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Lipoprotein lipase deficiency with pancreatitis in mink: biochemical characterization and pathology.

https://arctichealth.org/en/permalink/ahliterature61935
Source
J Lipid Res. 1997 May;38(5):837-46
Publication Type
Article
Date
May-1997
Author
B. Christophersen
K. Nordstoga
Y. Shen
T. Olivecrona
G. Olivecrona
Author Affiliation
Institute of Clinical Biochemistry, National Hospital, University of Oslo, Norway.
Source
J Lipid Res. 1997 May;38(5):837-46
Date
May-1997
Language
English
Publication Type
Article
Keywords
Animals
Diet
Disease Models, Animal
Humans
Lipids - blood
Lipoprotein Lipase - deficiency
Mink
Pancreatitis - enzymology - pathology - physiopathology
Research Support, Non-U.S. Gov't
Abstract
A severe hyperlipemia in mink, with a pattern that suggested recessive inheritance, was observed at a farm in Norway. On a normal mink diet, affected animals had grossly elevated levels of plasma triglycerides which decreased towards normal on a low-fat diet. Normal minks had the main part of their plasma cholesterol in the HDL fraction. Affected minks, although severely hypertriglyceridaemic, had almost normal levels of both LDL and HDL. Affected minks frequently had lipogranulomas in the mesentery and the pancreas. The lipogranulomatous tissue contained spaces filled with an amorphous, sudanophilic substance with many foamy macrophages in the fibrous tissue between the lesions. Separation of postheparin plasma on heparin-agarose revealed that the affected minks had no detectable lipoprotein lipase activity but normal activity of hepatic lipase. Both normal and affected minks had inactive lipoprotein lipase protein in pre- and post-heparin plasma. This protein, which eluted before the active lipase from heparin-agarose, probably corresponds to lipase monomers. The presence of lipoprotein lipase mass in the affected minks, but no activity, indicates that there might be a point mutation in the lipase gene. The minks provide a new animal model for studies on pancreatitis induced by hypertriglyceridemia and on lipoprotein metabolism in the lipoprotein lipase-deficient state and show features similar to those found in human hyperlipoproteinemia type I.
PubMed ID
9186902 View in PubMed
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Oral toxicity in mice of algal toxins from the diarrheic shellfish toxin (DST) complex and associated toxins.

https://arctichealth.org/en/permalink/ahliterature75582
Source
J Nat Toxins. 1998 Jun;7(2):141-58
Publication Type
Article
Date
Jun-1998
Author
T. Aune
O B Stabell
K. Nordstoga
K. Tjøtta
Author Affiliation
Department of Pharmacology, Microbiology and Food Hygiene, Norwegian College of Veterinary Medicine, Oslo, Norway.
Source
J Nat Toxins. 1998 Jun;7(2):141-58
Date
Jun-1998
Language
English
Publication Type
Article
Keywords
Administration, Oral
Animals
Bivalvia - chemistry
Dinoflagellida
Injections, Intraperitoneal
Intestines - drug effects - pathology
Jejunum - drug effects - pathology
Liver - drug effects - pathology
Marine Toxins - administration & dosage - analysis - toxicity
Mice
Norway
Okadaic Acid - administration & dosage - analysis - toxicity
Pyrans - administration & dosage - analysis - toxicity
Rats
Research Support, Non-U.S. Gov't
Shellfish
Abstract
Mussel samples from four locations along the Norweigian coast were extracted by methods for diarrheic shellfish toxins (DST) and tested by chemical and biological methods, including histopathology. All samples had previously been found to be highly toxic in mice, with symptoms indicating the presence of non-diarrheagenic toxins in the mouse bioassay. Chemical analysis revealed that the DST okadaic acid (OA) and dinophysistoxin-1 (DTX1) were present each one in one sample, but only a minor part of the total toxicity could be attributed to these toxions. In the other two samples, OA and DTX1 were absent. Incubation of the mussel extracts from all four samples with freshly prepared hepatocytes indicated the presence of unknown toxin(s) which may not be classified within the DST complex. Purified mussel samples were given to baby mice both via intraperitoneal (i.p.) injections and by oral intubation. Oral toxicity was about 25-50 times lower than toxicity obtained by i.p. injections, a result in accordance with acute toxic properties of many toxins. Risk assessment of the unknown toxin(s) requires chemical identification, but the preliminary results obtained indicate a large margin of safety, based on the large amounts of mussel extracts necessary to yield toxic effects in the intestine and liver in experimental animals upon oral exposure versus human intake.
PubMed ID
9678188 View in PubMed
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Source
Tidsskr Nor Laegeforen. 1995 Feb 28;115(6):714-7
Publication Type
Article
Date
Feb-28-1995
Author
K. Arnesen
H. Gamlem
E. Glattre
L. Moe
K. Nordstoga
Author Affiliation
Institutt for morfologi, genetikk og akvatisk biologi Norges veterinaerhøgskole, Oslo.
Source
Tidsskr Nor Laegeforen. 1995 Feb 28;115(6):714-7
Date
Feb-28-1995
Language
Norwegian
Publication Type
Article
Keywords
Animals
Dog Diseases - epidemiology
Dogs
English Abstract
Female
Humans
Male
Middle Aged
Neoplasms - epidemiology - veterinary
Norway - epidemiology
Registries
Risk factors
Species Specificity
Abstract
A Norwegian Canine Cancer Registry, covering four of 19 counties, has been operative since March 1990. Until the end of April 1994 about 6,000 tumours have been registered, more than 50% of these being manifestly or potentially malignant. Among 14 selected breeds the relative risk ratio for all tumours varies with factor 35 from boxer to dunker, the boxer having the highest tumour risk. The percentage distribution of specified tumour types also varies greatly between breeds, mammary cancer constituting 59% of all neoplasms in the dachshund, but only 4% in the Bernese mountain dog. Because of the genetic diversity between breeds the dog is a suitable species for differentiation between genetically determined predisposition and environmental influences in the etiology of cancer. Epidemiological surveillance of cancer morbidity in dogs may be a useful instrument for tracing carcinogens, even in the surroundings of man.
PubMed ID
7900133 View in PubMed
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