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G Brabant

Publications and source records attributed to G Brabant.

At least 37 records · Page 2Linked to original sources
PubMed2002

Secretion of free and protein-bound leptin from subcutaneous adipose tissue of lean and obese women.

Leptin circulates as a free (FL) and a protein-bound (BL) form, with the soluble leptin receptor (LR) as an important binding compound. Here we measured these components of leptin in serum and in the incubation medium of sc adipose tissue in healthy lean (n = 10) and obese (n = 13) female subjects using recently developed specific RIA systems. In addition, immunostaining for FL, BL, and LR in adipose tissue was performed. Serum FL levels were increased in the obese subjects (P < 0.0001), whereas BL and LR concentrations in serum of lean and obese subjects were similar. Both FL and BL were secreted from human preadipocytes and increased in parallel to the differentiation of the cells. In sc fat cell explants LR antibodies predominantly stained the fat cell membrane, whereas FL and BL antibodies revealed intracytoplasmatic adipocyte staining. The release of FL, BL, and LR from adipose tissue was increased in obese compared with lean subjects (P < 0.005 for FL; P < 0.02 for BL, and P < 0.01 for LR). In summary, fat cells are capable of releasing not only FL, but also BL and LR.

Adipocytes↗
PubMed2001

Noise enhanced hormonal signal transduction through intracellular calcium oscillations.

In a wide range of non-linear dynamical systems, noise may enhance the detection of weak deterministic input signals. Here, we demonstrate this phenomenon for transmembrane signaling in a hormonal model system of intracellular Ca(2+) oscillations. Adding Gaussian noise to a subthreshold extracellular pulsatile stimulus increased the sensitivity in the dose-response relation of the Ca(2+) oscillations compared to the same noise signal added as a constant mean level. These findings may have important physiological consequences for the operation of hormonal and other physiological signal transduction systems close to the threshold level.

Calcium↗
PubMed2001

[Reversible blindness caused by an invasive prolactinoma].

HISTORY: A 40-year-old man presented with severe headache, nausea and acute blindness. A CT-scan of the skull revealed a huge tumor along the basis of the skull. The patient was referred to our clinic for diagnostic and therapeutic evaluation. INVESTIGATIONS: MRT showed a large right-sided paramedian tumour displacing the brain stem with signs of increased intracranial pressure. Routine laboratory tests were normal except a normochromic anaemia. Endocrine tests demonstrated partial hypopituitarism with alteration of the somatotropic, gonadotropic and corticotropic axis and moderate hyperprolactinaemia. TREATMENT AND COURSE: On the day of admission a transnasal biopsy was taken. The preliminary histopathological diagnosis was a low differentiated carcinoma. Because of this diagnosis and because of the infiltrative tumour growth an operation was not performed but emergency irradiation was begun and dopamine agonist therapy was started because of hyperprolactinaemia. Several days later the final microscopic diagnosis of the transnasal biopsy specimen was reported to be an invasive prolactinoma. Under dopamine agonist therapy prolactin levels rose to a maximum of 6460 ng/ml to decline thereafter to normal values, and the visual disturbances recovered. After 5 weeks of therapy considerable shrinkage of the tumor was demonstrated by MRT. CONCLUSION: The differential diagnosis of acute visual deterioration caused by a large tumour along the basis of the skull includes an invasive prolactinoma. The diagnosis is made by demonstrating grossly elevated prolactin levels. To avoid falsely low prolactin measurements, caused by a hook-effect in the prolactin assay, serum dilution is mandatory in the diagnostic work-up. In the case of a prolactinoma medical treatment with dopamine receptor agonists is the therapy of choice because it causes rapid tumour shrinkage and symptomatic improvement in most patients, so that irradition of the tumour is not indicated. As dopamine agonist therapy is rapidly effective and well tolerated, it should be started even in case of doubt to lose no time until final diagnosis.

Acute Disease↗
PubMed2001

Wnts differentially regulate colony growth and differentiation of chondrogenic rat calvaria cells.

The wingless- and int-related proteins (Wnts) have an important role during embryonic development and limb patterning. To investigate their function during chondrocyte differentiation, we used NIH3T3 cells producing seven members of the Wnt family and secreted frizzled-related protein (sFRP-2) for co-culture experiments with the rat chondrogenic cell line pColl(II)-EGFP-5. Pilot experiments showed a negative effect of Wnt-7a on the proliferation of three rodent chondrogenic cell lines, RCJ3.1(C5.18), CFK-2, and C1. To establish a reporter system for chondrogenic differentiation we then produced a stably transfected chondrogenic cell line based on RCJ3.1(C5.18) for further experiments, which expresses green fluorescence protein (EGFP) under the collagen type II promoter (pColl(II)-EGFP-5). This cell line permits convenient observation of green fluorescence as a marker for differentiation in life cultures. The colony size of this cell line in agarose suspension cultures was reduced to 20-40% of control, when exposed to Wnt-1, 3a, 4, 7a, and 7b for 14 days. Similarly, reporter gene expression and the synthesis of cartilage-specific proteoglycans were inhibited by this group of Wnts. In contrast, pColl(II)-EGFP-5 cells exposed to Wnt-5a and Wnt-11 reached 140% of control, and reporter gene expression and proteoglycan synthesis were stimulated. The effects of Wnt-7a and Wnt-5a were additive in pColl(II)-EGFP-5 cells and some but not all Wnt effects were antagonized by the inhibition of proteoglycan sulfation with chlorate, by sFRP-2, which may modulate Wnt receptor binding, or by inhibitors of protein kinase C. These results suggest two functional Wnt subclasses that differentially regulate proliferation and chondrogenic differentiation in vitro which may have implications for cartilage differentiation in vivo. Since some, but not all Wnt effects were sensitive to inhibitors of proteoglycan synthesis or protein kinase C, multiple modes of signal transduction may be involved.

3T3 Cells↗
PubMed2001

Humoral coding and decoding.

Humoral communication systems are dynamically regulated. Most hormones are released in a pulsatile or burst-like manner into the bloodstream. It is well known that information coded in the frequency and amplitude of secretory pulses allows for the differential regulation of specific target cell function and structure. However, despite intensive study of transmembrane signalling relatively little is known about how the temporal dynamics of extracellular humoral stimuli specifically regulates the temporal pattern of intracellular signalling pathways, such as Ca2+-dependent signalling. Repetitive spikes of Ca2+ encode this information in their amplitude, duration and frequency, and are in turn decoded into the pattern of gene expression and phosphorylation of target proteins. Using a mathematical model for G protein-coupled Ca2+ signalling and information-theoretic approaches to stimulus reconstruction we have systematically quantified the amount of information coded in the Ca2+-signal about the dynamics of the stimulus, which allows us to explore the temporal bandwidth of transmembrane signalling. These in silico approaches permit us to differentiate the amount of information coded in the frequency, temporal precision, amplitude and the complete Ca2+-signal. This may open an avenue to the quantification of information flow and processing in the intra- and intercellular coding and decoding machinery.

Action Potentials↗
PubMed2001

Familial isolated parathyroid adenoma in a consanguineous family.

The 23-year-old Caucasian male propositus presented with symptomatic hypercalcemia, hypophosphatemia and normocalciuria for 2 months. His 29-year-old brother had undergone an operation for recurrent parathyroid adenoma at age 26 and 28. No other member of the family was affected. His father and mother were second-degree relatives. Laboratory studies showed primary hyperparathyroidism (pHPT), while the remaining endocrine studies and genetic testing for multiple endocrine neoplasia 1 and 2A were normal. Technetium-cardiolite scintigraphy and ultrasound scans revealed a parathyroid mass at the left lower neck. Apart from bilateral hearing loss due to gentamicin treatment as a pre-term child, the patient was in of good health. Signs or symptoms of other endocrinopathies were absent. The patient was referred for parathyroidectomy with subsequent autotransplantation of the remaining glands into his sternocleidomastoid muscle. Histological examination revealed an adenoma with oncocytic differentiation, similar to that seen in his brother. The disease may follow a recessive mode of inheritance or may be due to a dominant germ-cell mutation in one of the parents. The presented case may ultimately help in elucidating the molecular genetic basis of this rare form of pHPT.

Adenoma↗
PubMed2001

Identification of novel CBFA1/RUNX2 mutations causing cleidocranial dysplasia.

Core binding factor A1 (CBFA1/RUNX2) is a runt-like transcription factor essential for osteoblast differentiation. Haplotype insufficiency causes cleidocranial dysplasia (CCD), a syndrome featuring supernumerary tooth buds, delayed tooth eruption, patent fontanels, Wormian bones, short stature, dysplasia of the clavicles, growth retardation and hypoplasia of the distal phalanges. We identified novel CBFAI/RUNX2 mutations after PCR and direct sequencing of patient leukocyte DNA. In family 1 mother and son are affected by CCD. Both carry the missense mutation R190W (CGG > TGG). This nucleotide change introduced a BsmI restriction site, which was used to independently confirm the mutation. It was absent in healthy members of the family. Family 2, in which father and daughter are affected by CCD, shows a deletion of nucleotide C821. This deletion causes a frameshift mutation with premature stop after the insertion of 18 aberrant amino acids. Healthy family members did not have this mutation. The clavicular dysplasia was more pronounced with the R19OW mutation, while the bone density was markedly reduced in individuals with either mutation, suggesting a previously underemphasized increased risk for osteoporosis in CCD.

Adolescent↗
PubMed2001

Effects of insulin and glucocorticoids on the leptin system are mediated through free leptin.

OBJECTIVE: Insulin and glucocorticoids are known to increase total leptin levels. However, the effects of insulin and glucocorticoids on the components of the leptin system - free leptin (FL), bound leptin (BL) and soluble leptin receptor (SR) - have not been elucidated. The aim of this study was to determine if there is a differential effect of insulin and glucocorticoids on the leptin system. MATERIAL AND METHODS: In the first of two studies (study 1), we measured free leptin (FL), bound leptin (BL), a soluble leptin receptor (SR) and insulin, by specific RIA methods, in six healthy subjects on a control day, and subsequently during a hyperinsulinaemic euglycaemic clamp study. In the second study (study 2) we measured the same parameters in six healthy subjects, before (day 1) and during administration of dexamethasone over 3 consecutive days. RESULTS: In study 1, on the control day FL levels rose over the 16 h monitoring period (P = 0.057) and SR levels declined (P < 0.001), but there was no change of BL levels. Even after accounting for diurnal variation, FL levels increased even more substantially over 12 h of insulin infusion than observed on the control day (P < 0.001). In study 2, mean FL concentration doubled from day 1 to day 2 (P = 0.01) and remained elevated subsequently. In contrast to FL, BL and SR levels remained unchanged during the study. Fasting insulin levels (pmol/l) increased from day 1 to day 2, but this rise only approached significance on day 4 (P = 0.05). CONCLUSION: We conclude that insulin and dexamethasone increase free leptin levels, but do not change the concentrations of bound leptin and soluble leptin receptor. Furthermore, the dexamethasone-induced rise in leptin levels is (at least partially) independent of the effects of glucocorticoid-induced hyperinsulinaemia.

Adult↗
PubMed2001

Hepatitis C and the leptin system: bound leptin levels are elevated in patients with hepatitis C and decrease during antiviral therapy.

BACKGROUND: Serum leptin levels are elevated in alcoholic liver cirrhosis and thus might be involved in the anorexia and hypermetabolism often seen in those patients. We hypothesized that the leptin system is modulated in patients with hepatitis C and might be affected by antiviral therapy. The aim of this study was to investigate the different leptin components in serum of patients with hepatitis C before, during and after interferon alpha and ribavirin therapy and in controls. METHODS: 25 patients (11 female, 14 male) with chronic hepatitis C were compared with body mass index, gender and age-matched controls (n = 25). Patients were treated with interferon alpha alone (3 MU tiw) or in combination with ribavirin for 6-12 months. Free leptin and bound leptin levels were measured using specific radioimmunoassays before interferon therapy, at 12 weeks of therapy and after 3 months of follow-up. RESULTS: Free leptin levels were higher in female than in male subjects, both for patients (P < 0.01) and controls (P < 0.05). Bound leptin levels were elevated in both female (P < 0.05) and male (P < 0.001) patients compared to controls. No alteration of free leptin levels was found during therapy, whereas bound leptin levels decreased after 3 months of therapy (P < 0.005) and re-increased to the baseline levels 3 months after therapy was stopped. Responder but not non-responder had decreased bound leptin levels (P < 0.01) comparing pre- and posttreatment levels. However, no significant correlations were determined between any of the leptin components to virus load, ALT, TNF alpha receptor levels (sTNFR-75, sTNFR-55) and histopathology at any time point. CONCLUSION: Since no correlation was found between the different leptin components and any of the inflammatory markers, the decrease in bound leptin levels during antiviral therapy suggests either a direct interferon-dependent effect on the leptin system or an alteration of other leptin secretagogues.

Adult↗
PubMed2001

Alterations of cognitive functions induced by exogenous application of thyroid hormones in healthy men: a double-blind cross-over study using event-related brain potentials.

The influence of experimentally induced subclinical hyperthyroidism on cognitive functions was tested using exogenous thyroxine or placebo. In a double-blind cross-over design, 24 healthy young men received either 300 microg of levothyroxine or placebo for two consecutive 3-week periods. Determination of thyrotropin (TSH), total triiodothyronine (T3), thyroxine (T4), and sex hormone binding globulin (SHBG) confirmed the induction of subclinical hyperthyroidism. Three weeks after treatment with placebo or T4, subjects were tested in two visual search tasks, one requiring the serial scanning of a stimulus array of eight items in order to detect a missing feature (serial task), while the other task allowed the parallel processing of eight items in order to detect an extra feature. Reaction times varied greatly between the tasks while no effect of T4 medication was revealed on overt search behavior. The late cognitive components of the event-related brain potentials (ERP) were registered during the tasks using a multichannel recording. The late positive component (P300) to target stimuli showed a significant reduction in amplitude in the parallel search task in hyperthyroidism, while for the serial search task a significant frontal negativity was revealed for target stimuli, both suggesting an increased effort to be exerted for the execution of visual search tasks. Thus, short periods of subclinical hyperthyroidism in the range commonly induced in the treatment of thyroid cancer patients induce distinct alterations in brain-electric activity.

Adult↗
PubMed2001

Induction of autoantibodies to the adrenal cortex and pancreatic islet cells by interferon alpha therapy for chronic hepatitis C.

BACKGROUND/AIMS: Interferon alpha (IFN-alpha) therapy for chronic hepatitis C may trigger induction of autoimmunity against several organs. Immune reactions against distinct adrenocortical protein antigens involved in adrenal autoimmune disease have not been reported to date. Therefore, we investigated the development of highly sensitive and specific adrenal autoantibodies in patients with chronic hepatitis C in response to IFN-alpha treatment. In addition, we studied induction of pancreatic islet and thyroid autoantibodies. PATIENTS/METHODS: Sera of 75 patients (42 males, 33 females; mean age 47 (13) years) were analysed before, during, and after IFN-alpha therapy (9-18x10(6) IE/week; mean duration 8.3 (3.5) months). Autoantibodies (Abs) to adrenal 21-hydroxylase (21OH-Abs), and to islet glutamic acid decarboxylase (GAD65-Abs) and protein tyrosine phosphatase (IA2-Abs) were determined by a radiobinding assay using (35)S labelled protein generated by an in vitro translation system. Thyroid antibodies were measured by a commercially available ELISA. RESULTS: Thirteen of 75 patients were initially positive for some of the autoantibodies. During or after IFN-alpha therapy, 3/62 initially negative patients (4.8%) developed 21OH-Abs. GAD65-Abs or IA2-Abs appeared in 5/62 and 1/62 patients, respectively (9.7% in total). In 12/62 patients (19.4%), thyroid specific antibodies appeared. In none of the 21OH-Ab positive subjects was adrenal dysfunction observed, and no patient with islet autoantibodies developed diabetes mellitus or impaired glucose tolerance. CONCLUSIONS: IFN-alpha induces 21OH-Abs in some cases, while islet and thyroid specific autoantibodies are more frequently found. However, our results indicate for the first time that the adrenal cortex also has to be considered as a potential target of IFN-alpha related autoimmunity.

Adrenal Cortex↗
PubMed2001

Identification of a Wnt/beta-catenin signaling pathway in human thyroid cells.

beta-Catenin is a structural component of the adherens junctions. Outside the adherens junctions a complex consisting of glycogen synthase kinase 3beta, the tumor suppressor adenomatous polyposis coli, and axin constantly targets beta-Catenin for degradation to keep levels of free beta-Catenin low. Free beta-Catenin is able to bind to transcription factors of the T cell factor/lymphoid-enhancing factor family and to stimulate transcription of target genes. This signaling function of beta-Catenin is activated by extracellular Wnt factors that bind to Frizzled receptors and induce inhibition of beta-Catenin degradation. By RT-PCR and subcloning, we observed the expression of five Wnt factors, three members of the Frizzled receptor family, and all known Disheveled isoforms in thyroid cells. Immunoprecipitation studies demonstrated the formation of the complex targeting beta-Catenin for degradation. Introduction of a degradation resistant beta-Catenin into the thyroid carcinoma cell line WRO induced appearance of monomeric beta-Catenin as shown by size fractionation and nuclear beta-Catenin immunostaining. Reporter gene assays demonstrated a stimulation of T cell factor/lymphoid-enhancing factor-mediated transcription in these cells. In ARO cells, a thyroid carcinoma cell line carrying a mutated adenomatous polyposis coli gene, monomeric beta-Catenin and nuclear immunostaining were observed. In summary, our data indicate that elements of the Wnt signaling pathway are expressed in thyroid cells and that this pathway is functionally active.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Dyslipemia in familial partial lipodystrophy caused by an R482W mutation in the LMNA gene.

Lipatrophic diabetes, also referred to as familial partial lipodystrophy, is a rare disease that is metabolically characterized by hypertriglyceridemia and insulin resistance. Affected patients typically present with regional loss of body fat and muscular hypertrophic appearance. Variable symptoms may comprise pancreatitis and/or eruptive xanthomas due to severe hypertriglyceridemia, acanthosis nigricans, polycystic ovaria, and carpal tunnel syndrome. Mutations within the LMNA gene on chromosome 1q21.2 were recently reported to result in the phenotype of familial partial lipodystrophy. The genetic trait is autosomal dominant. We identified a family with partial lipodystrophy carrying the R482W (Arg(482)Trp) missense mutation within LMNA. Here we present the lipoprotein characteristics in this family in detail. Clinically, the loss of sc fat and muscular hypertrophy especially of the lower extremities started as early as in childhood. Acanthosis and severe hypertriglyceridemia developed later in life, followed by diabetes. The characterization of the lipoprotein subfractions revealed that affected children present with hyperlipidemia. The presence and severity of hyperlipidemia seem to be influenced by age, apolipoprotein E genotype, and the coexistence of diabetes mellitus. In conclusion, dyslipemia is an early and prominent feature in the presented lipodystrophic family carrying the R482W mutation within LMNA.

Adult↗
PubMed2001

Molecular cloning of a functional promoter of the human plakoglobin gene.

OBJECTIVE: Plakoglobin (Pg) is the only cytoplasmic protein component common to both junctional complexes mediating cell-cell adhesion, adherens junctions and desmosomes. In these complexes Pg appears to act as a linker protein anchoring transmembrane proteins of the cadherin superfamily to the actin cytoskeleton and intermediate filament system respectively. Intercellular adhesion is frequently disturbed in skin diseases and in carcinomas, enabling tumour progression and metastasis. Whereas Pg expression is lost in some thyroid tumours and carcinoma cell lines, little information on Pg gene regulation is currently available owing to a lack of promoter studies. DESIGN AND METHODS: We have cloned and sequenced genomic DNA from a human library that resulted in 979 bp upstream of the published Pg cDNA. The transcriptional start was mapped by rapid amplification of cDNA ends. Methylation-specific PCR of bisulfite-modified cell line DNA was applied to probe the methylation status of a promoter-associated CpG island. Reporter-gene constructs of various promoter fragments were transiently transfected in thyroid carcinoma cell lines and their activities were determined by luciferase measurements. RESULTS AND CONCLUSIONS: A 1 kb DNA fragment harbouring a functional promoter of the human Pg gene was cloned and characterized. The sequence lacks a canonical TATA box, but contains putative CCAAT boxes as well as various putative binding sites for transcription factors, among them SP1 and AP2, proximal to the transcriptional start. Considerable promoter activity was found in thyroid cell lines and deletion analysis indicated that a 300 bp region proximal to the 5'-untranslated region of the mRNA represents the minimal promoter of the human Pg gene. As cells lacking endogenous Pg expression were found to contain methylated CpG dinucleotides in a CpG island located around the transcriptional start site, it is suggested that epigenetic mechanisms such as DNA methylation contribute to dysregulated Pg expression.

5' Flanking Region↗
PubMed2000

Prediction and significance of the temporal pattern of hormone secretion in disease states.

Comparison of the temporal pattern of hormone secretion in health and disease reveals distinct differences in many systems. Analysis of these visually apparent differences conventionally rests on computer-assisted programs based on either model assumptions, or estimations of hormonal decay rates or threshold values, all of which may not accurately reflect physiological and/or pathophysiological states. Only recently have new methods evolved which are independent of preexisting knowledge of the system under study. Apart from the widely used approximate entropy statistic (ApEn), a measure for the regularity of a time-series, artificial neural networks are able to capture temporal structures in endocrine rhythms without any previous assumptions. In particular, non-linear dynamical systems may be delineated and separated from random behaviour. This is achieved by mapping complex input data to a given complex output by propagating data from the input layer to the output layer through a larger number of interconnections, so-called hidden layers. The networks are capable to extract relevant features from training samples and store this information in the distributed structure of interconnections. Using this approach on growth hormone (GH) rhythms of healthy controls, fasted healthy subjects, untreated acromegalic patients and acromegalics under octreotide suppressive therapy we were recently able to demonstrate the power of this approach to differentiate the temporal pattern of GH secretion following normalization of the data for absolute amplitudes. In a second approach we were able to significantly reduce the number of data points required to characterize the temporal structure of these rhythms. This latter quality of the networks may help to transfer analysis of changes in the temporal pattern of hormone secretion on a more routine basis.

Human Growth Hormone↗
PubMed2000

Free and protein bound leptin are distinct and independently controlled factors in energy regulation.

AIMS/HYPOTHESIS: Leptin exerts important regulating effects on energy homeostasis and could have a central role in our understanding of obesity, diabetes mellitus and the metabolic syndrome. Leptin circulates in a free and protein bound form. The aim of the present study was to test whether both fractions of the leptin system can be selectively regulated and thus serve independent physiological roles. METHODS: Using specific radioimmunoassays we measured both leptin components in relation to BMI in healthy subjects before and after weight reduction and in hyperthyroid patients during correction of thyrotoxicosis. In the latter group body composition and resting energy expenditure was monitored. In addition, we measured serum and cerebrospinal fluid concentrations of free and bound leptin in patients with neurological disorders. RESULTS: Under all conditions free leptin concentrations reflected body fat mass. Bound leptin concentrations decreased during weight reduction but also after treatment of hyperthyroidism despite an increase in fat mass. Direct measurement of resting energy expenditure and bound leptin in hyperthyroid patients and under thyrostatic treatment showed a significant positive correlation of both variables. In contrast to free leptin whose transport into the cerebrospinal fluid appears to be saturated at low physiological concentrations of serum free leptin, bound leptin concentrations in the cerebrospinal fluid increased in parallel to serum concentrations over the whole physiologically relevant range. CONCLUSION/INTERPRETATION: Our data indicate a distinct role of free and bound leptin in the feedback regulating energy intake and expenditure and could have important implications for our understanding of the physiology and pathophysiology of leptin-dependent signalling.

Adolescent↗
PubMed2000

Role of the intra-arterial calcium stimulation test in the preoperative localization of insulinomas.

The aim of this study was determination of the significance of the arterial stimulation test with venous sampling (ASVS) in the preoperative localization of insulinoma. Eleven patients with endogenous hyperinsulinism underwent preoperative transabdominal US, spiral computer tomography (spiral CT), MRI, endoscopic ultrasound (EUS) as well as angiography (DSA) combined with ASVS. The results were compared with intraoperative findings, intraoperative ultrasound (IOUS) and histopathology. There were no complications related to the ASVS test. In 11 patients the tumor could be localized with the various modalities as follows: US 1 of 11 (9%), MRI 3 of 10 (30%), spiral CT 4 of 11 (36%), EUS 5 of 10 (50%), DSA 8 of 11 (73%), and ASVS 10 of 11 (91%). In 2 patients the tumors were intraoperatively neither palpable nor detectable by IOUS, and consequently the intraoperative management was governed by information provided by DSA combined with the ASVS test. Ten patients had solitary benign insulinomas and 1 patient with multiple endocrine neoplasia I had two tumors adjacent to each other in the pancreatic tail. Arterial stimulation test with venous sampling was the most sensitive preoperative test for regionalizing the insulinoma in our set of patients. It can be performed safely in the course of a regular DSA examination and may affect intra-operative management in patients in whom the tumors are not detectable by palpation or IOUS.

Adolescent↗