Evidence map›Paper›PMID 20020218›Full record

ArticleLipids2010

Rapid development of fasting-induced hepatic lipidosis in the American mink (Neovison vison): effects of food deprivation and re-alimentation on body fat depots, tissue fatty acid profiles, hematology and endocrinology.

Kirsti Rouvinen-Watt, Anne-Mari Mustonen, Rebecca Conway, Catherine Pal, Lora Harris, Seppo Saarela, Ursula Strandberg, Petteri Nieminen

Abstract read
PubMed Publisher
In one paragraph

Article in Lipids, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Novel role of NLRP3-inflammasome in regulation of lipogenesis in fasting-induced hepatic steatosis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019
    Article
  6. Article
  7. Article
  8. Article
  9. Evidence of endoplasmic reticulum stress and liver inflammation in the American mink Neovison vison with benign hepatic steatosis.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2014
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

Kirsti Rouvinen-WattDepartment of Plant and Animal Sciences, Nova Scotia Agricultural College, Truro, NS, Canada. krouvinen@nsac.ca
Anne-Mari Mustonen
Rebecca Conway
Catherine Pal
Lora Harris
Seppo Saarela
Ursula Strandberg
Petteri Nieminen
Nova Scotia Department of Agriculture · CAJoensuu Science Park · FIUniversity of Eastern Finland · FIUniversity of Oulu · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic lipidosis is a common pathological finding in the American mink (Neovison vison) and can be caused by nutritional imbalance due to obesity or rapid body weight loss. The objectives of the present study were to investigate the timeline and characterize the development of hepatic lipidosis in mink in response to 0-7 days of food deprivation and liver recovery after 28 days of re-feeding. We report here the effects on hematological and endocrine variables, body fat mobilization, the development of hepatic lipidosis and the alterations in the liver lipid classes and tissue fatty acid (FA) sums. Food deprivation resulted in the rapid mobilization of body fat, most notably visceral, causing elevated hepatosomatic index and increased liver triacylglycerol content. The increased absolute amounts of liver total phospholipids and phosphatidylcholine suggested endoplasmic reticulum stress. The hepatic lipid infiltration and the altered liver lipid profiles were associated with a significantly reduced proportion of n-3 polyunsaturated FA (PUFA) in the livers and the decrease was more evident in the females. Likewise, re-feeding of the female mink resulted in a more pronounced recovery of the liver n-3 PUFA. The rapid decrease in the n-3/n-6 PUFA ratio in response to food deprivation could trigger an inflammatory response in the liver. This could be a key contributor to the pathophysiology of fatty liver disease in mink influencing disease progression.

Indexed as

FoodFood DeprivationAdipose TissueAnimalsBlood GlucoseFastingFatty Acids, Omega-3Fatty LiverFemaleHematologic TestsLeptinLipid MetabolismLiverMaleMinkPhosphatidylcholinesBlood GlucoseFatty Acids, Omega-3LeptinPhosphatidylcholinesPhospholipidsTriglycerides

Identifiers

PMID20020218
OpenAlexW2078114709

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.