Changes in bile composition and liver ultrastructure after TPN alone and TPN with ultra-short bowel syndrome

SummaryBackground & aimsTwo of the factors that can influence bile acid (BA) metabolism and biliary poles are long intestinal resections leading to short bowel syndrome (SBS) and prolonged starvation in total parenteral nutrition (TPN). These can act directly (by altering absorption) and/or indirectly (bacterial translocation, alterations of the hepato-intestinal hormonal complex,…). Our aim was to study the effects on bile metabolism and hepatic structure of the conditions of TPN with and without SBS in an animal model.MethodsWe used 3 experimental groups of Dunkin-Hartley guinea pigs: group A (GA: 10 animals), subjected to anæsthesia and a sham laparotomy, and fed for 10 days by TPN; group B (GB: 10 animals), subjected to a jejuno-ileal resection, and fed for 10 days by TPN; and a control group (6 animals) subjected to a sham laparotomy, and fed orally. At the end of the experimental period, bile samples were taken from the hepatic duct to study the bile composition, and blood samples from the vena cava for blood biochemistry. Following liver perfusion, samples of hepatic tissue were taken for electron microscopy.ResultsIn GA and GB, there were significant losses in weight and increases in glycæmia and serum triglycerides, but a decrease in plasma cholesterol only in GB. For the bile composition, the concentrations of cholic acid (ChA), ketolithocholic acid (KLChA), and total conjugated BA were lowered in both GA and GB, while bile phospholipids (BPh) and bile cholesterol (BCh) were raised in GB only. The electron microscopy showed microsteatosis and a major loss of microvilli in the biliary poles or canaliculi in GA and even more so in GB, with the latter group also showing signs of fibrogenesis.ConclusionsTPN and SBS affect the BPh, BCh, and BA composition, potentially increasing the risk of biliary lithogenicity. This was especially so in the association of SBS and TPN, with affection of the biliary duct anatomy, and induction of fibrogenesis and cholangitis.