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Title: INHIBITION OF GLUCONEOGENESIS IN CULTURED CHICKEN EMBRYO HEPATOCYTES BY FUSARIUM METABOLITES

Author
item WU, WEIDONG - UNIV OF WI, MADISON
item Vesonder, Ronald

Submitted to: Natural Toxins
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/12/1997
Publication Date: N/A
Citation: N/A

Interpretive Summary: Compounds produced by a mold called Fusarium solani (a mold associated with a disease in soybeans called sudden death syndrome) were studied for their ability to inhibit sugar formation. A bioassay using chicken embryo hepatocytes was developed to follow inhibition of sugar formation. This is the first report of the compounds moniliformin (a common toxin with potential to cause bad effects in chickens) and dehydrated sugars (for example, mannitol and sorbitol). The ability of these compounds to inhibit glucose (sugar) formation which may account for the symptoms observed in the sudden death syndrome of soybeans and sudden death syndrome in chickens. This information may be useful to plant pathologists and toxicologists.

Technical Abstract: Four Fusarium metabolites, 2,5-anhydro-D-mannitol, 2,5-anhydro-D-sorbitol, moniliformin, and fumonisin B1, were tested for their ability to inhibit gluconeogenesis and cell viability in a primary chicken embryo hepatocyte culture system. The hepatocyte system was established from fertilized chicken eggs that were incubated for 14 days. The hepatocytes produced and secreted glucose into the supernatant of a Krebs incubation solution amended with 3 mM of either lactate or fructose as a precursor for glucose formation. 2,5-Anhydro-D-mannitol and 2,5-anhydro-D-sorbitol inhibited gluconeogenesis in these cells from both lactate and fructose. The former anhydro sugar was more inhibitory when lactate was the precursor (50% inhibition, IC50, 6 mM) and the latter anhydro sugar more inhibitory when fructose was the precursor (IC50, 12 mM). Moniliformin was more inhibitory to glucose formation from lactate (IC50, 100 uM) than from fructose in these cells. The degrees of inhibition of gluconeogenesis by the two anhydro sugars and moniliformin were greater than their effect on cell viability. Fumonisin B1 as high as 1 mM neither inhibited gluconeogenesis, nor affected cell viability.