title: Serum bile acids and leptin interact with glucose metabolism in patients with liver cirrhosis.
abstract: OBJECTIVE
  We investigated possible involvements of bile acids (BA) and leptin in hepatogenous insulin resistance being present in up to 90% of cirrhotic patients.
  
  
  METHODS
  Blood was analysed in 10 cirrhotic patients (8m/2f, 48 ± 10.4 yrs) and 10 controls (8m/2f, 43 ± 9.3 yrs) after oral nutrition and during 1 h of parenteral feeding. In patients, leptin was additionally analysed from mesenteric and arterial blood.
  
  
  RESULTS
  Cirrhosis patients showed typical signs of hepatogenous insulin resistance (hyperinsulinaemia, normoglycaemia, hyperglucagonaemia). Both fasting BA (r = .714, p = 0.047) and fasting leptin (r = .867, p = 0.001) correlated to HOMA and predicted insulin response after oral feeding (R²adj = .783, p = 0.002). But during parenteral nutrition only leptin predicted insulin response (p = 0.005). The prandial glucose response was negatively correlated to the BA increase after oral nutrition (r = -.733, p = 0.028) and to the change in leptin during parenteral nutrition (r = -.738, p = 0.037) pointing towards a nutritional route-dependent positive impact on glucose tolerance of both substances. Prandial glucagon response was correlated to BA under both feeding conditions (p < 0.05). We found no relevant intestinal release of leptin during fasting or feeding conditions.
  
  
  CONCLUSIONS
  Our results suggest a substantial involvement of BA and leptin by improving postprandial glucose tolerance related to liver cirrhosis.
authors: Charité - Universitätsmedizin Berlin, Department of Gastroenterology, Infectiology and Rheumatology (incl. section on Clinical Nutrition), Charitéplatz 1, Berlin 10117, Germany. luzia.valentini@charite.de
authors: Luzia
authors: L
authors: Valentini
authors: Silja
authors: S
authors: Gläser
authors: Tatjana
authors: T
authors: Schuetz
authors: Ajmal
authors: A
authors: Omar
authors: Esmatollah
authors: E
authors: Kasim
authors: Thomas
authors: T
authors: Kroencke
authors: Uwe J F
authors: UJ
authors: Tietge
authors: Herbert
authors: H
authors: Lochs
authors: Jörg-Dieter
authors: JD
authors: Schulzke
authors: Georg
authors: G
authors: Brabant
authors: Johann
authors: J
authors: Ockenga
mesh_terms: D052436:Adipose Tissue, White / Q000378:metabolism; D000328:Adult; D001647:Bile Acids and Salts / Q000097:blood*; D005260:Female; D005934:Glucagon / Q000097:blood / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D006943:Hyperglycemia / Q000209:etiology; D007333:Insulin Resistance; D007413:Intestinal Mucosa / Q000378:metabolism; D020738:Leptin / Q000097:blood* / Q000378:metabolism; D008099:Liver / Q000378:metabolism*; D008103:Liver Cirrhosis / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010288:Parenteral Nutrition; D019518:Postprandial Period
chemical_list: D001647:Bile Acids and Salts; D020738:Leptin; D005934:Glucagon; D005947:Glucose