Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolated islets of Langerhans were obtained from sexually immature rats by means of collagenase. Interperitoneal isotransplantation of the islets to rats with alloxan diabetes caused an improvement of their condition, normoglycemia, and elevation of the immunoreactive insulin level, and prolonged survival of these rats, in the presence of coarse morphological changes in the endocrine part of the pancreas of the recipient (in 2--4 weeks). It is suggested that the insular cells of the islets of Langerhans isolated from the immature rats were viable.
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PMID:[Isolation of the islands of Langerhans and their transplantation under experimental conditions]. 9 54

Gingiva from alloxan and streptozotocin-diabetic rats exhibited markedly enhanced collagenolytic activity in tissue culture. This effect was eliminated by puromycin or by repeated freeze-thawing of the tissue prior to incubation. Soluble extracts of the diabetic gingiva in situ were found to contain breakdown products of collagen similar in size to the reaction products generated by tissue collagenase. These fragments were not detected in the control tissue. This study indicates that experimental diabetes stimulates the synthesis of gingival collagenase in culture and that a similar effect occurs in vivo.
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PMID:Enhanced collagenase activity in diabetic rat gingiva: in vitro and in vivo evidence. 21 Feb

In the present work, homogeneous isolated pancreatic islet-cells were transplanted to diabetic rats with the aim of verifying if the transplanted tissue could survive and reduce the plasma glucose concentration on the alloxan-induced diabetic receptors. For the isolation of the pancreatic islets, pancreas was incubated in collagenase solution for about 13 +/- 3 minutes, followed by centrifugation in Ficoll gradients. The islets, 3 000 to 5 000, were transplanted to alloxan diabetic recipients, in a territory, preferentially with portal-hepatic drainage (mesentery and spleen). Sixty per cent of the recipients exhibited a fall of the plasma glucose concentration, up to 70%, while in the control animals, the diabetes persisted. The islets were found in the recipients mesentery up to 10 days after transplantation, and all of them showed heavily granulated (aldehyde fuchsin positive) beta cells. After this time, islets were not found. These results indicate that islets can survive and attenuate diabetes in alloxan-treated rats, and that, probably, the number of islets transplanted as well as the receiving areas play an important role.
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PMID:Transplantation of islets of Langerhans in diabetic rats. 35 20

Pancreases from neonatal rats four to 16 days postpartum were grown in organ culture for from two to nine days. Approximately 10-20 explants, each measuring 1 mm.3 (1 mg.), were grown on a single Millipore filter placed at the gas-liquid interface of a medium consisting of 50 per cent horse serum and 50 per cent chick embryo extract. Following organ culture, an estimated 9-20 mg. of cultured islet tissue were dissociated with collagenase and isotransplanted into the peritoneal cavity of alloxan-diabetic recipients. In seven of eight recipients the diabetes was reversed between 11 and 53 days of posttransplantation. Animals receiving 12-16 mg. of cultured islet attained normoglycemia in 11-20 days; animals receiving 9-10 mg. of cultured islet tissue recovered between 45 and 53 days. These animals have remained symptom-free for over six months. Biopsies of grafts taken from the peritoneal cavity following reversal of diabetes contained well-vascularized islets compared primarily of heavily granulated beta cells. Quantitative analysis of host pancreases by the linear scanning method (biopsied at one to two weeks and four to five months following reversal of the diabetes) demonstrated that the total beta-cell mass was 3 per cent and the total insulin content was 6 per cent of the normal values. Little or no evidence of regeneration of host beta cells was observed. These studies show that a period of organ culture prior to isotransplantation does not impair the ability of islet tissue to reverse alloxan diabetes in the rat.
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PMID:Isotransplantation of organ-cultured neonatal pancreas: reversal of alloxan diabetes in the rat. 76 84

The in vitro inhibition of insulin released by alloxan (20 mg/100 ml) in collagenase isolated rat islets is preferentially prevented by alpha D-glucose at a concentration of 1.0 mg/ml, while at a higher anomer concentration (1.5 mg/ml) both alpha and beta D-glucose provide equal protection. The ability of alpha D-glucose compared with beta D-glucose to stimulate insulin release, in vitro, showed a similar dose-related response, as observed in the alloxan protective studies. Although, both alpha and beta D-glucose compete with mutorated D-glucose for transport into islet cells, neither anomer produced a significantly different degree of inhibition in the transport process. The shared alpha stereospecificity for D-glucose in protection against alloxan and in stimulating insulin secretion in these in vitro studies, suggest a common site of interaction which may involve the beta-cell membrane.
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PMID:Effect of anomers of D-glucose on alloxan inhibition of insulin release in isolated perifused pancreatic islets. 78 55

The in vitro effect of alloxan exposure on the permeability of collagenase isolated rat pancreatic islets to sucrose, D-mannitol, and L-glucose has been investigated. Determination of changes in cell volume with a non-wash double label isotope procedure indicates that alloxan treatment exerts no measurable effect on permeability to sucrose, D-mannitol, or L-glucose as compared to nonalloxan-treated islets. In addition, neither prior exposure nor the concomitant presence of alloxan alters the rate of D-glucose or 3-0-methyl-D-glucose transport into rat pancreatic islets. It is concluded that the in vitro effect of alloxan on abolishing glucose-induced insulin release in isolated rat pancreatic islets does not appear to be the result of permeability changes to small organic molecules or alteration in the transport of D-glucose into the beta-cell.
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PMID:Effect of alloxan on permeability and hexose transport in rat pancreatic islets. 109 63

Hepatocytes were isolated by collagenase in vitro perfusion technique. Net glucose production in isolated hepatocytes obtained from fed, fasted and alloxan diabetic rats was studied. Net glucose production from alanine, pyruvate and fructose was increased by 2-5 fold in isolated hepatocytes obtained from fasted and alloxan diabetic rats. Similar increases in the incorporation of 14C-bicarbonate into glucose was also observed. Net glucose production in isolated hepatocytes was also compared to other in vitro preparations. Net glucose production was much higher (2-5 fold) in isolated hepatocytes than that reported previously for liver slices or perfused liver. Studies on glycogen and protein synthesis show a 2 fold stimulation in the incorporation of 1-14C-glucoase into glycogen and U-14C-leucine into protein by the addition of 100 muU of insulin to isolated hepatocytes.
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PMID:Studies on gluconeogenesis and stimulation of glycogen and protein synthesis in isolated hepatocytes in alloxan diabetic, normal fed and fasted animals. 122 3

The apparent toxicity of alloxan was compared in nondiabetic rats and rats made diabetic by injection with streptozotocin during neonatal life (STZ). In the perfused pancreas of nondiabetic rats, 1 mM alloxan rapidly but evanescently stimulated insulin secretion; this effect was followed by pronounced inhibition of the insulin response to 27 mM glucose (94% inhibition) or 1 mM 3-isobutyl-1-methylxanthine (76% inhibition). Conversely, in STZ-diabetic rats the stimulatory effect of alloxan was reduced to 22% of that elicited in nondiabetic rats. In further contrast, the inhibitory effect of alloxan exposure was abolished with regard to subsequent glucose-induced insulin secretion and attenuated with regard to 3-isobutyl-1-methylxanthine-induced insulin secretion. A relative insensitivity to alloxan was also seen in collagenase-isolated islets, where alloxan completely abolished glucose-induced insulin secretion in islets from nondiabetic rats, but only nonsignificantly reduced secretion (by 37%) in islets from STZ-diabetic rats. Insensitivity to glucose in STZ diabetic rats is associated with insensitivity to alloxan. This implies a common defect in the initial recognition site of glucose and alloxan.
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PMID:Abnormal B-cell function in neonatally streptozotocin-diabetic rats: insensitivity to alloxan toxicity. 244 59

The author describes his findings pertaining to spontaneous diabetes mellitus in BB rats and the method and results in juvenile alloxan diabetes in neonatal and adolescent Wistar rats of his own inbreeding F8-10. The author presents also the results of attempts to treat juvenile alloxan diabetes in rats by intrafamilial renal-subscapular allotransplants of 2-5 neonatal collagenase nondigested pancreases. Six of eleven BB females developed latent or manifest insulin dependent diabetes mellitus during the third to fourth month of life. An intraperitoneal injection of alloxan to 2-5-day-old rats causes, after two months of prediabetes, latent or manifest disease, in particular in males. In one-two-month adolescent fasting F6--10 inbred rats (Wistar strain) intravenous injection of 50 mg/kg alloxan causes diabetes mellitus with hyperglycaemia (20-60 mmol/l), glycosuria, polyuria, arrested growth, development of cataract and early death due to pulmonary or intestinal infection. The author tries to prevent these sequelae and complications by insulin therapy or intrafamilial allotransplantations of 2-5 neonatal, collagenase nondigested pancreases beneath the renal capsule, using two-three--week immunosuppression with Cyclosporin A combined with Azathioprine. The author proves permanent cure, histologically and functionally, by repeated allotransplantation which, however, due to the intense thymolymphatic immunological barrier in adolescent rats is less frequent than cure repeatedly achieved by the author in adult diabetic rats.
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PMID:[Spontaneous and experimental models of human juvenile diabetes mellitus]. 275 53

In most previous studies of cryopreserved isolated pancreatic islets, a slow cooling rate has been employed. We recently observed that faster cooling (5 degrees C/min) resulted in better functional islet preservation than cooling at 0.5 degrees C/min. We found that a culture period after the collagenase isolation of the islets, but prior to freezing, is crucial for the preservation of the islet B cell function. In the present investigation the function of isolated mouse pancreatic islets cooled in Hanks' solution supplemented with 2 M dimethylsulphoxide was compared with that of nonfrozen, cultured islets prepared from the same donors. The islets were cultured in RPMI 1640 + 10% calf serum for 3 days before freezing, and for 3 days after rapid thawing at 37 degrees C. Islets were cooled at rates of 5, 15, or 25 degrees C/min to 70 degrees C and then plunged into liquid nitrogen. All three groups of cryopreserved islets responded with insulin secretion when challenged with high glucose concentrations in batch-type incubations. In further experiments it was found that glucose-stimulated (pro)insulin biosynthesis in islets frozen at 25 degrees C/min was the same as that in the controls. Similar observations were made with respect to glucose-stimulated insulin release in perifusion experiments. However, a 30% reduction in insulin content was observed in the rapidly frozen islets. There was no difference in the replicatory capacity of the islets cells in vitro, as determined by an autoradiographic technique, between control islets and islets cooled at 5 degrees C or 25 degrees C/min. Intrasplenic implantation of 600-800 cryopreserved syngeneic islets into alloxan-diabetic mice led to complete or partial normalization of the hyperglycemia in seven of nine mice. When splenectomy was performed in five animals the serum glucose concentrations increased promptly. We conclude that relatively rapid cooling rates may be useful for cryopreservation of isolated pancreatic islets.
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PMID:Cryopreservation of mouse pancreatic islets. Effects of fast cooling on islet B cell function and on the outcome of islet transplantation. 309 92


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