An amphotericin B (AmB)‐resistant mutant was isolated from a wild‐type AmB‐susceptible strain of Aspergillus flavus by serial transfer of conidia on agar plates containing stepwise increased concentrations of AmB up to 100 μtg ml−1. The acquired resistance of my celia was specific for polyene‐antibiotics AmB, nystatin and trichomycin. Spheroplasts derived from the resistant mycelia were as susceptible to AmB as the wild‐type. Chemical analysis of the cell wall revealed that levels of alkali‐soluble and ‐insoluble glucans were significantly higher in the resistant mycelia as compared to those in the wild‐type. When resistant mycelia were treated with SDS, they adsorbed as much AmB as wild‐type mycelia. These results suggest that alterations in the cell wall components of mycelia, especially 1,3‐α‐glucan and protein complex in the outermost wall layer, lead to AmB resistance in A. flavus.

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When isolated rat liver cells were incubated for 15 min in the presence of vasoactive intestinal peptide, secretin, gastrin, caerulein or glucagon at concentrations ranging from 0.2 microgram to 2 microgram per ml, glycogenolysis was stimulated. Among the gastrointestinal hormones or peptides tested, vasoactive intestinal peptide had the highest stimulatory activity. However, somatostatin was inhibitory for liver glycogenolysis. Combination experiments showed that somatostatin also inhibited the stimulatory effects of vasoactive intestinal peptide and secretin, but not that of glucagon, while glucagon and vasoactive intestinal peptide, or glucagon and secretin showed additive effects on glycogenolysis, but secretin and vasoactive intestinal peptide did not. The results suffest that the receptor site of glucagon is different from those of secretin and vasoactive intestinal peptide. Slight but significant stimulation of gluconeogenesis was also observed by vasoactive intestinal peptide and secretin. The evidence presented in this paper indicates that the so-called enterohepatic axis, in which a part of serum glucose levels is regulated directly by gastrointestinal hormones, exists and that the axis is inhibited by somatostatin.

When isolated rat liver cells were incubated for 15 min in the presence of vasoactive intestinal peptide, gastric inhibitory polypeptide, secretin or glucagon at a concentration of 2.0 micrograms/ml, glycogenolysis was stimulated by 30%-67% above the control. Slight but significant increase on gluconeogenesis was also observed by the addition vasoactive intestinal peptide, gastric inhibitory polypeptide or secretin. Somatostatin inhibited both glycogenolysis and gluconeogenesis induced by these hormones, but the degrees of inhibition are clearly much higher in the hormone-induced gluconeogenesis than glycogenolysis, and no significant inhibition of glycogenolysis was observed in case of glucagon and VIP. These results suggest the possibility that the so-called enterohepatic axis may play a part of roles in the regulation of serum glucose levels through gastrointestinal hormones belonging to the secretin family, and that it may be further regulated by somatostatin through gluconeogenesis.

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