Experimental pancreatitis in rabbits induces inhibition of lipoprotein lipase and elevates plasma triglycerides, suggesting the release of a circulating LPL inhibitor from necrotic pancreatic tissue.
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May link pancreatic necrosis to hypertriglyceridemia via LPL inhibitor; hypothesis-generating in rabbits and leaves open human relevance.
SummaryThe plasma of 9 of 10 rabbits with staphylococcal toxin pancreatitis inhibited the activity of post-heparin LYL. The pancreatitis resulted also in a significant elevation of plasma triglyceride level. The maximal triglyceride elevation, however, was not related to the maximal inhibition of LPL. The possibility that a circulating inhibitor(s) of LPL was liberated from the necrotic pancreatic tissue is discussed.
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Kessler et al. (1962) studied this question.
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