PubMed · 6298612
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R R Fink. 1983-01-28. [Hypoglycemia].. https://pubmed.ncbi.nlm.nih.gov/6298612/
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EAT/mcl-1 (EAT), a bcl-2 related anti-apoptotic gene, is up-regulated at the early stage of differentiation of human embryonal carcinoma cells; cells which serve as a model for early embryogenesis. We generated transgenic mice for the human EAT gene driven by the EF1 alpha promoter in order to elucidate its functional role in vivo. Histologically, these mice exhibited hyperplasia of Langerhans islet cells; pancreatic cell regions composed of both insulin- and glucagon-producing cells. Furthermore, Bax and Bag-1 -- possible heterodimeric partners for EAT in the anti-apoptotic process -- were up-regulated in islets isolated from the EAT transgenic mice. The insulin tolerance test exhibited no significant difference between the EAT transgenic mice and non-transgenic mice, indicating that islet cell hyperplasia was not due to insulin resistance. In conclusion, EAT transgenic mice exhibit hyperplasia of pancreatic beta cells. EAT may inhibit apoptosis of beta cells, allowing these cells to circumvent the process of apoptosis until the adult stage.
OBJECTIVE: To compare the value of the various imaging modalities in the detection of pancreatic islet cell tumors. METHODS: Analysis of the literature to compare the value of ultrasound, CT, MRI, angiography, venous sampling, scintigraphy and PET in the detection of neuroendocrine tumors of the pancreas. RESULTS: For transabdominal ultrasound a sensitivity of 60% has been reported; for endoscopic ultrasound a sensitivity of more than 90%. MRI with a sensitivity of 75-100% is more sensitive compared to CT with a sensitivity of 64-82%. Angiography and venous sampling have a reported sensitivity of 66% and 76%. Somatostatin receptor scintigraphy has a sensitivity of 81-88% with significant differences between the various histological subtypes of the pancreatic islet cell tumors. PET does not play an important role in the detection of neuroendocrine tumors of the pancreas. CONCLUSION: None of the various modalities is superior alone, so that it is often necessary to combine them for diagnostic imaging of pancreatic islet cell tumors.
The work-up of fasting hypoglycemia may be difficult but is crucially important because a wrong diagnosis can lead to either unnecessary pancreatectomy or a missed pancreatic tumor. We describe a patient with severe fasting hypoglycemia [22-32 mg/dl (1.2-1.8 mmol/liter) after 6-10 h of fasting] in which the diagnosis of a secretory islet-cell tumor was obscured, rather than facilitated, by use of a new, highly specific serum insulin assay. Insulin measured by the specific assay suppressed normally during fasting hypoglycemia [undetectable at < 2.0-3.8 micro IU/ml (26.4 pmol/liter)], whereas insulin measured by older, less specific assays was diagnostically elevated [34, 73 micro IU/ml (236.1, 507.0 pmol/liter)]. Serum proinsulin and C-peptide levels were abnormal, and further work-up revealed an islet-cell tumor that secreted predominantly proinsulin. The tumor was surgically removed, relieving the fasting hypoglycemia. We conclude that insulin levels as measured by new, highly specific insulin assays may obscure the diagnosis of a functional, proinsulin-secreting islet-cell tumor. Because proinsulin cross-reacts with insulin in older insulin assays, C-peptide or proinsulin should be measured to rule out a proinsulin-secreting islet-cell tumor. Normative values for new insulin assays must be established during prolonged fasting.