[Marfan's syndrome. A case report].
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Biomedical subjects
Publications and source records attributed to B Roca.
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BACKGROUND: There is a certain degree of peripheral cell resistance to insulin in the physiopathology of gestational diabetes. These disturbances may persist following pregnancy giving place to secondary hyperinsulinism. Insulin exerts a trophic action on the ovary and favors the production of androgens. The aim of this study was to verify whether the patients diagnosed of gestational diabetes present androgenic alterations following pregnancy. The existence of a correlation between the values of insulin and androgens was analyzed. METHODS: Fifty-one patients were studied. The study group (n = 297) was composed of patients diagnosed of gestational diabetes during their last week of pregnancy. The control group (n = 24) included patients with normal carbohydrate tolerance. The basal values of insulin, glucose, androstenedione, testosterone and SHBG were determined in a postmenstrual phase. RESULTS: Insulin was found to be higher in the study group (78.1 +/- 32.9 pmol/1 vs 63.0 +/- 27.6 pmol/1) although the differences were not significant. The insulin/glucose ratio was significantly higher in the study group (18.1 +/- 8.0 vs 13.9 +/- 7.7; p less than 0.05). Basal insulin and the insulin/glucose ratio were comparable among the obese and non obese patients of both groups. The remaining parameters studied dit not present any significant differences. No significant associations were observed between the values of insulin and insulin/glucose with the androgenic hormonal parameters. CONCLUSIONS: No elevated androgenic profile was observed in the women with previous gestational diabetes. The use of insulin and insulin/glucose values as indicators of insulin resistance did not demonstrate any correlation with the androgenic parameters.
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The present study is an investigation of the effects of 12- to 96-hours' starvation and 96-hours' starvation plus 48-hours' refeeding on both somatostatin-like immunoreactivity (SLI) and cytosolic somatostatin binding sites in rabbit small intestinal mucosa. The SLI concentration increased after 24 h in duodenal and jejunal mucosa, but not in ileal mucosa, and reached its highest value after 96 h of fasting. The number of specific high and low-affinity somatostatin binding sites, but not their affinity, decreased with the duration of fasting in the same gut segments, refeeding of fasted animals resulted in a return to normal control values for small intestine mucosal SLI and somatostatin binding.
To date, the effects of long-term growth hormone (GH)-releasing hormone [GHRH(1-29)-NH2] treatment on the plasma concentrations of somatostatin-like immunoreactivity (SLI) remain undefined. In the present study, the effect of GHRH(1-29)-NH2 therapy on plasma SLI levels has been studied in 11 non-GH-deficient children. The pattern of administration was 5 micrograms/kg body weight, given subcutaneously once every day. There was no significant change in plasma SLI levels after bolus injection of GHRH(1-29)-NH2 before and during GHRH(1-29)-NH2 therapy. However, plasma SLI rose in basal plasma and nocturnal sleep after 3 months of GHRH(1-29)-NH2 therapy and remained the same during 6 months of treatment with GHRH(1-29)-NH2. The reason for this finding is uncertain, but an increase in SLI release from the enteroinsular axis is a possible explanation. The association of our findings with the role of the circulating SLI on nutrient homeostasis and the effects of GNRH on growth velocity is discussed.
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Somatostatin like immunoreactivity and the density of somatostatin binding sites were measured in stomach (fundus and antrum) from either fed, 12 to 96 hours fasted, or 96 hours fasted plus 48 hours refed rabbits. The somatostatin concentration increased in fundic and antral mucosa after 24 h and reached its highest value after 96 h of fasting. The number of specific somatostatin binding sites with high and low affinity decreased with the duration of fasting. Refeeding of fasted animals resulted in a normalisation to control values of gastric mucosal somatostatin and somatostatin binding.