| 1. |
- Lundquist, Ingmar, et al.
(författare)
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Monoamines in pancreatic islets of guinea pig, hamster, rat, and mouse determined by high performance liquid chromatography
- 1989
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Ingår i: Pancreas. - 0885-3177. ; 4:6, s. 662-667
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Tidskriftsartikel (refereegranskat)abstract
- Previous studies on the occurrence of catecholamines and serotonin in pancreatic islets using various histochemical and chemical methods have given widely different results. We therefore performed a comparative analysis of these amines in whole pancreas and islet tissue from hamster, guinea pig, rat, and mouse by the use of high performance liquid chromatography. Whole pancreas of guinea pig, hamster, and rat had a norepinephrine concentration of approximately 1.1 [mu]mol/kg of pancreatic wet weight. The mouse pancreas had less than one-half of that concentration. Epinephrine and dopamine concentrations were on the order of 0.02 [mu]mol/kg of pancreatic wet weight in all four species. The serotonin concentration was 2.1 [mu]mol/kg of pancreatic wet weight in the guinea pig pancreas and approximately 0.2 [mu]mol/kg in the other three species studied. The catecholamine concentrations were much higher in the pancreatic islets than in the exocrine pancreas. Thus, the norepinephrine concentration was approximately 35 [mu]mol/kg of islet wet weight in hamster islets and 5-10 [mu]mol/kg in rat, guinea pig, and mouse islets. The epinephrine concentration in islet tissue ranged between 1 and 7 [mu]mol/kg of islet wet weight and the dopamine concentration between 0.5 and 4 [mu]mol/kg except for guinea pig islets (12 [mu]mol/kg). The islet tissue in the mouse, rat, and guinea pig contained disproportionately more epinephrine and dopamine relative to norepinephrine than did the exocrine pancreas. Chemical sympathectomy (6- hydroxydopamine treatment) in the mouse reduced the norepinephrine and epinephrine concentrations in islet tissue to nondetectable levels, whereas the dopamine concentration was essentially unchanged, thus suggesting an extraneuronal source of this amine in addition to its occurrence in adrenergic nerves. The islets of hamster, rat, and mouse contained no serotonin, whereas guinea pig islets contained approximately 275 [mu]mol/kg of islet wet weight. We conclude that, although species differences exist, the pancreatic islets have markedly higher levels of catecholamines than the exocrine pancreas, and that serotonin occurs in the exocrine pancreas of all four species studied but in the endocrine pancreas only in the guinea pig.
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| 2. |
- Xu, Ning, et al.
(författare)
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Down-regulation of apolipoprotein M expression is mediated by phosphatidylinositol 3-kinase in HepG2 cells.
- 2006
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Ingår i: Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids. - : Elsevier BV. - 1388-1981. ; 1761:2, s. 256-260
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Tidskriftsartikel (refereegranskat)abstract
- Apolipoprotein M (apoM) is a novel apolipoprotein present mostly in high-density lipoprotein (HDL) in human plasma. In the present study, we demonstrate that insulin, insulin-like growth factor I (IGF-I), and IGF-I potential peptide (IGF-IPP) significantly inhibits apoM expression, in a dose- and a time-dependent manner, in the human hepatoma cell line, HepG2 cells. Insulin-induced down-regulation of apoM was blocked by AG1024 (a specific insulin receptor inhibitor) and LY294002 (a phosphatidylinositol 3-kinase (PI3K) inhibitor), which indicates that it is mediated via the activation of PI3K pathway. In contrast, PD98059 (a MAP kinase inhibitor) did not influence insulin-induced down-regulation of apoM expression, and activation of neither PPAR-alpha agonist (GW7647) nor PPAR-gamma agonist (GW1929) influences apoM expression in HepG2 cells, which indicates that regulation of apoM expression is not related to the activation of PPAR-alpha and PPAR-gamma in hepatic cells, whereas, both PPAR-Of and PPAR-gamma agonists could inhibit apoB expression. Moreover, in the present study, we demonstrated that PPAR beta/delta agonist (GW501516) could inhibit both apoM and apoB expression in the HepG2 cells. In conclusion, this study shows that apoM expression is regulated by PI3-kinase in HepG2-cells. (c) 2006 Elsevier B.V. All rights reserved.
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| 3. |
- Bromander, Sara, et al.
(författare)
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Cerebrospinal fluid insulin during non-neurological surgery.
- 2010
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Ingår i: J Neural Transm (Vienna, Austria:1996). - : Springer Science and Business Media LLC. - 1435-1463 .- 0300-9564. ; 20, s. 328-329
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Tidskriftsartikel (refereegranskat)abstract
- Insulin plays an important metabolic and transmitter role in the central nervous system, but few studies have investigated the relationship between central and peripheral insulin concentrations. 35 patients undergoing knee surgery had cerebrospinal fluid (CSF) samples drawn before, 3 h after, and in the morning following surgery. Serum insulin concentrations increased after surgery and CSF insulin concentrations changed in the same direction with far smaller amplitude. These results indicate that the blood-brain barrier protects the brain from stress-induced peripheral hormonal fluctuations.
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| 4. |
- Evilevitch, L., et al.
(författare)
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Three-Day Enteral Exposure to a Red Kidney Bean Lectin Preparation Enhances the Pancreatic Response to CCK Stimulation in Suckling Pigs.
- 2005
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Ingår i: Biology of the Neonate. - : S. Karger AG. - 1421-9727. ; 87:1, s. 20-25
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Tidskriftsartikel (refereegranskat)abstract
- Background: A reason for the digestive problems that often occur around early weaning in piglets could be that the pancreas is not yet fully developed and the enzymes required for degradation of the solid food are not secreted in enough amounts. Objectives: The aim of the study was to investigate the possibility of inducing pancreas maturation with enhanced enzyme secretion. Methods: 10-day-old suckling pigs were gavage fed with a red kidney bean lectin preparation for 3 days, and the pancreatic response to intravenous infusion of CCK-33 was measured in the anaesthetized animals fitted with pancreatic duct catheters. Results: The pancreatic fluid secretion, protein output, and the trypsin and amylase outputs were significantly increased in response to CCK stimulation after the lectin treatment, as compared to those of the control littermates (p le 0.05). In addition, the plasma insulin basal levels and those observed during CCK-33 stimulation were lower in the lectin-treated piglets. Conclusion: The results suggested that the lectin treatment led to an increase in the capacity for pancreatic enzyme secretion in the suckling piglets. An enhanced pancreatic function might help to ameliorate the problems that may appear in modern pig production which are associated with weaning.
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| 5. |
- Karlsson, Sven, et al.
(författare)
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Beta cell adaptation to dexamethasone-induced insulin resistance in rats involves increased glucose responsiveness but not glucose effectiveness
- 2001
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Ingår i: Pancreas. - 0885-3177. ; 22:2, s. 148-156
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Tidskriftsartikel (refereegranskat)abstract
- Islet beta cell adaptation to dexamethasone-induced insulin resistance was characterized with respect to glucose-stimulated insulin secretion and islet innervation. Male Sprague-Dawley rats were injected daily with dexamethasone (2 mg/kg for 12 days), which resulted in hyperinsulinemia and hyperglycemia compared with controls (which were injected with sodium chloride). Insulin secretion was characterized in collagenase-isolated islets. Islet innervation was examined by immunocytochemical analysis of tyrosine hydroxylase, neuropeptide Y (sympathetic nerves), and vasoactive intestinal polypeptide (cholinergic nerves). In islets isolated from the insulin-resistant animals, the insulin response to 3.3 or 8.3 mM glucose was three times greater during perifusion compared with controls (p < 0.001). Incubation of islets at 0 to 20 mM glucose revealed a marked leftward shift of the glucose dose-response relation after dexamethasone treatment (potency ratio, 1.78; p < 0.01), with no difference at 0 or 20 mM glucose. Thus, the potency but not the efficacy of glucose was increased. The number of islet nerves did not differ between dexamethasone-treated rats and controls. Dexamethasone-induced insulin resistance leads to adaptively increased glucose responsiveness of the islet beta cells, with increased potency, but not increased efficacy, of glucose to stimulate insulin secretion without any evidence of altered islet innervation.
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| 6. |
- Kvist Reimer, Martina, et al.
(författare)
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Local growth factors are beneficial for the autonomic reinnervation of transplanted islets in rats
- 2003
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Ingår i: Pancreas. - 0885-3177. ; 26:4, s. 392-397
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Transplanted islets, being avascular and denervated, receive blood vessels and nerves from the recipient. Reinnervation may account in part for the normalization of islet function in islet transplants. Whether reinnervation is possible to augment is not known. Aims and Methodology: To explore whether reinnervation of transplanted islets is augmented by local addition of growth factors to the graft, syngeneic islets were transplanted to the pancreas of streptozotocin-diabetic Lewis rats with or without pellets locally releasing nerve growth factor (NGF) and vascular endothelial growth factor (VEGF), alone or in combination. The pellets released growth factors for 14 days at a rate of 20 ng/day. After 7 weeks, pancreatic tissue was processed for immunofluorescence of insulin and the neural markers neuropeptide Y (NPY) and tyrosine hydroxylase (TH). Results: Islets were larger and more numerous after treatment with NGF (p = 0.024) and with NGF in combination with VEGF (p = 0.044). Similarly, immunostaining for TH and the C-terminal flanking peptide of NPY (C-PON) was more pronounced after treatment with NGF in combination with VEGF than in controls (both p < 0.05). Conclusion: Local growth factor treatment has a beneficial effect on autonomic reinnervation as well as islet integrity and survival of the graft after islet transplantation in rats.
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| 7. |
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