Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glucocorticoid regulation of peptide hormone gene expression was studied in two cell lines derived from rodent islet cell tumors. In rat RIN1056A cells, dexamethasone reduced the levels of glucagon mRNA transcripts while markedly inducing the expression of the angiotensinogen gene. In contrast, dexamethasone had no effect on the regulation of glucagon gene expression in hamster InR1-G9 cells. Wild type InR1-G9 cells did not support the induction of the murine mammary tumor virus promoter by glucocorticoids, suggesting that these cells lacked the necessary cellular factor(s) for glucocorticoid responsiveness. Introduction of the glucocorticoid receptor into wild type InR1-G9 cells restored glucocorticoid induction of the murine mammary tumor virus promoter, but not glucocorticoid regulation of glucagon gene expression. Dexamethasone treatment of Sprague-Dawley rats had no effect on the levels of pancreatic glucagon mRNA transcripts. The results of these studies demonstrate that glucocorticoid regulation of glucagon gene expression is restricted to the immortalized RIN1056A cell line, providing additional evidence for cell-specific diversity in the regulation of peptide hormone gene expression in neuroendocrine tumors.
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PMID:Differential glucocorticoid regulation of glucagon gene expression in cell lines derived from rat and hamster islet cell tumors. 170 69

The blood glucose level and serum levels of insulin, glucagon, and free fatty acids were examined in 7- to 8-mo-old female SHN mice with or without spontaneous mammary tumors (MT). Blood glucose levels in the females with MT were significantly higher than in those without MT, rising in proportion to the increase in size of MT up to 30 mm in diameter. In 4-mo-old male SHN and 11-mo-old female C57BL mice bearing mammary tumor grafts (MTg), the blood glucose level was significantly higher than in mice without MTg. Serum insulin and free fatty acids in female SHN mice with MT rose to higher levels than in mice without MT, whereas serum glucagon levels were unaltered. In 50% of mice with MT, pancreatic islets contained a large number of pyknotic cells. Livers of mice with MT or MTg were significantly heavier than those of mice without MT or MTg. In both female SHN mice with spontaneous MT and male SHN and female C57BL mice with MTg, the total number of hepatocytes and the total amount of liver DNA increased significantly compared with values from corresponding controls without MT or MTg. These findings suggest that MT or MTg induce a hyperglycemic state and an enhanced production of free fatty acids and insulin, which may in turn stimulate the growth of mammary tumors and the liver.
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PMID:Correlation between mammary tumor and blood glucose, serum insulin, and free fatty acids in mice. 264 64

The effects of tumor growth on lipid metabolism were investigated by evaluating serum lipids, lipoprotein lipase activity (LPLA), the lipogenic enzymes, urinary catecholamines along with serum insulin and glucagon levels. We injected 1.5 X 10(6) cells of rat mammary tumor, AC33, and killed the rats on the 18th day. Serum triglycerides and free fatty acids of the tumor-bearing (TB) rats increased 4 and 5 times, respectively, more than the control (C) rats. Total liver lipids were not significantly different between the two groups. Tumor growth produced a 70% decrease in total epididymal fat pad LPLA; there were no changes in soleus muscle LPLA. Serum insulin levels of the TB rats were 49% less than the C rats. The TB rats had significantly lighter epididymal fat pads and lower activities of adipose fatty acid synthetase and citrate cleavage enzyme. Urinary catecholamines of the TB rats were reduced over 30% compared with the C rats. These results show that the hypertriglyceridemia of the TB rats may be due, in part, to a deficiency of adipose tissue LPLA. The data also suggest that the effects of the tumor on lipid metabolism may be mediated through insulin.
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PMID:Changes in the activities of lipoprotein lipase and the lipogenic enzymes in tumor-bearing rats. 698 80

Hepatic metabolism and gene expression are among other regulatory mechanisms controlled by the cellular hydration state, which changes rapidly in response to anisotonicity, concentrative substrate uptake, oxidative stress, and under the influence of hormones such as insulin and glucagon. Differential screening for cell volume sensitive transcripts in a human hepatoma cell line revealed a gene for a putative serine/threonine kinase, h-sgk, which has 98% sequence identity to a serum- and glucocorticoid regulated kinase, sgk, cloned from a rat mammary tumor cell line. h-sgk transcript levels were strongly altered during anisotonic and isotonic cell volume changes. Within 30 min h-sgk RNA was, independent of de novo protein synthesis, induced upon cell shrinkage and, due to a complete stop in h-sgk transcription, reduced upon cell swelling. Comparable changes of sgk transcript levels were observed in a renal epithelial cell line. h-sgk mRNA was detected in all human tissues tested, with the highest levels in pancreas, liver, and heart. The putative serine/threonine protein kinase h-sgk may provide a functional link between the cellular hydration state and metabolic control.
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PMID:Cloning and characterization of a putative human serine/threonine protein kinase transcriptionally modified during anisotonic and isotonic alterations of cell volume. 911 8