title: 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.
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.
authors.affiliation: Department of Plant and Animal Sciences, Nova Scotia Agricultural College, Truro, NS, Canada. krouvinen@nsac.ca
authors.forename: Kirsti
authors.initials: K
authors.lastname: Rouvinen-Watt
authors.forename: Anne-Mari
authors.initials: AM
authors.lastname: Mustonen
authors.forename: Rebecca
authors.initials: R
authors.lastname: Conway
authors.forename: Catherine
authors.initials: C
authors.lastname: Pal
authors.forename: Lora
authors.initials: L
authors.lastname: Harris
authors.forename: Seppo
authors.initials: S
authors.lastname: Saarela
authors.forename: Ursula
authors.initials: U
authors.lastname: Strandberg
authors.forename: Petteri
authors.initials: P
authors.lastname: Nieminen
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D005215:Fasting / Q000009:adverse effects / Q000378:metabolism; D015525:Fatty Acids, Omega-3 / Q000378:metabolism; D005234:Fatty Liver / Q000209:etiology / Q000378:metabolism / Q000662:veterinary*; D005260:Female; D005502:Food; D005508:Food Deprivation; D006403:Hematologic Tests; D020738:Leptin / Q000097:blood; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism*; D008297:Male; D008907:Mink / Q000378:metabolism*; D010713:Phosphatidylcholines / Q000378:metabolism; D010743:Phospholipids / Q000378:metabolism; D012737:Sex Factors; D014280:Triglycerides / Q000097:blood; D015431:Weight Loss
chemical_list: D001786:Blood Glucose; D015525:Fatty Acids, Omega-3; D020738:Leptin; D010713:Phosphatidylcholines; D010743:Phospholipids; D014280:Triglycerides