Evidence from both animal and human studies had been presented by various authors to suggest that reduction of pancreatic function increased iron absorption. The present experimental studies in rats showed that there was increased radioiron (59Fe) absorption after pancreatectomy, but this appeared to be due to the operative procedure as there was a similar increased absorption in animals who had sham operations performed. There was no certain evidence that pancreatic enzymes or extract had a specific inhibitory effect on the absorption of iron. But with increased doses of pancreatic extract, above the normal doses, the amount of radioiron absorption was greatly enhanced.
A significant increase in hepatic storage iron was found in the groups of rats who had been fed a diet supplemented with dl-ethionine. All these animals showed extensive damage and atrophy of the pancreas, with degeneration and considerable regenerative activity in the liver. The absolute increased hepatic storage iron was not due to the liberation and laying down of haemosiderin from the damaged cells or to decreased liver mass. Rats who had carbon tetrachloride-induced liver cirrhosis without pancreatic damage showed no increased hepatic storage iron.
It was observed that in liver damage with considerable cellular proliferation there was increased liver iron content. As this was found only when there was associated pancreatic injury, it is suggested that decreased pancreatic function in the presence of liver cell injury with cellular proliferation leads to increased iron absorption and storage. The relationship of liver injury with cellular proliferation and pancreatic damage to increased hepatic storage iron merits further study.
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