Specificity of the 3H-triolein assay for pancreatic lipase in blood plasma.

The aim of this study was to investigate the specificity of the 3H-triolein assay and to investigate the recovery of highly purified pancreatic lipase and pancreatic lipase in the form of pure non-activated pig pancreatic juice. Blood plasma from pigs was analysed for pancreatic lipase activity using the 3H-triolein substrate assay, with a method specific for lipoprotein lipase and with a method specific for hepatic lipase. The recovery of pancreatic lipase from pancreatic juice was approximately 100%, while the recovery of highly purified pancreatic lipase in plasma or whole blood was found to be approximately 1%.

The enzyme levels in blood are not affected by oral administration of a pancreatic enzyme preparation (Creon 10,000) in pancreas-insufficient pigs.

After oral intake, small amounts of intact protein may be absorbed into the blood circulation. The current study investigated whether orally administered pancreatic enzymes were absorbed from the intestine. The study included 28 pigs; 3 control pigs with intact pancreatic function and 25 pigs that were made exocrine pancreas insufficient by duct ligation (20 pigs) or total pancreatectomy (5 pigs).

Effects of dexamethasone on mitogen-activated protein kinases in mouse macrophages: implications for the regulation of 85 kDa cytosolic phospholipase A(2).

In mouse macrophages, arachidonate mobilisation in response to several stimuli is severely inhibited by prolonged (16-20 hr) treatment with nanomolar dexamethasone (dex). It was shown earlier that this inhibition was accompanied by a dual effect on cPLA(2); down-regulation of the enzyme protein and inhibition of its activation. We now report that cycloheximide, a protein synthesis inhibitor, caused an almost complete reversion of the inhibitory effects of dex on cPLA(2) activation.

Dexamethasone differentially regulates cytokine transcription and translation in macrophages responding to bacteria or okadaic acid.

Many microorganisms and microbial products induce expression of pro-inflammatory cytokines such as interleukin-1 (IL-1alpha/beta) and tumour necrosis factor-alpha (TNF-alpha) in macrophages, primarily by transcriptional activation. We show here, by using mouse macrophages in primary culture, that pre-treatment with dexamethasone inhibits bacteria-induced IL-1beta expression as mRNA and cellular pro-IL-1beta in parallel, consistent with an effect primarily on transcriptional activation. In contrast, the expression of TNF-alpha mRNA was only partly inhibited despite virtually complete inhibition of TNF-alpha protein formation.