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G Tamburrano

Publications and source records attributed to G Tamburrano.

At least 109 records · Page 6Linked to original sources

High insulin levels do not influence PC-1 gene expression and protein content in human muscle tissue and hepatoma cells.

BACKGROUND: To verify whether insulin levels influence PC-1 tissue content, we studied PC-1 gene expression and protein content in skeletal muscle of patients with insulinoma, a model of primary hyperinsulinemia. Data were compared with those obtained in matched insulin sensitive or resistant healthy subjects. In addition, the effect of high insulin concentration on PC-1 protein content was studied in HepG2 cells. METHODS: The following measurements were performed: insulin sensitivity by euglycemic clamp; PC-1 protein content and insulin receptor autophosphorylation by specific ELISAs; PC-1 gene expression by competitive polymerase chain reaction (PCR); phosphatidyl-inositol-3 kinase by immunoprecipitation and thin layer chromatography; glycogen synthesis by (14)C-glucose incorporation. RESULTS: Muscle PC-1 content was similar in the insulinoma patients and in insulin sensitive controls but higher (p<0.01) in insulin resistant controls (21.9+/-4.6 ng/mg protein, 23.8+/-3.9, 48.0+/-8.7, respectively). PC-1 protein content was inversely correlated with insulin sensitivity (r=-0.5, p<0.015) but with neither plasma insulin nor glucose levels. PC-1 protein content was correlated with PC-1 gene expression (r=0.53, p<0.05, n=14). Exposure to high insulin (100 nmol/l for 16 h) caused a significant (p<0.05-0.01) impairment of insulin receptor autophosphorylation, phosphatidyl-inositol-3 kinase activity and glycogen synthesis, but not of PC-1 protein content (114+/-3 vs 102+/-14 ng/mg protein) in HepG2 cells. CONCLUSION: These findings suggest that chronic high insulin levels do not influence PC-1 expression.

Carcinoma, Hepatocellular↗

Impaired alpha cell function in conditions with cortisol deficiency.

Plasma immunoreactive glucagon (IRG), insulin (IRI) and blood glucose (BG) were evaluated in the fasting state and during an arginine test (ATT) in 6 subjects with untreated hypopituitarism (H), in 2 hypopituitary subjects with normal cortisol production (H + C), in 3 subjects with Addison's disease (A) and in 14 normal volunteers (N). No increase in BG was observed in H and A after arginine, mean values being significantly lower than in N. Mean fasting and arginine-stimulated IRI levels were lower in H and A than in N; postabsorptive arginine-induced IRG levels were significantly reduced when compared to N. In contrast IRG levels in the two H + C patients were within the normal range. The impaired IRG production in A and in H (but not in H + C) suggests a close relationship between alpha pancreatic function and cortisol levels.

Addison Disease↗

Effects of somatostatin on insulin and glucagon in patients with insulinoma.

Effects of somatostatin on fasting and arginine-or tolbutamide-stimulated insulin release were studied in four patients with insulinoma. Somatostatin (bolus or bolus + infusion) reduced fasting insulin values in all patients; insulin response to tolbutamide was partially reduced in two patients; somatostatin bolus impaired the insulin response to arginine. Fasting glucagon levels and glucagon response to arginine were also reduced by somatostatin. These results indicate the potential usefulness of somatostatin in the diagnosis of insulinoma even if its effect on insulin is only partial.

Adenoma, Islet Cell↗

Plasma levels of glucagon-like polypeptides in patients with esophagoplasty.

Seven patients with interposition of a jejunal tract between the esophagus and stomach or duodenum (EP group) and ten healthy normal volunteers have been submitted to an oral glucose load (OGTT) to clarify the significance of glucagon-like polypeptides (GLI) induced by glucose in carbohydrate metabolism. Blood glucose (BG) and GLI plasma levels were significantly higher in the EP group than in the normal one (p less than 0.01), respectively 30, 60, 90 min for BG and during all the test for GLI. The fasting immunoreactive glucagon (IRG) plasma levels were significantly lower in patients than in normals (p less than 0.05) whereas a marked and significant increase was observed in the EP group (p less than 0.01) from 90 to 240 min. The precocious stimulation of jejunal mucosa and the rapid intestinal transit which occur in these patients may explain the elevated GLI (probably glicentin) plasma levels. The rise in IRG plasma levels might be due to the enzymatic transformation of glicentin. The role of these types of glucagon on carbohydrate metabolism is still to be fully clarified.

Aged↗

Occurrence of GH deficiency in adult patients who underwent neurosurgery in the hypothalamus-pituitary area for non-functioning tumour masses.

Hypothalamus-pituitary tumours and their treatments (neurosurgery and/or radiotherapy) are major causes of acquired hypopituitarism. Scientific and clinical evidences show the positive effect of GH replacement therapy in severe adult GH deficiency (GHD) pointed toward the need of diagnostic screening of conditions at high risk for GHD. We screened 152 adults (82 males, 70 females; age: 52.3+/-1.2 years, age-range: 20-80 years, BMI: 26.4+/-0.8 kg/m(2)) in order to disclose the presence of GHD after neurosurgery for hypothalamus-pituitary tumours. The whole group (studied at least 3 months after neurosurgery) included: 111 non-functioning pituitary adenomas and 41 peri-pituitary tumours (24 craniopharyngiomas, 7 meningiomas, 5 cysts, 2 chondrosarcomas, 1 colesteatoma, 1 germinoma and 1 hemangiopericitoma). In 14 patients who underwent both neurosurgery and radiotherapy due to a tumour remnant, the somatotroph function was evaluated again 6 months after the end of radiotherapy. GHD was assumed to be shown by GH peak <5 microg/L (severe <3 microg/L) after Insulin Tolerance Test (ITT) or <16.5 microg/L (severe <9 microg/L) after GH-releasing hormone+arginine test (GHRH+ARG) (3rd and 1st centile limits of normality, respectively), two widely accepted provocative tests. Before neurosurgery GHD was present in 97/152 (63.8%) and resulted severe in 66/152 (43.4%) patients. After neurosurgery GHD was present in 122/152 (80.2%) and severe in 106/152 (69.7%). While 26 patients developed severe GHD (GHD) as consequence of neurosurgery, only one patient who had been classified as GHD before neurosurgery showed normal GH response after surgery. After neurosurgery, 91.0% (81/89) of the pan-hypopituitaric patients showed severe GHD. Considering the 14 patients who underwent also radiotherapy after neurosurgery, 7/14 had GHD before neurosurgery while 12/14 became severe GHD after radiotherapy in a context of pan-hypopituitarism. IGF-I levels below the 3rd age-related normal limits were present in 39.0% of patients in whom severe GHD was showed by provocative tests. In conclusion, this study shows that the occurrence of acquired severe GHD is extremely common in adult patients bearing non-functioning tumour masses in the hypothalamus-pituitary area and further increases after neurosurgery. All patients bearing non-functioning hypothalamus-pituitary tumours should undergo evaluation of their somatotroph function before and after neurosurgery that represents a condition at obvious more than high risk for hypopituitarism.

Adenoma↗

Pancreatic beta-cell tumors: MRI.

Ten consecutive patients with surgically proven beta-islet cell tumors, strongly suspected clinically because of positive laboratory findings, were studied by MRI at 0.5 T. Results were correlated with CT and angiography. MRI detected all 10 insulinomas, with the location confirmed at surgery. Lesion size was < 1 cm in three cases, between 1 and 2 cm in five cases, and between 2 and 3 cm in two cases. A false-negative diagnosis was obtained with CT in 6 of 10 and with angiography in 3 of 10 cases. Our results suggest that if motion artifact can be controlled or reduced, MRI can be employed to localize insulinomas in patients with positive clinical and laboratory findings.

Adolescent↗