A mutation in the lipoprotein lipase gene associated with hyperlipoproteinemia type I in mink: studies on lipid and lipase levels in heterozygotes.

Lindberg, Anna‐Lena; Nordstoga, K.; Christophersen, Bjørn O.; Savonen, Roger; Tol, A. van; Olivecrona, Gunilla

doi:10.3892/ijmm.1.3.529

Cited by 11 publications

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“…The LPL-deficient mink produce an inactive form of the enzyme protein, and there is substantial LPL mass in tissues from these mink (18). Immunostaining of a kidney from an LPL-deficient mink showed staining over the tubular epithelial cells in the same overall pattern as seen in the normal mink, i.e., stronger immunoreaction over tubuli in the cortex than in the medulla and considerable variation in staining intensity among individual tubuli (Fig.…”

Section: Resultsmentioning

confidence: 72%

“…Mink, Chinese hamsters, and mice kidneys had high LPL activity, whereas the activity was lower in rats and very low in guinea pigs. In an earlier study in mink, LPL activity in kidney was 5.02 Ϯ 0.87 U/g wet wt in normal mink and about one-half that, 2.83 Ϯ 0.53 U/g, in mink heterozygous for the Pro214Leu mutation (18). In another study, the activity was 6.05 Ϯ 2.03 in a group of normal mink (28).…”

Section: Resultsmentioning

confidence: 93%

“…No LPL mRNA could be detected in any nearby cells by in situ hybridization, and the authors suggested that the lipase might have been picked up from the blood. On the other hand, there are reports of substantial amounts of LPL mRNA in mouse kidney (15), and some of us recently noted substantial levels of LPL mRNA, mass, and activity in kidneys from mink (18). This suggested that there may be large differences in the expression of LPL in kidneys between animal species.…”

mentioning

confidence: 89%

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Lipoprotein lipase in the kidney: activity varies widely among animal species

Ruge¹,

Neuger²,

Sukonina³

et al. 2004

American Journal of Physiology-Renal Physiology

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Much evidence points to a relationship among kidney disease, lipoprotein metabolism, and the enzyme lipoprotein lipase (LPL), but there is little information on LPL in the kidney. The range of LPL activity in the kidney in five species differed by >500-fold. The highest activity was in mink, followed by mice, Chinese hamsters, and rats, whereas the activity was low in guinea pigs. In contrast, the ranges for LPL activities in heart and adipose tissue were less than six- and fourfold, respectively. The activity in the kidney (in mice) decreased by >50% on food deprivation for 6 h without corresponding changes in mRNA or mass. This decrease in LPL activity did not occur when transcription was blocked with actinomycin D. Immunostaining for kidney LPL in mice and mink indicated that the enzyme is produced in tubular epithelial cells. To explore the previously suggested possibility that the negatively charged glomerular filter picks up LPL from the blood, bovine LPL was injected into rats and mice. This resulted in decoration of the glomerular capillary network with LPL. This study shows that in some species LPL is produced in the kidney and is subject to nutritional regulation by a posttranscriptional mechanism. In addition, LPL can be picked up from blood in the glomerulus.

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Section: Resultsmentioning

confidence: 72%

Section: Resultsmentioning

confidence: 93%

mentioning

confidence: 89%

See 1 more Smart Citation

Lipoprotein lipase in the kidney: activity varies widely among animal species

Ruge¹,

Neuger²,

Sukonina³

et al. 2004

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

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“…built a rat model of HTG-AP with TritonWR 1339 by tail vein injection, and plasma triglyceride level in this model could reach up to about 1000 mg/dl, but only lasting for 24 hours and it was difficult to keep the stable state of high blood triglycerides, what’s more, TritonWR 1339 was really expensive. LPL genetically deficient mink2324 and high-fat diet hamster25 both existed HTG, but the absence of antibodies was not in favor of the immunology and mechanism research on AP25. Along with the development of gene modification technology in recent years, the problem that stable and effective HTG-AP model can’t be established simply relying on drugs or high fat diet, has been solved by genetically modified animals, such as LPL-deficient mice91011 and ApoCIII-tg mice1213.…”

Section: Discussionmentioning

confidence: 99%

Development of a novel model of hypertriglyceridemic acute pancreatitis in mice

Pan

Yong

Gao

et al. 2017

Sci Rep

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The morbidity rate of hypertriglyceridemic acute pancreatitis (HTG-AP) increased rapidly over the last decade. However an appropriate animal model was lacking to recapitulate this complicated human disease. We established a novel mice model of HTG-AP by poloxamer 407 (P-407) combined with caerulein (Cae). In our study, serum triglyceride levels of P-407 induced mice were elevated in a dose-dependent manner, and the pancreatic and pulmonary injuries were much severer in HTG mice than normal mice when injected with conventional dose Cae (50 ug/kg), what’s more, the severity of AP was positively correlative with duration and extent of HTG. In addition, we found that a low dose Cae (5 ug/kg) could induce pancreatic injury in HTG mice while there was no obvious pathological injury in normal mice. Finally, we observed that HTG leaded to the increased infiltrations of macrophages and neutrophils in mice pancreatic tissues. In conclusion, we have developed a novel animal model of HTG-AP that can mimic physiological, histological, clinical features of human HTG-AP and it could promote the development of therapeutic strategies and advance the mechanism research on HTG-AP.

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“…For developing the qPCR assays for mRNA of the genes of interest, forward and reverse primers were designed based on reported sequences (Table 1). Published mink sequence data were available for LPL (Lindberg et al 1998) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH; GenBank accession number AF076283). In order to generate mink-specific sequences for GRP78, TNF-α, and MCP-1, forward and reverse primers were designed using the GenBank ® database (http://www.ncbi.nlm.nih.gov) and Primer3 software (Rozen and Skaletsky 2000) based on conserved regions of homologous mRNA sequences between several mammalian species, including the giant panda (Ailuropoda melanoleuca; GRP78, MCP-1), the cat (GRP78, MCP-1, TNF-α), the ferret (Mustela putorius furo; GRP78, TNF-α), and the dog (Canis lupus familiaris; TNF-α, MCP-1).…”

Section: Liver Histologymentioning

confidence: 99%

Evidence of endoplasmic reticulum stress and liver inflammation in the American mink Neovison vison with benign hepatic steatosis

et al. 2014

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We investigated the presence of inflammatory signs in the progression of fatty liver disease induced by fasting. Sixty standard black American mink (Neovison vison) were fasted for 0, 1, 3, 5, or 7 days and one group for 7 days followed by re-feeding for 28 days. Liver sections were evaluated histologically and liver mRNA levels indicating endoplasmic reticulum (ER) stress, adipogenic transformation, and inflammation were assessed by quantitative real-time PCR. After 3 days of fasting, the mink had developed moderate liver steatosis. Increased hyaluronan reactivity in lymphocytic foci but no Mallory-Denk bodies were seen in livers of the mink fasted for 5-7 days. Up-regulation of glucose-regulated protein, 78 kDa was observed on day 7 indicating ER stress, especially in the females. Liver lipoprotein lipase and monocyte chemoattractant protein 1 mRNA levels increased in response to 5-7 days of food deprivation, while tumor necrosis factor α (TNF-α) was the highest in the mink fasted for 5 days. The expression of the genes of interest, except for TNF-α, correlated with each other and with the liver fat content. The mRNA levels were found to change more rapidly below n-3/n-6 polyunsaturated fatty acid ratio threshold of 0.15. Following re-feeding, hepatocyte morphology and mRNA abundance returned to pre-fasting levels. Within the studied timeframe, evidence for ER stress, adipogenic transformation, and liver inflammation suggested incipient transition from steatosis to steatohepatitis with potential for development of more severe liver disease. This may present a possibility to influence disease progression before histologically observable steatohepatitis.

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A mutation in the lipoprotein lipase gene associated with hyperlipoproteinemia type I in mink: studies on lipid and lipase levels in heterozygotes.

Cited by 11 publications

References 0 publications

Lipoprotein lipase in the kidney: activity varies widely among animal species

Lipoprotein lipase in the kidney: activity varies widely among animal species

Development of a novel model of hypertriglyceridemic acute pancreatitis in mice

Evidence of endoplasmic reticulum stress and liver inflammation in the American mink Neovison vison with benign hepatic steatosis

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