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 |
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Authors: | Kirsti Rouvinen-Watt Anne-Mari Mustonen Rebecca Conway Catherine Pal Lora Harris Seppo Saarela Ursula Strandberg Petteri Nieminen |
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Affiliation: | (1) Department of Plant and Animal Sciences, Nova Scotia Agricultural College, P.O. Box 550, Truro, NS, B2N 5E3, Canada;(2) Faculty of Biosciences, University of Joensuu, P.O. Box 111, 80101 Joensuu, Finland;(3) Department of Biology, University of Oulu, P.O. Box 3000, 90014 Oulu, Finland;(4) Department of Anatomy and Cell Biology, Faculty of Medicine, Institute of Biomedicine, University of Oulu, P.O. Box 5000, 90014 Oulu, Finland;(5) Department of Biomedicine, Institute of Anatomy, University of Kuopio, P.O. Box 1627, 70211 Kuopio, Finland |
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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. |
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