Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess the contributions of glucose load to the working hindlimb and local contraction-related events (changes related to the microvasculature and/or intrinsic muscle metabolic properties) to the exercise-induced increases in muscle glucose uptake and metabolism in vivo, dogs were studied with somatostatin infused to suppress insulin release, and glucose and insulin were replaced 1) during rest and treadmill exercise at rates that recreate limb glucose and insulin loads evident during exercise (n = 5), 2) at rest to selectively normalize the limb glucose load to rates present during exercise while retaining basal limb insulin loads (GL, n = 5), or 3) at rest to normalize both the limb glucose and insulin loads to those present during exercise (IGL, n = 5). Limb arteriovenous difference and isotopic ([U-14C]glucose) techniques were used to quantify muscle glucose uptake and metabolism. Limb glucose load rose from 819 +/- 141 mumol/min in the basal state to 1,568 +/- 190 mumol/min with exercise. Limb glucose loads were 1,423 +/- 88 and 1,502 +/- 165 mumol/min in GL and IGL. The limb insulin load rose from basal rates of 12.9 +/- 2.3 to 22.9 +/- 5.9 nmol/min during exercise. Limb insulin loads were similar to basal loads in GL (8.8 +/- 1.9 nmol/min) and exercise in IGL (28.2 +/- 5.5 nmol/min).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of glucose and insulin loads to the exercising limb in increasing glucose uptake and metabolism. 836 92

Pancreatic ductal adenocarcinomas can display disseminated neuroendocrine (NE) cells. Controversies exist as to their relative incidence, histogenesis, hormone production, and the prognostic implications of their presence. These issues were elucidated by means of a broad immunohistochemical (IHC) investigation of the resected specimens from 47 patients. Chromogranin A (CgA) was chosen as the major NE marker. In addition, the sensitivity of the conventional IHC procedure was increased by means of the TSA (Tyramide Signal Amplification) technique. In tumours with CgA immunoreactive (IR) cells, detected by the conventional or the TSA methods, these NE cells were further IHC analyzed, using antisera raised against a broad spectrum of neurohormonal peptides, serotonin, and IGF-1. The IHC observations were correlated with clinical and histopathological data, the nuclear IR for the Ki67 antigen (proliferation) of the neoplastic cells, and their IR against the p53 protein. Distinct CgA IR cells were found in 5 out of 47 (11%) tumours when studied by the conventional method, and in 9 out of 47 (19%) when examined by the TSA technique. Corresponding figures, if tumours with only questionable IR against CgA were also included, were 14 (30%) and 23 (50%), respectively. Out of the 9 cases with unequivocal CgA IR, only 3 displayed an IR to an additional hormone or growth factor; this hormone turned out to be somatostatin (only minimal foci). Insulin and glucagon cells also appeared exceptionally. The NE differentiation was found to be unrelated to proliferation, p53 protein expression, and to the survival of the patients. It occurred mainly (7 out of 9) in poorly differentiated adenocarcinomas. Thus, the plain NE immunoprofile of the CgA IR cells, together with the increased IR observed when the TSA technique was used, indicates that the NE cells in these adenocarcinomas are only poorly differentiated. When the CgA IR cells exceptionally become highly differentiated, they can express islet hormones. Using strict structural and IHC criteria, a NE differentiation occurs in less than 20 % of cases; its clinico-pathological significance seems to be non relevant.
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PMID:Neuroendocrine cells in pancreatic duct adenocarcinoma: an immunohistochemical study. 1691 33