SUMMARY The process of iron absorption has been studied in 23 patients with idiopathic haemochromatosis, in eight with iron-deficiency anaemia, and in 20 control subjects. The initial uptake of iron by the intestinal mucosa was estimated by administering 59Fe-ferric citrate during a standard meal together with a non-absorbable marker, 51Cr-chromic chloride. Body iron absorption (iron retained at 14 days) was measured by whole body counting with discriminant analysis to separate the two isotopes. Thus, the fraction of the initial mucosal uptake finally retained in the body was calculated (the mucosal transport index of iron).In control subjects the mean values for mucosal uptake of iron and body iron absorption were 12-0 ± SD 4.9 % and 3.6 ± SD 2.4%, with a mean mucosal transport index of 031 i SD 0.21. Mucosal iron uptake and body absorption were both considerably increased in the patients with iron-deficiency anaemia (33.5 ± 15.6 and 29.8 ± 17-0% respectively) and in the eight patients with idiopathic haemochromatosis treated by venesection therapy until the excess iron stores were removed (27-2 + 12-0 and 26.6 ± 14.6% respectively). The mucosal transport index in all these subjects approached 1.0. Eight patients with haemochromatosis were studied before venesection therapy. The mucosal uptake of iron was within the normal range in all (mean 14-0 ± 2.8 %) but body iron absorptiorn was increased in five (mean 9.1 ± 4-8 %). The mean mucosal transport index of iron was significantly increased in this group (0.62 + 0.28; p <0.01).The findings suggest that the increased iron absorption in subjects with idiopathic haemochromatosis results from an abnormality of the intestinal mucosa and not from altered intraluminal factors. However, whether the aberrant mucosal cell function is a primary defect in the cell or an acquired change, dependent on humoral or corporeal factors, is unknown.While there is evidence that the absorption of iron in some patients with idiopathic haemochromatosis is increased, particularly in the early stages of the disease (Charlton
Summary: An experimental model, originally designed to study the effects of controlled interruption of the enterohepatic circulation (EHC), has been extensively modified and adapted to study the applied physiology of an “intact” EHC of bile in Rhesus monkeys.
Basically, the model consists of a surgically exteriorised extrahepatic biliary circuit in which an electronic stream splitter is interposed. This diverts every twentieth drop of bile which provides a representative sample for analysis while returning the remaining 95% of bile to the upper intestine.
During these studies, the monkeys were comfortably restrained in specially designed chairs whose construction is described in detail. Animal maintenance and the design of the electronic stream splitter are also described.
Analysis of the glycine: taurine and the dihydroxy: trihydroxy bile salt ratios both in gallbladder bile and in bile obtained with an “intact” EHC (by using the stream splitter), showed that the Rhesus monkey secretes a bile similar in composition to that of man.
The bile salt: cholesterol: phospholipid ratios in monkey gallbladder bile (81:6:13) were also similar to those found in human bile, indicating that this animal is suitable for studies of cholesterol solubility in bile – a factor of major importance in gallstone pathogenesis.
The model has been used to measure bile volume, bile salt secretion, pool size and the frequency of circulation of the bile salt pool. The diurnal variation in these variables has also been studied.
Bile salts are synthesized in the liver from cholesterol, conjugated with glycine or taurine and secreted in bile with cholesterol and lecithin. The molar concentrations of these three lipids determine solubility of cholesterol in bile. Within the gastrointestinal lumen bile salts play an essential role in lipid absorption and faty transport. An efficienct entero-hepatic circulation maintains hepatic bile salt secretion and provides a "feed-back" control of the bile salt and cholesterol metabolism. Potentially hepatotoxic lithocholic acid formed in the intestinal lumen by bacterial action on chenodeoxycholic acid is sulphated in the liver thus decreasing intestinal reabsorption. The total faecal excretion of bile salts balances hepatic synthesis and represents a major catabolic path in cholesterol metabolism.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.