone mineral density values, expressed as z-scores, in the treated group were significantly decreased in comparison with the control group (p < 0.01). We did not detect a significant relationship between different L-thyroxine doses administered and bone mineral density z-scores. On the contrary, an inverse correlation was detected between length of treatment and bone mineral density z-scores. Treated patients showed a significantly higher concentration of serum alkaline phosphatase, osteocalcin, urinary calcium/creatinine and hydroxyproline/creatinine in comparison with the controls. CONCLUSIONS: Our study suggests that thyroxine replacement therapy in patients with suppressed thyroid stimulating hormone levels increases postmenopausal bone loss.

Bone Density↗