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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glucose stimulates somatostatin release from perifused pancreatic islets of diabetic rats 42-47 days after the induction of diabetes, and 48 h after withdrawal of insulin replacement therapy. The glucose effect is augmented by theophylline or glucagon. Basal somatostatin release and glucose-induced secretion are significantly higher in diabetic islets than in controls. It is suggested that glucose promotes somatostatin release by directly interacting with islet D cells but not via indirect pathways. Glucose-induced stimulation appears to be modulated by a D-cell adenylate cyclase/phosphodiesterase system. Reasons responsible for increased somatostatin secretion by diabetic islets include reduction in B-cell mass, suggesting that B cells may normally suppress the secretory activity of D cells.
Mol Cell Endocrinol 1980 Dec
PMID:Increased somatostatin secretion from pancreatic islets of streptozotocin-diabetic rats in response to glucose. 611 May 94

1. The response of tyrosine aminotransferase activity in isolated liver cells has been studied under several conditions. 2. Activity is increased over a 5 h period by both glucagon and glucocorticoids in cells from adrenalectomized rats. The results do not support the view that glucagon action is dependent on preexposure of cells to steroid. 3. In cells from fed animals, significant stimulation is seen only when both glucagon and steroid are present together. 4. In cells from 48 h fasted rats steroid is effective, but glucagon is not significant so. 5. These anomalies are attributed to the differences in hormonal and nutritional status between the animals from which the cells are isolated.
Mol Cell Biochem 1981 Jan 20
PMID:Factors affecting induction of tyrosine aminotransferase in isolated rat liver cells. 611 64

Rat parenchymal hepatocytes isolated with collagenase were cultured as monolayers in Williams medium E supplemented with calf serum. Freshly isolated cells showed very low activities of various liver functions, and they had to be cultured for 6-24 h to allow recovery of these functions. Insulin and dexamethasone greatly increased cell viability in primary. After culture for 24 h, these cells showed various liver functions as seen in vivo and responded well to various added hormones and amino acids. The concentrations of amino acids in the medium regulated synthesis of serum proteins and insulin stimulated lipogenesis, which in turn regulated synthesis of lipoproteins. Insulin also stimulated glycogen synthesis and the stimulation was parallel with the number of insulin receptors. Glucagon stimulated glycogenolysis and its stimulation involved the function of the cytoskeleton. Glucagon and dexamethasone induced various enzymes of amino acid catabolism, such as tryptophan oxygenase, tyrosine aminotransferase and serine dehydratase. These inductions were inhibited by insulin or catecholamine. The effect of catecholamine was due to its alpha-adrenergic action. The beta-action of isoproterenol was low in freshly isolated cells, but increased during culture of the cells. Acquirement of hormonal responses during neonatal development can be studied in this culture system. Mature hepatocytes in culture are usually quiescent, but when insulin and epidermal growth factor were added, DNA synthesis by the cells increased markedly and they showed density-dependent growth. In this culture system, serum could be omitted for 2 days when the dishes were coated with fibronectin without appreciable change of functions, but serum was needed for longer culture of the cells. A factor that increased cell survival was found in serum and in pituitary gland. These results show that hepatocytes in primary culture are a simple and useful system for studies of liver functions in vitro and related works were also reviewed.
Mol Cell Biochem 1982 Apr 02
PMID:Use of hepatocytes in primary culture for biochemical studies on liver functions. 612 41

This study was performed to determine whether the enhanced hepatic autophagocytosis occurring in diabetes mellitus could be reversed by pancreatic transplantation despite the persistence of hyperglucagonemia in transplant recipients. Twenty weeks after pancreatic transplantation, hepatic lysosomes and autophagic vacuoles were quantitated morphometrically in untreated streptozotocin-diabetic rats and in streptozotocin-diabetic rats treated by pancreatic transplantation. Hyperglycemia and hypoinsulinemia in untreated diabetic rats were corrected after pancreatic transplantation. However, the peripheral plasma glucagon concentration remained significantly higher in transplant recipients than in non-diabetic controls. Light microscopic morphometry revealed no significant effect of the diabetic state or its reversal on the volume of the single hepatocyte or the volume density and numerical density of hepatocytes. However, electron microscopic examination showed that the number and volume density of lysosomes and autophagic vacuoles, which were significantly increased in diabetic rats, returned to control values after pancreatic transplantation. It is concluded that chronic hyperglucagonemia does not preserve enhanced hepatic autophagocytosis when the diabetic hypoinsulinemia is corrected by the pancreatic transplant.
Virchows Arch B Cell Pathol Incl Mol Pathol 1983
PMID:Normalization of hepatic lysosomal autophagy in streptozotocin diabetic rats after pancreatic transplantation. 613 7

Current studies on the synthesis of long-chain fatty acids by isolated rat liver cells are largely concerned with the regulation of the activity of previously existing acetyl-CoA carboxylase and fatty acid synthetase, and with the regulation of the quantity of these enzymes. These studies have required the development of methods for obtaining high yields of viable hepatocytes that respond to hormonal treatment. Such methods have been developed over the past 10-15 years through the efforts of several laboratories. These studies have also required the development of a method to determine whether a change in the activity of an enzyme is due to a modification of preexisting enzyme or to a change in quantity of that enzyme. The most satisfactory method to use for such studies is immunotitration of enzyme activity. In recent years studies on the regulation of acetyl-CoA carboxylase have largely centered upon the effect of phosphorylation-dephosphorylation on the activity of this enzyme and whether glucagon inhibits the activity of this enzyme through this process. Much data from a number of laboratories have suggested that glucagon regulates the activity of this enzyme through phosphorylation-dephosphorylation. However, several of these studies involved the use of crude systems in which competing enzymes and substrates that can significantly interfere with acetyl-CoA carboxylase activity measurements were still present. Hence, a confirmation of these studies needs to be carried out under conditions in which the effects of competing enzymes and substrates are eliminated. Studies on changes in quantity of acetyl-CoA carboxylase and fatty acid synthetase have shown that these enzymes are induced by the fasting and refeeding of animals. They have also shown that insulin stimulates (10- to 30-fold) the induction of these enzymes. This induction appears to be due to a change in the quantity of translatable mRNA which may, in turn, be due to a change in the rate of transcription of the genes coding for these enzymes.
Mol Cell Biochem 1983
PMID:Induction of fatty acid synthetase and acetyl-CoA carboxylase by isolated rat liver cells. 613 62

Antibodies against human prealbumin (HPA) give a strong immunoperoxidase staining of the A (glucagon) pancreatic cells and of glucagon-, insulin- and gastrin-producing pancreatic tumours. The majority of intestinal and bronchial carcinoids are also reactive. The staining may be related to presence in the C-terminal sequence of HPA of determinants in common with polypeptide (pro-) hormones.
Virchows Arch B Cell Pathol Incl Mol Pathol 1984
PMID:Binding of antibodies against human prealbumin to intestinal and bronchial carcinoids and to pancreatic endocrine tumours. 614 57

Pancreatic islet cell hyperplasia was studied in hamsters during one to eight weeks of cortisone treatment. Measurement of serum glucose and insulin; pancreatic insulin, glucagon, somatostatin, pancreatic polypeptide as well as islet tissue morphometry were performed. Serum glucose was highest at week 2, followed by mild to moderate hyperglycemia. Serum insulin was increasingly higher from week 1 to week 8. Pancreatic insulin was maximal at week 5 then declined through week 8 in the presence of beta cell neurosis in markedly hyperplastic islets. Pancreatic concentration of somatostatin and pancreatic polypeptide moderately increased more than the control levels; however, compared with the controls, glucagon was reduced by cortisone treatment. Effect of cortisone in the four types of islet cells is discussed, particularly on beta cell hyperplasia, which appears to be a response to decreased insulin binding to the target organs with no changes in receptor concentration.
Virchows Arch B Cell Pathol Incl Mol Pathol 1984
PMID:Cortisone-induced islet cell hyperplasia in hamsters. 614 61

Unique alpha-cell crystals, a herpes-like virus, islet amyloidosis, and immunohistochemical reactions of islets are compared in the rodent, Octodon degus, in animals with ordinary and high circulating glucose levels. Results suggest that crystals, virus, and amyloid are independent of blood sugar and bear no obvious relation to one another, although each is more common in older than in young animals. The crystals do not react with anti-glucagon. In the presence of high blood glucose, qualitative histochemical studies demonstrated diminished islet insulin and an unusual reaction with anti-somatostatin: (1) paucity of the usual cells that stain darkly for somatostatin and (2) striking staining of intermediate hue in most islet cells and in (3) multitudes of cell nests in exocrine parenchyma. The intermediate staining reaction may represent a visible demonstration of the paracrine phenomenon.
Exp Mol Pathol 1984 Jun
PMID:The pancreas in the degu. 614 70

Cyclosporine (CyA), formerly cyclosporin A, significantly inhibited the ability of prolactin (PRL) to elevate ornithine decarboxylase (ODC) activity in a variety of rat tissues. Administration of PRL to hypophysectomized rats also resulted in an induction of ODC activity which was inhibited markedly in all tissues studied in the presence of CyA. Transglutaminase ( TGase ) activity was not affected in any significant manner by PRL or CyA in most tissues studied. However, it was elevated in the adrenal by 10(-8) M PRL. Bromocryptine, which selectively antagonizes pituitary PRL release, decreased the kidney ODC basal levels to 30% of vehicle control and serum PRL level to 4.3 +/- 1.4 compared to 28 +/- 10 in controls, suggestive of PRL maintenance of steady-state ODC activity in the kidney. CyA administration did not affect the action of glucagon, a known cyclic AMP-mediated hormone, or 8-bromo-cyclic AMP on kidney ODC activity. The elevation of rat kidney ODC activity by dexamethasone and triiodothyronine (T3), compounds which elevated serum prolactin levels in all cases, was also blocked by administration of CyA. Epidermal growth factor (EGF), which did not induce rat kidney ODC activity by itself, was capable of producing a small increment in ODC activity in the presence of CyA. The marked effect of CyA to selectively block ODC induction by PRL may be due to the ability of CyA to interact with receptor-required phospholipids in membranes and thus to antagonize hormone-receptor interaction.
Mol Cell Endocrinol 1984 May
PMID:Cyclosporine inhibits prolactin induction of ornithine decarboxylase in rat tissues. 614 46

A microradioimmunoassay for cAMP was developed in order to analyse the effects of alpha-adrenergic agonists on vasopressin (AVP)-induced cAMP cell accumulation in single pieces of microdissected medullary (MCT) and cortical (CCT) rat collecting tubules. Under the experimental conditions chosen (4 min of incubation in the presence of a phosphodiesterase inhibitor), no cAMP could be detected either in the bathing solution or in non-stimulating samples of tubule. In MCT, 10(-6) M AVP stimulated cAMP generation up to 128.3 +/- 9.0 (SEM) fmoles per mm of tubule per 4 min, N = 11. The response was dose-dependent with a KA value below 10(-10) M AVP. The addition of norepinephrine (NE) (10(-5) M in the presence of propranolol) suppressed the larger part of the response to AVP (from 92% with 2 X 10(-11) M AVP to 76% with 10(-6) M AVP); the addition of 10(-7) M NE still reduced by 59% the MCT response to 10(-10) M AVP (26.2 +/- 5.9 vs. 64.0 +/- 6.4 fmoles/mm, N = 3). In CCT, 10(-5) M NE reduced by 84% the cAMP generation induced by 10(-10) M AVP (8.8 +/- 2.0 vs. 54.2 +/- 3.5 fmoles/mm, N = 3). This inhibitory action of NE against the AVP effect in CCT was mimicked by 10(-7) M clonidine; in MCT it was suppressed by phentolamine and yohimbine, but not by prazosin, suggesting that alpha 2-adrenoreceptors are involved. On the other hand, the addition of the alpha-agonists to the incubation solution produced no inhibition of the cAMP cell accumulations induced by glucagon, calcitonin and isoproterenol in CCT, or glucagon in MCT, an observation demonstrating that alpha 2-adrenergic agonists selectively inhibit vasopressin-dependent cAMP generation by these nephron segments.
Mol Cell Endocrinol 1984 Oct
PMID:Inhibition of alpha 2-adrenergic agonists on AVP-induced cAMP accumulation in isolated collecting tubule of the rat kidney. 614 67


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