From:
"SukieC"
Date: 2011-09-10 16:36:53 UTC
Subject: [ferrethealth] Re: abstract
To: ferrethealth@yahoogroups.com
It looks like what they found in those mink was a
marked reduction in lipase, enzymes that digest fats.
SOME questions then become:
"What can cause low lipase levels?"
"Genetic vulnerability?"
"Disease?"
"Injury (such as can happen with bile duct problems or other)?"
"Inflammatory processes themselves?"
"How easy is it to measure lipase levels or lipid levels
to see if the pancreas may be at risk from wrong levels? Will
blood levels accurately enough reflect what is happening at
the pancreas?"
"How much benefit might happen from adjusting diet in
these animals during the healing process?"
"How much benefit might come from artificially supplementing
lipase levels?"
"Do the outward symptoms of too low lipase levels
look at all similar to those of too high lipase levels?"
"Since some studies show that lipase levels increase with
purposeful weight loss, and since fat cells produce products
that can cause inflammation (and a recent study shows that
even too much subcutaneous fat can do that in some people
with genetic differences affecting which ones, so that MIGHT
apply or ferrets, too) is this possibly something to which obesity
can predispose an individual?"
"Are low lipase levels found in at least some of the ferrets who
get pancreatitis?"
As usual: I am not a vet, so check me, of course.
The abstract again:
Vet Pathol. 2011 Sep 7. [Epub ahead of print]
Pancreatitis in Hyperlipemic Mink (Mustela Vison).
Nordstoga K, Sørby R, Olivecrona G, Smith AJ, Christophersen B.
Abstract
In both man and animals, inflammatory changes in the pancreas often occur with disturbances in lipid metabolism, including hypertriglyceridemia and an excess of free fatty acids. Hyperlipoproteinemia type I is a human condition caused by a deficiency of lipoprotein lipase. A similar metabolic disturbance that occurs in mink is of considerable comparative interest, as it is also followed by pancreatitis. Pancreatic lesions in hyperlipoproteinemic mink included overt variably sized nodules with hemorrhage and necrosis. These lesions began as intralobular necrosis of exocrine cells and progressed to total lobular destruction, with eventual involvement of interlobular tissue. Remnants of epithelial cells and lipid-filled macrophages were seen in necrotic areas, along with other types of inflammatory cells scattered in a lipid-rich exudate. Granulation tissue developed rapidly in necrotic areas. Additional observations included ductal proliferation, replacement of epithelial cells with fat, and mural arterial thickening, most conspicuously with vacuolated cells and endothelial proliferation. Extravasation of lipid-rich plasma is thought to be a major intensifier of the inflammatory response.
PMID: 21900541 [PubMed - as supplied by publisher]
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